Critical Care Commentary

Bedside-focused cardiac ultrasound assessment, or cardiac point-of-care ultrasound (POCUS), has become common in intensive care units throughout the US and the world. Many clinicians argue a POCUS cardiac assessment should be completed in most hypotensive patients and all cases of undifferentiated shock.

However, obtaining images adequate for decision making via standard transthoracic echo (TTE) is not possible in a significant number of patients; as high as 30% of critically ill patients, according to The American Society of Echocardiography (ASE) guidelines.¹ Factors common to critically ill patients, such as invasive mechanical ventilation, external dressings, and limited mobility, contribute to poor image acquisition.

Proud_Kevin_TEXAS_web.jpg

In almost all these cases, the factors limiting image acquisition can be eliminated by utilizing a transesophageal approach. In a recent study, researchers were able to demonstrate that adding transesophageal echocardiography (TEE) to TTE in critically ill patients yielded a new diagnosis or a change in management about 45% of the time.²

Using transesophageal ultrasound for a focused cardiac assessment in hemodynamically unstable patients is not new—and is often referred to as rescue TEE or resuscitative TEE. A broader term, transesophageal ultrasound, has also been used to include sonographic evaluation of the lungs in patients with poor acoustic windows. At my institution, we use the term critical care TEE to define TEE performed by a noncardiology-trained intensivist in an intubated critically ill patient.

Regardless of the term, the use of transesophageal ultrasound by the noncardiologist in the ICU appears to be a developing trend. As with other uses of POCUS, ultrasound machines continue to be able to “do more” at a lower price point. In 2024, several cart-based ultrasound machines are compatible with transesophageal probes and contain software packages capable of common cardiac measurements.

Despite this growing interest, intensivists are likely to encounter barriers to implementing critical care TEE. Our division recently implemented adding TEE to our practice. Our practice involves two separate systems: a Veterans Administration hospital and a university-based county hospital. Our division has integrated the use of TEE in the medical ICU at both institutions. Having navigated the process at both institutions, I can offer some guidance in navigating barriers.

The development of a critical care TEE program must start with a strong base in transthoracic cardiac POCUS, at least for the foreseeable future. Having a strong background in TTE gives learners a solid foundation in cardiac anatomy, cardiac function, and ultrasound properties. Obtaining testamur status or board certification in critical care echocardiography is not an absolute must but is a definite benefit. Having significant experience in TTE image acquisition and interpretation will flatten the learning curve for TEE. Interestingly, image acquisition in TEE is often easier than in TTE, so the paradigm of learning TTE before TEE may reverse in the years to come.

Two barriers often work together to create a vicious cycle that stops the development of a TEE program at its start. These barriers include the lack of training and lack of equipment, specifically a TEE probe. Those who do not understand the value of TEE may ask, “Why purchase equipment for a procedure that you do not yet know how to do?” The opposite question can also be asked, “Why get trained to do something you don’t have the equipment to perform?”

My best advice to break this cycle is to “dive in” to whichever barrier seems easier to overcome first. I started with obtaining knowledge and training. Obtaining training and education in a procedure that is historically not done in your specialty is challenging but is not impossible. It takes a combination of high levels of self-motivation and at least one colleague with the training to support you. I approached a cardiac anesthesiologist, whom I knew from the surgical ICU. Cardiologists can also be a resource, but working with cardiac anesthesiologists offers several advantages. TEEs done by cardiac anesthesiologists are similar to those done in ICU patients (ie, all patients are intubated and sedated). The procedures are also scheduled several days in advance, making it easier to integrate training into your daily work schedule. Lastly, the TEE probe remains in place for several hours, so repeating the probe manipulations again as a learner does not add additional risk to the patient. In my case, we somewhat arbitrarily agreed that I participate in 25 TEE exams. (CME courses, both online and in-person simulation, exist and greatly supplement self-study.)

Obtaining equipment is also a common barrier, though this has become less restrictive in the last several years. As previously mentioned, many cart-based ultrasound machines can accommodate a TEE probe. This changes the request from purchasing a new machine to “just a probe.” Despite the higher cost than most other probes, those in charge of purchasing are often more open to purchasing “a probe” than to purchasing an ultrasound machine.

Additionally, the purchasing decision regarding probes may fall to a different person than it does for an ultrasound machine. If available, POCUS image archiving into the medical record can help offset the cost of equipment, both by increasing revenue via billing and by demonstrating that equipment is being used. If initially declined, continue to ask and work to integrate the purchase into the next year’s budget. Inquire about the process of making a formal request and follow that process. This will often involve obtaining a quote or quotes from the ultrasound manufacturer(s).

Keep in mind that the probe will require a special storage cabinet specifically designed for TEE probes. It is prudent to include this in budget requests. If needed, the echocardiography lab can be a useful resource for additional information regarding the cabinet requirements. It is strongly recommended to discuss TEE probe models with sterile processing before any purchasing. If options are available, it is wise to choose a model the hospital already uses, as the cleaning protocol is well established. Our unit purchased a model that did not have an established protocol, which took nearly 6 months to develop. If probe options are limited, involving sterile processing early to start developing a protocol will help decrease delays.

Obtaining hospital privileges is also a common barrier, though this may not be as challenging as expected. Hospitals typically have well-outlined policies on obtaining privileges for established procedures. One of our hospital systems had four different options; the most straightforward required 20 hours of CME specific to TEE and 10 supervised cases by a proctor currently holding TEE privileges (see Table 1).

166888_table_web.jpg

Dr. Proud is Associate Professor of Medicine, Division of Pulmonary and Critical Care Medicine, Pulmonary and Critical Care Medicine Program Director, UT Health San Antonio.

References:

1. Porter TR, Abdelmoneim S, Belcik FT, et al. Guidelines for the cardiac sonographer in the performance of contrast echocardiography: a focused update from the American Society of Echocardiography. J Am Soc Echocardiogr. 2024;27(8):797-810.

2. Si X, Ma J, Cao DY, et al. Transesophageal echocardiography instead or in addition to transthoracic echocardiography in evaluating haemodynamic problems in intubated critically ill patients. Ann Transl Med. 2020;8(12):785. 

3. Hahn RT, Abraham T, Adams MS, et al. Guidelines for performing a cmprehensive transesophageal echocardiographic examination: recommendations from the American Society of Echocardioraphy and the Society of Cardiovascular Anesthesiologists. J Am Soc Echocardiogr. 2013;26(9):921-964.

Bedside-focused cardiac ultrasound assessment, or cardiac point-of-care ultrasound (POCUS), has become common in intensive care units throughout the US and the world. Many clinicians argue a POCUS cardiac assessment should be completed in most hypotensive patients and all cases of undifferentiated shock.

However, obtaining images adequate for decision making via standard transthoracic echo (TTE) is not possible in a significant number of patients; as high as 30% of critically ill patients, according to The American Society of Echocardiography (ASE) guidelines.¹ Factors common to critically ill patients, such as invasive mechanical ventilation, external dressings, and limited mobility, contribute to poor image acquisition.

Proud_Kevin_TEXAS_web.jpg

In almost all these cases, the factors limiting image acquisition can be eliminated by utilizing a transesophageal approach. In a recent study, researchers were able to demonstrate that adding transesophageal echocardiography (TEE) to TTE in critically ill patients yielded a new diagnosis or a change in management about 45% of the time.²

Using transesophageal ultrasound for a focused cardiac assessment in hemodynamically unstable patients is not new—and is often referred to as rescue TEE or resuscitative TEE. A broader term, transesophageal ultrasound, has also been used to include sonographic evaluation of the lungs in patients with poor acoustic windows. At my institution, we use the term critical care TEE to define TEE performed by a noncardiology-trained intensivist in an intubated critically ill patient.

Regardless of the term, the use of transesophageal ultrasound by the noncardiologist in the ICU appears to be a developing trend. As with other uses of POCUS, ultrasound machines continue to be able to “do more” at a lower price point. In 2024, several cart-based ultrasound machines are compatible with transesophageal probes and contain software packages capable of common cardiac measurements.

Despite this growing interest, intensivists are likely to encounter barriers to implementing critical care TEE. Our division recently implemented adding TEE to our practice. Our practice involves two separate systems: a Veterans Administration hospital and a university-based county hospital. Our division has integrated the use of TEE in the medical ICU at both institutions. Having navigated the process at both institutions, I can offer some guidance in navigating barriers.

The development of a critical care TEE program must start with a strong base in transthoracic cardiac POCUS, at least for the foreseeable future. Having a strong background in TTE gives learners a solid foundation in cardiac anatomy, cardiac function, and ultrasound properties. Obtaining testamur status or board certification in critical care echocardiography is not an absolute must but is a definite benefit. Having significant experience in TTE image acquisition and interpretation will flatten the learning curve for TEE. Interestingly, image acquisition in TEE is often easier than in TTE, so the paradigm of learning TTE before TEE may reverse in the years to come.

Two barriers often work together to create a vicious cycle that stops the development of a TEE program at its start. These barriers include the lack of training and lack of equipment, specifically a TEE probe. Those who do not understand the value of TEE may ask, “Why purchase equipment for a procedure that you do not yet know how to do?” The opposite question can also be asked, “Why get trained to do something you don’t have the equipment to perform?”

My best advice to break this cycle is to “dive in” to whichever barrier seems easier to overcome first. I started with obtaining knowledge and training. Obtaining training and education in a procedure that is historically not done in your specialty is challenging but is not impossible. It takes a combination of high levels of self-motivation and at least one colleague with the training to support you. I approached a cardiac anesthesiologist, whom I knew from the surgical ICU. Cardiologists can also be a resource, but working with cardiac anesthesiologists offers several advantages. TEEs done by cardiac anesthesiologists are similar to those done in ICU patients (ie, all patients are intubated and sedated). The procedures are also scheduled several days in advance, making it easier to integrate training into your daily work schedule. Lastly, the TEE probe remains in place for several hours, so repeating the probe manipulations again as a learner does not add additional risk to the patient. In my case, we somewhat arbitrarily agreed that I participate in 25 TEE exams. (CME courses, both online and in-person simulation, exist and greatly supplement self-study.)

Obtaining equipment is also a common barrier, though this has become less restrictive in the last several years. As previously mentioned, many cart-based ultrasound machines can accommodate a TEE probe. This changes the request from purchasing a new machine to “just a probe.” Despite the higher cost than most other probes, those in charge of purchasing are often more open to purchasing “a probe” than to purchasing an ultrasound machine.

Additionally, the purchasing decision regarding probes may fall to a different person than it does for an ultrasound machine. If available, POCUS image archiving into the medical record can help offset the cost of equipment, both by increasing revenue via billing and by demonstrating that equipment is being used. If initially declined, continue to ask and work to integrate the purchase into the next year’s budget. Inquire about the process of making a formal request and follow that process. This will often involve obtaining a quote or quotes from the ultrasound manufacturer(s).

Keep in mind that the probe will require a special storage cabinet specifically designed for TEE probes. It is prudent to include this in budget requests. If needed, the echocardiography lab can be a useful resource for additional information regarding the cabinet requirements. It is strongly recommended to discuss TEE probe models with sterile processing before any purchasing. If options are available, it is wise to choose a model the hospital already uses, as the cleaning protocol is well established. Our unit purchased a model that did not have an established protocol, which took nearly 6 months to develop. If probe options are limited, involving sterile processing early to start developing a protocol will help decrease delays.

Obtaining hospital privileges is also a common barrier, though this may not be as challenging as expected. Hospitals typically have well-outlined policies on obtaining privileges for established procedures. One of our hospital systems had four different options; the most straightforward required 20 hours of CME specific to TEE and 10 supervised cases by a proctor currently holding TEE privileges (see Table 1).

166888_table_web.jpg

Dr. Proud is Associate Professor of Medicine, Division of Pulmonary and Critical Care Medicine, Pulmonary and Critical Care Medicine Program Director, UT Health San Antonio.

References:

1. Porter TR, Abdelmoneim S, Belcik FT, et al. Guidelines for the cardiac sonographer in the performance of contrast echocardiography: a focused update from the American Society of Echocardiography. J Am Soc Echocardiogr. 2024;27(8):797-810.

2. Si X, Ma J, Cao DY, et al. Transesophageal echocardiography instead or in addition to transthoracic echocardiography in evaluating haemodynamic problems in intubated critically ill patients. Ann Transl Med. 2020;8(12):785. 

3. Hahn RT, Abraham T, Adams MS, et al. Guidelines for performing a cmprehensive transesophageal echocardiographic examination: recommendations from the American Society of Echocardioraphy and the Society of Cardiovascular Anesthesiologists. J Am Soc Echocardiogr. 2013;26(9):921-964.

Bedside-focused cardiac ultrasound assessment, or cardiac point-of-care ultrasound (POCUS), has become common in intensive care units throughout the US and the world. Many clinicians argue a POCUS cardiac assessment should be completed in most hypotensive patients and all cases of undifferentiated shock.

However, obtaining images adequate for decision making via standard transthoracic echo (TTE) is not possible in a significant number of patients; as high as 30% of critically ill patients, according to The American Society of Echocardiography (ASE) guidelines.¹ Factors common to critically ill patients, such as invasive mechanical ventilation, external dressings, and limited mobility, contribute to poor image acquisition.

Proud_Kevin_TEXAS_web.jpg

In almost all these cases, the factors limiting image acquisition can be eliminated by utilizing a transesophageal approach. In a recent study, researchers were able to demonstrate that adding transesophageal echocardiography (TEE) to TTE in critically ill patients yielded a new diagnosis or a change in management about 45% of the time.²

Using transesophageal ultrasound for a focused cardiac assessment in hemodynamically unstable patients is not new—and is often referred to as rescue TEE or resuscitative TEE. A broader term, transesophageal ultrasound, has also been used to include sonographic evaluation of the lungs in patients with poor acoustic windows. At my institution, we use the term critical care TEE to define TEE performed by a noncardiology-trained intensivist in an intubated critically ill patient.

Regardless of the term, the use of transesophageal ultrasound by the noncardiologist in the ICU appears to be a developing trend. As with other uses of POCUS, ultrasound machines continue to be able to “do more” at a lower price point. In 2024, several cart-based ultrasound machines are compatible with transesophageal probes and contain software packages capable of common cardiac measurements.

Despite this growing interest, intensivists are likely to encounter barriers to implementing critical care TEE. Our division recently implemented adding TEE to our practice. Our practice involves two separate systems: a Veterans Administration hospital and a university-based county hospital. Our division has integrated the use of TEE in the medical ICU at both institutions. Having navigated the process at both institutions, I can offer some guidance in navigating barriers.

The development of a critical care TEE program must start with a strong base in transthoracic cardiac POCUS, at least for the foreseeable future. Having a strong background in TTE gives learners a solid foundation in cardiac anatomy, cardiac function, and ultrasound properties. Obtaining testamur status or board certification in critical care echocardiography is not an absolute must but is a definite benefit. Having significant experience in TTE image acquisition and interpretation will flatten the learning curve for TEE. Interestingly, image acquisition in TEE is often easier than in TTE, so the paradigm of learning TTE before TEE may reverse in the years to come.

Two barriers often work together to create a vicious cycle that stops the development of a TEE program at its start. These barriers include the lack of training and lack of equipment, specifically a TEE probe. Those who do not understand the value of TEE may ask, “Why purchase equipment for a procedure that you do not yet know how to do?” The opposite question can also be asked, “Why get trained to do something you don’t have the equipment to perform?”

My best advice to break this cycle is to “dive in” to whichever barrier seems easier to overcome first. I started with obtaining knowledge and training. Obtaining training and education in a procedure that is historically not done in your specialty is challenging but is not impossible. It takes a combination of high levels of self-motivation and at least one colleague with the training to support you. I approached a cardiac anesthesiologist, whom I knew from the surgical ICU. Cardiologists can also be a resource, but working with cardiac anesthesiologists offers several advantages. TEEs done by cardiac anesthesiologists are similar to those done in ICU patients (ie, all patients are intubated and sedated). The procedures are also scheduled several days in advance, making it easier to integrate training into your daily work schedule. Lastly, the TEE probe remains in place for several hours, so repeating the probe manipulations again as a learner does not add additional risk to the patient. In my case, we somewhat arbitrarily agreed that I participate in 25 TEE exams. (CME courses, both online and in-person simulation, exist and greatly supplement self-study.)

Obtaining equipment is also a common barrier, though this has become less restrictive in the last several years. As previously mentioned, many cart-based ultrasound machines can accommodate a TEE probe. This changes the request from purchasing a new machine to “just a probe.” Despite the higher cost than most other probes, those in charge of purchasing are often more open to purchasing “a probe” than to purchasing an ultrasound machine.

Additionally, the purchasing decision regarding probes may fall to a different person than it does for an ultrasound machine. If available, POCUS image archiving into the medical record can help offset the cost of equipment, both by increasing revenue via billing and by demonstrating that equipment is being used. If initially declined, continue to ask and work to integrate the purchase into the next year’s budget. Inquire about the process of making a formal request and follow that process. This will often involve obtaining a quote or quotes from the ultrasound manufacturer(s).

Keep in mind that the probe will require a special storage cabinet specifically designed for TEE probes. It is prudent to include this in budget requests. If needed, the echocardiography lab can be a useful resource for additional information regarding the cabinet requirements. It is strongly recommended to discuss TEE probe models with sterile processing before any purchasing. If options are available, it is wise to choose a model the hospital already uses, as the cleaning protocol is well established. Our unit purchased a model that did not have an established protocol, which took nearly 6 months to develop. If probe options are limited, involving sterile processing early to start developing a protocol will help decrease delays.

Obtaining hospital privileges is also a common barrier, though this may not be as challenging as expected. Hospitals typically have well-outlined policies on obtaining privileges for established procedures. One of our hospital systems had four different options; the most straightforward required 20 hours of CME specific to TEE and 10 supervised cases by a proctor currently holding TEE privileges (see Table 1).

166888_table_web.jpg

Dr. Proud is Associate Professor of Medicine, Division of Pulmonary and Critical Care Medicine, Pulmonary and Critical Care Medicine Program Director, UT Health San Antonio.

References:

1. Porter TR, Abdelmoneim S, Belcik FT, et al. Guidelines for the cardiac sonographer in the performance of contrast echocardiography: a focused update from the American Society of Echocardiography. J Am Soc Echocardiogr. 2024;27(8):797-810.

2. Si X, Ma J, Cao DY, et al. Transesophageal echocardiography instead or in addition to transthoracic echocardiography in evaluating haemodynamic problems in intubated critically ill patients. Ann Transl Med. 2020;8(12):785. 

3. Hahn RT, Abraham T, Adams MS, et al. Guidelines for performing a cmprehensive transesophageal echocardiographic examination: recommendations from the American Society of Echocardioraphy and the Society of Cardiovascular Anesthesiologists. J Am Soc Echocardiogr. 2013;26(9):921-964.

The practice of initiating early and adequate nutrition in critically ill patients is a cornerstone of ICU management. Adequate nutrition combats the dangerous catabolic state that accompanies critical illness. A few of the benefits of this practice are a decrease in disease severity with resultant lessened hospital and ICU lengths of stay, reduced infection rates, and a decrease in hospital mortality. Enteral nutrition (EN) is the route of nutritional support most associated with safe and effective provision of enhanced immunologic function and the ability to preserve the patient’s lean body mass while avoiding metabolic and infectious complications.

Gaillard_John_web.jpg

The practice of initiating early and adequate nutrition in critically ill patients is a cornerstone of ICU management. Adequate nutrition combats the dangerous catabolic state that accompanies critical illness. A few of the benefits of this practice are a decrease in disease severity with resultant lessened hospital and ICU lengths of stay, reduced infection rates, and a decrease in hospital mortality. Enteral nutrition (EN) is the route of nutritional support most associated with safe and effective provision of enhanced immunologic function and the ability to preserve the patient’s lean body mass while avoiding metabolic and infectious complications.

Gaillard_John_web.jpg

The practice of initiating early and adequate nutrition in critically ill patients is a cornerstone of ICU management. Adequate nutrition combats the dangerous catabolic state that accompanies critical illness. A few of the benefits of this practice are a decrease in disease severity with resultant lessened hospital and ICU lengths of stay, reduced infection rates, and a decrease in hospital mortality. Enteral nutrition (EN) is the route of nutritional support most associated with safe and effective provision of enhanced immunologic function and the ability to preserve the patient’s lean body mass while avoiding metabolic and infectious complications.

Gaillard_John_web.jpg

Patients admitted to ICUs require modifications to their medication regimen due to their critical illness and rapidly changing clinical status. Modifications to medication regimens may include stopping home medications for chronic conditions, dose adjustments for altered organ function, or initiating new treatments for acute illness(es). Common examples of changes to a critically ill patient’s medication regimen are stopping a chronic antihypertensive drug in the setting of shock, holding an oral medication that cannot be crushed or administered through a feeding tube, and initiating sedatives and analgesics to support invasive mechanical ventilation. Medication regimens are especially vulnerable to errors and omissions at transition points (i.e., ICU to ward transfers and home discharge). As critical illness resolves and patients transition to different care teams, the hospital discharge medication regimen may differ from the preadmission list with the omission of prehospital medications and/or the continuation of acute medications no longer needed without thorough medication review and reconciliation.

