Journal of Intensive Care Medicine

This study examined whether hypothermia (< 36.0°C) incidence among critically ill patients varied over time, the determinants of change, and the associated risk for ICU mortality.

Interrupted time series analysis among adults admitted to ICUs in Calgary, Canada over 8.5 years. Changes in the incidence of hypothermia within the first 24 hours of ICU admission were modelled using segmented regression.

Among 15,291 first admissions to ICU, hypothermia incidence decreased from 29% to 21% during the study period. Implementation of a new temporal artery thermometer (TAT) was associated with the majority of the decrease in incidence (10%; 95% CI 7.1-13%; P < .0001). However, subgroup analysis revealed important differences between medical and surgical patients. Hypothermia incidence decreased among surgical patients before TAT implementation (0.4% per quarter, 95% CI 0.1-0.7%, P = .009), but not after, whereas in medical patients, the incidence increased after (1.0% per quarter, 95% CI 0.6-1.4%, P < .0001) but not before TAT implementation. Segmented logistic regression suggested that increases in the proportion of patients with non-traumatic neurologic admission diagnoses were associated with hypothermia incidence among medical patients, whereas there was no measurable clinical factor associated with the observed time trends among surgical patients. Hypothermia at ICU admission was independently associated with ICU mortality in medical and surgical patients throughout the entire study.

The incidence of hypothermia at ICU admission was dependent on medical versus surgical status, and the method of non-invasive temperature measurement, but was persistently associated with ICU mortality.

Health care providers nationwide are routinely trained in Advanced Cardiac Life Support (ACLS), an American Heart Association program that teaches cardiac arrest management. Recent changes in the ACLS approach have de-emphasized routine pulse checks in an effort to promote uninterrupted chest compressions. We hypothesized that this new ACLS algorithm may lead to uncertainty regarding the appropriate action following detection of a pulse during a cardiac arrest.

We conducted an observational study in which a Web-based survey was sent to ACLS-trained medical providers at 4 major urban tertiary care centers in the United States. The survey consisted of 5 multiple-choice, scenario-based ACLS questions, including our question of interest. Adult staff members with a valid ACLS certification were included.

A total of 347 surveys were analyzed. The response rate was 28.1%. The majority (53.6%) of responders were between 18 and 32 years old, and 59.9% were female. The majority (54.2%) of responders incorrectly stated that they would continue CPR and possibly administer additional therapies when a team member detects a pulse immediately following defibrillation. Secondarily, only 51.9% of respondents correctly chose to perform a rhythm check following 2 minutes of CPR. The other 3 survey questions were correctly answered an average of 89.1% of the time.

Confusion exists regarding whether or not CPR and cardiac medications should be continued in the presence of a pulse. Education may be warranted to emphasize avoiding compressions and medications when a palpable pulse is detected.

Tissue hypoperfusion and hypoxia markers predict mortality in critically ill patients. This study evaluates the ability of serum lactate, central venous oxygen saturation (Scvo ₂), and venous-arterial carbon dioxide difference (GapCo ₂) to predict mortality in patients with postcardiac arrest (post-CA) syndrome.

A prospective observational study of patients with post-CA in a tertiary teaching hospital. Serial assessments of lactate, lactate clearance (Clac), GapCo ₂, and Scvo ₂ in the first 72 hours post-CA were analyzed. Adults (≥18 years) patients resuscitated from CA were included. The primary end point was 28-day mortality and secondary end points were 24- and 72-hour mortality.

A total of 54 patients were recruited, 33 (61,1%) of 54 were men, with a 28-day mortality of 75.9%. Cardiac arrest occurred in-hospital in 84.6% of survivors and 97.5% of nonsurvivors. Lactate and Clac were significantly associated with mortality at 28 days, yielding an area under the receiver–operating characteristic curve of 0.797 (lactate 6 hours) and 0.717 (Clac 6 hours) with a positive predictive value of 96% for lactate 6 hours (> 2.5 mmol/L) and 89.5% for Clac 6 hours (<50%). Survival analysis confirmed the difference between the groups from the 24th hour post-CA. Considering mortality at 24 hours, lactate, Clac, and Scvo ₂ (immediately post-CA, 6 and 18 hours) were different between the groups. In mortality at 72 hours, lactate, Clac, Scvo ₂ (48 hours), and GapCo ₂ (36 and 48 hours) were associated with mortality.

In post-CA syndrome, serum lactate and Clac were consistently able to predict mortality.

Venovenous extracorporeal membrane oxygenation (VV-ECMO) is a therapeutic option in the management of the most severe forms of acute respiratory distress syndrome. Oxygenation during VV-ECMO depends on many parameters, and its management is complex. The management of ECMO is still not completely codified. The aim of this study was to rationalize the management of hypoxemia during VV-ECMO.

To build a comprehensive flow diagram for management of hypoxemia during VV-ECMO, we considered (1) relationship between O₂ arterial saturation and its determinants; (2) analysis of physiopathology of oxygenation under VV-ECMO; and (3) main guidelines and recommendations recapitulated in troubleshooting charts.

We propose a stepwise approach that could guide specific intervention to improve oxygenation during VV-ECMO. The first step is to obtain adequate pump flow, the main determinant of oxygenation, by eliminating a mechanical problem or inadequate venous drainage. Second, if hypoxemia persists, algorithm considers multiple reasons for inadequate oxygenation, namely: (1) excessive recirculation, (2) excessive cardiac output (decrease of ratio pump flow/cardiac output), (3) decrease in SvO₂ (oxygen saturation in mixed venous blood), (4) malfunction of oxygenator, and (5) deterioration of residual lung function. Finally, for each modification of oxygenation parameters, specific measures are proposed to restore an adequate oxygenation by extracorporeal membrane oxygenation.

If hypoxemia occurs during VV-ECMO, collecting oxygenation parameters and a clear step-by-step algorithm could guide specific intervention to improve oxygenation. This flow diagram is in accordance with current recommendations recapitulated in guidelines or troubleshooting chart but more accurate and complete. Although rational and appealing, it remains to be tested together with a number of still unsolved issues.