Role of tricuspid regurgitation and left ventricular damage in the treatment of right ventricular infarction-induced low cardiac output syndrome.

To evaluate, in right ventricular (RV) myocardial infarction, the role of tricuspid regurgitation (TR) and left ventricular (LV) damage and the response to treatment of low cardiac output, 20 patients were prospectively studied. Volume infusion increased cardiac output only slightly (11%, p less than 0.001), despite a dramatic increase in ventricular filling pressures. Dobutamine (4 micrograms.kg-1.min-1) markedly increased cardiac output (24%, p less than 0.001) with a decrease in ventricular filling pressures. In the 5 patients with TR, dobutamine only modestly increased cardiac output (9 vs 26%, p less than 0.001), while stroke index and LV end-diastolic dimensions decreased in comparison (-5 vs 33% and -6 vs 9%, respectively, p less than 0.001). In the absence of TR (n = 15), there was no significant difference in response to volume expansion between patients with normal (n = 7) and depressed LV ejection fraction (n = 8). In contrast, dobutamine, in patients with depressed LV function, induced a greater increase in cardiac output (38 vs 17%, p less than 0.01) and RV ejection fraction (36 vs 12%, p less than 0.05). All patients with RV infarction-induced low cardiac output responded only modestly to volume loading. Dobutamine is particularly efficacious in patients without TR who have depressed LV function by improving RV function and, consequently, LV preload. In the 5 patients with TR, increasing RV contractility failed to improve the forward stroke volume by increasing the regurgitant fraction.

Right ventricular performance in patients with acute respiratory failure.

To examine the right ventricular response to acute respiratory failure, serial studies of biventricular performance were analysed in 34 such patients, specifically detailing the role of associated underlying disease. During the initial study, the 34 patients with acute respiratory failure had a higher right ventricular end-diastolic volume than the control group (+21%), associated with a decrease in right ventricular ejection fraction, abnormalities which tended to return to normal values in the 15 survivors. In the 9 patients who died of refractory hypoxemia with severe pulmonary hypertension, the right ventricular dilation allowed to maintain stroke volume. In contrast, in 8 patients who died of septic shock, biventricular function was progressively altered (right and left ventricular ejection fraction = -37% and -35%). In 4 patients who died of cardiogenic shock (viral myocarditis), the cardiac function was the lowest (right and left ventricular ejection fraction = -59% and -60%). Only patients with acute respiratory failure associated with septic shock or viral myocarditis are unable to maintain their stroke volume.

Right ventricular dysfunction in patients with septic shock.

Using a rapid computerized thermodilution method, we examined the evolution of right ventricular performance in 23 patients with septic shock. Nine survived the episode of septic shock. The other 14 patients died of refractory circulatory shock. Significant right ventricular systolic dysfunction, defined as decreased ejection fraction (-39%) and right ventricular dilation (+38%) was observed in all patients with septic shock. However, in the survivors, increased right ventricular preload may prevent hemodynamic evidence of right ventricular pump failure by utilizing the Frank-Starling mechanism to maintain stroke volume. Conversely, in the nonsurvivors, right ventricular dysfunction was more prononced two days after the onset of septic shock, leading to a fall in stroke. In the last patients, a decrease in contractility appears to be the major factor accounting for decreased right ventricular performance, as evidenced by the marked increase in end-systolic volume (+27%) without significant change in pulmonary artery pressure, during the later stage of septic shock. The observed right ventricular pump failure then appears associated with an alteration in diastolic mechanical properties of this ventricle, as suggested by a leftward displacement of the individual pressure-volume curves.

Coronary hemodynamics and myocardial metabolism of lactate, free fatty acids, glucose, and ketones in patients with septic shock.

To investigate disturbances in the coronary circulation and myocardial metabolism during septic shock, we examined coronary sinus blood flow and myocardial substrate extraction in 40 patients with septic shock and 13 control patients. Patients with coronary artery disease were excluded from this study. The global hemodynamic pattern of the septic patients was characterized by a lower stroke volume, despite an elevated cardiac index. Coronary sinus blood flow was high (187 +/- 47 vs 130 +/- 21 ml/min in the control group, p less than .001) due to marked coronary vasodilation, especially in the subgroup of nonsurvivors. In contrast to the control group, myocardial lactate uptake was elevated, while that of free fatty acids, glucose, and ketone bodies was diminished in patients with septic shock. These findings were especially prominent in the nonsurvivors. Expressed as oxygen equivalents, the contribution of free fatty acids as an energy source of the myocardium was markedly diminished in septic patients (12% vs 54% in the control group, p less than .005), while that of lactate was increased (36% vs 12%, p less than .01). The observed shift in myocardial substrate extraction was associated with a discrepancy between measured myocardial oxygen consumption and that calculated chemically from commonly available exogenous substrates: 41% of myocardial oxygen consumption was not explained by the utilization of commonly available substrates extracted from coronary circulation in all patients with septic shock.(ABSTRACT TRUNCATED AT 250 WORDS)

Bedside evaluation of right ventricular performance using a rapid computerized thermodilution method.

