Blood flow beta-blocker effects

VASODILATOR ANTIHYPERTENSIVES BETA-BLOCKERS t hypotensive effect Additive hypotensive effect with diazoxide, hydralazine, minoxidil and sodium nitroprusside. In addition, hydralazine may T the bioavailability of beta-blockers with a high first-pass metabolism (e.g. propanolol and metoprolol), possibly due to alterations in hepatic blood flow or inhibited hepatic metabolism Monitor BP closely... 

BETA-BLOCKERS LIDOCAINE 1. Risk of bradycardia (occasionally severe), 1 BP and heart failure with intravenous lidocaine 2. Risk of lidocaine toxicity due to t plasma concentrations of lidocaine, particularly with propranolol and nadolol 3. t plasma concentrations of propranolol and possibly some other beta-blockers 1. Additive negative inotropic and chronotropic effects 2. Uncertain, but possibly a combination of beta-blocker-induced reduction in hepatic blood flow (due to 1 cardiac output) and inhibition of metabolism of lidocaine 3. Attributed to inhibition of metabolism by lidocaine 1. Monitor PR, BP and ECG closely watch for development of heart failure when intravenous lidocaine is administered to patients on beta-blockers 2. Watch for lidocaine toxicity 3. Be aware. Regional anaesthetics should be used cautiously in patients with bradycardia. Beta-blockers could cause dangerous hypertension due to stimulation of alpha-receptors if epinephrine is used with focal anaesthetic... 

Many beta-adrenoceptor antagonists undergo substantial first-pass hepatic metabolism these include alprenolol, metoprolol, oxprenolol, and propranolol. Hepatic cirrhosis, with consequent portosystemic shunting, can therefore result in increased systemic availability and higher plasma concentrations, perhaps resulting in adverse effects. Beta-blockers may also reduce liver blood flow and cause interactions with drugs with flow-dependent hepatic clearance. 

A single 20-mg dose of nisoldipine increased the steady-state AUC and peak plasma level of propranolol 160 mg daily by 35% and 55%, respectively. After combined treatment for 7 days, the AUC of propranolol was increased by 60% and the peak plasma level was increased by 55%. The combination enhanced blood pressure reduction to a small extent, but nisoldipine did not significantly reduce the effect of propranolol on heart rate. Similarly, another study found that a single 20-mg dose of nisoldipine increased the AUC and peak plasma level of a single 40-mg dose of propranolol by 43% and 68%, respectively, and that the AUC and peak plasma level of nisoldipine increased 30% and 57%, respectively. In this study, nisoldipine was reported to enhance beta-blockade. However, the same research group later found that the steady-state pharmacokinetics of propranolol 80 mg twice daily and nisoldipine 10 mg twice daily were not affected by concurrent use for 7 days, but nisoldipine attenuated the decrease in forearm blood flow seen with propranolol. The manufacturer of nisoldipine notes that severe hypotension can occur when it is given at the same time as beta blockers, and that, in isolated cases, signs of heart failure can also occur. ... 

Not understood. Where pharmaeokinetie ehanges are seen, a possible reason is that the metabolism of the beta bloekers is altered by changes in blood flow through the liver. The pharmacodynamic changes with nifedipine may be explained by the fact that nifedipine reduces the contractility of the heart muscle. This is counteracted by a sympathetic reflex increase in heart rate due to nifedipine-induced peripheral vasodilation, so that the ventricular output stays the same or is even improved. The presence of a beta blocker may oppose this to some extent by slowing the heart rate, which allows the negative inotropic effects of nifedipine to go unchecked. 

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