Burry_Lisa_D_CANADA_web.jpg

While admitted to ICU, many critically ill patients – particularly those who are mechanically ventilated – receive intravenous or enteral sedatives such as benzodiazepines and antipsychotics. Sedatives are prescribed to more than two-thirds of critically ill patients for disturbing symptoms of agitation, delirium, anxiety, and insomnia and to facilitate invasive procedures (Burry LD, et al. J Crit Care. 2017;42:268). Current sedation practice guidelines endorse the use of sedatives when indicated for the shortest duration possible, given the known associated serious short- and long-term adverse drug events (Devlin JW, et al. Crit Care Med. 2018;46[9]:e825). Previous research has demonstrated that benzodiazepines initiated in-hospital are often continued on discharge for older adults and that patients from the ICU are at greater risk of benzodiazepine continuation than patients hospitalized without an ICU admission (Scales DC, et al. J Gen Intern Med. 2016;31[2]:196; Bell C, et al. J Gen Intern Med. 2007;22[7]:1024). This is particularly concerning for older adults as sedatives have been associated with serious adverse events in community-dwelling older adults, including falls and cognitive impairment (American Geriatrics Society. J Am Geriatr Soc. 2015;63[11]:2227)

Williamson_David_R_CANADA_web.jpg

The cohort of patients included all adults aged 66 years or more, who were discharged alive from the hospital and who were sedative-naive prior to hospitalization. Sedative-naive status was defined as no sedative prescription filled for any class, dose, or duration in the 180 days before hospital admission. The proportion of ICU survivors who filled a sedative prescription within 1 week of hospital discharge was the primary outcome. The secondary outcomes were the proportion of patients that filled each sedative class (e.g., antipsychotic, benzodiazepine, nonbenzodiazepine sedative) within 1 week of hospital discharge and persistent sedative prescription (additional prescriptions filled within 6 months after discharge).

The cohort included 250,428 sedative-naive older adults. The mean age was 75.8 years, 61.0% were male, 26.3% received invasive mechanical ventilation, and 14.8% had sepsis. In total, 6.1% (n=15,277) of patients filled a sedative prescription within 1 week of discharge; 57.7% (n = 8824) filled a benzodiazepine, 18.0% (n = 2749) filled a non-benzodiazepine sedative, 17.9% (n = 2745) filled an antipsychotic, and 6.2% (n = 959) filled more than 1 sedative drug class. Most patients filled prescriptions on the day of discharge (median 0 days (interquartile range (IQR) 0-3). The study found considerable variation in the primary outcome across the 153 hospitals: 2.1% (95% confidence interval [CI] 1.2% to 2.8%) to 44.0% (95% CI 3.0% to –57.8%) filled a sedative prescription within a week of hospital discharge. The factors strongly associated with an increased odds of a sedative prescription filled within a week of discharge included: discharge to long-term care (adjusted OR (aOR) 4.00, 95% CI 3.72 to 4.31), receipt of inpatient geriatric (aOR 1.95, 95% CI 1.80 to 2.10) or psychiatry consultation (aOR 2.76, 95% CI 2.62, 2.91), mechanical ventilation (aOR 1.59, 95% CI 1.53 to 1.66), and admitted ≥ 7 days to the ICU (aOR 1.50, 95% CI 1.42 to 1.58). Among hospital factors, a community hospital (vs academic) (aOR 1.40, 95% CI 1.16 to 1.70) and rural location (vs urban) (aOR 1.67, 95% CI 1.36 to 2.05) were also associated with new sedative prescriptions. Even after adjusting for patient and site characteristics, there was considerable remaining variability between sites quantified by the median odds ratio (aMOR) of 1.43. By drug class, there were similar findings with the exception of different associations for sex and frailty. For benzodiazepine prescriptions, female sex was associated with increased odds of a prescription (aOR 1.13, 95% CI 1.08 to 1.18), while frailty was inversely associated (aOR 0.82, 95% CI 0.75 to 0.89). The opposite associations were identified for antipsychotics: female sex (aOR 0.75, 95% CI 0.69 to 0.81) and frailty (aOR 1.41, 95% CI 1.28 to 1.55). No associations were identified for sex and frailty and non-benzodiazepine sedative prescriptions.

Persistent sedative prescription was common as 55% met the definition of persistence, filling a median of 2 prescriptions (IQR 1,3) in the 6 months after hospital discharge. The factors associated with persistent sedative prescriptions were similar to those identified above except female sex was associated with persistent sedative prescription (sHR 1.07, 95% CI 1.02 to 1.13). Those who filled an antipsychotic prescription (sHR 1.45, 95% CI 1.35 to 1.56), a non-benzodiazepine sedative prescription (sHR 1.44, 955 CI 1.34 to 1.53), or prescriptions for more than 1 sedative class filled (sHR 2.16, 95% CI 1.97 to 2.37) were more likely to fill persistent prescriptions compared with those who filled a prescription for a benzodiazepine alone as their first sedative.

In summary, 1 in 15 sedative-naive older adults filled a sedative prescription within a week of hospital discharge following a critical illness, and many continued to fill sedative prescriptions in the next 6 months. We were able to identify factors associated with new sedative prescriptions that could be targeted for stewardship programs or quality improvement projects that focus on medication safety and reconciliation. Medication stewardship and reconciliation processes have been broadly studied in many patient care settings but not the ICU. There is still much to determine regarding de-escalating and discontinuing sedatives as critical illness resolves and patients are liberated from intensive clinical interventions as well as the consequences of sedative exposure after hospital discharge for this population.
 

Dr. Burry is with the Departments of Pharmacy and Medicine, Sinai Health; Leslie Dan Faculty of Pharmacy and Interdepartmental Division of Critical Care, University of Toronto, Toronto, Canada. Dr. Williamson is with the Faculté de Pharmacie, Université de Montréal; Pharmacy Département, Hôpital du Sacré-Cœur de Montréal; and Research center, CIUSSS du Nord-de-l’Île-de-Montréal, Canada.

Patients admitted to ICUs require modifications to their medication regimen due to their critical illness and rapidly changing clinical status. Modifications to medication regimens may include stopping home medications for chronic conditions, dose adjustments for altered organ function, or initiating new treatments for acute illness(es). Common examples of changes to a critically ill patient’s medication regimen are stopping a chronic antihypertensive drug in the setting of shock, holding an oral medication that cannot be crushed or administered through a feeding tube, and initiating sedatives and analgesics to support invasive mechanical ventilation. Medication regimens are especially vulnerable to errors and omissions at transition points (i.e., ICU to ward transfers and home discharge). As critical illness resolves and patients transition to different care teams, the hospital discharge medication regimen may differ from the preadmission list with the omission of prehospital medications and/or the continuation of acute medications no longer needed without thorough medication review and reconciliation.

Burry_Lisa_D_CANADA_web.jpg

While admitted to ICU, many critically ill patients – particularly those who are mechanically ventilated – receive intravenous or enteral sedatives such as benzodiazepines and antipsychotics. Sedatives are prescribed to more than two-thirds of critically ill patients for disturbing symptoms of agitation, delirium, anxiety, and insomnia and to facilitate invasive procedures (Burry LD, et al. J Crit Care. 2017;42:268). Current sedation practice guidelines endorse the use of sedatives when indicated for the shortest duration possible, given the known associated serious short- and long-term adverse drug events (Devlin JW, et al. Crit Care Med. 2018;46[9]:e825). Previous research has demonstrated that benzodiazepines initiated in-hospital are often continued on discharge for older adults and that patients from the ICU are at greater risk of benzodiazepine continuation than patients hospitalized without an ICU admission (Scales DC, et al. J Gen Intern Med. 2016;31[2]:196; Bell C, et al. J Gen Intern Med. 2007;22[7]:1024). This is particularly concerning for older adults as sedatives have been associated with serious adverse events in community-dwelling older adults, including falls and cognitive impairment (American Geriatrics Society. J Am Geriatr Soc. 2015;63[11]:2227)

Williamson_David_R_CANADA_web.jpg

The cohort of patients included all adults aged 66 years or more, who were discharged alive from the hospital and who were sedative-naive prior to hospitalization. Sedative-naive status was defined as no sedative prescription filled for any class, dose, or duration in the 180 days before hospital admission. The proportion of ICU survivors who filled a sedative prescription within 1 week of hospital discharge was the primary outcome. The secondary outcomes were the proportion of patients that filled each sedative class (e.g., antipsychotic, benzodiazepine, nonbenzodiazepine sedative) within 1 week of hospital discharge and persistent sedative prescription (additional prescriptions filled within 6 months after discharge).

The cohort included 250,428 sedative-naive older adults. The mean age was 75.8 years, 61.0% were male, 26.3% received invasive mechanical ventilation, and 14.8% had sepsis. In total, 6.1% (n=15,277) of patients filled a sedative prescription within 1 week of discharge; 57.7% (n = 8824) filled a benzodiazepine, 18.0% (n = 2749) filled a non-benzodiazepine sedative, 17.9% (n = 2745) filled an antipsychotic, and 6.2% (n = 959) filled more than 1 sedative drug class. Most patients filled prescriptions on the day of discharge (median 0 days (interquartile range (IQR) 0-3). The study found considerable variation in the primary outcome across the 153 hospitals: 2.1% (95% confidence interval [CI] 1.2% to 2.8%) to 44.0% (95% CI 3.0% to –57.8%) filled a sedative prescription within a week of hospital discharge. The factors strongly associated with an increased odds of a sedative prescription filled within a week of discharge included: discharge to long-term care (adjusted OR (aOR) 4.00, 95% CI 3.72 to 4.31), receipt of inpatient geriatric (aOR 1.95, 95% CI 1.80 to 2.10) or psychiatry consultation (aOR 2.76, 95% CI 2.62, 2.91), mechanical ventilation (aOR 1.59, 95% CI 1.53 to 1.66), and admitted ≥ 7 days to the ICU (aOR 1.50, 95% CI 1.42 to 1.58). Among hospital factors, a community hospital (vs academic) (aOR 1.40, 95% CI 1.16 to 1.70) and rural location (vs urban) (aOR 1.67, 95% CI 1.36 to 2.05) were also associated with new sedative prescriptions. Even after adjusting for patient and site characteristics, there was considerable remaining variability between sites quantified by the median odds ratio (aMOR) of 1.43. By drug class, there were similar findings with the exception of different associations for sex and frailty. For benzodiazepine prescriptions, female sex was associated with increased odds of a prescription (aOR 1.13, 95% CI 1.08 to 1.18), while frailty was inversely associated (aOR 0.82, 95% CI 0.75 to 0.89). The opposite associations were identified for antipsychotics: female sex (aOR 0.75, 95% CI 0.69 to 0.81) and frailty (aOR 1.41, 95% CI 1.28 to 1.55). No associations were identified for sex and frailty and non-benzodiazepine sedative prescriptions.

Persistent sedative prescription was common as 55% met the definition of persistence, filling a median of 2 prescriptions (IQR 1,3) in the 6 months after hospital discharge. The factors associated with persistent sedative prescriptions were similar to those identified above except female sex was associated with persistent sedative prescription (sHR 1.07, 95% CI 1.02 to 1.13). Those who filled an antipsychotic prescription (sHR 1.45, 95% CI 1.35 to 1.56), a non-benzodiazepine sedative prescription (sHR 1.44, 955 CI 1.34 to 1.53), or prescriptions for more than 1 sedative class filled (sHR 2.16, 95% CI 1.97 to 2.37) were more likely to fill persistent prescriptions compared with those who filled a prescription for a benzodiazepine alone as their first sedative.

In summary, 1 in 15 sedative-naive older adults filled a sedative prescription within a week of hospital discharge following a critical illness, and many continued to fill sedative prescriptions in the next 6 months. We were able to identify factors associated with new sedative prescriptions that could be targeted for stewardship programs or quality improvement projects that focus on medication safety and reconciliation. Medication stewardship and reconciliation processes have been broadly studied in many patient care settings but not the ICU. There is still much to determine regarding de-escalating and discontinuing sedatives as critical illness resolves and patients are liberated from intensive clinical interventions as well as the consequences of sedative exposure after hospital discharge for this population.
 

Dr. Burry is with the Departments of Pharmacy and Medicine, Sinai Health; Leslie Dan Faculty of Pharmacy and Interdepartmental Division of Critical Care, University of Toronto, Toronto, Canada. Dr. Williamson is with the Faculté de Pharmacie, Université de Montréal; Pharmacy Département, Hôpital du Sacré-Cœur de Montréal; and Research center, CIUSSS du Nord-de-l’Île-de-Montréal, Canada.

Patients admitted to ICUs require modifications to their medication regimen due to their critical illness and rapidly changing clinical status. Modifications to medication regimens may include stopping home medications for chronic conditions, dose adjustments for altered organ function, or initiating new treatments for acute illness(es). Common examples of changes to a critically ill patient’s medication regimen are stopping a chronic antihypertensive drug in the setting of shock, holding an oral medication that cannot be crushed or administered through a feeding tube, and initiating sedatives and analgesics to support invasive mechanical ventilation. Medication regimens are especially vulnerable to errors and omissions at transition points (i.e., ICU to ward transfers and home discharge). As critical illness resolves and patients transition to different care teams, the hospital discharge medication regimen may differ from the preadmission list with the omission of prehospital medications and/or the continuation of acute medications no longer needed without thorough medication review and reconciliation.

Burry_Lisa_D_CANADA_web.jpg

While admitted to ICU, many critically ill patients – particularly those who are mechanically ventilated – receive intravenous or enteral sedatives such as benzodiazepines and antipsychotics. Sedatives are prescribed to more than two-thirds of critically ill patients for disturbing symptoms of agitation, delirium, anxiety, and insomnia and to facilitate invasive procedures (Burry LD, et al. J Crit Care. 2017;42:268). Current sedation practice guidelines endorse the use of sedatives when indicated for the shortest duration possible, given the known associated serious short- and long-term adverse drug events (Devlin JW, et al. Crit Care Med. 2018;46[9]:e825). Previous research has demonstrated that benzodiazepines initiated in-hospital are often continued on discharge for older adults and that patients from the ICU are at greater risk of benzodiazepine continuation than patients hospitalized without an ICU admission (Scales DC, et al. J Gen Intern Med. 2016;31[2]:196; Bell C, et al. J Gen Intern Med. 2007;22[7]:1024). This is particularly concerning for older adults as sedatives have been associated with serious adverse events in community-dwelling older adults, including falls and cognitive impairment (American Geriatrics Society. J Am Geriatr Soc. 2015;63[11]:2227)

Williamson_David_R_CANADA_web.jpg

The cohort of patients included all adults aged 66 years or more, who were discharged alive from the hospital and who were sedative-naive prior to hospitalization. Sedative-naive status was defined as no sedative prescription filled for any class, dose, or duration in the 180 days before hospital admission. The proportion of ICU survivors who filled a sedative prescription within 1 week of hospital discharge was the primary outcome. The secondary outcomes were the proportion of patients that filled each sedative class (e.g., antipsychotic, benzodiazepine, nonbenzodiazepine sedative) within 1 week of hospital discharge and persistent sedative prescription (additional prescriptions filled within 6 months after discharge).

The cohort included 250,428 sedative-naive older adults. The mean age was 75.8 years, 61.0% were male, 26.3% received invasive mechanical ventilation, and 14.8% had sepsis. In total, 6.1% (n=15,277) of patients filled a sedative prescription within 1 week of discharge; 57.7% (n = 8824) filled a benzodiazepine, 18.0% (n = 2749) filled a non-benzodiazepine sedative, 17.9% (n = 2745) filled an antipsychotic, and 6.2% (n = 959) filled more than 1 sedative drug class. Most patients filled prescriptions on the day of discharge (median 0 days (interquartile range (IQR) 0-3). The study found considerable variation in the primary outcome across the 153 hospitals: 2.1% (95% confidence interval [CI] 1.2% to 2.8%) to 44.0% (95% CI 3.0% to –57.8%) filled a sedative prescription within a week of hospital discharge. The factors strongly associated with an increased odds of a sedative prescription filled within a week of discharge included: discharge to long-term care (adjusted OR (aOR) 4.00, 95% CI 3.72 to 4.31), receipt of inpatient geriatric (aOR 1.95, 95% CI 1.80 to 2.10) or psychiatry consultation (aOR 2.76, 95% CI 2.62, 2.91), mechanical ventilation (aOR 1.59, 95% CI 1.53 to 1.66), and admitted ≥ 7 days to the ICU (aOR 1.50, 95% CI 1.42 to 1.58). Among hospital factors, a community hospital (vs academic) (aOR 1.40, 95% CI 1.16 to 1.70) and rural location (vs urban) (aOR 1.67, 95% CI 1.36 to 2.05) were also associated with new sedative prescriptions. Even after adjusting for patient and site characteristics, there was considerable remaining variability between sites quantified by the median odds ratio (aMOR) of 1.43. By drug class, there were similar findings with the exception of different associations for sex and frailty. For benzodiazepine prescriptions, female sex was associated with increased odds of a prescription (aOR 1.13, 95% CI 1.08 to 1.18), while frailty was inversely associated (aOR 0.82, 95% CI 0.75 to 0.89). The opposite associations were identified for antipsychotics: female sex (aOR 0.75, 95% CI 0.69 to 0.81) and frailty (aOR 1.41, 95% CI 1.28 to 1.55). No associations were identified for sex and frailty and non-benzodiazepine sedative prescriptions.

Persistent sedative prescription was common as 55% met the definition of persistence, filling a median of 2 prescriptions (IQR 1,3) in the 6 months after hospital discharge. The factors associated with persistent sedative prescriptions were similar to those identified above except female sex was associated with persistent sedative prescription (sHR 1.07, 95% CI 1.02 to 1.13). Those who filled an antipsychotic prescription (sHR 1.45, 95% CI 1.35 to 1.56), a non-benzodiazepine sedative prescription (sHR 1.44, 955 CI 1.34 to 1.53), or prescriptions for more than 1 sedative class filled (sHR 2.16, 95% CI 1.97 to 2.37) were more likely to fill persistent prescriptions compared with those who filled a prescription for a benzodiazepine alone as their first sedative.

In summary, 1 in 15 sedative-naive older adults filled a sedative prescription within a week of hospital discharge following a critical illness, and many continued to fill sedative prescriptions in the next 6 months. We were able to identify factors associated with new sedative prescriptions that could be targeted for stewardship programs or quality improvement projects that focus on medication safety and reconciliation. Medication stewardship and reconciliation processes have been broadly studied in many patient care settings but not the ICU. There is still much to determine regarding de-escalating and discontinuing sedatives as critical illness resolves and patients are liberated from intensive clinical interventions as well as the consequences of sedative exposure after hospital discharge for this population.
 

Dr. Burry is with the Departments of Pharmacy and Medicine, Sinai Health; Leslie Dan Faculty of Pharmacy and Interdepartmental Division of Critical Care, University of Toronto, Toronto, Canada. Dr. Williamson is with the Faculté de Pharmacie, Université de Montréal; Pharmacy Département, Hôpital du Sacré-Cœur de Montréal; and Research center, CIUSSS du Nord-de-l’Île-de-Montréal, Canada.

After much anticipation, the inaugural issues of both CHEST^®Critical Care and CHEST^®Pulmonary officially launched in late June. These new open access additions to the journal CHEST^® portfolio feature content that is permanently and freely available online for all – promoting transparency, inclusiveness, and collaboration in research – and offer authors more avenues to share their practice-changing research.

The first issue of CHEST Critical Care featured research into ICU mortality across prepandemic and pandemic cohorts in resource-limited settings in South Africa, an exploration into symptom trajectory in recipients of hematopoietic stem-cell transplantation, a narrative review of post-intensive care syndrome, and an investigation into early echocardiographic and ultrasonographic findings in critically ill patients with COVID-19.

In addition, an editorial from Hayley Gershengorn, MD, Editor in Chief of CHEST Critical Care, offers readers more insights into the need for a publication focused on the breadth of clinical topics in critical care and her goals for the new publication.

“I’m ecstatic for this launch. We are grateful to our authors for the trust they put in us and are excited to share their work with our critical care colleagues around the world,” Dr. Gershengorn said. “The editorial team and the American College of Chest Physicians staff have worked tirelessly on this journal, and it’s incredibly gratifying to see the first issue publish.”

Read the full issue and new research from the journal at www.chestcc.org.

In his own editorial featured in the inaugural issue of CHEST Pulmonary, Editor in Chief Matthew Miles, MD, MEd, FCCP, shares how the flagship journal’s proud heritage of sharing impactful clinical research – and the need to target areas of pulmonary and sleep medicine research not covered by other journals – inspired the creation of this new publication.

The issue also includes research into mobile health opportunities for asthma management, an exploration into telemedicine for patients with interstitial lung diseases, an in-depth review into the rare and often underdiagnosed disorder primary ciliary dyskinesia, research on the impact of the social vulnerability index on pulmonary embolism mortality, and an investigation into pneumothorax complications after percutaneous lung biopsy.

“I am deeply grateful to our authors, reviewers, editorial board, and staff who have contributed to the launch of our first issue,” Dr. Miles said. “The journal CHEST is known for excellence in clinically relevant research and patient management guidance. CHEST Pulmonary expands the CHEST portfolio with additional opportunity for researchers to share their work in an exclusively open access format to reach the broadest possible audience. I know our readers will enjoy learning from the research and reviews in issue one.”

Review the full issue and new articles from CHEST Pulmonary at www.chestpulmonary.org.

After much anticipation, the inaugural issues of both CHEST^®Critical Care and CHEST^®Pulmonary officially launched in late June. These new open access additions to the journal CHEST^® portfolio feature content that is permanently and freely available online for all – promoting transparency, inclusiveness, and collaboration in research – and offer authors more avenues to share their practice-changing research.

The first issue of CHEST Critical Care featured research into ICU mortality across prepandemic and pandemic cohorts in resource-limited settings in South Africa, an exploration into symptom trajectory in recipients of hematopoietic stem-cell transplantation, a narrative review of post-intensive care syndrome, and an investigation into early echocardiographic and ultrasonographic findings in critically ill patients with COVID-19.

In addition, an editorial from Hayley Gershengorn, MD, Editor in Chief of CHEST Critical Care, offers readers more insights into the need for a publication focused on the breadth of clinical topics in critical care and her goals for the new publication.

“I’m ecstatic for this launch. We are grateful to our authors for the trust they put in us and are excited to share their work with our critical care colleagues around the world,” Dr. Gershengorn said. “The editorial team and the American College of Chest Physicians staff have worked tirelessly on this journal, and it’s incredibly gratifying to see the first issue publish.”

Read the full issue and new research from the journal at www.chestcc.org.

In his own editorial featured in the inaugural issue of CHEST Pulmonary, Editor in Chief Matthew Miles, MD, MEd, FCCP, shares how the flagship journal’s proud heritage of sharing impactful clinical research – and the need to target areas of pulmonary and sleep medicine research not covered by other journals – inspired the creation of this new publication.

