Transient Bradycardia Induced by Carotid Sinus Pressure Increases Outflow Obstruction in Hypertrophic Obstructive Cardiomyopathy but Not in Valvular Aortic Stenosis: Discussion

Possible Mechanisms
Transient and sudden slowing of the heart, by-applying CSP or by manipulating the pacing rate, may increase LV outflow obstruction by one or more of several mechanisms: Starling’s law, the Woodworth effect, or decreased afterload.
First, based on Starling’s law of the heart, the long diastolic period could allow more complete LV filling (notwithstanding the marked stiffness of the hypertrophied myocardium) leading to increased fiber length and tension, which then enhance the force of contraction at the next systole. No tangible proof exists for this. Angiographic evidence suggests just the opposite, and no increase in septal-posterior wall diastolic dimension could be seen in any of our patients. There is also no proof that a longer diastole automatically means increased blood transfer from the left atrium into the noncompliant left ventricle (as opposed to sustained bradycardia induced by (3-blockers or calcium-channel blockers, which may exert complex effects). Finally, ventricular pressure was not consistently increased during the longer diastole, as seen in Figure 5. Click Here However, this mechanism cannot be completely ruled out.
Second, as Woodworth showed in 1902, the “recuperative effect” of a long pause may lead to a transient increase in the force of contraction (increased contractility; positive inotropic effect) in isolated cardiac muscle preparations, independent of any ventricular volume considerations. Sonnenblick et al demonstrated a similar phenomenon in the intact human heart during cardiopulmonary bypass: sudden heart rate reduction caused an immediate increase in peak force above control levels. In their study of postextrasystolic potentiation, Sung et al concluded that improved contractility (and not the Frank-Starling mechanism) is responsible for the enhanced performance of the postextrasystolic beat. A similar phenomenon could indeed also occur in the first beat after the long pause induced by CSP or cessation of atrial pacing.
The third possible mechanism is the effect of decreased afterload. Earlier and faster ventricular ejection into the more completely decompressed aorta after the long diastole might facilitate mitral valvular motion into the LV outflow tract. Theoretically, CSP could also induce peripheral vasodilation, thus enhancing even further the influence of heart rate slowing on afterload.

Category: Bradycardia

Tags: carotid sinus pressure, hypertrophic obstructive cardiomyopathy, murmurs