Etiologies, clinical features and outcome of cardiac arrest in HIV-infected patients.

BACKGROUND: Compared to many other cardiovascular diseases, there is a paucity of data on the characteristics of successfully resuscitated cardiac arrest (CA) patients with human immunodeficiency virus (HIV) infection. We investigated causes, clinical features and outcome of these patients, and assessed the specific burden of HIV on outcome. METHODS: Retrospective analysis of HIV-infected patients admitted to 20 French ICUs for successfully resuscitated CA (2000-2012). Characteristics and outcome of HIV-infected patients were compared to those of a large cohort of HIV-uninfected patients admitted after CA in the Cochin Hospital ICU during the same period. RESULTS: 99 patients were included (median CD4 lymphocyte count 233/mm(3), viral load 43 copies/ml). When compared with the control cohort of 1701 patients, HIV-infected patients were younger, with a predominance of male, a majority of in-hospital CA (52%), and non-shockable initial rhythm (80.8%). CA was mostly related to respiratory cause (n=36, including 23 pneumonia), cardiac cause (n=33, including 16 acute myocardial infarction), neurologic cause (n=8) and toxic cause (n=5). CA was deemed directly related to HIV infection in 18 cases. Seventy-one patients died in the ICU, mostly for care withdrawal after post-anoxic encephalopathy. After propensity score matching, ICU mortality was not significantly affected by HIV infection. Similarly, HIV disease characteristics had no impact on ICU outcome. CONCLUSIONS: Etiologies of CA in HIV-infected patients are miscellaneous and mostly not related to HIV infection. Outcome remains bleak but is similar to outcome of HIV-negative patients.

Ten good reasons why everybody can and should perform cardiac ultrasound in the ICU.

Critical care ultrasonography (CCUS) has been defined as an ultrasound evaluation of the heart, abdomen, pleura and lungs at the bedside by the intensivist, 24/7. Within CCUS, critical care echocardiography (CCE) is used to assess cardiac function and more generally haemodynamics. Experts in haemodynamics have published a 'consensus of 16' regarding an update on haemodynamic monitoring. They reported the ten key properties of an 'ideal' haemodynamic monitoring system, which perfectly match the ten good reasons we describe here for performing CCE in critically ill patients. Even though unfortunately no evidence-based medicine study is available to support this review, especially regarding CCE-related improvement of outcome, many clinical studies have demonstrated that CCE provides measurements of relevant, accurate, reproducible and interpretable variables, is easy to use, readily available, has a rapid response time, causes no harm, and is cost-effective. Whether it is operator-independent is obviously more debatable and is discussed in this review. All these characteristics are arguments for the extensive use of CCE by intensivists. This is why experts in the field have recommended that a basic level of CCE should be included in the training of all intensivists.

Myocardial dysfunction during H1N1 influenza infection.

PURPOSE: The purpose of the study is to evaluate the incidence and hemodynamic consequences of right ventricular (RV) and left ventricular (LV) dysfunction in critically ill patients with H1N1 infection. PATIENTS AND METHODS: This is a retrospective analysis of all patients admitted to the intensive care unit of an academic hospital between October 2009 and March 2011 with severe H1N1 infection. Hemodynamic measurements and respiratory conditions were noted daily during the intensive care unit stay. RESULTS: Forty-six patients were admitted with severe H1N1 infection. Echocardiography was obtained in 39 patients on admission: 28 (72%) had abnormal ventricular function, of whom 13 (46%) had isolated LV abnormalities, 11 (39%) had isolated RV dysfunction, and 4 (14%) had biventricular dysfunction. Echocardiography was repeated in 19 of the 39 patients during their hospitalization: RV function tended to worsen with time, but LV function tended to normalize. The ventricular abnormalities were not associated with history, severity of the respiratory failure, or hemodynamic status. However, patients with ventricular dysfunction needed more aggressive therapy, including more frequent use of vasopressor and inotropic agents and of rescue ventilatory strategies, such as inhaled nitric oxide, prone positioning, and extracorporeal membrane oxygenation. CONCLUSIONS: These observations emphasize the high incidence of cardiac dysfunction in patients with H1N1 influenza infections.

Assessment of left ventricular function by pulse wave analysis in critically ill patients.