The issue also includes research into mobile health opportunities for asthma management, an exploration into telemedicine for patients with interstitial lung diseases, an in-depth review into the rare and often underdiagnosed disorder primary ciliary dyskinesia, research on the impact of the social vulnerability index on pulmonary embolism mortality, and an investigation into pneumothorax complications after percutaneous lung biopsy.

“I am deeply grateful to our authors, reviewers, editorial board, and staff who have contributed to the launch of our first issue,” Dr. Miles said. “The journal CHEST is known for excellence in clinically relevant research and patient management guidance. CHEST Pulmonary expands the CHEST portfolio with additional opportunity for researchers to share their work in an exclusively open access format to reach the broadest possible audience. I know our readers will enjoy learning from the research and reviews in issue one.”

Review the full issue and new articles from CHEST Pulmonary at www.chestpulmonary.org.

After much anticipation, the inaugural issues of both CHEST^®Critical Care and CHEST^®Pulmonary officially launched in late June. These new open access additions to the journal CHEST^® portfolio feature content that is permanently and freely available online for all – promoting transparency, inclusiveness, and collaboration in research – and offer authors more avenues to share their practice-changing research.

The first issue of CHEST Critical Care featured research into ICU mortality across prepandemic and pandemic cohorts in resource-limited settings in South Africa, an exploration into symptom trajectory in recipients of hematopoietic stem-cell transplantation, a narrative review of post-intensive care syndrome, and an investigation into early echocardiographic and ultrasonographic findings in critically ill patients with COVID-19.

In addition, an editorial from Hayley Gershengorn, MD, Editor in Chief of CHEST Critical Care, offers readers more insights into the need for a publication focused on the breadth of clinical topics in critical care and her goals for the new publication.

“I’m ecstatic for this launch. We are grateful to our authors for the trust they put in us and are excited to share their work with our critical care colleagues around the world,” Dr. Gershengorn said. “The editorial team and the American College of Chest Physicians staff have worked tirelessly on this journal, and it’s incredibly gratifying to see the first issue publish.”

Read the full issue and new research from the journal at www.chestcc.org.

In his own editorial featured in the inaugural issue of CHEST Pulmonary, Editor in Chief Matthew Miles, MD, MEd, FCCP, shares how the flagship journal’s proud heritage of sharing impactful clinical research – and the need to target areas of pulmonary and sleep medicine research not covered by other journals – inspired the creation of this new publication.

The issue also includes research into mobile health opportunities for asthma management, an exploration into telemedicine for patients with interstitial lung diseases, an in-depth review into the rare and often underdiagnosed disorder primary ciliary dyskinesia, research on the impact of the social vulnerability index on pulmonary embolism mortality, and an investigation into pneumothorax complications after percutaneous lung biopsy.

“I am deeply grateful to our authors, reviewers, editorial board, and staff who have contributed to the launch of our first issue,” Dr. Miles said. “The journal CHEST is known for excellence in clinically relevant research and patient management guidance. CHEST Pulmonary expands the CHEST portfolio with additional opportunity for researchers to share their work in an exclusively open access format to reach the broadest possible audience. I know our readers will enjoy learning from the research and reviews in issue one.”

Review the full issue and new articles from CHEST Pulmonary at www.chestpulmonary.org.

Cardiogenic shock (CS) is being recognized more often in critically ill patients. This increased prevalence is likely due to a better understanding of CS and the benefit of improving cardiac output (CO) to ensure adequate oxygen delivery (DO₂). There is no one specific definition of CS; rather, CS describes a clinical condition in which a patient is suffering from cellular hypoperfusion due to an ineffective CO with normal or elevating intravascular filling pressures.

CS is often, but not always, caused by a cardiac dysfunction. The heart is not able to provide adequate DO₂ to the tissues. Hypoperfusion ensues. The body attempts to compensate for the poor perfusion by increasing heart rate, vasoconstriction, and shunting blood flow to vital organs. These compensatory mechanisms worsen perfusion by increasing myocardial ischemia which further worsens cardiac dysfunction. This is known as the downward spiral of CS (Ann Intern Med. 1999 Jul 6;131[1]).

Gaillard_John_web.jpg

There is a number of different etiologies for CS. Historically, acute myocardial infarctions (AMI) was the most common cause. In the last 20 years, AMI-induced CS has become less prevalent due to more aggressive reperfusion strategies. CS due to etiologies such as cardiomyopathy, myocarditis, right ventricle failure, and valvular pathologies have become more common. While the overarching goal is to restore DO₂ to the tissue, the optimal treatment may differ based on the etiology of the CS. The Society for Cardiovascular Angiography and Intervention (SCAI) published CS classification stages in 2019 and then updated the stages 2022 (J Am Coll Cardiol. 2022 Mar 8;79[9]:933-46). In addition to the stages, there is now a three-axis model to address risk stratification. These classifications are a practically means of identifying and treating patients presenting with or concern for acute CS.

Stage A (At Risk) patients are not experiencing CS, but they are the at risk population. The patient’s hemodynamics, physical exam, and markers of hypoperfusion are normal. Stage A includes patients who have had a recent AMI or have heart failure.

Stage B (Beginning) patients have evidence of hemodynamic instability but are able to maintain tissue perfusion. These patients will have true or relative hypotension or tachycardia (in an attempt to maintain CO). Distal perfusion is adequate, but signs of ensuing decompensation (eg, elevated jugular venous pressure [JVP]) are present. Lactate is <2.0 mmol/L. Clinicians must be vigilant and treat these patients aggressively, so they do not decompensate further. It can be difficult to identify these patients because their blood pressure may be “normal,” but upon investigation, the blood pressure is actually a drop from the patient’s baseline.

Chronic heart failure patients with a history of depressed cardiac function will often have periods of cardiac decompensation between stages A and B. These patients are able to maintain perfusion for longer periods of time before further decompensation with hypoperfusion. If and when they do decompensate, they will often have a steep downward trajectory, so it is advantageous to the patient to be aggressive early.

Stage C (Classic) patients have evidence of tissue hypoperfusion. While these patients will often have true or relative hypotension, it is not a definition of stage C. These patients have evidence of volume overload with elevated JVP and rales throughout their lung fields. They will have poor distal perfusion and cool extremities that may become mottled. Lactate is ≥ 2 mmol/L. B-type natriuretic peptide (BNP) and liver function test (LFTs) results are elevated, and urine output is diminished. If a pulmonary arterial catheter is placed (highly recommended), the cardiac index (CI) is < 2.2 L/min/m² and the pulmonary capillary wedge pressure (PCWP) is > 15 mm Hg. These patients look like what many clinicians think of when they think of CS.

These patients need better tissue perfusion. Inotropic support is needed to augment CO and DO₂. Pharmacologic support is often the initial step. These patients also benefit from volume removal. This is usually accomplished with aggressive diuresis with a loop diuretic.

Stage D (Deteriorating) patients have failed initial treatment with single inotropic support. Hypoperfusion is not getting better and is often worsening. Lactate is staying > 2 mmol/L or rising. BNP and LFTs are also rising. These patients require additional inotropes and usually need vasopressors. Mechanical cardiac support (MCS) is often needed in addition to pharmacologic inotropic support.

Stage E (Extremis) patients have actual or impending circulatory collapse. These patients are peri-arrest with profound hypotension, lactic acidosis (often > 8 mmol/L), and unconsciousness. These patients are worsening despite multiple strategies to augment CO and DO₂. These patients will likely die without emergent veno-arterial (VA) extracorporeal membrane oxygenation (ECMO). The goal of treatment is to stabilize the patient as quickly as possible to prevent cardiac arrest.

In addition to the stage of CS, SCAI developed the three-axis model of risk stratification as a conceptual model to be used for evaluation and prognostication. Etiology and phenotype, shock severity, and risk modifiers are factors related to patient outcomes from CS. This model is a way to individualize treatment to a specific patient.

Shock severity: What is the patient’s shock stage? What are the hemodynamics and metabolic abnormalities? What are the doses of the inotropes or vasopressors? Risk goes up with higher shock stages and vasoactive agent doses and worsening metabolic disturbances or hemodynamics.

Phenotype and etiology: what is the clinical etiology of the patient’s CS? Is this acute or acute on chronic? Which ventricle is involved? Is this cardiac driven or are other organs the driving factor? Single ventricle involvement is better than bi-ventricular failure. Cardiogenic collapse due to an overdose may have a better outcome than a massive AMI.

Risk modifiers: how old is the patient? What are the comorbidities? Did the patient have a cardiac arrest? What is the patient’s mental status? Some factors are modifiable, but others are not. The concept of chronologic vs. physiologic age may come into play. A frail 40 year old with stage 4 cancer and end stage renal failure may be assessed differently than a 70 year old with mild hypertension and an AMI.

The SCAI stages of CS are a pragmatic way to assess patients with an acute presentation of CS. These stages have defined criteria and treatment recommendations for all patients. The three-axis model allows the clinician to individualize patient care based on shock severity, etiology/phenotype, and risk modification. The goal of these stages is to identify and aggressively treat patients with CS, as well as identify when treatment is failing and additional therapies may be needed.

Dr. Gaillard is Associate Professor in the Departments of Anesthesiology, Section on Critical Care; Internal Medicine, Section on Pulmonology, Critical Care, Allergy, and Immunologic Diseases; and Emergency Medicine; Wake Forest School of Medicine, Winston-Salem, N.C.

Cardiogenic shock (CS) is being recognized more often in critically ill patients. This increased prevalence is likely due to a better understanding of CS and the benefit of improving cardiac output (CO) to ensure adequate oxygen delivery (DO₂). There is no one specific definition of CS; rather, CS describes a clinical condition in which a patient is suffering from cellular hypoperfusion due to an ineffective CO with normal or elevating intravascular filling pressures.

CS is often, but not always, caused by a cardiac dysfunction. The heart is not able to provide adequate DO₂ to the tissues. Hypoperfusion ensues. The body attempts to compensate for the poor perfusion by increasing heart rate, vasoconstriction, and shunting blood flow to vital organs. These compensatory mechanisms worsen perfusion by increasing myocardial ischemia which further worsens cardiac dysfunction. This is known as the downward spiral of CS (Ann Intern Med. 1999 Jul 6;131[1]).

Gaillard_John_web.jpg

There is a number of different etiologies for CS. Historically, acute myocardial infarctions (AMI) was the most common cause. In the last 20 years, AMI-induced CS has become less prevalent due to more aggressive reperfusion strategies. CS due to etiologies such as cardiomyopathy, myocarditis, right ventricle failure, and valvular pathologies have become more common. While the overarching goal is to restore DO₂ to the tissue, the optimal treatment may differ based on the etiology of the CS. The Society for Cardiovascular Angiography and Intervention (SCAI) published CS classification stages in 2019 and then updated the stages 2022 (J Am Coll Cardiol. 2022 Mar 8;79[9]:933-46). In addition to the stages, there is now a three-axis model to address risk stratification. These classifications are a practically means of identifying and treating patients presenting with or concern for acute CS.

Stage A (At Risk) patients are not experiencing CS, but they are the at risk population. The patient’s hemodynamics, physical exam, and markers of hypoperfusion are normal. Stage A includes patients who have had a recent AMI or have heart failure.

Stage B (Beginning) patients have evidence of hemodynamic instability but are able to maintain tissue perfusion. These patients will have true or relative hypotension or tachycardia (in an attempt to maintain CO). Distal perfusion is adequate, but signs of ensuing decompensation (eg, elevated jugular venous pressure [JVP]) are present. Lactate is <2.0 mmol/L. Clinicians must be vigilant and treat these patients aggressively, so they do not decompensate further. It can be difficult to identify these patients because their blood pressure may be “normal,” but upon investigation, the blood pressure is actually a drop from the patient’s baseline.

Chronic heart failure patients with a history of depressed cardiac function will often have periods of cardiac decompensation between stages A and B. These patients are able to maintain perfusion for longer periods of time before further decompensation with hypoperfusion. If and when they do decompensate, they will often have a steep downward trajectory, so it is advantageous to the patient to be aggressive early.

Stage C (Classic) patients have evidence of tissue hypoperfusion. While these patients will often have true or relative hypotension, it is not a definition of stage C. These patients have evidence of volume overload with elevated JVP and rales throughout their lung fields. They will have poor distal perfusion and cool extremities that may become mottled. Lactate is ≥ 2 mmol/L. B-type natriuretic peptide (BNP) and liver function test (LFTs) results are elevated, and urine output is diminished. If a pulmonary arterial catheter is placed (highly recommended), the cardiac index (CI) is < 2.2 L/min/m² and the pulmonary capillary wedge pressure (PCWP) is > 15 mm Hg. These patients look like what many clinicians think of when they think of CS.

These patients need better tissue perfusion. Inotropic support is needed to augment CO and DO₂. Pharmacologic support is often the initial step. These patients also benefit from volume removal. This is usually accomplished with aggressive diuresis with a loop diuretic.

Stage D (Deteriorating) patients have failed initial treatment with single inotropic support. Hypoperfusion is not getting better and is often worsening. Lactate is staying > 2 mmol/L or rising. BNP and LFTs are also rising. These patients require additional inotropes and usually need vasopressors. Mechanical cardiac support (MCS) is often needed in addition to pharmacologic inotropic support.

Stage E (Extremis) patients have actual or impending circulatory collapse. These patients are peri-arrest with profound hypotension, lactic acidosis (often > 8 mmol/L), and unconsciousness. These patients are worsening despite multiple strategies to augment CO and DO₂. These patients will likely die without emergent veno-arterial (VA) extracorporeal membrane oxygenation (ECMO). The goal of treatment is to stabilize the patient as quickly as possible to prevent cardiac arrest.

In addition to the stage of CS, SCAI developed the three-axis model of risk stratification as a conceptual model to be used for evaluation and prognostication. Etiology and phenotype, shock severity, and risk modifiers are factors related to patient outcomes from CS. This model is a way to individualize treatment to a specific patient.

Shock severity: What is the patient’s shock stage? What are the hemodynamics and metabolic abnormalities? What are the doses of the inotropes or vasopressors? Risk goes up with higher shock stages and vasoactive agent doses and worsening metabolic disturbances or hemodynamics.

Phenotype and etiology: what is the clinical etiology of the patient’s CS? Is this acute or acute on chronic? Which ventricle is involved? Is this cardiac driven or are other organs the driving factor? Single ventricle involvement is better than bi-ventricular failure. Cardiogenic collapse due to an overdose may have a better outcome than a massive AMI.

Risk modifiers: how old is the patient? What are the comorbidities? Did the patient have a cardiac arrest? What is the patient’s mental status? Some factors are modifiable, but others are not. The concept of chronologic vs. physiologic age may come into play. A frail 40 year old with stage 4 cancer and end stage renal failure may be assessed differently than a 70 year old with mild hypertension and an AMI.

The SCAI stages of CS are a pragmatic way to assess patients with an acute presentation of CS. These stages have defined criteria and treatment recommendations for all patients. The three-axis model allows the clinician to individualize patient care based on shock severity, etiology/phenotype, and risk modification. The goal of these stages is to identify and aggressively treat patients with CS, as well as identify when treatment is failing and additional therapies may be needed.

Dr. Gaillard is Associate Professor in the Departments of Anesthesiology, Section on Critical Care; Internal Medicine, Section on Pulmonology, Critical Care, Allergy, and Immunologic Diseases; and Emergency Medicine; Wake Forest School of Medicine, Winston-Salem, N.C.

Cardiogenic shock (CS) is being recognized more often in critically ill patients. This increased prevalence is likely due to a better understanding of CS and the benefit of improving cardiac output (CO) to ensure adequate oxygen delivery (DO₂). There is no one specific definition of CS; rather, CS describes a clinical condition in which a patient is suffering from cellular hypoperfusion due to an ineffective CO with normal or elevating intravascular filling pressures.

CS is often, but not always, caused by a cardiac dysfunction. The heart is not able to provide adequate DO₂ to the tissues. Hypoperfusion ensues. The body attempts to compensate for the poor perfusion by increasing heart rate, vasoconstriction, and shunting blood flow to vital organs. These compensatory mechanisms worsen perfusion by increasing myocardial ischemia which further worsens cardiac dysfunction. This is known as the downward spiral of CS (Ann Intern Med. 1999 Jul 6;131[1]).

Gaillard_John_web.jpg

There is a number of different etiologies for CS. Historically, acute myocardial infarctions (AMI) was the most common cause. In the last 20 years, AMI-induced CS has become less prevalent due to more aggressive reperfusion strategies. CS due to etiologies such as cardiomyopathy, myocarditis, right ventricle failure, and valvular pathologies have become more common. While the overarching goal is to restore DO₂ to the tissue, the optimal treatment may differ based on the etiology of the CS. The Society for Cardiovascular Angiography and Intervention (SCAI) published CS classification stages in 2019 and then updated the stages 2022 (J Am Coll Cardiol. 2022 Mar 8;79[9]:933-46). In addition to the stages, there is now a three-axis model to address risk stratification. These classifications are a practically means of identifying and treating patients presenting with or concern for acute CS.

Stage A (At Risk) patients are not experiencing CS, but they are the at risk population. The patient’s hemodynamics, physical exam, and markers of hypoperfusion are normal. Stage A includes patients who have had a recent AMI or have heart failure.

Stage B (Beginning) patients have evidence of hemodynamic instability but are able to maintain tissue perfusion. These patients will have true or relative hypotension or tachycardia (in an attempt to maintain CO). Distal perfusion is adequate, but signs of ensuing decompensation (eg, elevated jugular venous pressure [JVP]) are present. Lactate is <2.0 mmol/L. Clinicians must be vigilant and treat these patients aggressively, so they do not decompensate further. It can be difficult to identify these patients because their blood pressure may be “normal,” but upon investigation, the blood pressure is actually a drop from the patient’s baseline.

Chronic heart failure patients with a history of depressed cardiac function will often have periods of cardiac decompensation between stages A and B. These patients are able to maintain perfusion for longer periods of time before further decompensation with hypoperfusion. If and when they do decompensate, they will often have a steep downward trajectory, so it is advantageous to the patient to be aggressive early.

Stage C (Classic) patients have evidence of tissue hypoperfusion. While these patients will often have true or relative hypotension, it is not a definition of stage C. These patients have evidence of volume overload with elevated JVP and rales throughout their lung fields. They will have poor distal perfusion and cool extremities that may become mottled. Lactate is ≥ 2 mmol/L. B-type natriuretic peptide (BNP) and liver function test (LFTs) results are elevated, and urine output is diminished. If a pulmonary arterial catheter is placed (highly recommended), the cardiac index (CI) is < 2.2 L/min/m² and the pulmonary capillary wedge pressure (PCWP) is > 15 mm Hg. These patients look like what many clinicians think of when they think of CS.

These patients need better tissue perfusion. Inotropic support is needed to augment CO and DO₂. Pharmacologic support is often the initial step. These patients also benefit from volume removal. This is usually accomplished with aggressive diuresis with a loop diuretic.

Stage D (Deteriorating) patients have failed initial treatment with single inotropic support. Hypoperfusion is not getting better and is often worsening. Lactate is staying > 2 mmol/L or rising. BNP and LFTs are also rising. These patients require additional inotropes and usually need vasopressors. Mechanical cardiac support (MCS) is often needed in addition to pharmacologic inotropic support.

Stage E (Extremis) patients have actual or impending circulatory collapse. These patients are peri-arrest with profound hypotension, lactic acidosis (often > 8 mmol/L), and unconsciousness. These patients are worsening despite multiple strategies to augment CO and DO₂. These patients will likely die without emergent veno-arterial (VA) extracorporeal membrane oxygenation (ECMO). The goal of treatment is to stabilize the patient as quickly as possible to prevent cardiac arrest.

In addition to the stage of CS, SCAI developed the three-axis model of risk stratification as a conceptual model to be used for evaluation and prognostication. Etiology and phenotype, shock severity, and risk modifiers are factors related to patient outcomes from CS. This model is a way to individualize treatment to a specific patient.

Shock severity: What is the patient’s shock stage? What are the hemodynamics and metabolic abnormalities? What are the doses of the inotropes or vasopressors? Risk goes up with higher shock stages and vasoactive agent doses and worsening metabolic disturbances or hemodynamics.

Phenotype and etiology: what is the clinical etiology of the patient’s CS? Is this acute or acute on chronic? Which ventricle is involved? Is this cardiac driven or are other organs the driving factor? Single ventricle involvement is better than bi-ventricular failure. Cardiogenic collapse due to an overdose may have a better outcome than a massive AMI.

Risk modifiers: how old is the patient? What are the comorbidities? Did the patient have a cardiac arrest? What is the patient’s mental status? Some factors are modifiable, but others are not. The concept of chronologic vs. physiologic age may come into play. A frail 40 year old with stage 4 cancer and end stage renal failure may be assessed differently than a 70 year old with mild hypertension and an AMI.

The SCAI stages of CS are a pragmatic way to assess patients with an acute presentation of CS. These stages have defined criteria and treatment recommendations for all patients. The three-axis model allows the clinician to individualize patient care based on shock severity, etiology/phenotype, and risk modification. The goal of these stages is to identify and aggressively treat patients with CS, as well as identify when treatment is failing and additional therapies may be needed.

Dr. Gaillard is Associate Professor in the Departments of Anesthesiology, Section on Critical Care; Internal Medicine, Section on Pulmonology, Critical Care, Allergy, and Immunologic Diseases; and Emergency Medicine; Wake Forest School of Medicine, Winston-Salem, N.C.

