Hello! Let's talk about cocaine and beta blockers! :)
But just to cover the basics:
Cocaine blocks the reuptake of norepinephrine and dopamine at the presynaptic adrenergic terminals, causing an accumulation of catecholamines at the postsynaptic receptor (Mnemonic). That makes it a powerful sympathomimetic agent. Cocaine causes increased heart rate and blood pressure.
Cocaine causes myocardial ischemia or MI for a number of reasons:
(1) increasing myocardial oxygen demand by increasing heart rate, blood pressure, and contractility;
(2) decreasing oxygen supply via vasoconstriction;
(3) inducing a prothrombotic state by stimulating platelet activation and altering the balance between procoagulant and anticoagulant factors; and
(4) accelerating atherosclerosis.
Usually, in non–cocaine-using patients, β-blockers benefit numerous end points, including mortality, during and after acute MI, and in patients with cardiomyopathy.
BUT in cocaine-using patients, however, β- blockade can potentially leave α-stimulation unopposed, resulting in pronounced systemic and coronary vasoconstriction. They increase the risk of hypertension and coronary artery vasoconstriction. An anecdotal report of crushing chest pain, cardiac arrest, and death ensuing minutes after metoprolol administration illustrates the potential risk of mixing β-blockers with cocaine :O
So that's why, all β-blockers should be avoided in cocaine-using patients in the acute setting.
That's all!
-IkaN
You might also like:
Vasomotor reversal of Dale
Autonomic system drugs mnemonic
Uses of alpha and beta blockers
But just to cover the basics:
Cocaine blocks the reuptake of norepinephrine and dopamine at the presynaptic adrenergic terminals, causing an accumulation of catecholamines at the postsynaptic receptor (Mnemonic). That makes it a powerful sympathomimetic agent. Cocaine causes increased heart rate and blood pressure.
Cocaine causes myocardial ischemia or MI for a number of reasons:
(1) increasing myocardial oxygen demand by increasing heart rate, blood pressure, and contractility;
(2) decreasing oxygen supply via vasoconstriction;
(3) inducing a prothrombotic state by stimulating platelet activation and altering the balance between procoagulant and anticoagulant factors; and
(4) accelerating atherosclerosis.
Usually, in non–cocaine-using patients, β-blockers benefit numerous end points, including mortality, during and after acute MI, and in patients with cardiomyopathy.
BUT in cocaine-using patients, however, β- blockade can potentially leave α-stimulation unopposed, resulting in pronounced systemic and coronary vasoconstriction. They increase the risk of hypertension and coronary artery vasoconstriction. An anecdotal report of crushing chest pain, cardiac arrest, and death ensuing minutes after metoprolol administration illustrates the potential risk of mixing β-blockers with cocaine :O
So that's why, all β-blockers should be avoided in cocaine-using patients in the acute setting.
That's all!
-IkaN
You might also like:
Vasomotor reversal of Dale
Autonomic system drugs mnemonic
Uses of alpha and beta blockers
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