PURPOSE: Left ventricular (LV) performance is often quantified by echocardiography in critically ill patients. Pulse wave analysis (PWA) systems can also monitor cardiac function but in a continuous fashion. We compared echocardiographic and PWA-derived indices of LV function. METHODS: We enrolled 70 critically ill patients equipped with invasive arterial pressure monitoring who required echocardiography. We simultaneously assessed LV ejection fraction (LVEF), the rate of LV pressure rise during systole (dP/dt MAX) obtained with echocardiography (EC-dP/dt MAX), the ratio of effective arterial elastance to LV end-systolic elastance (E a/E es) determined by echocardiography, the dP/dt MAX estimated from the arterial pressure waveform (AP-dP/dt MAX) and the cardiac cycle efficiency (CCE) using PWA. RESULTS: Mean LVEF was 53 ± 18 % and CCE 0.16 ± 0.26. CCE was correlated linearly with LVEF (r = 0.88, 95 % CI 0.81 to 0.92, P < 0.001), and the dP/dt MAX values from the two techniques were linearly correlated (r = 0.93, 95 % CI 0.87 to 0.96, P < 0.001). There was minimal bias between the techniques for measurement of dP/dt MAX (23.7 mmHg/ms; 95 % CI -23.6 to 71.0). E a/E es and CCE were inversely correlated (r = -0.81, 95 % CI -0.88 to -0.71, P < 0.001). A CCE value of <0.07 predicted LVEF <40 % with a sensitivity of 0.93 and a specificity of 0.96 (AUC 0.98, 95 % CI 0.90 to 1.0, P < 0.001). A CCE value of >0.12 predicted LVEF ≥50 % with a sensitivity of 0.96 and a specificity of 0.82 (AUC 0.94, 95 % CI 0.87 to 1.0, P < 0.001). A CCE value <0.12 predicted E a/E es ≥1.3 with a sensitivity of 0.93 and a specificity of 0.89 (AUC 0.94, 95 % CI 0.83 to 1.0, P < 0.001). CONCLUSIONS: PWA-derived variables provide relevant information on cardiac contractility and performance in critically ill patients. PWA provides an easy method for online hemodynamic evaluation in critically ill patients.

Doppler echocardiography in shocked patients.

PURPOSE OF REVIEW: To reiterate the necessity of integrating echocardiography in the management of shocked patients and to propose a step-by-step functional evaluation of hemodynamics proven to optimize hemodynamic monitoring and to adapt the treatment. RECENT FINDINGS: Echocardiography has become the cornerstone to hemodynamic monitoring. By providing real-time images, echocardiography has the advantage over 'blind' technologies of an excellent diagnostic performance and of quick provision of information about the pathophysiology of circulatory failure. Critical care echocardiography (CCE) has been defined as echocardiography performed and interpreted by intensivists themselves, 7/7 and 24/24, at the bedside. Basic CCE is mainly a diagnostic approach, allowing quick and focused examination of cardiac function. Advanced CCE is the core of functional hemodynamic monitoring. It is based not only on transthoracic echocardiography but also strongly on transesophageal echocardiography, a very useful approach in ventilated patients. However, this monitoring is discontinuous. A single-use 72-h indwelling transesophageal probe was recently tested, allowing functional hemodynamic monitoring more continuously. SUMMARY: Echocardiography has become a hemodynamic monitoring technique used worldwide. It allows to make a quick and simple diagnosis of typical hemodynamic situations, by means of basic CCE, and also to achieve real functional hemodynamic monitoring, through advanced CCE.

Respiratory variation in inferior vena cava diameter: surrogate of central venous pressure or parameter of fluid responsiveness? Let the physiology reply.

In the previous issue of Critical Care, Muller and colleagues investigated whether respiratory variation in inferior vena cava diameter (ΔIVC) could be a useful predictor of fluid responsiveness in spontaneously breathing patients. The study concludes that accuracy was not very good and therefore that this parameter should be used with caution in these patients. There is still confusion about the meaning of IVC respiratory variations, whether the patient is spontaneously breathing or mechanically ventilated. In this brief commentary, we try to summarize as clearly as possible the significance of IVC variation in different clinical settings.

Organ failure in the ICU: cardiac alterations.