In recent months, we have seen the results of the much awaited Crystalloid Liberal or Vasopressors Early Resuscitation in Sepsis (CLOVERS) trial showing that a restrictive fluid and early vasopressor strategy initiated on arrival of patients with sepsis and hypotension in the ED did not result in decreased mortality compared with a liberal fluid approach (PETAL Network. www.nejm.org/doi/10.1056/NEJMoa2202707). The March 2023 issue of CHEST Physician provided a synopsis of the trial highlighting several limitations (Splete H. CHEST Physician. 2023;18[3]:1). Last year in 2022, the Conservative versus Liberal Approach to Fluid Therapy in Septic Shock (CLASSIC) trial also showed no difference in mortality with restrictive fluid compared with standard fluid in patients with septic shock in the ICU already receiving vasopressor therapy (Meyhoff TS, et al. N Engl J Med. 2022;386[26]:2459). Did CLOVERS and CLASSIC resolve the ongoing debate about the timing and quantity of fluid resuscitation in sepsis? Did their results suggest a “you can do what you want” approach? Is the management of sepsis and septic shock limited to fluids vs vasopressors? Hopefully, the ongoing studies ARISE FLUIDS (NCT04569942), EVIS (NCT05179499), FRESHLY (NCT05453565), 1BED (NCT05273034), and REDUCE (NCT04931485) will further address these questions.

In the meantime, I continue to admit and care for patients with sepsis in the ICU. One example was a 72-year-old woman with a history of stroke, coronary artery disease, diabetes, and chronic kidney disease presenting with 3 days of progressive cough and dyspnea. In the ED, temperature was 38.2° C, heart rate 120 beats per min, respiratory rate 28/min, blood pressure 82/48 mm Hg, and weight 92 kg. She had audible crackles in the left lower lung. Her laboratory and imaging results supported a diagnosis of sepsis due to severe community-acquired pneumonia, including the following values: white blood cell 18.2 million/mm3; lactate 3.8 mmol/L; and creatinine 4.3 mg/dL.

While in the ED, the patient received 1 liter of crystalloid fluids and appropriate broad spectrum antibiotics. Repeat lactate value was 2.8 mmol/L. Patient’s blood pressure then decreased to 85/42 mm Hg. Norepinephrine was started peripherally and titrated to 6 mcg/min to achieve blood pressure 104/56 mm Hg. No further fluid administration was given, and the patient was admitted to the medical ICU. On admission, a repeat lactate had increased to 3.4 mmol/L with blood pressure of 80/45 mm Hg. Instead of further escalating vasopressor administration, she received 2 L of fluid and continued at 150 mL/h. Shortly after, norepinephrine was titrated off. Fluid resuscitation was then deescalated. We transfered the patient to the general ward within 12 hours of ICU admission.

Could we have avoided ICU admission and critical care resource utilization if the patient had received more optimal fluid resuscitation in the ED?

While our fear of fluids (or hydrophobia) may be unwarranted, the management of this patient was a common example of fluid restriction in sepsis (Jaehne AK, et al. Crit Care Med. 2016;44[12]:2263). By clinical criteria, she was in septic shock (requiring vasopressor) and appropriately required ICU admission. But, I would posit that the patient had severe sepsis based on pre-Sepsis 3 criteria. Optimal initial fluid resuscitation would have prevented her from requiring vasopressor and progressing to septic shock with ICU admission. Unfortunately, the patient’s care reflected the objective of CLOVERS and its results. Other than the lack of decreased mortality, decreased ventilator use, decreased renal replacement therapy, and decreased hospital length of stay, restricting fluids resulted in an increase of 8.1% (95% confidence interval 3.3 to 12.8) ICU utilization. Furthermore, the data and safety monitoring committee halted the trial for futility at two-thirds of enrollment. One must wonder if CLOVERS had completed its intended enrollment of 2,320 patients, negative outcomes would have occurred.

Should an astute clinician interpret the results of the CLOVERS and CLASSIC trials as “Fluids, it doesn’t matter, so I can do what I want?” Absolutely not! The literature is abundant with studies showing that increasing dose and/or number of vasopressors is associated with higher mortality in septic shock. One example is a recent multicenter prospective cohort study examining the association of vasopressor dosing during the first 24 hours and 30-day mortality in septic shock over 33 hospitals (Roberts RJ, et al. Crit Care Med. 2020;48[10]:1445).

Six hundred and sixteen patients were enrolled with 31% 30-day mortality. In 24 hours after shock diagnosis, patients received a median of 3.4 (1.9-5.3) L of fluids and 8.5 mcg/min norepinephrine equivalent. During the first 6 hours, increasing vasopressor dosing was associated with increased odds of mortality. Every 10 mcg/min increase in norepinephrine over the 24-hour period was associated with a 33% increased odds of mortality. Patients who received no fluids but 35 mcg/min norepinephrine in 6 hours had the highest mortality of 50%. As fluid volume increased, the association between vasopressor dosing and mortality decreased, such that at least 2 L of fluid during the first 6 hours was required for this association to become nonsignificant. Based on these results and a number of past studies, we should be cautious in believing that a resuscitation strategy favoring vasopressors would result in a better outcome.

Shock resuscitation is complex, and there is no one-size-fits-all approach. With the present climate, the success of resuscitation has been simplified to assessing fluid responsiveness. Trainees learn to identify the inferior vena cava and lung B-lines by ultrasound. With more advanced technology, stroke volume variation is considered. And, let us not forget the passive leg raise. Rarely can our fellows and residents recite the components of oxygen delivery as targets of shock resuscitation: preload, afterload, contractility, hemoglobin, and oxygen saturation. Another patient example comes to mind when fluid responsiveness alone is inadequate.

Our patient was a 46-year-old man now day 4 in the ICU with Klebsiella bacteremia and acute cholecystitis undergoing medical management. His comorbidities included diabetes, obesity, hypertension, and cardiomyopathy with ejection fraction 35%. He was supported sson mechanical ventilation, norepinephrine 20 mcg/min, and receiving appropriate antibiotics. For hemodynamic monitoring, a central venous and arterial catheter have been placed. The patient had a heart rate 92 beats per min, mean arterial pressure (MAP) 57 mm Hg, central venous pressure (CVP) 26 mm Hg, stroke volume variation (SVV) 9%, cardiac output (CO) 2.5 L/min, and central venous oxygen saturation (ScvO₂) 42%.

Based on these parameters, we initiated dobutamine at 2.5 mcg/kg/min, which was then titrated to 20 mcg/kg/min over 2 hours to achieve ScvO₂ 72%. Interestingly, CVP had decreased to 18 mm Hg, SVV increased to 16%, with CO 4.5 L/min. MAP also increased to 68 mm Hg. We then administered 1-L fluid bolus with the elevated SVV. Given the patient’s underlying cardiomyopathy, CVP < 20 mm Hg appeared to indicate a state of fluid responsiveness. After our fluid administration, heart rate 98 beats per min, MAP 70 mm Hg, CVP increased to 21 mm Hg, SVV 12%, CO 4.7 L/min, and ScvO₂ 74%. In acknowledging a mixed hypovolemic, cardiogenic, and septic shock, we had optimized his hemodynamic state. Importantly, during this exercise of hemodynamic manipulation, we were able to decrease norepinephrine to 8 mcg/min, maintaining dobutamine at 20 mcg/kg/min.

The above case illustrates that the hemodynamic perturbations in sepsis and septic shock are not simple. Patients do not present with a single shock state. An infection progressing to shock often is confounded by hypovolemia and underlying comorbidities, such as cardiac dysfunction. Without considering the complex physiology, our desire to continue the debate of fluids vs vasopressors is on the brink of taking us back several decades when the management of sepsis was to start a fluid bolus, administer “Rocephin,” and initiate dopamine. But I remind myself that we have made advances – now it’s 1 L lactated Ringer’s, administer “vanco and zosyn,” and initiate norepinephrine.

In recent months, we have seen the results of the much awaited Crystalloid Liberal or Vasopressors Early Resuscitation in Sepsis (CLOVERS) trial showing that a restrictive fluid and early vasopressor strategy initiated on arrival of patients with sepsis and hypotension in the ED did not result in decreased mortality compared with a liberal fluid approach (PETAL Network. www.nejm.org/doi/10.1056/NEJMoa2202707). The March 2023 issue of CHEST Physician provided a synopsis of the trial highlighting several limitations (Splete H. CHEST Physician. 2023;18[3]:1). Last year in 2022, the Conservative versus Liberal Approach to Fluid Therapy in Septic Shock (CLASSIC) trial also showed no difference in mortality with restrictive fluid compared with standard fluid in patients with septic shock in the ICU already receiving vasopressor therapy (Meyhoff TS, et al. N Engl J Med. 2022;386[26]:2459). Did CLOVERS and CLASSIC resolve the ongoing debate about the timing and quantity of fluid resuscitation in sepsis? Did their results suggest a “you can do what you want” approach? Is the management of sepsis and septic shock limited to fluids vs vasopressors? Hopefully, the ongoing studies ARISE FLUIDS (NCT04569942), EVIS (NCT05179499), FRESHLY (NCT05453565), 1BED (NCT05273034), and REDUCE (NCT04931485) will further address these questions.

In the meantime, I continue to admit and care for patients with sepsis in the ICU. One example was a 72-year-old woman with a history of stroke, coronary artery disease, diabetes, and chronic kidney disease presenting with 3 days of progressive cough and dyspnea. In the ED, temperature was 38.2° C, heart rate 120 beats per min, respiratory rate 28/min, blood pressure 82/48 mm Hg, and weight 92 kg. She had audible crackles in the left lower lung. Her laboratory and imaging results supported a diagnosis of sepsis due to severe community-acquired pneumonia, including the following values: white blood cell 18.2 million/mm3; lactate 3.8 mmol/L; and creatinine 4.3 mg/dL.

While in the ED, the patient received 1 liter of crystalloid fluids and appropriate broad spectrum antibiotics. Repeat lactate value was 2.8 mmol/L. Patient’s blood pressure then decreased to 85/42 mm Hg. Norepinephrine was started peripherally and titrated to 6 mcg/min to achieve blood pressure 104/56 mm Hg. No further fluid administration was given, and the patient was admitted to the medical ICU. On admission, a repeat lactate had increased to 3.4 mmol/L with blood pressure of 80/45 mm Hg. Instead of further escalating vasopressor administration, she received 2 L of fluid and continued at 150 mL/h. Shortly after, norepinephrine was titrated off. Fluid resuscitation was then deescalated. We transfered the patient to the general ward within 12 hours of ICU admission.

Could we have avoided ICU admission and critical care resource utilization if the patient had received more optimal fluid resuscitation in the ED?

While our fear of fluids (or hydrophobia) may be unwarranted, the management of this patient was a common example of fluid restriction in sepsis (Jaehne AK, et al. Crit Care Med. 2016;44[12]:2263). By clinical criteria, she was in septic shock (requiring vasopressor) and appropriately required ICU admission. But, I would posit that the patient had severe sepsis based on pre-Sepsis 3 criteria. Optimal initial fluid resuscitation would have prevented her from requiring vasopressor and progressing to septic shock with ICU admission. Unfortunately, the patient’s care reflected the objective of CLOVERS and its results. Other than the lack of decreased mortality, decreased ventilator use, decreased renal replacement therapy, and decreased hospital length of stay, restricting fluids resulted in an increase of 8.1% (95% confidence interval 3.3 to 12.8) ICU utilization. Furthermore, the data and safety monitoring committee halted the trial for futility at two-thirds of enrollment. One must wonder if CLOVERS had completed its intended enrollment of 2,320 patients, negative outcomes would have occurred.

Should an astute clinician interpret the results of the CLOVERS and CLASSIC trials as “Fluids, it doesn’t matter, so I can do what I want?” Absolutely not! The literature is abundant with studies showing that increasing dose and/or number of vasopressors is associated with higher mortality in septic shock. One example is a recent multicenter prospective cohort study examining the association of vasopressor dosing during the first 24 hours and 30-day mortality in septic shock over 33 hospitals (Roberts RJ, et al. Crit Care Med. 2020;48[10]:1445).

Six hundred and sixteen patients were enrolled with 31% 30-day mortality. In 24 hours after shock diagnosis, patients received a median of 3.4 (1.9-5.3) L of fluids and 8.5 mcg/min norepinephrine equivalent. During the first 6 hours, increasing vasopressor dosing was associated with increased odds of mortality. Every 10 mcg/min increase in norepinephrine over the 24-hour period was associated with a 33% increased odds of mortality. Patients who received no fluids but 35 mcg/min norepinephrine in 6 hours had the highest mortality of 50%. As fluid volume increased, the association between vasopressor dosing and mortality decreased, such that at least 2 L of fluid during the first 6 hours was required for this association to become nonsignificant. Based on these results and a number of past studies, we should be cautious in believing that a resuscitation strategy favoring vasopressors would result in a better outcome.

Shock resuscitation is complex, and there is no one-size-fits-all approach. With the present climate, the success of resuscitation has been simplified to assessing fluid responsiveness. Trainees learn to identify the inferior vena cava and lung B-lines by ultrasound. With more advanced technology, stroke volume variation is considered. And, let us not forget the passive leg raise. Rarely can our fellows and residents recite the components of oxygen delivery as targets of shock resuscitation: preload, afterload, contractility, hemoglobin, and oxygen saturation. Another patient example comes to mind when fluid responsiveness alone is inadequate.

Our patient was a 46-year-old man now day 4 in the ICU with Klebsiella bacteremia and acute cholecystitis undergoing medical management. His comorbidities included diabetes, obesity, hypertension, and cardiomyopathy with ejection fraction 35%. He was supported sson mechanical ventilation, norepinephrine 20 mcg/min, and receiving appropriate antibiotics. For hemodynamic monitoring, a central venous and arterial catheter have been placed. The patient had a heart rate 92 beats per min, mean arterial pressure (MAP) 57 mm Hg, central venous pressure (CVP) 26 mm Hg, stroke volume variation (SVV) 9%, cardiac output (CO) 2.5 L/min, and central venous oxygen saturation (ScvO₂) 42%.

Based on these parameters, we initiated dobutamine at 2.5 mcg/kg/min, which was then titrated to 20 mcg/kg/min over 2 hours to achieve ScvO₂ 72%. Interestingly, CVP had decreased to 18 mm Hg, SVV increased to 16%, with CO 4.5 L/min. MAP also increased to 68 mm Hg. We then administered 1-L fluid bolus with the elevated SVV. Given the patient’s underlying cardiomyopathy, CVP < 20 mm Hg appeared to indicate a state of fluid responsiveness. After our fluid administration, heart rate 98 beats per min, MAP 70 mm Hg, CVP increased to 21 mm Hg, SVV 12%, CO 4.7 L/min, and ScvO₂ 74%. In acknowledging a mixed hypovolemic, cardiogenic, and septic shock, we had optimized his hemodynamic state. Importantly, during this exercise of hemodynamic manipulation, we were able to decrease norepinephrine to 8 mcg/min, maintaining dobutamine at 20 mcg/kg/min.

The above case illustrates that the hemodynamic perturbations in sepsis and septic shock are not simple. Patients do not present with a single shock state. An infection progressing to shock often is confounded by hypovolemia and underlying comorbidities, such as cardiac dysfunction. Without considering the complex physiology, our desire to continue the debate of fluids vs vasopressors is on the brink of taking us back several decades when the management of sepsis was to start a fluid bolus, administer “Rocephin,” and initiate dopamine. But I remind myself that we have made advances – now it’s 1 L lactated Ringer’s, administer “vanco and zosyn,” and initiate norepinephrine.

In recent months, we have seen the results of the much awaited Crystalloid Liberal or Vasopressors Early Resuscitation in Sepsis (CLOVERS) trial showing that a restrictive fluid and early vasopressor strategy initiated on arrival of patients with sepsis and hypotension in the ED did not result in decreased mortality compared with a liberal fluid approach (PETAL Network. www.nejm.org/doi/10.1056/NEJMoa2202707). The March 2023 issue of CHEST Physician provided a synopsis of the trial highlighting several limitations (Splete H. CHEST Physician. 2023;18[3]:1). Last year in 2022, the Conservative versus Liberal Approach to Fluid Therapy in Septic Shock (CLASSIC) trial also showed no difference in mortality with restrictive fluid compared with standard fluid in patients with septic shock in the ICU already receiving vasopressor therapy (Meyhoff TS, et al. N Engl J Med. 2022;386[26]:2459). Did CLOVERS and CLASSIC resolve the ongoing debate about the timing and quantity of fluid resuscitation in sepsis? Did their results suggest a “you can do what you want” approach? Is the management of sepsis and septic shock limited to fluids vs vasopressors? Hopefully, the ongoing studies ARISE FLUIDS (NCT04569942), EVIS (NCT05179499), FRESHLY (NCT05453565), 1BED (NCT05273034), and REDUCE (NCT04931485) will further address these questions.

In the meantime, I continue to admit and care for patients with sepsis in the ICU. One example was a 72-year-old woman with a history of stroke, coronary artery disease, diabetes, and chronic kidney disease presenting with 3 days of progressive cough and dyspnea. In the ED, temperature was 38.2° C, heart rate 120 beats per min, respiratory rate 28/min, blood pressure 82/48 mm Hg, and weight 92 kg. She had audible crackles in the left lower lung. Her laboratory and imaging results supported a diagnosis of sepsis due to severe community-acquired pneumonia, including the following values: white blood cell 18.2 million/mm3; lactate 3.8 mmol/L; and creatinine 4.3 mg/dL.

While in the ED, the patient received 1 liter of crystalloid fluids and appropriate broad spectrum antibiotics. Repeat lactate value was 2.8 mmol/L. Patient’s blood pressure then decreased to 85/42 mm Hg. Norepinephrine was started peripherally and titrated to 6 mcg/min to achieve blood pressure 104/56 mm Hg. No further fluid administration was given, and the patient was admitted to the medical ICU. On admission, a repeat lactate had increased to 3.4 mmol/L with blood pressure of 80/45 mm Hg. Instead of further escalating vasopressor administration, she received 2 L of fluid and continued at 150 mL/h. Shortly after, norepinephrine was titrated off. Fluid resuscitation was then deescalated. We transfered the patient to the general ward within 12 hours of ICU admission.

Could we have avoided ICU admission and critical care resource utilization if the patient had received more optimal fluid resuscitation in the ED?

While our fear of fluids (or hydrophobia) may be unwarranted, the management of this patient was a common example of fluid restriction in sepsis (Jaehne AK, et al. Crit Care Med. 2016;44[12]:2263). By clinical criteria, she was in septic shock (requiring vasopressor) and appropriately required ICU admission. But, I would posit that the patient had severe sepsis based on pre-Sepsis 3 criteria. Optimal initial fluid resuscitation would have prevented her from requiring vasopressor and progressing to septic shock with ICU admission. Unfortunately, the patient’s care reflected the objective of CLOVERS and its results. Other than the lack of decreased mortality, decreased ventilator use, decreased renal replacement therapy, and decreased hospital length of stay, restricting fluids resulted in an increase of 8.1% (95% confidence interval 3.3 to 12.8) ICU utilization. Furthermore, the data and safety monitoring committee halted the trial for futility at two-thirds of enrollment. One must wonder if CLOVERS had completed its intended enrollment of 2,320 patients, negative outcomes would have occurred.

Should an astute clinician interpret the results of the CLOVERS and CLASSIC trials as “Fluids, it doesn’t matter, so I can do what I want?” Absolutely not! The literature is abundant with studies showing that increasing dose and/or number of vasopressors is associated with higher mortality in septic shock. One example is a recent multicenter prospective cohort study examining the association of vasopressor dosing during the first 24 hours and 30-day mortality in septic shock over 33 hospitals (Roberts RJ, et al. Crit Care Med. 2020;48[10]:1445).

Six hundred and sixteen patients were enrolled with 31% 30-day mortality. In 24 hours after shock diagnosis, patients received a median of 3.4 (1.9-5.3) L of fluids and 8.5 mcg/min norepinephrine equivalent. During the first 6 hours, increasing vasopressor dosing was associated with increased odds of mortality. Every 10 mcg/min increase in norepinephrine over the 24-hour period was associated with a 33% increased odds of mortality. Patients who received no fluids but 35 mcg/min norepinephrine in 6 hours had the highest mortality of 50%. As fluid volume increased, the association between vasopressor dosing and mortality decreased, such that at least 2 L of fluid during the first 6 hours was required for this association to become nonsignificant. Based on these results and a number of past studies, we should be cautious in believing that a resuscitation strategy favoring vasopressors would result in a better outcome.

Shock resuscitation is complex, and there is no one-size-fits-all approach. With the present climate, the success of resuscitation has been simplified to assessing fluid responsiveness. Trainees learn to identify the inferior vena cava and lung B-lines by ultrasound. With more advanced technology, stroke volume variation is considered. And, let us not forget the passive leg raise. Rarely can our fellows and residents recite the components of oxygen delivery as targets of shock resuscitation: preload, afterload, contractility, hemoglobin, and oxygen saturation. Another patient example comes to mind when fluid responsiveness alone is inadequate.

Our patient was a 46-year-old man now day 4 in the ICU with Klebsiella bacteremia and acute cholecystitis undergoing medical management. His comorbidities included diabetes, obesity, hypertension, and cardiomyopathy with ejection fraction 35%. He was supported sson mechanical ventilation, norepinephrine 20 mcg/min, and receiving appropriate antibiotics. For hemodynamic monitoring, a central venous and arterial catheter have been placed. The patient had a heart rate 92 beats per min, mean arterial pressure (MAP) 57 mm Hg, central venous pressure (CVP) 26 mm Hg, stroke volume variation (SVV) 9%, cardiac output (CO) 2.5 L/min, and central venous oxygen saturation (ScvO₂) 42%.

Based on these parameters, we initiated dobutamine at 2.5 mcg/kg/min, which was then titrated to 20 mcg/kg/min over 2 hours to achieve ScvO₂ 72%. Interestingly, CVP had decreased to 18 mm Hg, SVV increased to 16%, with CO 4.5 L/min. MAP also increased to 68 mm Hg. We then administered 1-L fluid bolus with the elevated SVV. Given the patient’s underlying cardiomyopathy, CVP < 20 mm Hg appeared to indicate a state of fluid responsiveness. After our fluid administration, heart rate 98 beats per min, MAP 70 mm Hg, CVP increased to 21 mm Hg, SVV 12%, CO 4.7 L/min, and ScvO₂ 74%. In acknowledging a mixed hypovolemic, cardiogenic, and septic shock, we had optimized his hemodynamic state. Importantly, during this exercise of hemodynamic manipulation, we were able to decrease norepinephrine to 8 mcg/min, maintaining dobutamine at 20 mcg/kg/min.

