Heart failure hypokalemia causing

It is important to note that, even more than in heart failure, overly aggressive use of diuretics in this setting can be disastrous. Vigorous diuretic therapy can cause marked depletion of intravascular volume, hypokalemia, and metabolic alkalosis. Hepatorenal syndrome and hepatic encephalopathy are the unfortunate consequences of excessive diuretic use in the cirrhotic patient. 

Sodium removal is the next important step—by dietary salt restriction or a diuretic—especially if edema is present. In mild failure, it is reasonable to start with a thiazide diuretic, switching to more powerful agents as required. Sodium loss causes secondary loss of potassium, which is particularly hazardous if the patient is to be given digitalis. Hypokalemia can be treated with potassium supplementation or through the addition of a potassium-sparing diuretic such as spironolactone. As noted above, spironolactone should probably be considered in all patients with moderate or severe heart failure since it appears to reduce both morbidity and mortality. 

The mineralocorticoid properties of carbenoxolone are probably exerted by displacement of aldosterone from non-specific receptor sites in cells, thus making it more available to affect mineral metabolism. What this means in practice is that in normal doses carbenoxolone can cause salt and water retention, with occasional hypokalemia. These effects are common but usually mUd they are detected more often during treatment if patients are weighed, their blood pressure measured, and serum potassium concentrations checked. Those who take prolonged courses, elderly patients, and those with hepatic, cardiac, or renal impairment are at special risk severe effects, with serious hypertension, heart failure, and hypokalemia of sufficient degree to induce myopathy and tubular necrosis, can usually be ascribed to ill-advised treatment of people in whom carbenoxolone is contraindicated, to its use in elderly patients, or to prolonged intake without supervision. 

In a randomized, open, parallel-group study of the hemodynamic effects of milrinone and glyceryl trinitrate in 119 patients with advanced decompensated heart failure, milrinone was significantly more effective than glyceryl trinitrate (7). Adverse effects caused the withdrawal of milrinone in three of the 58 patients who took it one had ventricular extra beats, one had renal insufficiency, and one had hypokalemia. Headache was the most common adverse effect in both groups, but was less common in those who took milrinone (12 versus 29%). 

Like all diuretics, the thiazides can cause electrolyte abnormalities, such as hypokalemia and hyponatremia, and dehydration. These complications are uncommon in patients with uncomplicated hypertension, but are more common in patients with heart failure or decompensated hepatic cirrhosis with secondary hyperaldosteronism. Until a patient is accustomed to the effect of a diuretic, dizziness may be experienced. Serum lipid concentrations are slightly raised acutely and hyperglycemia can occur during long-term therapy. Rare effects are thrombocytopenia, rashes, drug fever, cholestatic jaundice, pancreatitis, and precipitation of hepatic... 

Answer E. In approaching the answer to this question, try to sort out the incorrect statements. Spironolactone does not cause hypokalemia, but hyperkalemia. Although loop diuretics may cause hyperuricemia, there is no connection between elevations of uric add and fainting episodes. When used with ACEIs in the treatment of heart failure, spironolactone is reported to increase survival, but there is no evidence of similar efficacy in patients with HTN. Obviously, statement B is erroneous (never choose never ). Although postural hypotension from the combination of antihypertensive drugs is most likely responsible for the fainting episode in this patient, there could also be alternative explanations ... 

Amiloride is used with thiazide or loop diuretics in hypertension, in congestive heart failure, in digitalis-induced hypokalemia, and in arrhythmias resulting from hypokalemia. Inappropriate use of amiloride may cause hyperkalemia (potassium >5.5 mEq/L), which may be fatal if not corrected, and may be more deleterious in elderly individuals and in patients with diabetes mellitus and renal impairment. The symptoms of hyperkalemia include fatigue, flaccid paralysis of the extremities, paresthesias, bradycardia, ECG abnormalities, and shock. Amiloride is not metabolized but is contraindicated in anuria, acute or chronic renal insufficiency, or in diabetic nephropathy. It should not be used with potassium preparations, and should be used cautiously with ACE inhibitors because these agents cause hyperkalemia. 

Cardiovascular Long QT syndrome and torsade de pointes occurred postpartum in a woman with heart failure who was taking ciprofloxacin for a urinary tract infection. Other causative factors included hypokalemia and hypomagnesemia [36 ]. The electrolyte disturbances were corrected, a pacemaker was implanted, and she was... 

Adults. 3 g PO q6h x 4 PRN Supl 1-2 g IM or IV repeat PRN Preeclampsia/pre-mature labor 4 g load then g/h IV inf Cardiac arrest 1-2 g IV push (2-4 mL 50% soln) in 10 mL DjW AMI Load 1-2 g in 50-100 mL D5W, over 5-60 min IV then 0.5-1.0 g/h IV up to 24 h (ECC 2005) Feds. 25-50 mg/kg/dose IM or IV q4-6h for 3-4 doses repeat PRN dose w/ low urine output or renal insuff Caution [B, +] Contra Heart block, renal failure Disp Inj 10, 20, 40, 80, 125, 500 mg/mL bulk powder SE CNS depression, D, flushing, heart block Interactions T CNS depression W/ antidepressants, antipsychotics, anxiolytics, barbiturates, hypnotics, narcotics EtOH T neuromuscular blockade Wf aminoglycosides, atracurium, gallamine, pancuronium, tubocurarine, vecuronium EMS Check for absent patellar reflexes this may indicate tox may cause hypokalemia (flattened T waves) and hypocalcemia OD May cause hypotension, resp arrest, T PR, QRS, and QT interval, AV block, and cardiac arrest calcium salts can be given to reverse resp depression... 

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