Cardiac alterations may be defined as changes that lead to abnormal cardiac function. They include decrease in preload, increase in afterload, and depressed cardiac contractility. Cardiac dysfunction differs from cardiac failure: cardiac performance is altered, but this does not necessarily mean that the cardiovascular system is failing. Several tools are available to detect cardiac alterations. Some may continuously assess cardiac performance by mainly or exclusively measuring cardiac output, but no information is given about the mechanisms underlying the cardiac output decrease. Doppler echocardiography allows noncontinuous cardiac monitoring, but it is perfectly adapted to evaluation of cardiac performance. It directly visualizes cardiac contractility and assesses cardiac preload. Only when there is an imbalance between oxygen demand and oxygen transport is correction of cardiac alterations required. But the truth is that no study supports the use of one treatment rather than another. Changes in respiratory settings or in respiratory mechanics induce changes in cardiac function and must then be considered in the strategy.

Cardiac tamponade.

PURPOSE OF REVIEW: To re-emphasize the epidemiology, pathophysiology, diagnosis, and treatment of cardiac tamponade. RECENT FINDINGS: Cardiac tamponade is a cause of obstructive shock. Incidence of cardiac tamponade is poorly documented. In cardiac tamponade, the pericardial pressure may reach 15-20  mmHg, leading to an equalization of pressures into the cardiac chambers and to a huge decrease in the systemic venous return. The right atrial transmural pressure becomes negligible. A competition between the right atrium and the right ventricle and between both ventricles is occurring. Deep inspiration allows the patients to maintain the systemic venous return at a certain level. Echocardiography is the key tool to diagnose a pericardial effusion, to detect its bad-tolerance, and to guide the treatment. In some situations following cardiac surgery, transesophageal echocardiography is mandatory. Treatment aims to restore a 'normal' blood pressure by fluid loading (with caution) and catecholamines and to drain the pericardium in emergency. SUMMARY: Cardiac tamponade is responsible for an obstructive shock. Causes of pericardial effusion are numerous. Echocardiography is the fundamental tool for the diagnosis and therapeutic management. Volume resuscitation and catecholamines are temporary treatments, pericardial drainage remaining the only effective treatment.

PaCO2 and alveolar dead space are more relevant than PaO2/FiO2 ratio in monitoring the respiratory response to prone position in ARDS patients: a physiological study.

INTRODUCTION: Our aims in this study were to report changes in the ratio of alveolar dead space to tidal volume (VDalv/VT) in the prone position (PP) and to test whether changes in partial pressure of arterial CO2 (PaCO2) may be more relevant than changes in the ratio of partial pressure of arterial O2 to fraction of inspired O2 (PaO2/FiO2) in defining the respiratory response to PP. We also aimed to validate a recently proposed method of estimation of the physiological dead space (VDphysiol/VT) without measurement of expired CO2. METHODS: Thirteen patients with a PaO2/FiO2 ratio < 100 mmHg were included in the study. Plateau pressure (Pplat), positive end-expiratory pressure (PEEP), blood gas analysis and expiratory CO2 were recorded with patients in the supine position and after 3, 6, 9, 12 and 15 hours in the PP. Responders to PP were defined after 15 hours of PP either by an increase in PaO2/FiO2 ratio > 20 mmHg or by a decrease in PaCO2 > 2 mmHg. Estimated and measured VDphysiol/VT ratios were compared. RESULTS: PP induced a decrease in Pplat, PaCO2 and VDalv/VT ratio and increases in PaO2/FiO2 ratios and compliance of the respiratory system (Crs). Maximal changes were observed after six to nine hours. Changes in VDalv/VT were correlated with changes in Crs, but not with changes in PaO2/FiO2 ratios. When the response was defined by PaO2/FiO2 ratio, no significant differences in Pplat, PaCO2 or VDalv/VT alterations between responders (n = 7) and nonresponders (n = 6) were observed. When the response was defined by PaCO2, four patients were differently classified, and responders (n = 7) had a greater decrease in VDalv/VT ratio and in Pplat and a greater increase in PaO2/FiO2 ratio and in Crs than nonresponders (n = 6). Estimated VDphysiol/VT ratios significantly underestimated measured VDphysiol/VT ratios (concordance correlation coefficient 0.19 (interquartile ranges 0.091 to 0.28)), whereas changes during PP were more reliable (concordance correlation coefficient 0.51 (0.32 to 0.66)). CONCLUSIONS: PP induced a decrease in VDalv/VT ratio and an improvement in respiratory mechanics. The respiratory response to PP appeared more relevant when PaCO2 rather than the PaO2/FiO2 ratio was used. Estimated VDphysiol/VT ratios systematically underestimated measured VDphysiol/VT ratios.