The above case illustrates that the hemodynamic perturbations in sepsis and septic shock are not simple. Patients do not present with a single shock state. An infection progressing to shock often is confounded by hypovolemia and underlying comorbidities, such as cardiac dysfunction. Without considering the complex physiology, our desire to continue the debate of fluids vs vasopressors is on the brink of taking us back several decades when the management of sepsis was to start a fluid bolus, administer “Rocephin,” and initiate dopamine. But I remind myself that we have made advances – now it’s 1 L lactated Ringer’s, administer “vanco and zosyn,” and initiate norepinephrine.

The overnight shift in the MCU began as it does for many intensivists, by hearing about ED admissions, transfers from outside hospitals, sick floor patients, and high-risk patients in the MICU. Earlier in the day, the MICU team had admitted a 39-year-old woman with a severe asthma attack that required endotracheal intubation and mechanical ventilation in the ED for hypercarbic respiratory failure. After intubation, she had no audible air movement on chest exam, severe hypercarbic respiratory acidosis determined by an arterial blood gas, a clear chest radiograph, and negative findings on a respiratory viral panel. Her family said that she had run out of her steroid inhaler a month earlier and could not afford a refill. She had been using increasing amounts of albuterol over the past week before developing severe shortness of breath on the day of admission. The ED and MICU teams aggressively treated her with high-dose inhaled albuterol, ipratropium, and IV magnesium sulfate for bronchodilation; methylprednisolone for airway inflammation; and continuous ketamine for sedation, analgesia, and bronchodilation (Rehder KJ, et al. Respir Care. 2017;62[6]:849). Her airway pressures continued to be high despite using lung protective ventilation, so she was shifted to a permissive hypercapnia ventilation strategy using neuromuscular blockade, deep sedation, and low minute-ventilation (Laher AE, et al. J Intensive Care Med. 2018;33[9]:491).

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Two hours into the shift, the bedside nurse noted that the patient had become hypotensive. Her ventilator pressures remained stable with peak inspiratory pressures of 38-42 cm H₂O, plateau pressures of 28-30 cm H₂O, auto-positive end-expiratory pressure (auto-PEEP) of 10-12 cm H₂O, and fractional inspiratory oxygen (FiO₂) of 40%. A repeat chest radiograph showed no signs of barotrauma, but arterial blood gas values showed severe respiratory acidosis with a pH of 7.05 and a PCO₂ > 100 mm Hg. Her condition stabilized when she received a continuous infusion of bicarbonate to control her acidosis and low-dose IV norepinephrine for blood pressure control. It was at that moment that the bedside nurse astutely asked whether we should consider starting ECMO for the patient, as coauthor Dr. Arun Kannappan had done for a similar patient with asthma a month earlier. Dr. Vandivier notes, “My first response was that ECMO was not needed, because our patient had stabilized, and I had taken care of many patients like this in the past. But as I considered the situation more carefully, it was clear that any further decompensation could put our patient’s life at risk by not leaving enough time to start ECMO in a controlled setting. In short, my ‘traditional’ approach left little room for error in a patient with high ventilator pressures and hemodynamic instability.”

Kannappan_Anum_web.jpg

ECMO is a technique used to add oxygen or remove CO₂ from the blood of people with different forms of respiratory failure (Fan E, et al. Intensive Care Med. 2016;2:712) that was first used by Hill and colleagues in 1966 for trauma-induced ARDS (Hill JD, et al. N Engl J Med. 1972;286:629). The ECMO circuit pumps blood from the venous system into an oxygenator that adds oxygen and removes CO₂ before blood is returned to either the venous or arterial circulation (Intensive Care Med. 2016;42:712). Venovenous ECMO (vvECMO) is used in clinical scenarios where only oxygenation and/or CO₂ removal is needed, whereas venoarterial ECMO (vaECMO) is reserved for situations where additional hemodynamic support is necessary. ECMO is traditionally thought of as a means to increase blood oxygenation, but it is less widely appreciated that ECMO is particularly effective at removing blood CO₂. In addition to ECMO helping to normalize oxygenation or eliminate CO₂, it can also be used to lower tidal volumes, decrease airway pressures, and allow “lungs to rest” with the goal of avoiding ventilator-induced lung injury (VILI).

Vandivier_William_R_web.jpg

Standing at the bedside, it seemed to the authors that it was the right time to think about instituting a salvage therapy. But was there evidence that ECMO could improve survival? Were there clear guidelines for when to initiate ECMO, and was ECMO more effective than other salvage therapies such as inhaled volatile anesthetics?

Since McDonnell and colleagues first described the use of ECMO for a severe asthma exacerbation in 1981 (Ann Thoracic Surg. 1981;31[2]:171), about 95 articles have been published. Other than two registry studies and a recent epidemiologic study, all of these publications were case reports, case series, and reviews. Mikkelsen and colleagues (ASAIO J. 2009;55[1]:47) performed a retrospective, cohort study using the International Extracorporeal Life Support (ECLS) Organization Registry to determine whether ECMO use for status asthmaticus was associated with greater survival than the use of ECMO for other causes of respiratory failure. From 1986 through 2006, a total of 2,127 cases of respiratory failure were identified that required ECMO, including 27 for status asthmaticus and 1,233 for other causes. Their analysis showed that 83.3% of asthmatics treated with ECMO survived to hospital discharge, compared with 50.8% of people treated with ECMO for respiratory failure not due to asthma, with an odds ratio (OR) of 4.86 favoring survival of asthmatics (OR = 4.86; 95% CI, 1.65-14.31, P = .004).

Yeo and colleagues (Yeo HJ, et al. Critical Care. 2017;21:297) also used the ECLS Organization Registry to measure survival to hospital discharge, complications, and clinical factors associated with in-hospital mortality for asthmatics treated with ECMO. They included 272 people treated with ECMO for asthma between 1992 and 2016, after excluding people treated with ECMO for cardiopulmonary resuscitation or cardiac dysfunction. ECMO was associated with improvements in ventilator mechanics, including a reduction in respiratory rate, FiO₂, peak inspiratory pressure, mean airway pressure, and driving pressure. Use of ECMO for status asthmaticus was also associated with an 83.5% survival to hospital discharge, similar to the study by Mikkelsen and colleagues. Hemorrhage, the most common complication, occurred in roughly a quarter of people treated with ECMO. In the multivariate analysis, age, bleeding, pre-ECMO PEEP, post-ECMO FiO₂, and driving pressure were all associated with higher in-hospital mortality.

Although there are no formal criteria to guide use of ECMO for asthma exacerbations with respiratory failure, a number of physicians and a physician organization have recommended that ECMO be considered for persistently high ventilator pressures, uncontrolled respiratory acidosis, or hemodynamic instability. Because our patient qualified for ECMO based on all three suggested criteria, we consulted cardiac surgery who quickly started her on vvECMO. She remained on ECMO for 4 days until she was decannulated, extubated, and discharged home.

Despite this positive outcome, the lack of a high-quality, controlled study to help guide our decision was surprising given the ability of ECMO to efficiently remove CO₂ and to decrease ventilator pressures. The lack of guidance prompted us to perform a retrospective, epidemiologic cohort study to determine whether treatment with ECMO for asthma exacerbations with respiratory failure was associated with reduced mortality, compared with people treated without ECMO (Zakrajsek JK, Chest. 2023;163[1]:38). The study included 13,714 people admitted to an ECMO-capable hospital with respiratory failure that required invasive ventilation because of an asthma exacerbation between 2010 and 2020, of which 127 were treated with ECMO and 13,587 were not. During this period, use of ECMO as a salvage therapy for severe asthma exacerbations was a rare event, but it became more common over time. With the limitation that 40% of asthma patients were transferred from an outside hospital, 74% were started on ECMO in the first 2 hospital days, and 94% were started within the first week of hospitalization. Once started, ECMO was continued for a median of 1.0 day and range of 1-49 days. Hospital mortality was 14.6% in the ECMO group versus 26.2% in the no ECMO group, which equated to an 11.6% absolute risk reduction (P = 0.03) and 52% relative risk reduction (P = 0.04) in mortality. ECMO was associated with hospital costs that were $114,000 higher per patient, compared with the no ECMO group, but did not affect intensive care unit length of stay, hospital length of stay, or time on invasive mechanical ventilation.

We were pleased that our patient had a good outcome, and were reassured by our study results. But we were left to wonder whether ECMO really was the best salvage therapy for asthma exacerbations with respiratory failure, and if it was initiated for the right indications at the best time. These are important treatment considerations that take on new urgency given that physicians are increasingly looking to ECMO as a salvage therapy for refractory asthma, and the recent FDA approval of low-flow, extracorporeal CO₂ removal systems that could make CO₂ removal a more available, and perhaps less expensive, strategy. Despite promising epidemiological data, it will be important that these questions are answered with well-designed clinical trials so that physicians can be armed with the knowledge needed to navigate complex clinical scenarios, and ultimately to prevent unfortunate deaths from a reversible disease.

The overnight shift in the MCU began as it does for many intensivists, by hearing about ED admissions, transfers from outside hospitals, sick floor patients, and high-risk patients in the MICU. Earlier in the day, the MICU team had admitted a 39-year-old woman with a severe asthma attack that required endotracheal intubation and mechanical ventilation in the ED for hypercarbic respiratory failure. After intubation, she had no audible air movement on chest exam, severe hypercarbic respiratory acidosis determined by an arterial blood gas, a clear chest radiograph, and negative findings on a respiratory viral panel. Her family said that she had run out of her steroid inhaler a month earlier and could not afford a refill. She had been using increasing amounts of albuterol over the past week before developing severe shortness of breath on the day of admission. The ED and MICU teams aggressively treated her with high-dose inhaled albuterol, ipratropium, and IV magnesium sulfate for bronchodilation; methylprednisolone for airway inflammation; and continuous ketamine for sedation, analgesia, and bronchodilation (Rehder KJ, et al. Respir Care. 2017;62[6]:849). Her airway pressures continued to be high despite using lung protective ventilation, so she was shifted to a permissive hypercapnia ventilation strategy using neuromuscular blockade, deep sedation, and low minute-ventilation (Laher AE, et al. J Intensive Care Med. 2018;33[9]:491).

Zakrajsek_Jonathan_web.jpg

Two hours into the shift, the bedside nurse noted that the patient had become hypotensive. Her ventilator pressures remained stable with peak inspiratory pressures of 38-42 cm H₂O, plateau pressures of 28-30 cm H₂O, auto-positive end-expiratory pressure (auto-PEEP) of 10-12 cm H₂O, and fractional inspiratory oxygen (FiO₂) of 40%. A repeat chest radiograph showed no signs of barotrauma, but arterial blood gas values showed severe respiratory acidosis with a pH of 7.05 and a PCO₂ > 100 mm Hg. Her condition stabilized when she received a continuous infusion of bicarbonate to control her acidosis and low-dose IV norepinephrine for blood pressure control. It was at that moment that the bedside nurse astutely asked whether we should consider starting ECMO for the patient, as coauthor Dr. Arun Kannappan had done for a similar patient with asthma a month earlier. Dr. Vandivier notes, “My first response was that ECMO was not needed, because our patient had stabilized, and I had taken care of many patients like this in the past. But as I considered the situation more carefully, it was clear that any further decompensation could put our patient’s life at risk by not leaving enough time to start ECMO in a controlled setting. In short, my ‘traditional’ approach left little room for error in a patient with high ventilator pressures and hemodynamic instability.”

Kannappan_Anum_web.jpg

ECMO is a technique used to add oxygen or remove CO₂ from the blood of people with different forms of respiratory failure (Fan E, et al. Intensive Care Med. 2016;2:712) that was first used by Hill and colleagues in 1966 for trauma-induced ARDS (Hill JD, et al. N Engl J Med. 1972;286:629). The ECMO circuit pumps blood from the venous system into an oxygenator that adds oxygen and removes CO₂ before blood is returned to either the venous or arterial circulation (Intensive Care Med. 2016;42:712). Venovenous ECMO (vvECMO) is used in clinical scenarios where only oxygenation and/or CO₂ removal is needed, whereas venoarterial ECMO (vaECMO) is reserved for situations where additional hemodynamic support is necessary. ECMO is traditionally thought of as a means to increase blood oxygenation, but it is less widely appreciated that ECMO is particularly effective at removing blood CO₂. In addition to ECMO helping to normalize oxygenation or eliminate CO₂, it can also be used to lower tidal volumes, decrease airway pressures, and allow “lungs to rest” with the goal of avoiding ventilator-induced lung injury (VILI).

Vandivier_William_R_web.jpg

Standing at the bedside, it seemed to the authors that it was the right time to think about instituting a salvage therapy. But was there evidence that ECMO could improve survival? Were there clear guidelines for when to initiate ECMO, and was ECMO more effective than other salvage therapies such as inhaled volatile anesthetics?

Since McDonnell and colleagues first described the use of ECMO for a severe asthma exacerbation in 1981 (Ann Thoracic Surg. 1981;31[2]:171), about 95 articles have been published. Other than two registry studies and a recent epidemiologic study, all of these publications were case reports, case series, and reviews. Mikkelsen and colleagues (ASAIO J. 2009;55[1]:47) performed a retrospective, cohort study using the International Extracorporeal Life Support (ECLS) Organization Registry to determine whether ECMO use for status asthmaticus was associated with greater survival than the use of ECMO for other causes of respiratory failure. From 1986 through 2006, a total of 2,127 cases of respiratory failure were identified that required ECMO, including 27 for status asthmaticus and 1,233 for other causes. Their analysis showed that 83.3% of asthmatics treated with ECMO survived to hospital discharge, compared with 50.8% of people treated with ECMO for respiratory failure not due to asthma, with an odds ratio (OR) of 4.86 favoring survival of asthmatics (OR = 4.86; 95% CI, 1.65-14.31, P = .004).

Yeo and colleagues (Yeo HJ, et al. Critical Care. 2017;21:297) also used the ECLS Organization Registry to measure survival to hospital discharge, complications, and clinical factors associated with in-hospital mortality for asthmatics treated with ECMO. They included 272 people treated with ECMO for asthma between 1992 and 2016, after excluding people treated with ECMO for cardiopulmonary resuscitation or cardiac dysfunction. ECMO was associated with improvements in ventilator mechanics, including a reduction in respiratory rate, FiO₂, peak inspiratory pressure, mean airway pressure, and driving pressure. Use of ECMO for status asthmaticus was also associated with an 83.5% survival to hospital discharge, similar to the study by Mikkelsen and colleagues. Hemorrhage, the most common complication, occurred in roughly a quarter of people treated with ECMO. In the multivariate analysis, age, bleeding, pre-ECMO PEEP, post-ECMO FiO₂, and driving pressure were all associated with higher in-hospital mortality.

Although there are no formal criteria to guide use of ECMO for asthma exacerbations with respiratory failure, a number of physicians and a physician organization have recommended that ECMO be considered for persistently high ventilator pressures, uncontrolled respiratory acidosis, or hemodynamic instability. Because our patient qualified for ECMO based on all three suggested criteria, we consulted cardiac surgery who quickly started her on vvECMO. She remained on ECMO for 4 days until she was decannulated, extubated, and discharged home.

Despite this positive outcome, the lack of a high-quality, controlled study to help guide our decision was surprising given the ability of ECMO to efficiently remove CO₂ and to decrease ventilator pressures. The lack of guidance prompted us to perform a retrospective, epidemiologic cohort study to determine whether treatment with ECMO for asthma exacerbations with respiratory failure was associated with reduced mortality, compared with people treated without ECMO (Zakrajsek JK, Chest. 2023;163[1]:38). The study included 13,714 people admitted to an ECMO-capable hospital with respiratory failure that required invasive ventilation because of an asthma exacerbation between 2010 and 2020, of which 127 were treated with ECMO and 13,587 were not. During this period, use of ECMO as a salvage therapy for severe asthma exacerbations was a rare event, but it became more common over time. With the limitation that 40% of asthma patients were transferred from an outside hospital, 74% were started on ECMO in the first 2 hospital days, and 94% were started within the first week of hospitalization. Once started, ECMO was continued for a median of 1.0 day and range of 1-49 days. Hospital mortality was 14.6% in the ECMO group versus 26.2% in the no ECMO group, which equated to an 11.6% absolute risk reduction (P = 0.03) and 52% relative risk reduction (P = 0.04) in mortality. ECMO was associated with hospital costs that were $114,000 higher per patient, compared with the no ECMO group, but did not affect intensive care unit length of stay, hospital length of stay, or time on invasive mechanical ventilation.

We were pleased that our patient had a good outcome, and were reassured by our study results. But we were left to wonder whether ECMO really was the best salvage therapy for asthma exacerbations with respiratory failure, and if it was initiated for the right indications at the best time. These are important treatment considerations that take on new urgency given that physicians are increasingly looking to ECMO as a salvage therapy for refractory asthma, and the recent FDA approval of low-flow, extracorporeal CO₂ removal systems that could make CO₂ removal a more available, and perhaps less expensive, strategy. Despite promising epidemiological data, it will be important that these questions are answered with well-designed clinical trials so that physicians can be armed with the knowledge needed to navigate complex clinical scenarios, and ultimately to prevent unfortunate deaths from a reversible disease.

The overnight shift in the MCU began as it does for many intensivists, by hearing about ED admissions, transfers from outside hospitals, sick floor patients, and high-risk patients in the MICU. Earlier in the day, the MICU team had admitted a 39-year-old woman with a severe asthma attack that required endotracheal intubation and mechanical ventilation in the ED for hypercarbic respiratory failure. After intubation, she had no audible air movement on chest exam, severe hypercarbic respiratory acidosis determined by an arterial blood gas, a clear chest radiograph, and negative findings on a respiratory viral panel. Her family said that she had run out of her steroid inhaler a month earlier and could not afford a refill. She had been using increasing amounts of albuterol over the past week before developing severe shortness of breath on the day of admission. The ED and MICU teams aggressively treated her with high-dose inhaled albuterol, ipratropium, and IV magnesium sulfate for bronchodilation; methylprednisolone for airway inflammation; and continuous ketamine for sedation, analgesia, and bronchodilation (Rehder KJ, et al. Respir Care. 2017;62[6]:849). Her airway pressures continued to be high despite using lung protective ventilation, so she was shifted to a permissive hypercapnia ventilation strategy using neuromuscular blockade, deep sedation, and low minute-ventilation (Laher AE, et al. J Intensive Care Med. 2018;33[9]:491).

Zakrajsek_Jonathan_web.jpg

Two hours into the shift, the bedside nurse noted that the patient had become hypotensive. Her ventilator pressures remained stable with peak inspiratory pressures of 38-42 cm H₂O, plateau pressures of 28-30 cm H₂O, auto-positive end-expiratory pressure (auto-PEEP) of 10-12 cm H₂O, and fractional inspiratory oxygen (FiO₂) of 40%. A repeat chest radiograph showed no signs of barotrauma, but arterial blood gas values showed severe respiratory acidosis with a pH of 7.05 and a PCO₂ > 100 mm Hg. Her condition stabilized when she received a continuous infusion of bicarbonate to control her acidosis and low-dose IV norepinephrine for blood pressure control. It was at that moment that the bedside nurse astutely asked whether we should consider starting ECMO for the patient, as coauthor Dr. Arun Kannappan had done for a similar patient with asthma a month earlier. Dr. Vandivier notes, “My first response was that ECMO was not needed, because our patient had stabilized, and I had taken care of many patients like this in the past. But as I considered the situation more carefully, it was clear that any further decompensation could put our patient’s life at risk by not leaving enough time to start ECMO in a controlled setting. In short, my ‘traditional’ approach left little room for error in a patient with high ventilator pressures and hemodynamic instability.”

Kannappan_Anum_web.jpg

ECMO is a technique used to add oxygen or remove CO₂ from the blood of people with different forms of respiratory failure (Fan E, et al. Intensive Care Med. 2016;2:712) that was first used by Hill and colleagues in 1966 for trauma-induced ARDS (Hill JD, et al. N Engl J Med. 1972;286:629). The ECMO circuit pumps blood from the venous system into an oxygenator that adds oxygen and removes CO₂ before blood is returned to either the venous or arterial circulation (Intensive Care Med. 2016;42:712). Venovenous ECMO (vvECMO) is used in clinical scenarios where only oxygenation and/or CO₂ removal is needed, whereas venoarterial ECMO (vaECMO) is reserved for situations where additional hemodynamic support is necessary. ECMO is traditionally thought of as a means to increase blood oxygenation, but it is less widely appreciated that ECMO is particularly effective at removing blood CO₂. In addition to ECMO helping to normalize oxygenation or eliminate CO₂, it can also be used to lower tidal volumes, decrease airway pressures, and allow “lungs to rest” with the goal of avoiding ventilator-induced lung injury (VILI).

Vandivier_William_R_web.jpg

Standing at the bedside, it seemed to the authors that it was the right time to think about instituting a salvage therapy. But was there evidence that ECMO could improve survival? Were there clear guidelines for when to initiate ECMO, and was ECMO more effective than other salvage therapies such as inhaled volatile anesthetics?

Since McDonnell and colleagues first described the use of ECMO for a severe asthma exacerbation in 1981 (Ann Thoracic Surg. 1981;31[2]:171), about 95 articles have been published. Other than two registry studies and a recent epidemiologic study, all of these publications were case reports, case series, and reviews. Mikkelsen and colleagues (ASAIO J. 2009;55[1]:47) performed a retrospective, cohort study using the International Extracorporeal Life Support (ECLS) Organization Registry to determine whether ECMO use for status asthmaticus was associated with greater survival than the use of ECMO for other causes of respiratory failure. From 1986 through 2006, a total of 2,127 cases of respiratory failure were identified that required ECMO, including 27 for status asthmaticus and 1,233 for other causes. Their analysis showed that 83.3% of asthmatics treated with ECMO survived to hospital discharge, compared with 50.8% of people treated with ECMO for respiratory failure not due to asthma, with an odds ratio (OR) of 4.86 favoring survival of asthmatics (OR = 4.86; 95% CI, 1.65-14.31, P = .004).

