CARDIAC HYPERTROPHY
H︎ypertrophy is an increase in the size of cells resulting in an increase in the size of the organ. Stated another way, in pure hypertrophy there are no new cells, just bigger cells containing increased amounts of structural proteins and organelles. Hypertrophy of cardiac muscle can be caused by genetic disease or by certain pathophysiologic circumstances. Myocardium subjected to a persistently increased workload, as in hypertension or with a narrowed (stenotic) valve, adapts by undergoing hypertrophy to generate the required higher contractile force.
Let's take it one side at a time. The left heart squeezes blood to the body, namely to the entire systemic vascular tree via the aorta.
Afterload is the pressure that the heart must work against to eject blood during systole (ventricular contraction). Afterload is proportional to the average arterial pressure.Thus, one cause of increased strain on the left heart is increased blood pressure in the arteries (hypertension).
What else might cause the left ventricle to have to work extra
hard?
Blood goes from the left ventricle through the aortic valve to the aorta. In aortic stenosis, aortic valve narrows. This narrowing prevents the valve from opening fully, which reduces or blocks blood flow from your heart into the main artery to your body (aorta) and onward to the rest of your body. The left ventricle has to squeeze hard against the resistance posed by the stenotic aortic valve. Over time, this can cause left ventricular hypertrophy.
What causes right ventricular hypertrophy?
Using the same logic, what site of increased resistance would
cause the right heart to have to work harder? Since the right
heart ejects into the lungs, any process that increases
resistance in the pulmonary vasculature (pulmonary hypertension) can lead to right ventricular hypertrophy.
If any process increases the resistance that the heart must pump against, the heart will have to work harder to squeeze, and can eventually grow big and thick. Although this growth may initially be compensatory, it eventually reaches diminishing returns.
Consequences of Cardiac Hypertrophy.
First, the increased thickness of the hypertrophied ventricular wall also makes it more difficult to adequately perfuse. As the cardiac muscle outgrows its blood supply, ischemia (decreased blood flow) can occur, which can result in angina, and/or infarction. Second the hypertrophy allows the heart to squeeze better, but its thick walls do not relax as well. In addition, the muscle can get so thick that the chamber becomes quite small. Poor relaxation and small chamber size lead to decreased filling of the ventricles, which results in decreased cardiac output.
Ventricular relaxation occurs during diastole, so since the hypertrophied heart cannot relax as well, cardiac hypertrophy causes diastolic dysfunction. If the heart cannot relax opti mally, it cannot fill optimally; thus, forward flow decreases and backup of flow occurs. Hypertrophy of the left ventricle can eventually lead to left heart failure symptoms and signs, and right ventricular hypertrophy can lead to right heart failure symptoms and signs
Treatment of Cardiac Hypertrophy.
If the hypertrophied heart has a smaller chamber size, and does not fill optimally, the treatment of choice should de crease heart rate and contractile force, allowing for in creased filling and increased cardiac output. Beta blockers which are competitive antagonists that block the receptor sites for epinephrine and norepinephrine on adrenergic beta

receptors, of the sympathetic nervous system, and calcium channel blockers by blocking calcium entry into the cell, cause decreased myocardial force generation and decreased heart rate. So beta blockers and calcium channel blockers accomplish these goals.







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