Question

A. B. is a 67 year old gentleman who was admitted to the cardiac floor for monitoring after he presented to the ER with chest pain and a sensation that his heart was beating irregularly. His initial workup to R/O an MI was negative but he had multi-focal PVC's on the monitor. Vital signs are normal including a pulse of 72 and BP of 98/78. All his blood work was normal except for a K+ level of 6.2. His past medical history is positive for heart failure secondary to many years of poorly controlled HTN. He has no other medical problems. His medications include the ACEI lisinopril and the non-selective beta blocker carvedilol (Coreg). He is on no other medications. 1. Why would a negative inotropic medication such as a beta blocker be prescribed for a patient with heart failure? To prevent excess stimulation from catecholamines. 2. If A. B. developed decompensated heart failure would you anticipate that his beta blocker be continued? 3. Why would a beta blocker usually not be given with digoxin for a patient with heart failure? 4. Why couldn't A. B. fix the hyperkalemia with endogenous aldosterone? 5. If A. B. was on a thiazide diuretic such as hydrochlorothiazide (HCTZ) could his hyperkalemia perhaps have been avoided?

Answer 1

1. Beta blocker help to decrease heart rate and heart gets more time to fill with blood. This allows left ventricle to fill more completely and there will be increase in volume of blood to be pumped with each heartbeat i. E. Ejection fraction increases.

2. acute decompensated heart failure is a sudden worsening of the signs and symptoms of heart failure, which typically includes difficulty breathing (dyspnea), leg or feet swelling, and fatigue. It is caused by pooling of blood in organs due to failure of heart to pump. Beta blockers are contraindicated in acute decompensated heart failure because they decrease heart rate therefore worsen heart pumping action. This aggravates sign and symptoms.

3. Beta blockers will not be given with digoxin in patients with heart failure because these both drugs have negative ionotropic effect. Thereby these drugs together will worsen heart failure symptoms.

4. Hyperkalemia cant be fixed by endogenous aldosterone because patient is on angiotensin converting enzyme inhibitor that causes hypoaldosteronism. Therefore there is no sufficient alsosterone to fix hyperkalemia.

5. Yes thiazide diuretics can avoid hyperkalemia as they increase sodium delivery to the distal segment of the distal tubule. Thisincrease in distal tubular sodium concentration stimulates the aldosterone-sensitive sodium pump to increase sodium reabsorption in exchange for potassium and hydrogen ion, which are lost to the urine. This leads to resolution of hyperkalemia.