Yeo and colleagues (Yeo HJ, et al. Critical Care. 2017;21:297) also used the ECLS Organization Registry to measure survival to hospital discharge, complications, and clinical factors associated with in-hospital mortality for asthmatics treated with ECMO. They included 272 people treated with ECMO for asthma between 1992 and 2016, after excluding people treated with ECMO for cardiopulmonary resuscitation or cardiac dysfunction. ECMO was associated with improvements in ventilator mechanics, including a reduction in respiratory rate, FiO₂, peak inspiratory pressure, mean airway pressure, and driving pressure. Use of ECMO for status asthmaticus was also associated with an 83.5% survival to hospital discharge, similar to the study by Mikkelsen and colleagues. Hemorrhage, the most common complication, occurred in roughly a quarter of people treated with ECMO. In the multivariate analysis, age, bleeding, pre-ECMO PEEP, post-ECMO FiO₂, and driving pressure were all associated with higher in-hospital mortality.

Although there are no formal criteria to guide use of ECMO for asthma exacerbations with respiratory failure, a number of physicians and a physician organization have recommended that ECMO be considered for persistently high ventilator pressures, uncontrolled respiratory acidosis, or hemodynamic instability. Because our patient qualified for ECMO based on all three suggested criteria, we consulted cardiac surgery who quickly started her on vvECMO. She remained on ECMO for 4 days until she was decannulated, extubated, and discharged home.

Despite this positive outcome, the lack of a high-quality, controlled study to help guide our decision was surprising given the ability of ECMO to efficiently remove CO₂ and to decrease ventilator pressures. The lack of guidance prompted us to perform a retrospective, epidemiologic cohort study to determine whether treatment with ECMO for asthma exacerbations with respiratory failure was associated with reduced mortality, compared with people treated without ECMO (Zakrajsek JK, Chest. 2023;163[1]:38). The study included 13,714 people admitted to an ECMO-capable hospital with respiratory failure that required invasive ventilation because of an asthma exacerbation between 2010 and 2020, of which 127 were treated with ECMO and 13,587 were not. During this period, use of ECMO as a salvage therapy for severe asthma exacerbations was a rare event, but it became more common over time. With the limitation that 40% of asthma patients were transferred from an outside hospital, 74% were started on ECMO in the first 2 hospital days, and 94% were started within the first week of hospitalization. Once started, ECMO was continued for a median of 1.0 day and range of 1-49 days. Hospital mortality was 14.6% in the ECMO group versus 26.2% in the no ECMO group, which equated to an 11.6% absolute risk reduction (P = 0.03) and 52% relative risk reduction (P = 0.04) in mortality. ECMO was associated with hospital costs that were $114,000 higher per patient, compared with the no ECMO group, but did not affect intensive care unit length of stay, hospital length of stay, or time on invasive mechanical ventilation.

We were pleased that our patient had a good outcome, and were reassured by our study results. But we were left to wonder whether ECMO really was the best salvage therapy for asthma exacerbations with respiratory failure, and if it was initiated for the right indications at the best time. These are important treatment considerations that take on new urgency given that physicians are increasingly looking to ECMO as a salvage therapy for refractory asthma, and the recent FDA approval of low-flow, extracorporeal CO₂ removal systems that could make CO₂ removal a more available, and perhaps less expensive, strategy. Despite promising epidemiological data, it will be important that these questions are answered with well-designed clinical trials so that physicians can be armed with the knowledge needed to navigate complex clinical scenarios, and ultimately to prevent unfortunate deaths from a reversible disease.

Since the first SARS-CoV-2 (COVID-19) outbreak in Wuhan, China, in December 2019, more than 6.6 million deaths have occurred. Management strategies for patients with COVID-19 pneumonia/ARDS have continued to evolve during the pandemic. One of the strategies for those cases refractory to traditional ARDS treatments has been the use of extracorporeal membrane oxygenation (ECMO).

Before the COVID-19 pandemic, a substantial amount of data regarding the use of ECMO in ARDS was gathered during the H1N1 influenza outbreak in 2009. Mortality ranged from 8% to 65% (Zangrillo, et al. Crit Care. 2013;17[1]:R30). From these data, we learned the importance of patient selection. Young patients with few co-morbidities and less than 7 days supported by mechanical ventilation did remarkably better than elderly patients or those who had prolonged positive-pressure ventilation prior to ECMO.  

To date, the mortality rate for COVID-19 patients with ARDS requiring ECMO is 48% based on data from ELSO. Interestingly though, using May 1, 2020, as a cutoff date, mortality rates for patients with COVID-19 receiving ECMO significantly increased from 37% to 52% (Barbaro, et al. Lancet. 2021;398[10307]:1230). This escalation in mortality engendered concern that ECMO may not be useful in treating patients with COVID-19 and ARDS.

Several factors can be cited for this increase in mortality. First, many new ECMO programs launched after May 1. These new programs had a higher mortality rate (59%) compared with established programs, suggesting that program and provider experience play a significant role in patient outcomes (Barbaro, et al. Lancet. 2021;398[10307]:1230). Second, patients in the latter part of 2020 experienced much longer intervals between the onset of symptoms and time of intubation. Clinicians had a tendency to delay intubation as long as possible. Subsequently, the number of days receiving high flow nasal oxygen or noninvasive ventilation (NIV) was significantly longer (Schmidt, et al. Crit Care. 2021;25[1]:355). These data suggest that prolonged NIV on high Fio2 may be a negative prognostic indicator and should be considered when assessing a patient’s candidacy for ECMO.

Early in the pandemic, clinicians realized that average ECMO run times for patients with COVID-19 and ARDS were significantly longer, 15 vs 9 days, respectively (Jacobs, et al. Ann Thorac Surg. 2022;113[5]:1452). With such long run times, beds were slow to turn over, and a shortage of ECMO beds resulted during the height of the pandemic. In a retrospective study, Gannon looked at 90 patients, all of whom were deemed medically appropriate for ECMO. Two groups were created: (1) no capacity for ECMO vs (2) ECMO provided. Mortality rates were staggering at 89% and 43%, respectively (P =.001) (Gannon, et al. Am J Respir Crit Care Med. 2022;205[11]:1354). This study demonstrated a profound point: during a pandemic, when demand overcomes supply, there is a unique opportunity to see the effect of lifesaving therapies, such as ECMO, on outcomes. This study was particularly poignant, as the average age of the patients was 40 years old.  

It is now widely accepted that prone positioning has survival benefit in ARDS. Prone positioning while receiving ECMO has generally been avoided due to concern for potential complications associated with the cannula(s). However, it has been shown that prone positioning while receiving veno-venous (VV) -ECMO reduces mortality rates, 37% proned vs 50% supine positioning (P =.02) (Giani, et al. Ann Am Thorac Soc. 2021;18[3]:495). In this study, no major complications occurred, and minor complications occurred in 6% of the proning events. Prone positioning improves ventilation-perfusion mismatch and reduces hypoxic vasoconstriction, which is thought to be right-sided heart-protective.  

Right-sided heart dysfunction (RHD) is common in ARDS, whether COVID-19-related or not. The pathogenesis includes hypoxic vasoconstriction, pulmonary fibrosis, and ventilator-induced lung injury. Pulmonary microthrombi and patient-specific characteristics, such as obesity, are additional factors leading to RHD in patients with COVID-19. During the pandemic, several articles described using right-sided heart protective cannulation strategies for patients with COVID-19 requiring ECMO with favorable results (Mustafa, et al. JAMA Surg. 2020;155[10]:990; Cain, et al. J Surg Res. 2021;264:81-89). This right-sided heart protective strategy involves inserting a single access dual lumen cannula into the right internal jugular vein, which is advanced into the pulmonary artery, effectively bypassing the right ventricle. This setup is more typical of right ventricle assist device (RVAD), rather than typical VV-ECMO, which returns blood to the right atrium. Unfortunately, these studies did not include echocardiographic information to evaluate the effects of this intervention on RVD, and this is an area for future research. However, this vein to pulmonary artery strategy was found to facilitate decreased sedation, earlier liberation from mechanical ventilation, reduced need for tracheostomy, improved mobilization out of bed, and ease in prone positioning (Mustafa, et al. JAMA Surg. 2020;155[10]:990).

In conclusion, there is evidence to support the use of ECMO in patients with COVID-19 patients and ARDS failing conventional mechanical ventilation. The success of ECMO therapy is highly dependent on patient selection. Prolonged use of NIV on high Fio2 may be a negative predictor of ECMO survival and should be considered when assessing a patient for ECMO candidacy. Prone positioning with ECMO has been shown to have survival benefit and should be considered in all patients receiving ECMO.
 

Dr. Gaillard, Dr. Staples, and Dr. Kapoor are with the Department of Anesthesiology, Section on Critical Care, at Wake Forest School of Medicine in Winston-Salem, N.C. Dr. Gaillard is also with the Department of Emergency Medicine and Department of Internal Medicine, Section on Pulmonary, Critical Care, Allergy, and Immunology at Wake Forest School of Medicine.

Since the first SARS-CoV-2 (COVID-19) outbreak in Wuhan, China, in December 2019, more than 6.6 million deaths have occurred. Management strategies for patients with COVID-19 pneumonia/ARDS have continued to evolve during the pandemic. One of the strategies for those cases refractory to traditional ARDS treatments has been the use of extracorporeal membrane oxygenation (ECMO).

Before the COVID-19 pandemic, a substantial amount of data regarding the use of ECMO in ARDS was gathered during the H1N1 influenza outbreak in 2009. Mortality ranged from 8% to 65% (Zangrillo, et al. Crit Care. 2013;17[1]:R30). From these data, we learned the importance of patient selection. Young patients with few co-morbidities and less than 7 days supported by mechanical ventilation did remarkably better than elderly patients or those who had prolonged positive-pressure ventilation prior to ECMO.  

To date, the mortality rate for COVID-19 patients with ARDS requiring ECMO is 48% based on data from ELSO. Interestingly though, using May 1, 2020, as a cutoff date, mortality rates for patients with COVID-19 receiving ECMO significantly increased from 37% to 52% (Barbaro, et al. Lancet. 2021;398[10307]:1230). This escalation in mortality engendered concern that ECMO may not be useful in treating patients with COVID-19 and ARDS.

Several factors can be cited for this increase in mortality. First, many new ECMO programs launched after May 1. These new programs had a higher mortality rate (59%) compared with established programs, suggesting that program and provider experience play a significant role in patient outcomes (Barbaro, et al. Lancet. 2021;398[10307]:1230). Second, patients in the latter part of 2020 experienced much longer intervals between the onset of symptoms and time of intubation. Clinicians had a tendency to delay intubation as long as possible. Subsequently, the number of days receiving high flow nasal oxygen or noninvasive ventilation (NIV) was significantly longer (Schmidt, et al. Crit Care. 2021;25[1]:355). These data suggest that prolonged NIV on high Fio2 may be a negative prognostic indicator and should be considered when assessing a patient’s candidacy for ECMO.

Early in the pandemic, clinicians realized that average ECMO run times for patients with COVID-19 and ARDS were significantly longer, 15 vs 9 days, respectively (Jacobs, et al. Ann Thorac Surg. 2022;113[5]:1452). With such long run times, beds were slow to turn over, and a shortage of ECMO beds resulted during the height of the pandemic. In a retrospective study, Gannon looked at 90 patients, all of whom were deemed medically appropriate for ECMO. Two groups were created: (1) no capacity for ECMO vs (2) ECMO provided. Mortality rates were staggering at 89% and 43%, respectively (P =.001) (Gannon, et al. Am J Respir Crit Care Med. 2022;205[11]:1354). This study demonstrated a profound point: during a pandemic, when demand overcomes supply, there is a unique opportunity to see the effect of lifesaving therapies, such as ECMO, on outcomes. This study was particularly poignant, as the average age of the patients was 40 years old.  

It is now widely accepted that prone positioning has survival benefit in ARDS. Prone positioning while receiving ECMO has generally been avoided due to concern for potential complications associated with the cannula(s). However, it has been shown that prone positioning while receiving veno-venous (VV) -ECMO reduces mortality rates, 37% proned vs 50% supine positioning (P =.02) (Giani, et al. Ann Am Thorac Soc. 2021;18[3]:495). In this study, no major complications occurred, and minor complications occurred in 6% of the proning events. Prone positioning improves ventilation-perfusion mismatch and reduces hypoxic vasoconstriction, which is thought to be right-sided heart-protective.  

Right-sided heart dysfunction (RHD) is common in ARDS, whether COVID-19-related or not. The pathogenesis includes hypoxic vasoconstriction, pulmonary fibrosis, and ventilator-induced lung injury. Pulmonary microthrombi and patient-specific characteristics, such as obesity, are additional factors leading to RHD in patients with COVID-19. During the pandemic, several articles described using right-sided heart protective cannulation strategies for patients with COVID-19 requiring ECMO with favorable results (Mustafa, et al. JAMA Surg. 2020;155[10]:990; Cain, et al. J Surg Res. 2021;264:81-89). This right-sided heart protective strategy involves inserting a single access dual lumen cannula into the right internal jugular vein, which is advanced into the pulmonary artery, effectively bypassing the right ventricle. This setup is more typical of right ventricle assist device (RVAD), rather than typical VV-ECMO, which returns blood to the right atrium. Unfortunately, these studies did not include echocardiographic information to evaluate the effects of this intervention on RVD, and this is an area for future research. However, this vein to pulmonary artery strategy was found to facilitate decreased sedation, earlier liberation from mechanical ventilation, reduced need for tracheostomy, improved mobilization out of bed, and ease in prone positioning (Mustafa, et al. JAMA Surg. 2020;155[10]:990).

In conclusion, there is evidence to support the use of ECMO in patients with COVID-19 patients and ARDS failing conventional mechanical ventilation. The success of ECMO therapy is highly dependent on patient selection. Prolonged use of NIV on high Fio2 may be a negative predictor of ECMO survival and should be considered when assessing a patient for ECMO candidacy. Prone positioning with ECMO has been shown to have survival benefit and should be considered in all patients receiving ECMO.
 

Dr. Gaillard, Dr. Staples, and Dr. Kapoor are with the Department of Anesthesiology, Section on Critical Care, at Wake Forest School of Medicine in Winston-Salem, N.C. Dr. Gaillard is also with the Department of Emergency Medicine and Department of Internal Medicine, Section on Pulmonary, Critical Care, Allergy, and Immunology at Wake Forest School of Medicine.

Since the first SARS-CoV-2 (COVID-19) outbreak in Wuhan, China, in December 2019, more than 6.6 million deaths have occurred. Management strategies for patients with COVID-19 pneumonia/ARDS have continued to evolve during the pandemic. One of the strategies for those cases refractory to traditional ARDS treatments has been the use of extracorporeal membrane oxygenation (ECMO).

Before the COVID-19 pandemic, a substantial amount of data regarding the use of ECMO in ARDS was gathered during the H1N1 influenza outbreak in 2009. Mortality ranged from 8% to 65% (Zangrillo, et al. Crit Care. 2013;17[1]:R30). From these data, we learned the importance of patient selection. Young patients with few co-morbidities and less than 7 days supported by mechanical ventilation did remarkably better than elderly patients or those who had prolonged positive-pressure ventilation prior to ECMO.  

To date, the mortality rate for COVID-19 patients with ARDS requiring ECMO is 48% based on data from ELSO. Interestingly though, using May 1, 2020, as a cutoff date, mortality rates for patients with COVID-19 receiving ECMO significantly increased from 37% to 52% (Barbaro, et al. Lancet. 2021;398[10307]:1230). This escalation in mortality engendered concern that ECMO may not be useful in treating patients with COVID-19 and ARDS.

Several factors can be cited for this increase in mortality. First, many new ECMO programs launched after May 1. These new programs had a higher mortality rate (59%) compared with established programs, suggesting that program and provider experience play a significant role in patient outcomes (Barbaro, et al. Lancet. 2021;398[10307]:1230). Second, patients in the latter part of 2020 experienced much longer intervals between the onset of symptoms and time of intubation. Clinicians had a tendency to delay intubation as long as possible. Subsequently, the number of days receiving high flow nasal oxygen or noninvasive ventilation (NIV) was significantly longer (Schmidt, et al. Crit Care. 2021;25[1]:355). These data suggest that prolonged NIV on high Fio2 may be a negative prognostic indicator and should be considered when assessing a patient’s candidacy for ECMO.

Early in the pandemic, clinicians realized that average ECMO run times for patients with COVID-19 and ARDS were significantly longer, 15 vs 9 days, respectively (Jacobs, et al. Ann Thorac Surg. 2022;113[5]:1452). With such long run times, beds were slow to turn over, and a shortage of ECMO beds resulted during the height of the pandemic. In a retrospective study, Gannon looked at 90 patients, all of whom were deemed medically appropriate for ECMO. Two groups were created: (1) no capacity for ECMO vs (2) ECMO provided. Mortality rates were staggering at 89% and 43%, respectively (P =.001) (Gannon, et al. Am J Respir Crit Care Med. 2022;205[11]:1354). This study demonstrated a profound point: during a pandemic, when demand overcomes supply, there is a unique opportunity to see the effect of lifesaving therapies, such as ECMO, on outcomes. This study was particularly poignant, as the average age of the patients was 40 years old.  

It is now widely accepted that prone positioning has survival benefit in ARDS. Prone positioning while receiving ECMO has generally been avoided due to concern for potential complications associated with the cannula(s). However, it has been shown that prone positioning while receiving veno-venous (VV) -ECMO reduces mortality rates, 37% proned vs 50% supine positioning (P =.02) (Giani, et al. Ann Am Thorac Soc. 2021;18[3]:495). In this study, no major complications occurred, and minor complications occurred in 6% of the proning events. Prone positioning improves ventilation-perfusion mismatch and reduces hypoxic vasoconstriction, which is thought to be right-sided heart-protective.  

Right-sided heart dysfunction (RHD) is common in ARDS, whether COVID-19-related or not. The pathogenesis includes hypoxic vasoconstriction, pulmonary fibrosis, and ventilator-induced lung injury. Pulmonary microthrombi and patient-specific characteristics, such as obesity, are additional factors leading to RHD in patients with COVID-19. During the pandemic, several articles described using right-sided heart protective cannulation strategies for patients with COVID-19 requiring ECMO with favorable results (Mustafa, et al. JAMA Surg. 2020;155[10]:990; Cain, et al. J Surg Res. 2021;264:81-89). This right-sided heart protective strategy involves inserting a single access dual lumen cannula into the right internal jugular vein, which is advanced into the pulmonary artery, effectively bypassing the right ventricle. This setup is more typical of right ventricle assist device (RVAD), rather than typical VV-ECMO, which returns blood to the right atrium. Unfortunately, these studies did not include echocardiographic information to evaluate the effects of this intervention on RVD, and this is an area for future research. However, this vein to pulmonary artery strategy was found to facilitate decreased sedation, earlier liberation from mechanical ventilation, reduced need for tracheostomy, improved mobilization out of bed, and ease in prone positioning (Mustafa, et al. JAMA Surg. 2020;155[10]:990).

In conclusion, there is evidence to support the use of ECMO in patients with COVID-19 patients and ARDS failing conventional mechanical ventilation. The success of ECMO therapy is highly dependent on patient selection. Prolonged use of NIV on high Fio2 may be a negative predictor of ECMO survival and should be considered when assessing a patient for ECMO candidacy. Prone positioning with ECMO has been shown to have survival benefit and should be considered in all patients receiving ECMO.
 

Dr. Gaillard, Dr. Staples, and Dr. Kapoor are with the Department of Anesthesiology, Section on Critical Care, at Wake Forest School of Medicine in Winston-Salem, N.C. Dr. Gaillard is also with the Department of Emergency Medicine and Department of Internal Medicine, Section on Pulmonary, Critical Care, Allergy, and Immunology at Wake Forest School of Medicine.

The COVID-19 pandemic has caused unprecedented and unpredictable strain on health care systems worldwide, forcing rapid organizational modifications and innovations to ensure availability of critical care resources during acute surge events. Yet, while much attention has been paid to the availability of ICU beds and ventilators, COVID-19 has insidiously and significantly harmed the most precious critical care resource of all – the human beings who are the lifeblood of critical care delivery. We are now at a crucial moment in history to better understand the pandemic’s impact on our human resources and enact changes to reverse the damage that it has inflicted on our workforce.

To understand the impact of the pandemic on critical care clinicians, we must first acknowledge the context in which they work. ICUs, where critical care delivery predominantly occurs, increasingly utilize interprofessional staffing models in which clinicians from multiple disciplines – physicians, nurses, clinical pharmacists, respiratory therapists, and dieticians, among others – bring their unique expertise to team-based clinical decisions and care delivery. Such a multidisciplinary approach helps enable the provision of more comprehensive, higher-quality critical care. In this way, the interprofessional ICU care team is an embodiment of the notion that the “whole” is more than just the sum of its parts. Therefore, we must consider the impact of the pandemic on interprofessional critical care clinicians as the team that they are.

