The Heart Is Not Always in Good Hands: SQUARE WAVE BLOOD PRESSURE RESPONSE TO VALSALVA MANEUVER IN HEART FAILURE

Posted by James

This is also explicable by the analogy of the disten­sible segment in the siphon tubing. In failure, the intrathoracic and intra-abdominal vessels are dis­tended. Raising the pressure surrounding them in the chest squeezes them toward a normal caliber and the elevated extracardiac pressure lessens left ventricular load. The sustained output and the blood pressure increase from the high intrathoracic pressure is helped by the increased venous return from the compression of the engorged abdominal vessels by the equally raised intra-abdominal pressure. Since, when there is heart failure, there is little fall in systemic pressure during the Valsalva maneuver, the reflex overshoot of systemic pressure and consequent bradycardia does not occur.

Ventricular Hypertrophy

Cor Pulmonale. The conundrum of cor pulmonale in obstructed airflow disease is particularly baffling. It seems that neither pulmonary vascular disease due to emphysematous changes, nor pulmonary vasocon­striction due to alveolar hypoxia are the significant factors related to right ventricular hypertrophy and eventual right heart failure. A thought-provoking pos­sibility is that it could be due to the effects of lung distension in raising pulmonary vascular resistance and restricting the cardiogenic movement of the walls of the cardiac fossa. It has been shown that distended lungs are many times more difficult to deform than lungs at normal volumes. Because of this there could be an added load on the ventricles that is not imposed by vascular impedances, but by the need to deform surrounding tissues as the heart beats. In spite of the unchanging heart volume between systole and dias­tole, obvious conformational changes could be ex­pected to load ventricular movement externally when the walls of the cardiac fossa are noncompliant. The effect would be more marked on the weaker, thin walled right ventricle. This potential load cannot be measured with present-day techniques and so remains highly speculative. However, it would explain the association of cor pulmonale, and the morbidity and mortality experienced by patients, with the severity of the obstructive pulmonary disease rather than the pulmonary hypertension. The improvement with oxygen could be due to the effect of oxygen breathing in reducing hyperpnea and gas trapping rather than hypoxic pulmonary vasoconstriction. An external load imposed by the tense walls of the cardiac fossa could also explain the previously inexplicable finding of left ventricular hypertrophy in patients with cor pulmonale due to obstructed airflow disease. Al­though the strong left ventricle might be expected to be unaffected by its surroundings under normal con­ditions, it is possible that a poorly deformable cardiac fossa could, in time, lead to its hypertrophy. cialis professional online

Conclusion

As is usual when the results of research in applied physiology are looked at in terms of clinical medicine, the view is incomplete and distorted by the bias of the reviewer. Most of the concepts in the preceding analysis are extensions of basic science studies beyond the limit of the factual data. The heart is normally held rather gently in the soft bed of the cardiac fossa and this has been amply demonstrated by observation and physiologic studies. The idea that external restrictions imposed by the harder hands of a tense cardiac fossa in a distended lung could add to the load of the heart in obstructed airflow disease may be provocative but remains to be proved.