MOA: Calcium channel blockers (CCB) prevent the release of internal calcium stores into the cell cytosol. Heart muscle cell does not respond to calcium ion signal as a result. Therefore, there is a decrease in intercellular calcium. CCB attach to alpha 1 subunit on L-type voltage-gated slow calcium ion channels.
Dosage: 5-10mg (0.075-0.15mg/kg) over 2 min; may give additional 10mg after 30 min if no response.
Onset: 1-3 min IV
Duration: 15 min IV
Half-Life: 3-7 hours
Protein Binding: 90%
Metabolism: Renal 70% Hepatic 15% has an active metabolite (prolong action)
S/E's: Hypotension, flushing, HA, weakness, palpitations, constipation, peripheral edema, myocardial ischemia r/t coronary steal
Uses: Supraventricular tachydysrhythmias (AV node), Vasospastic angina, symptomatic hypertrophic cardiomyopathy; if liver disease (give 20-50% normal dose), geriatrics (give slower IV), DO NOT GIVE WITH: heart failure, severe bradycardia, AV node block, WPW, A fib/flutter, cardiogenic shock, hypotension <90SBP, LV EF <30%, SSS, 2nd or 3rd AV block w/out Pacemaker. CAUTION (pt's treated with digitalis or beta-blockers)
MOA: Inhibits extracellular Ca ion influx across membranes of myocardial cells and vascular smooth muscle cells, without changing serum calcium concentrations, resulting in inhibition of cardiac and vascular smooth muscle contraction, thereby dilating main coronary and systemic arteries.
Dosage: 0.25-0.35 mg/kg over 2 min; may repeat after 15 min. Drip after bolus: 5-15 mg/hr. up to 24 hours.
Onset: 2-5 min IV
Duration: SVT: IV: 1-3 hr.; continuous IV infusion: 0.5-10 hr.
Half-Life: 4-6 hours
Protein Binding: 70-80%
Metabolism: Renal 35% Hepatic 60% Has an active metabolite
S/E's: Headache, edema, Atrioventricular block, hypotension, Brady arrhythmia
Uses: ***1st line Treatment for SVT! Angina, Hypertension, Afib/flutter. DO NOT GIVE WITH: WPW, cardiogenic shock, hypotension <90SBP, SSS, 2nd or 3rd AV block w/out Pacemaker.
CAUTION (AV block, CHF, hepatic/renal impairment)
MOA: Inhibits the trans membrane influx of extracellular Ca++ across myocardial and vascular smooth muscle cell membranes without changing serum calcium concentrations, resulting in inhibition of cardiac and vascular smooth muscle contraction, thereby dilating the main coronary and systemic arteries. Vasodilation with decreased peripheral resistance and increased heart rate.
Dosage: 5-15 mcg/kg IV
Onset: 1-3 min IV
Duration: 2-6 hours (if taken orally)
Half-Life: 3-7 hours
Protein Binding: 92-98%
Metabolism: Renal 80% Hepatic <15%
S/E's: flushing, vertigo, and headache.
Uses: Treatment of angina due to coronary artery vasospasm, Raynaud's syndrome
GREATEST VASODILATING EFFECTS!!!
MOA: Inhibits trans membrane influx of extracellular Ca ions across membranes of myocardial cells & vascular smooth muscle cells, without changing serum calcium concentrations, resulting in inhibition of cardiac & vascular smooth muscle contraction, thereby dilating main coronary & systemic arteries. Produces vasodilation and decreases peripheral resistance. **Pure Afterload Reducer.
Dosage: Initial 5 mg/hr. slowly (50 mL/hr.), may increase q15min by 2.5 mg/hr.; no more than 15 mg/hr
Onset: 1-3 min IV
Duration: 3 hour IV
Half-Life: 3-5 hours
Protein Binding: 95%
Metabolism: Renal 55% Hepatic 45%
S/E's: Headache, hypotension, tachycardia, nausea/vomiting
Uses: Hypertension. Tocolytic, Electroconvulsive therapy, useful in patients with residual hypertension despite beta-adrenergic blockade.
