A primary goal of the cardiopulmonary system is to continuously deliver adequate amounts of oxygen (O2) to meet the metabolic demands of the organism. Persistent tissue hypoperfusion results in end-organ dysfunction and death. Preventing initial tissue dysoxia by optimizing cardio-pulmonary function in post-operative surgical patients at risk for the development of multiple organ failure substantially increases the changes of a successful outcome [1]. Often such optimization requires the use of artificial mechanical ventilation, invasive monitoring and potent pharmacological therapies. Although artificial ventilation, in particular, may improve pulmonary gas exchange and restore arterial blood acid-base balance in those in whom it was previously deranged, it may also disrupt an already fragile hemodynamic balance developed in response to these disturbances. Presently, clinical practice defends a therapeutic approach which favors maintaining a minimal level of systemic O2 delivery to tissues so as to prevent tissue hypoxia. In practice this is accomplished by maintaining cardiac output and arterial perfusion pressure with the patient in a stable metabolic condition. Ventilation may modify all of these processes. Thus, an understanding of cardiopulmonary interactions is central to the effective implementation of intensive care treatment programs.

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The hemodynamic consequences of mechanical ventilation: an evolving story

Acute liver failure (ALF) is a syndrome of diverse etiology, in which patients without previously recognized liver disease sustain a liver injury that results in rapid loss of hepatic function. Depending on the etiology and severity of the insult, some patients undergo rapid hepatic regeneration and spontaneously recover. However, nearly 60% of patients with ALF in the US require and undergo orthotopic liver transplantation or die. Management decisions made by clinicians who initially assess individuals with ALF can drastically affect these patients' outcomes. Even with optimal early management, however, many patients with ALF develop a cascade of complications often presaged by the systemic inflammatory response syndrome, which involves failure of nearly every organ system. We highlight advances in the intensive care management of patients with ALF that have contributed to a marked improvement in their overall survival over the past 20 years. These advances include therapies that limit the extent of liver injury and maximize the likelihood of spontaneous recovery and approaches to enable prevention, recognition and early treatment of complications that lead to multi-organ-system failure, the most common cause of death. Finally, we summarize the role of orthotopic liver transplantation in salvage of the most severely affected patients.

Management of acute liver failure

Effects of induced hypothermia in patients with septic adult respiratory distress syndrome

Objective:The approach to applying positive end-expiratory pressure in morbidly obese patients is not well defined. These patients frequently require prolonged mechanical ventilation, increasing the risk for failed liberation from ventilatory support. We hypothesized that lung recruitment maneuvers

Recruitment Maneuvers and Positive End-Expiratory Pressure Titration in Morbidly Obese ICU Patients.

Electrophysiologic and proarrhythmic effects of intravenous inotropic agents

The effects of positive end-expiratory pressure on heart-lung interactions

Augmentation of cardiac function in end-stage heart failure by combined use of dobutamine and amrinone.

In the anesthetized closed-chest canine model of Gram-negative endotoxemia (n = 10), we tested the hypothesis that the effect of cardiac cycle-specific intrathoracic pressure pulses delivered by a heart rate-(HR) synchronized high-frequency jet ventilator (sync HFJV) on systolic ventricular performance is dependent on the level of preload. To control for HFJV frequency, hemodynamic responses were also measured at fixed frequency within 15% of HR (async HFJV). Biventricular stroke volumes (SV) were measured by electromagnetic flow probes. Measurements were made before (baseline) and 30 min after infusion of 1 mg/kg Escherichia coli endotoxin (serotype 055:B5) and then after 2 mg/kg propranolol at both low (less than 10 mmHg) left ventricular filling pressure (LVFP) and high (greater than 10 mmHg) LVFP. Ventricular function curves, aortic pressure-flow (P-Q) relationships, and venous return (VR) curves were analyzed. We found that endotoxin did not alter VR curves but shifted the aortic P-Q curves to the left with pressure on the x-axis (P less than 0.05). Volume loading increased SV (P less than 0.01) because of a rightward shift of the VR curve. No specific differences occurred with either sync or async HFJV during endotoxin, presumably because of preserved VR and shifted aortic P-Q. The lack of cardiac cycle-specific effects of ITP appears to be due to the selective endotoxin-induced changes in peripheral vasomotor tone that counterbalance any depressed myocardial contractility.

Jean-Gilles Guimond

Papers

The effects of positive end-expiratory pressure on heart-lung interactions

Augmentation of cardiac function in end-stage heart failure by combined use of dobutamine and amrinone.

Effect of synchronous increase in intrathoracic pressure on cardiac performance during acute endotoxemia