Left-Sided Heart Failure
ID: ANM10003
MEDICAL ANIMATION TRANSCRIPT: In left-sided heart failure, the left ventricle cannot pump an adequate amount of blood, a volume known as preload, out of the heart. This condition causes pulmonary congestion, a buildup of blood in the pulmonary vessels causes fluid in lung tissues that impedes normal respiration. Systolic left-sided heart failure describes the left ventricle's inability to contract with enough force to drive blood out of the heart against resistance called afterload to the rest of the body. After a left ventricular contraction, the blood left behind in the chamber causes blood to back up into the left atrium and pulmonary circulation, leading to pulmonary congestion. Diastolic left-sided heart failure describes the inability of the left ventricle to expand sufficiently to accommodate oxygenated blood entering from the left atrium. In this condition, the left ventricle contracts with normal force, but the blood volume that is pumped out is insufficient to meet the body's needs. Long-standing diseases, such as coronary artery disease, hypertension, and diabetes, can thicken and stiffen the ventricular muscle, making it a non-compliant, inefficient pump. As a result of reduced myocardial contractility, the unexpelled blood pools inside the left ventricle, and the chamber expands to hypertrophic size. This hypertrophy of the heart muscle results in the insufficient delivery of nutrients and oxygen to tissues. In both systolic and diastolic left-sided heart failure, the buildup of unexpelled blood increases pressure in the pulmonary circulation, causing serosanguineous fluid to seep into the alveoli and interstitium. This fluid buildup is heard as crackles and rhonchi when the lungs are auscultated. As the lungs saturate with fluid, patients may develop difficulty breathing, called dyspnea, trouble breathing while lying flat, called orthopnea, or rapid breathing, called tachypnea. The heart rate increases to compensate for the left ventricle's weakened state, which in time leads to thickening the myocardium as it labors to push blood out of the heart against the increasing pressure in the pulmonary vessels and fluid in the lungs and continuing the cycle of cardiac muscle damage. Treatment for heart failure involves changes in lifestyle, such as diet and exercise, medication, surgery, or a combination of approaches. Medications commonly prescribed for heart failure include diuretics, which reduce fluid volume and venous return by inhibiting sodium and water reabsorption along the kidney's renal tubular system; ACE inhibitors, which block hormones in the renin-angiotensin-aldosterone system, dilating vessels, lowering blood volume and venous return, decreasing the heart's workload, and halting ventricular hypertrophy; digoxin, a cardiac glycoside medication that increases the force of myocardial contractility by raising intracellular sodium and calcium concentrations; and beta-blockers, which compete with norepinephrine molecules for binding sites on cardiomyocytes, preventing norepinephrine's effects, resulting in reduced speed and strength of the contractions, which can support more efficient circulation through the body.
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