**DO NOT GIVE- premixed cardene to pt.'s with Advanced Aortic Stenosis!
MOA: Highly lipid soluble (Crosses BBB). Prevent Ca entry into the vascular smooth cells by extracellular allosteric modulation of the L-type voltage-gated calcium ion channels.
Dosage: 10 mcg/kg IV
Onset: 1-3 min IV
Duration: unable to find.
Protein Binding: 99%
Metabolism: Renal 20% Hepatic 80%, has an active metabolite
S/E's: Reduction in systemic blood pressure, diarrhea, headache, abdominal pain
Uses: Cerebral Vasospasm (give PO X21 days)
MOA: Inhibits extracellular Ca ions across the membranes of myocardial cells and vascular smooth muscle cells, without changing serum calcium concentrations, resulting in inhibition of cardiac and vascular smooth muscle contraction, thereby dilating the main coronary and systemic arteries
Dosage: 2.5-10mg PO
Onset: 24-96 hour
Duration: 24-48 Hour
Half-Life: 35-50 Hour
Protein Binding: 93-98%
Metabolism: Extensively metabolized in liver
S/E's: Flushing, HA, weakness, palpitations, peripheral edema, nausea, abdominal pain.
Uses: Hypertension, Angina. CAUTION (CHF, hepatic impairment, symptomatic hypotension, worsening of angina and acute MI)
Verapamil and diltiazem slow heart rate by working on what phase of the SA node action potential?
Verapamil and diltiazem slow heart rate by slowing phase 4 depolarization of the SA node action potential.
Calcium channel blockers such as verapamil act on what phase of the ventricular action potential?
Verapamil and other calcium channel blockers decrease myocardial (ventricular) contractility by blocking the entry of calcium during phase 2 (plateau) of the ventricular action potential. (This action of the calcium channel blockers is a side-effect, not a therapeutic effect).
On what tissue of the heart does verapamil work: atrial muscle, ventricular muscle, nodal tissue, Purkinje network?
For therapeutic effect, verapamil works on nodal tissue where it slows phase 4 depolarization. Verapamil secondarily works on phase 2 (plateau) of the ventricular muscle action potential, but this is not the best answer to the question as written.
What are five uses of calcium entry blockers?
supraventricular tachydysrhythmia (verapamil)
coronary artery vasospasm (nifedipine and diltiazem )
cerebral artery vasospasm (nimodipine)
How does verapamil effect systemic vascular resistance (SVR) and heart rate?
Verapamil decreases both SVR (by relaxing vascular smooth muscle) and heart rate.
Verapamil potentiates the actions of what drugs used in anesthesia?
Verapamil potentiates the actions of nondepolarizing and depolarizing muscle relaxants.
Why is verapamil a poor choice when treat in patients with WoIff-Parkinson-White syndrome?
Verapamil may increase conduction velocity in the accessory tract and increase heart rate excessively.
Why should verapamil be avoided or used cautiously in the patient taking either a beta blocker (propranolol) or digitalis?
Verapamil and propranolol or verapamil and digitalis, can produce complete heart block.
What are the cardiovascular actions of diltiazem?
Diltiazem is a good coronary vasodilator but a poor peripheral vasodilator. Diltiazem also decreases heart rate.
How does nifedipine affect systemic vascular resistance (SVR) and heart rate?
Nifedipine decreases systemic vascular resistance (SVR) and causes a reflex increase in heart rate.
When would you use sublingual nifedipine?
Sublingual nifedipine might be used to treat intraoperative myocardial ischemia when hemodynamics are normal.
What is the mechanism of action of CCB's?
CCBs attach to alpha1 subunit on L-type voltage-gated slow calcium ion channels resulting in negative inotropy, negative chronotropy, negative dromotropy and peripheral vasodilation.
If a patient on chronic beta-blocker therapy was administered Verapamil, what cardiovascular event could occur?
Drug induced complete heart block.
What is the treatment for a complete heart block caused from the administration of both verapamil and a beta-blocker?