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Cardiovascular Physiology Concepts

Richard E. Klabunde, PhD

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Cardiovascular Physiology Concepts textbook cover

Click here for information on Cardiovascular Physiology Concepts, 2nd edition, a textbook published by Lippincott Williams & Wilkins (2012)


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Click here for information on Normal and Abnormal Blood Pressure, a textbook published by Richard E. Klabunde (2013)


 


Ventricular Diastolic Dysfunction

diastolic dysfunction effects on ventricular pressure-volume loops

Ventricular function is highly dependent upon preload as demonstrated by the Frank-Starling relationship. Therefore, if ventricular filling (preload) is impaired, this will lead to a decrease in stroke volume. The term "diastolic dysfunction" refers to changes in ventricular diastolic properties that have an adverse effect on ventricular filling and stroke volume. About 50% of heart failure patients have diastolic dysfunction, with or without normal systolic function as determined by normal ejection fractions.

Ventricular filling (i.e., end-diastolic volume and hence sarcomere length) depends upon the venous return and the compliance of the ventricle during diastole. A reduction in ventricular compliance, as occurs in ventricular hypertrophy, will result in less ventricular filling (decreased end-diastolic volume) and a greater end-diastolic pressure (and pulmonary capillary wedge pressures) as shown to the right by changes in the ventricular pressure-volume loop. Stroke volume, therefore, will decrease. Depending on the relative change in stroke volume and end-diastolic volume, there may or may not be a small decrease in ejection fraction. Heart failure caused by diastolic dysfunction is now often refered to as heart failure with preserved ejection fraction (HFpEF). Because stroke volume is decreased, there will also be a decrease in ventricular stroke work.

A second mechanism can also contribute to diastolic dysfunction: impaired ventricular relaxation (reduced lusitropy). Near the end of the cycle of excitation-contraction coupling in the myocyte, the sarcoplasmic reticulum actively sequesters Ca++ so that the concentration of Ca++ in the vicinity of troponin-C is reduced allowing the Ca++ to leave its binding sites on the troponin-C and thereby permit disengagement of actin from myosin. This is a necessary step to achieve rapid and complete relaxation of the myocyte. If this mechanism is impaired (e.g., by reduced rate of Ca++ uptake by the sarcoplasmic reticulum), or by other mechanisms that contribute to myocyte relaxation, then the rate and perhaps the extent of relaxation are decreased. This will reduce the rate of ventricular filling, particularly during the phase of rapid filling.

An important and deleterious consequence of diastolic dysfunction is the rise in end-diastolic pressure. If the left ventricle is involved, then left atrial and pulmonary venous pressures will also rise. This can lead to pulmonary congestion and edema. If the right ventricle is in diastolic failure, the increase in end-diastolic pressure will be reflected back into the right atrium and systemic venous vessels. This can lead to peripheral edema and ascites. The rise in venous pressures also occur because of an increase in blood volume due to activation of the renin-angiotensin-aldosterone system, which causes renal retention of sodium and water.

Revised 06/30/2015



DISCLAIMER: These materials are for educational purposes only, and are not a source of medical decision-making advice.