Drug Interactions between KIE and nebivolol / valsartan

MONITOR CLOSELY: Concomitant use of angiotensin II receptor blockers (ARBs) and potassium salts may increase the risk of hyperkalemia. Inhibition of angiotensin II results in decreased aldosterone secretion, which in turn causes potassium retention. Risk factors for developing severe or life-threatening hyperkalemia may include renal impairment, diabetes, old age, severe or worsening heart failure, dehydration, and concomitant use of other agents that block the renin-angiotensin-aldosterone system or otherwise increase serum potassium levels.

MANAGEMENT: Caution is advised if angiotensin II receptor blockers must be used concurrently with potassium salts, particularly in patients with renal impairment, diabetes, old age, severe or worsening heart failure, dehydration, or concomitant therapy with other agents that increase serum potassium such as nonsteroidal anti-inflammatory drugs, beta-blockers, cyclosporine, heparin, tacrolimus, and trimethoprim. The combination should generally be avoided in these patients unless absolutely necessary and the benefits outweigh the potential risks. Serum potassium and renal function should be checked prior to initiating therapy and regularly thereafter. Patients should be given counseling on the appropriate levels of potassium and fluid intake, and advised to seek medical attention if they experience signs and symptoms of hyperkalemia such as nausea, vomiting, weakness, listlessness, tingling of the extremities, paralysis, confusion, weak pulse, and a slow or irregular heartbeat.

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MONITOR: Beta-blockers may antagonize the cardiostimulatory effects of ephedrine by blocking beta-1 adrenergic receptors in the heart. Parenteral ephedrine may be less effective in the treatment of shock and hypotension if the patient is receiving, or has recently received, a beta-blocking drug. In addition, peripheral vascular resistance may increase due to unopposed alpha-adrenergic effect of ephedrine in the presence of beta-blockade. Theoretically, the interaction may also occur with beta-blocker ophthalmic preparations, since they may be systemically absorbed and can produce clinically significant systemic effects even at low or undetectable plasma levels.

MANAGEMENT: Clinicians should be alert to the potential for diminished cardiac response when parenteral ephedrine is used in patients treated with beta-blockers, including ophthalmic formulations.

GENERALLY AVOID: Noncardioselective beta-blockers can antagonize the bronchodilating effects of ephedrine by blocking beta-2 adrenergic receptors in smooth muscles of the bronchial tree. The interaction is less likely to occur with cardioselective beta-blockers, which generally have little effect on beta-2 adrenergic receptors at therapeutic dosages. However, cardioselectivity is not absolute and may be lost with larger doses.

MANAGEMENT: Noncardioselective beta-blockers, including ophthalmic formulations, should generally be avoided in patients using ephedrine-containing preparations for bronchospastic diseases. If beta-blocker therapy is necessary, an agent with beta-1 selectivity (e.g., atenolol, metoprolol, betaxolol) is considered safer. However, caution is advised, especially with higher dosages of the beta-blocker.

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GENERALLY AVOID: In the Valsartan Heart Failure Trial, the combination of valsartan with a beta-blocker and an ACE inhibitor was associated with unfavorable outcomes on morbidity and mortality in heart failure patients. The mechanism is unknown.

MANAGEMENT: The manufacturer recommends that the triple combination of valsartan with a beta-blocker and an ACE inhibitor be avoided in heart failure patients.

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