Even before the COVID-19 pandemic, the well-being of critical care clinicians was compromised. Across multiple disciplines, they had among the highest rates of burnout syndrome of all health care professionals (Moss M, et al. Am J Respir Crit Care Med. 2016;194[1]:106-113). As the pandemic has dragged on, their well-being has only further declined. Burnout rates are at all-time highs, and symptoms of posttraumatic stress disorder, anxiety, and depression are common and have increased with each subsequent surge (Azoulay E, et al. Chest. 2021;160[3]:944-955). Offsets to burnout, such as fulfillment and recognition, have declined over time (Kerlin MP, et al. Ann Amer Thorac Soc. 2022;19[2]:329-331). These worrisome trends pose a significant threat to critical care delivery. Clinician burnout is associated with worse patient outcomes, increased medical errors, and lower patient satisfaction (Moss M, et al. Am J Respir Crit Care Med. 2016;194[1]:106-113; Poghosyan L, et al. Res Nurs Health. 2010;33[4]:288-298). It is also associated with mental illness and substance use disorders among clinicians (Dyrbye LN, et al. Ann Intern Med. 2008;149[5]:334-341). Finally, it has contributed to a workforce crisis: nearly 500,000 health care workers have left the US health care sector since the beginning of the pandemic, and approximately two-thirds of acute and critical care nurses have considered doing so (Wong E. “Why Healthcare Workers are Quitting in Droves”. The Atlantic. Accessed November 7, 2022). Such a “brain drain” of clinicians – whose expertise cannot be easily replicated or replaced – represents a staffing crisis that threatens our ability to provide high-quality, safe care for the foreseeable future.

To combat burnout, it is first necessary to identify the mechanisms by which the pandemic has induced harm. Early during the pandemic, critical care clinicians feared for their own safety with little information of how the virus was spread. At a time when the world was under lockdown, vaccines were not yet available, and hospitals were overwhelmed with surges of critically ill patients, clinicians struggled like the rest of the world to meet their own basic needs such as childcare, grocery shopping, and time with family. They experienced distress from high volumes of patients with extreme mortality rates, helplessness due to lack of treatment options, and moral injury over restrictive visitation policies (Vranas KC, et al. Chest. 2022;162[2]:331-345; Vranas KC, et al. Chest. 2021;160[5]:1714-1728). Over time, critical care clinicians have no doubt experienced further exhaustion related to the duration of the pandemic, often without adequate time to recover and process the trauma they have experienced. More recently, a new source of distress for clinicians has emerged from variability in vaccine uptake among the public. Clinicians have experienced compassion fatigue and even moral outrage toward those who chose not to receive a vaccine that is highly effective at preventing severe illness. They also suffered from ethical conflicts over how to treat unvaccinated patients and whether they should be given equal priority and access to limited therapies (Shaw D. Bioethics. 2022;36[8]:883-890).

Furthermore, the pandemic has damaged the relationship between clinicians and their institutions. Early in the pandemic, the widespread shortages of personal protective equipment harmed trust among clinicians due to their perception that their safety was not prioritized. Hospitals have also struggled with having to make rapid decisions on how to equitably allocate fixed resources in response to unanticipated and unpredictable demands, while also maintaining financial solvency. In some cases, these challenging policy decisions (eg, whether to continue elective procedures during acute surge events) lacked transparency and input from the team at the frontlines of patient care. As a result, clinicians have felt undervalued and without a voice in decisions that directly impact both the care they can provide their patients and their own well-being.

It is incumbent upon us now to take steps to repair the damage inflicted on our critical care workforce by the pandemic. To this end, there have been calls for the urgent implementation of strategies to mitigate the psychological burden experienced by critical care clinicians. However, many of these focus on interventions to increase coping strategies and resilience among individual clinicians. While programs such as mindfulness apps and resilience training are valuable, they are not sufficient. The very nature of these solutions implies that the solution (and therefore, the problem) of burnout lies in the individual clinician. Yet, as described above, many of the mechanisms of harm to clinicians’ well-being are systems-level issues that will necessarily require systems-level solutions.

Therefore, we propose a comprehensive, layered approach to begin to reverse the damage inflicted by the pandemic on critical care clinicians’ well-being, with solutions organized by ecological levels of individual clinicians, departments, institutions, and society. With this approach, we hope to address specific aspects of our critical care delivery system that, taken together, will fortify the well-being of our critical care workforce as a whole. We offer suggestions below that are both informed by existing evidence, as well as our own opinions as intensivists and researchers.
 

At the level of the individual clinician:

• Proactively provide access to mental health resources. Clinicians have limited time or energy to navigate mental health and support services and find it helpful when others proactively reach out to them.
• Provide opportunities for clinicians to experience community and support among peers. Clinicians find benefit in town halls, debrief sessions, and peer support groups, particularly during times of acute strain.

At the level of the department:

• Allow more flexibility in work schedules. Even prior to the pandemic, the lack of scheduling flexibility and the number of consecutive days worked had been identified as key contributors to burnout; these have been exacerbated during times of caseload surges, when clinicians have been asked or even required to increase their hours and work extra shifts.
• Promote a culture of psychological safety in which clinicians feel empowered to say “I cannot work” for whatever reason. This will require the establishment of formalized backup systems that easily accommodate call-outs without relying on individual clinicians to find their own coverage.

At the level of the health care system:

• Prioritize transparency, and bring administrators and clinicians together for policy decisions. Break down silos between the frontline workers involved in direct patient care and hospital executives, both to inform those decisions and demonstrate the value of clinicians’ perspectives.
• Compensate clinicians for extra work. Consider hazard pay or ensure extra time off for extra time worked.
• Make it “easier” for clinicians to do their jobs by helping them meet their basic needs. Create schedules with designated breaks during shifts. Provide adequate office space and call rooms. Facilitate access to childcare. Provide parking.
• Minimize moral injury. Develop protocols for scarce resource allocation that exclude the treatment team from making decisions about allocation of scarce resources. Avoid visitor restrictions given the harm these policies inflict on patients, families, and members of the care team.

At the level of society:

• Study mechanisms to improve communication about public health with the public. Both science and communication are essential to promoting and protecting public health; more research is needed to improve the way scientific knowledge and evidence-based recommendations are communicated to the public.

In conclusion, the COVID-19 pandemic has forever changed our critical care workforce and the way we deliver care. The time is now to act on the lessons learned from the COVID-19 pandemic through implementation of systems-level solutions to combat burnout and ensure both the health and sustainability of our critical care workforce for the season ahead.
 

Dr. Vranas is with the Center to Improve Veteran Involvement in Care, VA Portland Health Care System, the Division of Pulmonary and Critical Care, Oregon Health & Science University; Portland, OR; and the Palliative and Advanced Illness Research (PAIR) Center, University of Pennsylvania; Philadelphia, PA. Dr. Kerlin is with the Palliative and Advanced Illness Research (PAIR) Center, and Division of Pulmonary, Allergy and Critical Care, Perelman School of Medicine, University of Pennsylvania; Philadelphia, PA.

The COVID-19 pandemic has caused unprecedented and unpredictable strain on health care systems worldwide, forcing rapid organizational modifications and innovations to ensure availability of critical care resources during acute surge events. Yet, while much attention has been paid to the availability of ICU beds and ventilators, COVID-19 has insidiously and significantly harmed the most precious critical care resource of all – the human beings who are the lifeblood of critical care delivery. We are now at a crucial moment in history to better understand the pandemic’s impact on our human resources and enact changes to reverse the damage that it has inflicted on our workforce.

To understand the impact of the pandemic on critical care clinicians, we must first acknowledge the context in which they work. ICUs, where critical care delivery predominantly occurs, increasingly utilize interprofessional staffing models in which clinicians from multiple disciplines – physicians, nurses, clinical pharmacists, respiratory therapists, and dieticians, among others – bring their unique expertise to team-based clinical decisions and care delivery. Such a multidisciplinary approach helps enable the provision of more comprehensive, higher-quality critical care. In this way, the interprofessional ICU care team is an embodiment of the notion that the “whole” is more than just the sum of its parts. Therefore, we must consider the impact of the pandemic on interprofessional critical care clinicians as the team that they are.

Even before the COVID-19 pandemic, the well-being of critical care clinicians was compromised. Across multiple disciplines, they had among the highest rates of burnout syndrome of all health care professionals (Moss M, et al. Am J Respir Crit Care Med. 2016;194[1]:106-113). As the pandemic has dragged on, their well-being has only further declined. Burnout rates are at all-time highs, and symptoms of posttraumatic stress disorder, anxiety, and depression are common and have increased with each subsequent surge (Azoulay E, et al. Chest. 2021;160[3]:944-955). Offsets to burnout, such as fulfillment and recognition, have declined over time (Kerlin MP, et al. Ann Amer Thorac Soc. 2022;19[2]:329-331). These worrisome trends pose a significant threat to critical care delivery. Clinician burnout is associated with worse patient outcomes, increased medical errors, and lower patient satisfaction (Moss M, et al. Am J Respir Crit Care Med. 2016;194[1]:106-113; Poghosyan L, et al. Res Nurs Health. 2010;33[4]:288-298). It is also associated with mental illness and substance use disorders among clinicians (Dyrbye LN, et al. Ann Intern Med. 2008;149[5]:334-341). Finally, it has contributed to a workforce crisis: nearly 500,000 health care workers have left the US health care sector since the beginning of the pandemic, and approximately two-thirds of acute and critical care nurses have considered doing so (Wong E. “Why Healthcare Workers are Quitting in Droves”. The Atlantic. Accessed November 7, 2022). Such a “brain drain” of clinicians – whose expertise cannot be easily replicated or replaced – represents a staffing crisis that threatens our ability to provide high-quality, safe care for the foreseeable future.

To combat burnout, it is first necessary to identify the mechanisms by which the pandemic has induced harm. Early during the pandemic, critical care clinicians feared for their own safety with little information of how the virus was spread. At a time when the world was under lockdown, vaccines were not yet available, and hospitals were overwhelmed with surges of critically ill patients, clinicians struggled like the rest of the world to meet their own basic needs such as childcare, grocery shopping, and time with family. They experienced distress from high volumes of patients with extreme mortality rates, helplessness due to lack of treatment options, and moral injury over restrictive visitation policies (Vranas KC, et al. Chest. 2022;162[2]:331-345; Vranas KC, et al. Chest. 2021;160[5]:1714-1728). Over time, critical care clinicians have no doubt experienced further exhaustion related to the duration of the pandemic, often without adequate time to recover and process the trauma they have experienced. More recently, a new source of distress for clinicians has emerged from variability in vaccine uptake among the public. Clinicians have experienced compassion fatigue and even moral outrage toward those who chose not to receive a vaccine that is highly effective at preventing severe illness. They also suffered from ethical conflicts over how to treat unvaccinated patients and whether they should be given equal priority and access to limited therapies (Shaw D. Bioethics. 2022;36[8]:883-890).

Furthermore, the pandemic has damaged the relationship between clinicians and their institutions. Early in the pandemic, the widespread shortages of personal protective equipment harmed trust among clinicians due to their perception that their safety was not prioritized. Hospitals have also struggled with having to make rapid decisions on how to equitably allocate fixed resources in response to unanticipated and unpredictable demands, while also maintaining financial solvency. In some cases, these challenging policy decisions (eg, whether to continue elective procedures during acute surge events) lacked transparency and input from the team at the frontlines of patient care. As a result, clinicians have felt undervalued and without a voice in decisions that directly impact both the care they can provide their patients and their own well-being.

It is incumbent upon us now to take steps to repair the damage inflicted on our critical care workforce by the pandemic. To this end, there have been calls for the urgent implementation of strategies to mitigate the psychological burden experienced by critical care clinicians. However, many of these focus on interventions to increase coping strategies and resilience among individual clinicians. While programs such as mindfulness apps and resilience training are valuable, they are not sufficient. The very nature of these solutions implies that the solution (and therefore, the problem) of burnout lies in the individual clinician. Yet, as described above, many of the mechanisms of harm to clinicians’ well-being are systems-level issues that will necessarily require systems-level solutions.

Therefore, we propose a comprehensive, layered approach to begin to reverse the damage inflicted by the pandemic on critical care clinicians’ well-being, with solutions organized by ecological levels of individual clinicians, departments, institutions, and society. With this approach, we hope to address specific aspects of our critical care delivery system that, taken together, will fortify the well-being of our critical care workforce as a whole. We offer suggestions below that are both informed by existing evidence, as well as our own opinions as intensivists and researchers.
 

At the level of the individual clinician:

• Proactively provide access to mental health resources. Clinicians have limited time or energy to navigate mental health and support services and find it helpful when others proactively reach out to them.
• Provide opportunities for clinicians to experience community and support among peers. Clinicians find benefit in town halls, debrief sessions, and peer support groups, particularly during times of acute strain.

At the level of the department:

• Allow more flexibility in work schedules. Even prior to the pandemic, the lack of scheduling flexibility and the number of consecutive days worked had been identified as key contributors to burnout; these have been exacerbated during times of caseload surges, when clinicians have been asked or even required to increase their hours and work extra shifts.
• Promote a culture of psychological safety in which clinicians feel empowered to say “I cannot work” for whatever reason. This will require the establishment of formalized backup systems that easily accommodate call-outs without relying on individual clinicians to find their own coverage.

At the level of the health care system:

• Prioritize transparency, and bring administrators and clinicians together for policy decisions. Break down silos between the frontline workers involved in direct patient care and hospital executives, both to inform those decisions and demonstrate the value of clinicians’ perspectives.
• Compensate clinicians for extra work. Consider hazard pay or ensure extra time off for extra time worked.
• Make it “easier” for clinicians to do their jobs by helping them meet their basic needs. Create schedules with designated breaks during shifts. Provide adequate office space and call rooms. Facilitate access to childcare. Provide parking.
• Minimize moral injury. Develop protocols for scarce resource allocation that exclude the treatment team from making decisions about allocation of scarce resources. Avoid visitor restrictions given the harm these policies inflict on patients, families, and members of the care team.

At the level of society:

• Study mechanisms to improve communication about public health with the public. Both science and communication are essential to promoting and protecting public health; more research is needed to improve the way scientific knowledge and evidence-based recommendations are communicated to the public.

In conclusion, the COVID-19 pandemic has forever changed our critical care workforce and the way we deliver care. The time is now to act on the lessons learned from the COVID-19 pandemic through implementation of systems-level solutions to combat burnout and ensure both the health and sustainability of our critical care workforce for the season ahead.
 

Dr. Vranas is with the Center to Improve Veteran Involvement in Care, VA Portland Health Care System, the Division of Pulmonary and Critical Care, Oregon Health & Science University; Portland, OR; and the Palliative and Advanced Illness Research (PAIR) Center, University of Pennsylvania; Philadelphia, PA. Dr. Kerlin is with the Palliative and Advanced Illness Research (PAIR) Center, and Division of Pulmonary, Allergy and Critical Care, Perelman School of Medicine, University of Pennsylvania; Philadelphia, PA.

The COVID-19 pandemic has caused unprecedented and unpredictable strain on health care systems worldwide, forcing rapid organizational modifications and innovations to ensure availability of critical care resources during acute surge events. Yet, while much attention has been paid to the availability of ICU beds and ventilators, COVID-19 has insidiously and significantly harmed the most precious critical care resource of all – the human beings who are the lifeblood of critical care delivery. We are now at a crucial moment in history to better understand the pandemic’s impact on our human resources and enact changes to reverse the damage that it has inflicted on our workforce.

To understand the impact of the pandemic on critical care clinicians, we must first acknowledge the context in which they work. ICUs, where critical care delivery predominantly occurs, increasingly utilize interprofessional staffing models in which clinicians from multiple disciplines – physicians, nurses, clinical pharmacists, respiratory therapists, and dieticians, among others – bring their unique expertise to team-based clinical decisions and care delivery. Such a multidisciplinary approach helps enable the provision of more comprehensive, higher-quality critical care. In this way, the interprofessional ICU care team is an embodiment of the notion that the “whole” is more than just the sum of its parts. Therefore, we must consider the impact of the pandemic on interprofessional critical care clinicians as the team that they are.

Even before the COVID-19 pandemic, the well-being of critical care clinicians was compromised. Across multiple disciplines, they had among the highest rates of burnout syndrome of all health care professionals (Moss M, et al. Am J Respir Crit Care Med. 2016;194[1]:106-113). As the pandemic has dragged on, their well-being has only further declined. Burnout rates are at all-time highs, and symptoms of posttraumatic stress disorder, anxiety, and depression are common and have increased with each subsequent surge (Azoulay E, et al. Chest. 2021;160[3]:944-955). Offsets to burnout, such as fulfillment and recognition, have declined over time (Kerlin MP, et al. Ann Amer Thorac Soc. 2022;19[2]:329-331). These worrisome trends pose a significant threat to critical care delivery. Clinician burnout is associated with worse patient outcomes, increased medical errors, and lower patient satisfaction (Moss M, et al. Am J Respir Crit Care Med. 2016;194[1]:106-113; Poghosyan L, et al. Res Nurs Health. 2010;33[4]:288-298). It is also associated with mental illness and substance use disorders among clinicians (Dyrbye LN, et al. Ann Intern Med. 2008;149[5]:334-341). Finally, it has contributed to a workforce crisis: nearly 500,000 health care workers have left the US health care sector since the beginning of the pandemic, and approximately two-thirds of acute and critical care nurses have considered doing so (Wong E. “Why Healthcare Workers are Quitting in Droves”. The Atlantic. Accessed November 7, 2022). Such a “brain drain” of clinicians – whose expertise cannot be easily replicated or replaced – represents a staffing crisis that threatens our ability to provide high-quality, safe care for the foreseeable future.

To combat burnout, it is first necessary to identify the mechanisms by which the pandemic has induced harm. Early during the pandemic, critical care clinicians feared for their own safety with little information of how the virus was spread. At a time when the world was under lockdown, vaccines were not yet available, and hospitals were overwhelmed with surges of critically ill patients, clinicians struggled like the rest of the world to meet their own basic needs such as childcare, grocery shopping, and time with family. They experienced distress from high volumes of patients with extreme mortality rates, helplessness due to lack of treatment options, and moral injury over restrictive visitation policies (Vranas KC, et al. Chest. 2022;162[2]:331-345; Vranas KC, et al. Chest. 2021;160[5]:1714-1728). Over time, critical care clinicians have no doubt experienced further exhaustion related to the duration of the pandemic, often without adequate time to recover and process the trauma they have experienced. More recently, a new source of distress for clinicians has emerged from variability in vaccine uptake among the public. Clinicians have experienced compassion fatigue and even moral outrage toward those who chose not to receive a vaccine that is highly effective at preventing severe illness. They also suffered from ethical conflicts over how to treat unvaccinated patients and whether they should be given equal priority and access to limited therapies (Shaw D. Bioethics. 2022;36[8]:883-890).

Furthermore, the pandemic has damaged the relationship between clinicians and their institutions. Early in the pandemic, the widespread shortages of personal protective equipment harmed trust among clinicians due to their perception that their safety was not prioritized. Hospitals have also struggled with having to make rapid decisions on how to equitably allocate fixed resources in response to unanticipated and unpredictable demands, while also maintaining financial solvency. In some cases, these challenging policy decisions (eg, whether to continue elective procedures during acute surge events) lacked transparency and input from the team at the frontlines of patient care. As a result, clinicians have felt undervalued and without a voice in decisions that directly impact both the care they can provide their patients and their own well-being.

It is incumbent upon us now to take steps to repair the damage inflicted on our critical care workforce by the pandemic. To this end, there have been calls for the urgent implementation of strategies to mitigate the psychological burden experienced by critical care clinicians. However, many of these focus on interventions to increase coping strategies and resilience among individual clinicians. While programs such as mindfulness apps and resilience training are valuable, they are not sufficient. The very nature of these solutions implies that the solution (and therefore, the problem) of burnout lies in the individual clinician. Yet, as described above, many of the mechanisms of harm to clinicians’ well-being are systems-level issues that will necessarily require systems-level solutions.

Therefore, we propose a comprehensive, layered approach to begin to reverse the damage inflicted by the pandemic on critical care clinicians’ well-being, with solutions organized by ecological levels of individual clinicians, departments, institutions, and society. With this approach, we hope to address specific aspects of our critical care delivery system that, taken together, will fortify the well-being of our critical care workforce as a whole. We offer suggestions below that are both informed by existing evidence, as well as our own opinions as intensivists and researchers.
 

At the level of the individual clinician:

• Proactively provide access to mental health resources. Clinicians have limited time or energy to navigate mental health and support services and find it helpful when others proactively reach out to them.
• Provide opportunities for clinicians to experience community and support among peers. Clinicians find benefit in town halls, debrief sessions, and peer support groups, particularly during times of acute strain.

At the level of the department:

• Allow more flexibility in work schedules. Even prior to the pandemic, the lack of scheduling flexibility and the number of consecutive days worked had been identified as key contributors to burnout; these have been exacerbated during times of caseload surges, when clinicians have been asked or even required to increase their hours and work extra shifts.
• Promote a culture of psychological safety in which clinicians feel empowered to say “I cannot work” for whatever reason. This will require the establishment of formalized backup systems that easily accommodate call-outs without relying on individual clinicians to find their own coverage.

At the level of the health care system:

• Prioritize transparency, and bring administrators and clinicians together for policy decisions. Break down silos between the frontline workers involved in direct patient care and hospital executives, both to inform those decisions and demonstrate the value of clinicians’ perspectives.
• Compensate clinicians for extra work. Consider hazard pay or ensure extra time off for extra time worked.
• Make it “easier” for clinicians to do their jobs by helping them meet their basic needs. Create schedules with designated breaks during shifts. Provide adequate office space and call rooms. Facilitate access to childcare. Provide parking.
• Minimize moral injury. Develop protocols for scarce resource allocation that exclude the treatment team from making decisions about allocation of scarce resources. Avoid visitor restrictions given the harm these policies inflict on patients, families, and members of the care team.

At the level of society:

• Study mechanisms to improve communication about public health with the public. Both science and communication are essential to promoting and protecting public health; more research is needed to improve the way scientific knowledge and evidence-based recommendations are communicated to the public.

In conclusion, the COVID-19 pandemic has forever changed our critical care workforce and the way we deliver care. The time is now to act on the lessons learned from the COVID-19 pandemic through implementation of systems-level solutions to combat burnout and ensure both the health and sustainability of our critical care workforce for the season ahead.
 

Dr. Vranas is with the Center to Improve Veteran Involvement in Care, VA Portland Health Care System, the Division of Pulmonary and Critical Care, Oregon Health & Science University; Portland, OR; and the Palliative and Advanced Illness Research (PAIR) Center, University of Pennsylvania; Philadelphia, PA. Dr. Kerlin is with the Palliative and Advanced Illness Research (PAIR) Center, and Division of Pulmonary, Allergy and Critical Care, Perelman School of Medicine, University of Pennsylvania; Philadelphia, PA.

