Impaired atrial contraction that can result from atrial arrhythmias such as atrial fibrillation. Increased heart rate e. Decreased ventricular afterload , which enhances forward flow i. Ventricular diastolic failure decreased ventricular compliance caused, for example, by ventricular hypertrophy or impaired relaxation lusitropy. Inflow mitral and tricuspid valve stenosis , which reduces ventricular filling.
Cardiovascular Physiology Concepts Richard E. Klabunde, PhD. This was very helpful, thank you. Thank you! Krishna gopal. Me a nurse in a conmunity as a community nurse. Plz subscribe me. Shahzad Ahmed Malik. Evonne Smith. We have the patient restrict fluid intake to about 2 liters daily and keep a low sodium diet. Also ACE inhibitors i. Spironolactone works in heart failure by inhibiting aldosterone. Lastly, hydralazine a direct arterial vasodilator decreases afterload and nitrates i.
The combination of hydralazine and nitrates are used in systolic congestive heart failure when ACE inhibitors and ARBs are contraindicated i. It is simply like taking a load off the wagon making the work of the donkey much easier:. We use beta-blockers i. I remember as a student asking "If beta-blockers decrease heart rate and contractility, then don't they also decrease cardiac output?
Wouldn't that make congestive heart failure worse since this is just a state of low cardiac output? Recall that cardiac output is calculated by heart rate multiplied by stroke volume Well, when a beta-blocker is FIRST started in systolic congestive heart failure, it can indeed lessen the cardiac output in the short term.
That is why it is nice to be sure the patient is clinically stable before you give it somewhat diuresed and certainly no pulmonary edema. Beta-blockers are like saying to the donkey "Slow down a bit and rest. Don't work so hard! Regain your strength! There are two types of drugs used in congestive heart failure that can do this by directly increasing the cardiac output: Digoxin and sympathomimetics i.
Digoxin is unique and is reviewed here. Through unknown mechanisms perhaps heightened tone of the parasympathetic nervous system , digoxin actually decreases heart rate. Digoxin ends up increasing the overall cardiac output and relieving the symptoms of congestive heart failure, but has never been shown to reduce mortality and certainly has some risk of toxicity.
This results from a decline in stroke volume that is due to systolic dysfunction, diastolic dysfunction, or a combination of the two. Briefly, systolic dysfunction results from a loss of intrinsic inotropy contractility , which can be caused by alterations in signal transduction mechanisms responsible for regulating inotropy. Systolic dysfunction can also result from the loss of viable, contracting muscle as occurs following acute myocardial infarction.
Diastolic dysfunction refers to the diastolic properties of the ventricle and occurs when the ventricle becomes less compliant i. Reduced filling of the ventricle results in less ejection of blood. Both systolic and diastolic dysfunction result in a higher ventricular end-diastolic pressure , which serves as a compensatory mechanism by utilizing the Frank-Starling mechanism to augment stroke volume. In some types of heart failure e.
Therapeutic interventions to improve cardiac function in heart failure include the use of cardiostimulatory drugs e. Neurohumoral responses occur during heart failure. These include activation of sympathetic nerves and the renin-angiotensin system , and increased release of antidiuretic hormone vasopressin and atrial natriuretic peptide. The net effect of these neurohumoral responses is to produce arterial vasoconstriction to help maintain arterial pressure , venous constriction to increase venous pressure , and increased blood volume to increase ventricular filling.
In general, these neurohumoral responses can be viewed as compensatory mechanisms, but they can also aggravate heart failure by increasing ventricular afterload which depresses stroke volume and increasing preload to the point where pulmonary or systemic congestion and edema occur. Therefore, it is important to understand the pathophysiology of heart failure because it serves as the rationale for therapeutic intervention.
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