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12 views3 pages

Step 2 of UW3

Uploaded by

sunnykratnani
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© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Calcium channel blockers

● Types
○ Dihydropyridines: targeting vascular smooth muscle
■ Use: Hypertension, Angina (including vasospastic), Raynaud
phenomenon; dilated arteries
■ Amlodipine: systemic arterial dilation and reduced afterload to decrease
myocardial oxygen demand
■ clevidipine, nicardipine: both used for hypertensive urgency/emergency
■ nifedipine,
■ Nimodipine: Subarachnoid hemorrhage -> prevent cerebral
vasospasm
○ Nondihydropyridines: acting on the heart
■ Use: Hypertension, angina, AFib/Aflutter
■ diltiazem, verapamil.
● Mechanism: They block voltage-dependent L-type calcium channels in cardiac and
smooth muscle, reducing muscle contractility.
○ Potency in vascular smooth muscle: amlodipine = nifedipine > diltiazem >
verapamil.
○ Potency in the heart: verapamil > diltiazem > amlodipine = nifedipine.
● Side effect
○ Both: Gingival hyperplasia
○ Dihydropyridine
■ Peripheral edema
● Mechanism: Preferential arteriolar vasodilation and increased
peripheral capillary hydrostatic pressure.
● Addition of ACEi/ARBs reduce edema: post-capillary
venodilation
■ Flushing
■ Dizziness
○ Nondihydropyridine
■ Cardiac depression
■ AV block
■ Hyperprolactinemia: verapamil
■ Constipation

Nitrates: Nitroglycerin, isosorbide dinitrate, isosorbide mononitrate.


- Mechanism: Vasodilate via releasing NO in vascular smooth muscle, leading to an increase in
cGMP and smooth muscle relaxation. They dilate veins more than arteries (systemic
venodilation) w/ reduction in LVEDV and wallstress, reducing preload, decreased
myocardial oxygen demand
- Clinical use: Angina, acute coronary syndrome, pulmonary edema.
- Adverse effects: Reflex tachycardia (manage with β-blockers), methemoglobinemia,
hypotension, flushing, headache. "Monday disease" in industrial nitrate exposure may occur,
where tolerance develops during the work week but decreases over the weekend, resulting in
tachycardia, dizziness, and headache upon reexposure. Contraindicated in right ventricular
infarction, hypertrophic cardiomyopathy, and when using concurrent PDE-5 inhibitors.

β1 receptors: Increase heart rate, increase contractility (one heart), reduce renin release,
reduce lipolysis.
● Blockade: cardiac suppression with bradycardia and hypotension, Confusion due to
cerebral hypoperfusion
- β2 receptors: Cause vasodilation, bronchodilation (two lungs), reduce lipolysis, reduce
insulin release, reduce glycogenolysis/glucogenesis, relax uterine tone (tocolysis), reduce
aqueous humor production, decrease cellular K+ uptake.
● Blockade: Bronchospasm, Hypoglycemia, Confusion & seizure due to hypoglycemia

β-blockers: Atenolol, betaxolol, bisoprolol, carvedilol, esmolol, labetalol, metoprolol, nadolol,


nebivolol, propranolol, timolol.
● Angina pectoris: Decrease heart rate and contractility, leading to reduced oxygen
consumption.
● Glaucoma: Reduce production of aqueous humor (Timolol).
● Heart failure: Block neurohormonal stress to prevent deleterious cardiac remodeling and
decrease mortality (Bisoprolol, carvedilol, metoprolol).
● Hypertension: Reduce cardiac output and renin secretion (β1-receptor blockade on JG
cells).
● Hyperthyroidism/thyroid storm: Control symptoms like heart rate and tremor
(Propranolol).
● Hypertrophic cardiomyopathy: Decrease heart rate to improve filling time and relieve
obstruction.
● Myocardial infarction: Decrease oxygen demand in the short term and reduce mortality
in the long term.
● Supraventricular tachycardia: Reduce AV conduction velocity (Metoprolol, esmolol).
● Variceal bleeding: Decrease hepatic venous pressure gradient and portal hypertension
prophylactically (Nadolol, propranolol, carvedilol).
● Adverse Effects
○ Erectile dysfunction,
○ cardiovascular effects (bradycardia, AV block, heart failure),
○ CNS effects (seizures, sleep alterations),
○ dyslipidemia (metoprolol),
○ masked hypoglycemia,
○ exacerbations of asthma/COPD.
○ Controversy surrounds the use of β-blockers for acute cocaine-associated chest
pain due to concerns about unopposed α-adrenergic stimulation.
● Toxicity
○ Diagnosis: ECG: sinus node dysfunction, AV block, consistent clinical
presentation (drug level not useful)
○ Treatment: IV fluid for hypotension & atropine for bradycardia; Glucagon to
directly counter toxicity (increased intracellular cAMP), calcium gluconate
given to increase BP
● Selectivity
○ β1-selective antagonists (β1 > β2): Atenolol, betaxolol, bisoprolol, esmolol,
metoprolol:
○ Nonselective antagonists (β1 = β2): Nadolol, propranolol, timolol.
○ Nonselective α- and β-antagonists: Carvedilol, labetalol.
○ Nebivolol combines β1-adrenergic blockade with stimulation of β3-receptors,
activating NO synthase in the vasculature and reducing systemic vascular
resistance.
● Overdose
●

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