Intensive care telemedicine was first described in 1982 after implementation in a seven-bed, inner-city ICU using 19-inch television screens connected with intensivists at the University Hospitals of Cleveland (Grundy, et al. Crit Care Med. 1982;10[7]:471). After this proof-of-concept report, however, ICU telemedicine gained little traction for nearly 20 years, until Johns Hopkins Hospital established a continuously monitored ICU telemedicine service in a nonintensivist staffed surgical ICU. Their pre/post analysis suggested a 64% decrease in severity-adjusted ICU mortality and greater than 30% decrease in ICU length of stay, ICU complications, and costs (Rosenfeld, et al. Crit Care Med. 2000;28[12]:3925).

Along with better and less costly telemedicine technology, rapid adoption of electronic medical records, and a nationwide intensivist shortage, this and other evidence for the service’s clinical and cost effectiveness has spurred explosive growth in ICU telemedicine in the succeeding 2 decades, with at least 18% of hospitals and 28% of ICU beds supported by ICU telemedicine by 2018 (Ofoma, et al. Crit Care Explor. 2021;4[3]:e0468).

Importantly, what “ICU telemedicine” represents varies substantially across hospitals and even across ICUs within systems. Two-way audiovisual technology is the defining feature, and at a minimum, programs provide intensivists and/or nurses who respond to consultation requests. Commonly, telemedicine clinicians directly connect with patients; monitor labs, hemodynamics, and alarms; and proactively contact on-site clinicians with recommendations or place orders directly into the electronic health record depending on whether the clinician acts as the patients’ primary, co-managing, or consultant provider. A centralized hub and spoke model with telemedicine personnel located at a single, remote center is the most common and best studied ICU telemedicine design. Additional staffing may include respiratory therapists, pharmacists, and advanced practice clinicians in coverage models that range from 24/7 to nocturnal and can also differ in whether patients are monitored continuously or on an as needed basis, triggered by alarms or clinician/nursing concerns.

On-demand services may extend to support for teams responding to medical emergencies inside and sometimes outside the ICU. Another equally important role that ICU telemedicine can provide is helping ensure facilities adhere to ICU quality metrics, such as ventilator bundles, DVT prophylaxis, and daily SAT/SBT.

Unsurprisingly, integrating ICU telemedicine into an existing system is very costly and complex, requiring substantial and thoughtful process redesign to maximize fiscal and clinical return on investment. One vendor of proprietary telemedicine technology, Philips eICU, estimates an implementation cost of $50,000 to $100,000 per bed with annual overhead, software maintenance, and IT staffing of ~20% of implementation costs in addition to clinician staffing of $1-2 million per 100 beds. However, some (but not all) evidence suggests that ICU telemedicine programs pay for themselves over time. An influential report from Sentara Healthcare, an early adopter of ICU telemedicine, described equipment costs of more than $1 million for a total of 103 critical care beds but attributed savings of $460,000 per month to decreased length of stay (Coustasse, et al. The Permanente Journal. 2014;18[4]:76).

Cost savings are great, of course, but ICU telemedicine’s potential to improve clinical outcomes is the real priority. While Sentara’s early report included a 27% decrease in ICU mortality after telemedicine adoption, a 2011 meta-analysis of 13 studies, including 35 ICUs and over 40,000 patients, suggested decreased ICU mortality and LOS with a statistically significant effect on overall hospital mortality and LOS (Young, et al. Arch Intern Med. 2011;171[6]:498). This highlights the Achilles heel of ICU telemedicine evidence: the pretest/posttest studies that dominate this field and likely contribute substantially to the inconsistencies in the evidence base.

In the absence of risk adjustment and control groups, many studies observed postimplementation changes that may reflect trends in patient mix or the effects of unrelated practice changes rather than the causal influence of ICU telemedicine. In fact, in studies using more robust methods, ICU telemedicine’s effect size has been smaller or nonexistent. For example, in 2016, Kahn and colleagues used CMS data to evaluate 132 ICU telemedicine programs using 389 matched controlled hospitals. There was a slight reduction in 90-day mortality (OR=0.96, CI 0.94-0.98) with only 12% showing a statistically significant reduction in mortality. Interestingly, hospitals in urban areas demonstrated greater benefit than rural facilities (Kahn, et al. Medical Care. 2016;54[3]:319).

The heterogeneity of the studied programs (e.g., primary vs consultative role, on-demand vs proactive involvement) and recipient ICUs (e.g., rural vs tertiary care facility, presence of bedside intensivists) further hinders a clear answer to the key question: Would ICU telemedicine benefit my hospital? Fortunately, some recent, well-designed studies have attempted to understand which attributes of ICU telemedicine programs provide results and which ICUs will see the most benefit. In a cohort of 118,990 patients across 56 ICUs, four interventions were associated with lower mortality and reduced LOS: (1) evaluation of patients within 1 hour of ICU admission, (2) frequent leadership review of performance data, (3) ICU best practice compliance, and (4) prompt response to alerts (Lilly, et al. Chest. 2014;145[3]:500). Kahn and colleagues have also investigated this issue, conducting an in-depth ethnographic evaluation of 10 hospitals identified in their 2016 study to have positive, neutral, or negative outcomes after ICU telemedicine implementation (Kahn, et al. Am J Respir Crit Care Med. 2019;199[8]:970). They found that successful programs:

(1) provided consistent services matched to recipient needs;

(2) provided services both proactively and reactively without being obtrusive;

(3) embedded routine engagements unobtrusively into usual routines;

(4) had engaged leadership who set clear expectations and mediated conflicts; and

(5) had bedside clinicians who valued and sought out telemedicine participation in care.

The authors concluded that, “the true value of ICU telemedicine lies not in whether the technology exists but in how it is applied.” However, another recent analysis also suggested that, rather than telemedicine or recipient ICU design, targeting underperforming recipient ICU performance may be the key determinant of whether ICU telemedicine implementation improves outcomes (Fusaro, et al. Crit Care Med. 2019; 47[4]:501). While the finding may reflect regression to the mean, the idea that ICUs with above-expected mortality derive greater benefit from ICU telemedicine support than already well-performing ICUs is certainly logical.

As COVID-19 strained health care systems across the country, we and others found ways to use ICU telemedicine to preserve optimal care delivery for critically ill patients. Our program at Intermountain Healthcare – already supporting 17 ICUs within our 24-hospital health system, as well as 10 external ICUs with experienced critical care physicians, nurses, respiratory therapists, and pharmacists – took on increased responsibility for ICU load balancing and interhospital transfers.

Leveraging telemedicine services also helped community ICUs care for sicker, more complex patients than usual and aided nonintensivist physicians called upon to manage critically ill patients in ad hoc ICUs at referral hospitals. While the pandemic certainly stressed ICU staff, we suspect that telemedicine’s ability to balance caseloads and distribute clinical tasks helped mitigate these stresses. At age 40, ICU telemedicine is both mature and still growing, with continued expansion of bed coverage and the range of services available. Looking ahead, as we confront a national shortage of intensivists, ICU telemedicine likely represents a cost effective and efficient strategy to maintain critical care capacity with the potential to ensure low-cost, high-quality care for all, regardless of location.
 

Dr. Graham and Dr. Peltan are with the Division of Pulmonary & Critical Care Medicine, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, Utah; and Dr. Peltan is also with the Division of Pulmonary & Critical Care Medicine, Department of Medicine, Intermountain Medical Center, Murray, Utah.

Intensive care telemedicine was first described in 1982 after implementation in a seven-bed, inner-city ICU using 19-inch television screens connected with intensivists at the University Hospitals of Cleveland (Grundy, et al. Crit Care Med. 1982;10[7]:471). After this proof-of-concept report, however, ICU telemedicine gained little traction for nearly 20 years, until Johns Hopkins Hospital established a continuously monitored ICU telemedicine service in a nonintensivist staffed surgical ICU. Their pre/post analysis suggested a 64% decrease in severity-adjusted ICU mortality and greater than 30% decrease in ICU length of stay, ICU complications, and costs (Rosenfeld, et al. Crit Care Med. 2000;28[12]:3925).

Along with better and less costly telemedicine technology, rapid adoption of electronic medical records, and a nationwide intensivist shortage, this and other evidence for the service’s clinical and cost effectiveness has spurred explosive growth in ICU telemedicine in the succeeding 2 decades, with at least 18% of hospitals and 28% of ICU beds supported by ICU telemedicine by 2018 (Ofoma, et al. Crit Care Explor. 2021;4[3]:e0468).

Importantly, what “ICU telemedicine” represents varies substantially across hospitals and even across ICUs within systems. Two-way audiovisual technology is the defining feature, and at a minimum, programs provide intensivists and/or nurses who respond to consultation requests. Commonly, telemedicine clinicians directly connect with patients; monitor labs, hemodynamics, and alarms; and proactively contact on-site clinicians with recommendations or place orders directly into the electronic health record depending on whether the clinician acts as the patients’ primary, co-managing, or consultant provider. A centralized hub and spoke model with telemedicine personnel located at a single, remote center is the most common and best studied ICU telemedicine design. Additional staffing may include respiratory therapists, pharmacists, and advanced practice clinicians in coverage models that range from 24/7 to nocturnal and can also differ in whether patients are monitored continuously or on an as needed basis, triggered by alarms or clinician/nursing concerns.

On-demand services may extend to support for teams responding to medical emergencies inside and sometimes outside the ICU. Another equally important role that ICU telemedicine can provide is helping ensure facilities adhere to ICU quality metrics, such as ventilator bundles, DVT prophylaxis, and daily SAT/SBT.

Unsurprisingly, integrating ICU telemedicine into an existing system is very costly and complex, requiring substantial and thoughtful process redesign to maximize fiscal and clinical return on investment. One vendor of proprietary telemedicine technology, Philips eICU, estimates an implementation cost of $50,000 to $100,000 per bed with annual overhead, software maintenance, and IT staffing of ~20% of implementation costs in addition to clinician staffing of $1-2 million per 100 beds. However, some (but not all) evidence suggests that ICU telemedicine programs pay for themselves over time. An influential report from Sentara Healthcare, an early adopter of ICU telemedicine, described equipment costs of more than $1 million for a total of 103 critical care beds but attributed savings of $460,000 per month to decreased length of stay (Coustasse, et al. The Permanente Journal. 2014;18[4]:76).

Cost savings are great, of course, but ICU telemedicine’s potential to improve clinical outcomes is the real priority. While Sentara’s early report included a 27% decrease in ICU mortality after telemedicine adoption, a 2011 meta-analysis of 13 studies, including 35 ICUs and over 40,000 patients, suggested decreased ICU mortality and LOS with a statistically significant effect on overall hospital mortality and LOS (Young, et al. Arch Intern Med. 2011;171[6]:498). This highlights the Achilles heel of ICU telemedicine evidence: the pretest/posttest studies that dominate this field and likely contribute substantially to the inconsistencies in the evidence base.

In the absence of risk adjustment and control groups, many studies observed postimplementation changes that may reflect trends in patient mix or the effects of unrelated practice changes rather than the causal influence of ICU telemedicine. In fact, in studies using more robust methods, ICU telemedicine’s effect size has been smaller or nonexistent. For example, in 2016, Kahn and colleagues used CMS data to evaluate 132 ICU telemedicine programs using 389 matched controlled hospitals. There was a slight reduction in 90-day mortality (OR=0.96, CI 0.94-0.98) with only 12% showing a statistically significant reduction in mortality. Interestingly, hospitals in urban areas demonstrated greater benefit than rural facilities (Kahn, et al. Medical Care. 2016;54[3]:319).

The heterogeneity of the studied programs (e.g., primary vs consultative role, on-demand vs proactive involvement) and recipient ICUs (e.g., rural vs tertiary care facility, presence of bedside intensivists) further hinders a clear answer to the key question: Would ICU telemedicine benefit my hospital? Fortunately, some recent, well-designed studies have attempted to understand which attributes of ICU telemedicine programs provide results and which ICUs will see the most benefit. In a cohort of 118,990 patients across 56 ICUs, four interventions were associated with lower mortality and reduced LOS: (1) evaluation of patients within 1 hour of ICU admission, (2) frequent leadership review of performance data, (3) ICU best practice compliance, and (4) prompt response to alerts (Lilly, et al. Chest. 2014;145[3]:500). Kahn and colleagues have also investigated this issue, conducting an in-depth ethnographic evaluation of 10 hospitals identified in their 2016 study to have positive, neutral, or negative outcomes after ICU telemedicine implementation (Kahn, et al. Am J Respir Crit Care Med. 2019;199[8]:970). They found that successful programs:

(1) provided consistent services matched to recipient needs;

(2) provided services both proactively and reactively without being obtrusive;

(3) embedded routine engagements unobtrusively into usual routines;

(4) had engaged leadership who set clear expectations and mediated conflicts; and

(5) had bedside clinicians who valued and sought out telemedicine participation in care.

The authors concluded that, “the true value of ICU telemedicine lies not in whether the technology exists but in how it is applied.” However, another recent analysis also suggested that, rather than telemedicine or recipient ICU design, targeting underperforming recipient ICU performance may be the key determinant of whether ICU telemedicine implementation improves outcomes (Fusaro, et al. Crit Care Med. 2019; 47[4]:501). While the finding may reflect regression to the mean, the idea that ICUs with above-expected mortality derive greater benefit from ICU telemedicine support than already well-performing ICUs is certainly logical.

As COVID-19 strained health care systems across the country, we and others found ways to use ICU telemedicine to preserve optimal care delivery for critically ill patients. Our program at Intermountain Healthcare – already supporting 17 ICUs within our 24-hospital health system, as well as 10 external ICUs with experienced critical care physicians, nurses, respiratory therapists, and pharmacists – took on increased responsibility for ICU load balancing and interhospital transfers.

Leveraging telemedicine services also helped community ICUs care for sicker, more complex patients than usual and aided nonintensivist physicians called upon to manage critically ill patients in ad hoc ICUs at referral hospitals. While the pandemic certainly stressed ICU staff, we suspect that telemedicine’s ability to balance caseloads and distribute clinical tasks helped mitigate these stresses. At age 40, ICU telemedicine is both mature and still growing, with continued expansion of bed coverage and the range of services available. Looking ahead, as we confront a national shortage of intensivists, ICU telemedicine likely represents a cost effective and efficient strategy to maintain critical care capacity with the potential to ensure low-cost, high-quality care for all, regardless of location.
 

Dr. Graham and Dr. Peltan are with the Division of Pulmonary & Critical Care Medicine, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, Utah; and Dr. Peltan is also with the Division of Pulmonary & Critical Care Medicine, Department of Medicine, Intermountain Medical Center, Murray, Utah.

Intensive care telemedicine was first described in 1982 after implementation in a seven-bed, inner-city ICU using 19-inch television screens connected with intensivists at the University Hospitals of Cleveland (Grundy, et al. Crit Care Med. 1982;10[7]:471). After this proof-of-concept report, however, ICU telemedicine gained little traction for nearly 20 years, until Johns Hopkins Hospital established a continuously monitored ICU telemedicine service in a nonintensivist staffed surgical ICU. Their pre/post analysis suggested a 64% decrease in severity-adjusted ICU mortality and greater than 30% decrease in ICU length of stay, ICU complications, and costs (Rosenfeld, et al. Crit Care Med. 2000;28[12]:3925).

Along with better and less costly telemedicine technology, rapid adoption of electronic medical records, and a nationwide intensivist shortage, this and other evidence for the service’s clinical and cost effectiveness has spurred explosive growth in ICU telemedicine in the succeeding 2 decades, with at least 18% of hospitals and 28% of ICU beds supported by ICU telemedicine by 2018 (Ofoma, et al. Crit Care Explor. 2021;4[3]:e0468).

Importantly, what “ICU telemedicine” represents varies substantially across hospitals and even across ICUs within systems. Two-way audiovisual technology is the defining feature, and at a minimum, programs provide intensivists and/or nurses who respond to consultation requests. Commonly, telemedicine clinicians directly connect with patients; monitor labs, hemodynamics, and alarms; and proactively contact on-site clinicians with recommendations or place orders directly into the electronic health record depending on whether the clinician acts as the patients’ primary, co-managing, or consultant provider. A centralized hub and spoke model with telemedicine personnel located at a single, remote center is the most common and best studied ICU telemedicine design. Additional staffing may include respiratory therapists, pharmacists, and advanced practice clinicians in coverage models that range from 24/7 to nocturnal and can also differ in whether patients are monitored continuously or on an as needed basis, triggered by alarms or clinician/nursing concerns.

On-demand services may extend to support for teams responding to medical emergencies inside and sometimes outside the ICU. Another equally important role that ICU telemedicine can provide is helping ensure facilities adhere to ICU quality metrics, such as ventilator bundles, DVT prophylaxis, and daily SAT/SBT.

Unsurprisingly, integrating ICU telemedicine into an existing system is very costly and complex, requiring substantial and thoughtful process redesign to maximize fiscal and clinical return on investment. One vendor of proprietary telemedicine technology, Philips eICU, estimates an implementation cost of $50,000 to $100,000 per bed with annual overhead, software maintenance, and IT staffing of ~20% of implementation costs in addition to clinician staffing of $1-2 million per 100 beds. However, some (but not all) evidence suggests that ICU telemedicine programs pay for themselves over time. An influential report from Sentara Healthcare, an early adopter of ICU telemedicine, described equipment costs of more than $1 million for a total of 103 critical care beds but attributed savings of $460,000 per month to decreased length of stay (Coustasse, et al. The Permanente Journal. 2014;18[4]:76).

Cost savings are great, of course, but ICU telemedicine’s potential to improve clinical outcomes is the real priority. While Sentara’s early report included a 27% decrease in ICU mortality after telemedicine adoption, a 2011 meta-analysis of 13 studies, including 35 ICUs and over 40,000 patients, suggested decreased ICU mortality and LOS with a statistically significant effect on overall hospital mortality and LOS (Young, et al. Arch Intern Med. 2011;171[6]:498). This highlights the Achilles heel of ICU telemedicine evidence: the pretest/posttest studies that dominate this field and likely contribute substantially to the inconsistencies in the evidence base.

In the absence of risk adjustment and control groups, many studies observed postimplementation changes that may reflect trends in patient mix or the effects of unrelated practice changes rather than the causal influence of ICU telemedicine. In fact, in studies using more robust methods, ICU telemedicine’s effect size has been smaller or nonexistent. For example, in 2016, Kahn and colleagues used CMS data to evaluate 132 ICU telemedicine programs using 389 matched controlled hospitals. There was a slight reduction in 90-day mortality (OR=0.96, CI 0.94-0.98) with only 12% showing a statistically significant reduction in mortality. Interestingly, hospitals in urban areas demonstrated greater benefit than rural facilities (Kahn, et al. Medical Care. 2016;54[3]:319).

The heterogeneity of the studied programs (e.g., primary vs consultative role, on-demand vs proactive involvement) and recipient ICUs (e.g., rural vs tertiary care facility, presence of bedside intensivists) further hinders a clear answer to the key question: Would ICU telemedicine benefit my hospital? Fortunately, some recent, well-designed studies have attempted to understand which attributes of ICU telemedicine programs provide results and which ICUs will see the most benefit. In a cohort of 118,990 patients across 56 ICUs, four interventions were associated with lower mortality and reduced LOS: (1) evaluation of patients within 1 hour of ICU admission, (2) frequent leadership review of performance data, (3) ICU best practice compliance, and (4) prompt response to alerts (Lilly, et al. Chest. 2014;145[3]:500). Kahn and colleagues have also investigated this issue, conducting an in-depth ethnographic evaluation of 10 hospitals identified in their 2016 study to have positive, neutral, or negative outcomes after ICU telemedicine implementation (Kahn, et al. Am J Respir Crit Care Med. 2019;199[8]:970). They found that successful programs:

(1) provided consistent services matched to recipient needs;

(2) provided services both proactively and reactively without being obtrusive;

(3) embedded routine engagements unobtrusively into usual routines;

(4) had engaged leadership who set clear expectations and mediated conflicts; and

(5) had bedside clinicians who valued and sought out telemedicine participation in care.

The authors concluded that, “the true value of ICU telemedicine lies not in whether the technology exists but in how it is applied.” However, another recent analysis also suggested that, rather than telemedicine or recipient ICU design, targeting underperforming recipient ICU performance may be the key determinant of whether ICU telemedicine implementation improves outcomes (Fusaro, et al. Crit Care Med. 2019; 47[4]:501). While the finding may reflect regression to the mean, the idea that ICUs with above-expected mortality derive greater benefit from ICU telemedicine support than already well-performing ICUs is certainly logical.

As COVID-19 strained health care systems across the country, we and others found ways to use ICU telemedicine to preserve optimal care delivery for critically ill patients. Our program at Intermountain Healthcare – already supporting 17 ICUs within our 24-hospital health system, as well as 10 external ICUs with experienced critical care physicians, nurses, respiratory therapists, and pharmacists – took on increased responsibility for ICU load balancing and interhospital transfers.

Leveraging telemedicine services also helped community ICUs care for sicker, more complex patients than usual and aided nonintensivist physicians called upon to manage critically ill patients in ad hoc ICUs at referral hospitals. While the pandemic certainly stressed ICU staff, we suspect that telemedicine’s ability to balance caseloads and distribute clinical tasks helped mitigate these stresses. At age 40, ICU telemedicine is both mature and still growing, with continued expansion of bed coverage and the range of services available. Looking ahead, as we confront a national shortage of intensivists, ICU telemedicine likely represents a cost effective and efficient strategy to maintain critical care capacity with the potential to ensure low-cost, high-quality care for all, regardless of location.
 

Dr. Graham and Dr. Peltan are with the Division of Pulmonary & Critical Care Medicine, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, Utah; and Dr. Peltan is also with the Division of Pulmonary & Critical Care Medicine, Department of Medicine, Intermountain Medical Center, Murray, Utah.