Cardio Pharm Flashcards by Steffanie Nelson

Where do dihydropyridine calcium channel blockers act?

On vascular smooth muscle

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Where do non-dihydropyridine calcium channel blockers act?

On heart

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Nimodipine use

Subarachnoid hemorrhage (prevents cerebral vasospasm)

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Dihydropyridine clinical uses

HTN, angina, Raynaud phenomenon

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Drugs used in hypertensive urgency or emergency

Nicardipine, Clevidipine, Fenoldopam, Labetalol, or Notroprusside

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Non-dihydropyridine clinical uses

HTN, angina, atrial fibrillation/flutter

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Adverse effects of non-dihydropyridines

Cardiac depression, AV block, hyperprolactinemia, constipation, gingival hyperplasia

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Adverse effects of dihydropyridines

Peripheral edema, flushing, dizziness

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Mechanism of Hydralazine

Increase cGMP leading to smooth muscle relaxation. Vasodilates arterioles > veins; afterload reduction

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Clinical uses of hydralazine

Severe HTN, HF,

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Nitroprusside MOA

Increase cGMP via direct release of NO

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MOA for Fenoldopam

Dopamine D1 receptor agonist - causes coronary, peripheral, renal, and splanchnic vasodilation. Decreases BP and increases natriuresis.

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What are the adverse effects of nitrates?

Reflex tachycardia, hypotension, flushing, headache, “Monday disease”

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When are nitrates contraindicated?

In right ventricular infarction

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MOA for Ranolazine

Inhibits the late phase of sodium current thereby reducing diastolic wall tension and oxygen consumption. Does not affect HR or contractility

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Clinical use of Ranolazine

Angina refractory to other medical therapies

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Adverse effects of Ranolazine

Constipation, dizziness, headache, nausea, QT prolongation

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MOA of Milrinone

Selective PDE-3 inhibitor.
In cardiomyocytes: Increase cAMP accumulation, leading to increase calcium influx, and increased inotropy and chronotropy.
In vascular smooth muscle: Increase cAMP accumulation, inhibition of MLCK activity, and general vasodilation

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Adverse effects of Milrinone

Arrhythmias, hypotension

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Name the HMG-CoA reductase inhibitors

Lovastatin, Pravastatin

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MOA of Lovastatin, Pravastatin

Inhibit conversion of HMG-CoA to mevalonate, a cholesterol precursor; decrease mortality in CAD patients

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Adverse effects of HMG-CoA reductase inhibitors

Hepatotoxicity (increase LFTs), myopathy (when used with fibrates or niacin)

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Name the bile acid resins

Cholestyramine, colestipol, colesevelam

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MOA for bile acid resins

Prevent intestinal reabsorption of bile acids; liver must use cholesterol to make more

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MOA of Ezetimibe

Prevent cholesterol absorption at small intestine brush border

MOA of Fibrates

Upregulate LPL leading to increased triglyceride clearance. Activates PPAR-alpha to induce HDL synthesis.

Adverse effects of fibrates

Myopathy (increased risk with statins), cholesterol gallstones (via inhibition of cholesterol 7alpha-hydroxlase)

MOA of Niacin

Inhibits lipolysis (hormone sensitive lipase) in adipose tissue; reduces hepatic VLDL synthesis

Adverse effects of Niacin

Red, flushed face; hyperglycemia, hyperuricemia

Name the PCSK9 inhibitors

Alirocumab, evolocumab

MOA of PCSK9 inhibitors

Inactivation of LDL-receptor degradation, increasing amount of LDL removed from bloodstream

Adverse effects of PCSK9 inhibitors

Myalgias, delirium, dementia, other neurocognitive effects

MOA of Digoxin

Direct inhibition of Na+/K+ ATPase, leading to indirect inhibition of Na+/Ca2+ exchanger. Increased Ca2+ leads to positive inotropy. Also stimulates the vagus nerve leading to decreased HR.

Clinical uses of Digoxin

HF (increase contractility); atrial fibrillation (decrease conduction at AV node and depression of SA node)

Adverse effects of Digoxin

Cholinergic, hyperkalemia

Antidote for Digoxin

Slowly normalize K+, cardiac pacer, anti-digoxin Fab fragments, Mg2+

Quinidine, Procainamide, Disopyramide are in which class of drugs?

Class 1A Antiarrhythmics

MOA of class 1A antiarrhythmics

Increase AP duration, increase effective refractory period, increase QT interval, some potassium channel blocking effects

Adverse effects of class 1A antiarrhythmics?

Cinchonism, reversible SLE-like syndrome, HF, thrombocytopenia, torsades de pointes

Lidocaine, Mexiletine are in which class of drugs?

Class 1B Antiarrhythmics

MOA of class 1B antiarrhythmics

Decrease AP duration. Preferentially affect ischemic or depolarized Purkinje and ventricular tissue

Flecainide, Propafenone are in which class of drugs?

Class 1C Antiarrhythmics

MOA of class 1C antiarrythmics

Prolongs ERP in AV node and accessory bypass tracts

Adverse effects of class 1C antiarrhythmics

Pro-arrythmic, especially post MI

What kind of drugs are class II antiarrhythmics?

Beta blockers

MOA of class II antiarrythmics

Decrease SA and AV nodal activity by decreasing cAMP and Ca2+ currents. Suppress abnormal pacemakers by decreasing the slope of phase 4. Increase PR interval.

How is beta blocker overdose treated?

With saline, atropine, glucagon

What kind of drugs are class III antiarrhythmics?

Potassium channel blockers

Amiodarone, Ibutilide, Dofetilide, Sotalol

Class III antiarrhythmics

MOA of class III antiarrythmics

Increase AP duration, increase ERP, increase QT interval

What is an adverse affect of class III antiarrythmics

Torsades de pointes

Adverse effects of Amiodarone

Pulmonary fibrosis, hepatotoxicity, hypothyroidism or hyperthyroidism, acts as hapten, neurologic effects, constipation, cardiovascular effects

What type of drugs are class IV antiarrhythmics?

Calcium channel blockers

Verapamil, Diltiazem

Class IV antiarrhythmics

MOA of class IV antiarrhythmics

Decrease conduction velocity, increase ERP, increase PR interval

Adverse effects of class IV antiarrhythmics

Constipation, flushing, edema, cardiovascular effects

Adenosine MOA

Increase K+ out of cells leading to hyperpolarization of the cell and decreased Ca2+ influx, decreasing AV node conduction

Adverse effects of Adenosine

Flushing, hypotension, chest pain, sense of impending doom, bronchospasm

How are torsades de pointes and digoxin toxicity treated?

Mg2+

MOA of Ivabradine

Selective inhibition of funny sodium channels, prolonging slow depolarization phase (phase 4). Decreased SA node firing; negative chronotropic effect without inotropy. Reduces cardiac O2 requirement.

When is Ivabradine used?

Chronic stable angina in pts who can't take beta blockers. Chronic HF with reduced EF