In 34 patients, we assessed the reproducibility and accuracy of a new, computerized, thermodilution method that determines right ventricular ejection fraction (RVEF). We compared the results from this new algorithm with simultaneous results from the conventional plateau thermodilution method and from both first-pass and gated nuclear techniques. Using this new method improved the reproducibility of thermal determinations of RVEF. Although the thermal values were lower, the correlations between thermal and nuclear measurements were close [r = .92 (first-pass technique), r = .81 (gated technique)]. This new method seems particularly appropriate for serial monitoring of RV performance.

Mechanisms of decreased left ventricular preload during continuous positive pressure ventilation in ARDS.

Continuous positive pressure ventilation is associated with a reduction in left ventricular preload and cardiac output, but the mechanisms responsible are controversial. The decrease in left ventricular preload may result exclusively from a decreased systemic venous return due to increased pleural pressure, or from an additional effect such as decreased left ventricular compliance. To determine the mechanisms responsible, we studied the changes in cardiac output induced by continuous positive pressure ventilation in eight patients with the adult respiratory distress syndrome. We measured cardiac output by thermodilution, and biventricular ejection fraction by equilibrium gated blood pool scintigraphy. Biventricular end-diastolic volumes were then calculated by dividing stroke volume by ejection fraction. As positive end-expiratory pressure increased from 0 to 20 cm H2O, stroke volume and biventricular end-diastolic volumes fell about 25 percent, and biventricular ejection fraction remained unchanged. At 20 cm H2O positive end-expiratory pressure, volume expansion for normalizing cardiac output restored biventricular end-diastolic volumes without markedly changing biventricular end-diastolic transmural pressures. The primary cause of the reduction in left ventricular preload with continuous positive pressure ventilation appears to be a fall in venous return and hence in right ventricular stroke volume, without evidence of change in left ventricular diastolic compliance.

Oxygen consumption during septic shock. Effects of inotropic drugs.

Septic shock may be defined as a clinical entity wherein a patient has an inadequate peripheral metabolism in the presence of circulating bacteria. The demands for metabolic requirements of the tissues and hence for oxygen transport to these tissues are then markedly high. The average response to increased metabolism in such patients is a percentage increase in cardiac output that is comparable to the percentage increase in oxygen consumption while oxygen extraction rate does not change or even decreases in severe or/and advanced septic shock. This emphasizes the high priority placed by the body on the ability to increase blood flow from the heart in the presence of increased metabolic demands due to sepsis. Concerning the myocardium, oxygen consumption is low in hyper- and hypodynamic states of septic shock, probably and partially due to marked arterial vasodilatation. However, in hypodynamic states, the lower value of perfusion pressure may account for a decrease in myocardial oxygen supply, especially in subendocardial areas and may be responsible for myocardial ischaemia, more especially as myocardial oxygen extraction as well as systemic oxygen extraction is impaired. The goal of therapeutics is to improve oxygen availability through: (1) maintenance of haemoglobin levels and (2) increases in stroke volume using inotropic drugs since these drugs may produce a rise in myocardial oxygen supply higher than their drug-induced increase in oxygen requirements in hypodynamic states of septic shock.

[Traumatic left ventricular aneurysm disclosed by systemic emboli. Value of platelet labelling with indium]. / Anévrysme ventriculaire gauche traumatique révélé par des embolies systémiques. Intérêt du marquage plaquettaire à l'indium.

The authors report a case of traumatic left ventricular aneurysm, presenting with recurrent cerebral embolism, 36 years after a thoraco-brachial bullet wound. The 58 year old man had no symptoms of angina or particular cardiovascular risk factors. The ECG showed changes of chronic anterior wall infarction, observed 10 years previously on a routine preoperative recording. There was a calcified circular para-apical shadow on chest X-Ray. The antero-apical region showed hypofixation on myocardial scintigraphy, and hypokinesia on isotopic angiography. The coronary arteries were normal. Indium III platelet marking revealed a focus of hyperfixation within the left ventricle. At surgery, a true calcific para-apical left ventricular aneurysm was discovered, containing a fresh thrombus. This lesion was resected. Peroperative Indium III platelet test confirmed that the thrombus was the site of high uptake. The surgical result was good at 6 months follow-up. This case illustrates: the value of the Indium test which would appear to be a very specific and sensitive method of detecting intraventricular thrombi. This test, which appreciates the thrombotic activity of intracardiac masses is a useful complement to other non-invasive methods such as 2D echocardiography; the special characteristics of post-trauma left ventricular aneurysms which are rare, often diagnosed late, at the time of complications such as systemic embolism, commonly pose medico-legal problems, and for which surgical treatment seems to be indicated in symptomatic patients.