Mechanisms of the cardiac output decrease

Nearly all authors agree that the drop in cardiac output in HBO is

00 1 dependent on the decrease in heart rate (Keys , Otis , Dripps & Comroe ,

Kenmure21). However, Whitehorn16 have reported a combined decrease in systolic ejection volume (SEV). In patients with myocardial infarction,

Cameron32 also showed a decrease in the SEV. Interestingly, in their patients, cardiac output decreased whereas the heart rate remained the same.

Arterial blood pressure rose, indicating a marked increase in systemic arterial resistance. However, these harmful effects on patients with compromised hearts have not been observed by all authors. In fact, several have reported an improvement of heart performance for this type of patient

(Smetnev33, Deepika34).

There is little available literature on the ventricular function and the effects of HBO. Savitt35 observed a decrease in cardiac output, in myocardial oxygen consumption (VO2) and in coronary output in HBO at 3 ata in anaesthetized dogs, but the changes were proportional so that myocardial contractility remained unchanged. Ishikawa36 reported an increase of 11% of myocardial contractility when PO2 was increased to 460 mmHg. They interpreted this increase as the result of a direct beneficial effect of oxygen on the myocardial fibre. However, Ask & Tyssebotn reported a positive inotropic effect related to the barometric pressure itself. But this effect only seems to appear at pressures above those used in HBO37-39.

In contrast with the findings of Savitt, Kioschos40 and Abel41 observed a slight but significant decrease (10-15 %) in the indexes of ventricular performance in anaesthetized animals. This decrease in myocardial contractility was only observed in the left ventricle and Abel41 made the hypothesis that the relative decrease in left ventricle function combined with a preserved function of the right ventricle could be the cause of spurious cases of pulmonary oedema occurring during HBO exposure.

To clarify this point, we have carried out a study on the global haemodynamic changes induced by HBO (2.5 ata) in 10 critical sedated patients under controlled ventilation42. We observed a decrease in heart rate, a moderate increase in systemic and pulmonary blood pressures, and no change in cardiac output. The absence of variation in cardiac output was due to an increase in the SEV mainly related to an increase in ventricular end diastolic volume with the ejection fraction remaining the same.

In our study, no decrease in myocardial contractility was observed. The increase in ventricular afterload due to the hyperoxic arterial vasoconstriction was balanced by an increase in ventricular preload evidenced by an increase in end diastolic filling volume. The increasing effect on preload was mainly related to the hyperbaric pressure rather than to the hyperoxia. These observations are consistent with the finding that hyperbaric pressure rather than hyperoxia increases auricular natriuretic factor release due to an increase in auricular volume43. Two mechanisms can account for the increase in preload: the increase in ventricular filling time caused by the bradycardia, and a decrease in ventricular compliance which is made evident by the pressure / volume curves (i.e., Starling curve).

However, these compensatory mechanisms are finite: increasing ventricular work in the presence of pre-existing ventricular dilatation (i.e., a reduction in ventricular compliance) explains why patients with dilated cardiomyopathies or coronary artery diseases may decompensate.

Hence two situations can arise: (1) the myocardium is able to oppose the increase in peripheral resistance by maintaining the systolic ejection volume, either because it has the necessary reserves or because the conditions of hyperoxygenation provide the required oxygen, or (2) the degraded myocardium is no longer able to counter the increase in peripheral resistance and cannot therefore maintain the SEV leading to manifestations of left heart (pulmonary oedema) or cardiac failure during HBO.

If one remembers that it is not so much the body itself but its metabolic requirements - particularly the need for oxygen delivery and CO2 elimination - that determines cardiac output, it makes sense that the increase in oxygen content by HBO would result in a decrease in cardiac output while peripheral oxygen delivery remains the same.

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