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Cardiovascular - Pharmacology Flashcards

1
Q

Antihypertensive therapy

  • Primary (essential) hypertension
  • Hypertension with CHF
  • Hypertension with diabetes mellitus
A
  • Primary (essential) hypertension
    • Diuretics, ACE inhibitors, angiotensin II receptor blockers (ARBs), calcium channel blockers.
  • Hypertension with CHF
    • Diuretics, ACE inhibitors/ARBs, β-blockers (compensated CHF), aldosterone antagonists.
    • β-blockers must be used cautiously in decompensated CHF and are contraindicated in cardiogenic shock.
  • Hypertension with diabetes mellitus
    • ACE inhibitors/ARBs, calcium channel blockers, diuretics, β-blockers, α-blockers.
    • ACE inhibitors/ARBs are protective against diabetic nephropathy.
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2
Q

Calcium channel blockers

  • Examples
  • Mechanism
  • Clinical use
  • Toxicity
A
  • Examples
    • Amlodipine, nimodipine, nifedipine (dihydropyridine)
    • Diltiazem, verapamil (non-dihydropyridine).
  • Mechanism
    • Block voltage-dependent L-type calcium channels of cardiac and smooth muscle, thereby reduce muscle contractility.
    • Vascular smooth muscle
      • Amlodipine = nifedipine > diltiazem > verapamil.
    • Heart
      • Verapamil > diltiazem > amlodipine = nifedipine
      • Verapamil = ventricle
  • Clinical use
    • Dihydropyridine (except nimodipine): hypertension, angina (including Prinzmetal), Raynaud phenomenon.
    • Non-dihydropyridine: hypertension, angina, atrial fibrillation/flutter.
    • Nimodipine: subarachnoid hemorrhage (prevents cerebral vasospasm).
  • Toxicity
    • Cardiac depression, AV block, peripheral edema, flushing, dizziness, hyperprolactinemia, and constipation.
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3
Q

Hydralazine

  • Mechanism
  • Clinical use
  • Toxicity
A
  • Mechanism
    • Increases cGMP –>Ž smooth muscle relaxation.
    • Vasodilates arterioles > veins
      • Afterload reduction.
  • Clinical use
    • Severe hypertension, CHF.
    • First-line therapy for hypertension in pregnancy, with methyldopa.
    • Frequently coadministered with a β-blocker to prevent reflex tachycardia.
  • Toxicity
    • Compensatory tachycardia (contraindicated in angina/CAD), fluid retention, nausea, headache, angina, Lupus-like syndrome.
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4
Q

Hypertensive emergency

  • Commonly used drugs
  • Nitroprusside
  • Fenoldopam
A
  • Commonly used drugs
    • Nitroprusside, nicardipine, clevidipine, labetalol, and fenoldopam.
  • Nitroprusside
    • Short acting
    • Increases cGMP via direct release of NO.
    • Can cause cyanide toxicity (releases cyanide).
  • Fenoldopam
    • Dopamine D1 receptor agonist—coronary, peripheral, renal, and splanchnic vasodilation.
    • Decreases BP and increases natriuresis.
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5
Q

Nitroglycerin, isosorbide dinitrate

  • Mechanism
  • Clinical use
  • Toxicity
A
  • Mechanism
    • Vasodilate by increasing NO in vascular smooth muscle –> increase in cGMP and smooth muscle relaxation.
    • Dilate veins >> arteries.
    • Decreases preload.
  • Clinical use
    • Angina, acute coronary syndrome, pulmonary edema.
  • Toxicity
    • Reflex tachycardia (treat with β-blockers), hypotension, flushing, headache
    • “Monday disease” in industrial exposure: development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekend results in tachycardia, dizziness, and headache upon reexposure.
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6
Q

Antianginal therapy

  • Goal
  • Calcium channel blockers
  • Pindolol and acebutolol
  • Nitrates
  • β-blockers
A
  • Goal
    • Reduction of myocardial O2 consumption (MVO2) by decreasing 1 or more of the determinants of MVO2: end-diastolic volume, blood pressure, heart rate, contractility.
  • Calcium channel blockers
    • Nifedipine is similar to nitrates in effect
    • Verapamil is similar to β-blockers in effect.
  • Pindolol and acebutolol
    • Partial β-agonists contraindicated in angina.
  • Nitrates
    • Affect preload.
  • β-blockers
    • Affect afterload.
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7
Q

Antianginal therapy

  • For each: increased, decreased, or little/no effect
    • Nitrates
    • β-blockers
    • Nitrates + β-blockers
  • End-diastolic volume
  • Blood pressure
  • Contractility
  • Heart rate
  • Ejection time
  • MVO2
A
  • End-diastolic volume
    • Nitrates: Decreased
    • β-blockers: Increased
    • Nitrates + β-blockers: No effect or decreased
  • Blood pressure
    • Nitrates: Decreased
    • β-blockers: Decreased
    • Nitrates + β-blockers: Decreased
  • Contractility
    • Nitrates: Increased (reflex response)
    • β-blockers: Decreased
    • Nitrates + β-blockers: Little/no effect
  • Heart rate
    • Nitrates: Increased (reflex response)
    • β-blockers: Decreased
    • Nitrates + β-blockers: Decreased
  • Ejection time
    • Nitrates: Decreased
    • β-blockers: Increased
    • Nitrates + β-blockers: Little/no effect
  • MVO2
    • Nitrates: Decreased
    • β-blockers: Decreased
    • Nitrates + β-blockers: Really decreased
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8
Q

Lipid-lowering agents:
HMG-CoA reductase inhibitors (lovastatin, pravastatin, simvastatin, atorvastatin, rosuvastatin)

  • Effect on LDL
  • Effect on HDL
  • Effect on triglycerides
  • Mechanisms of action
  • Side effects / problems
A
  • Effect on LDL (“bad cholesterol”)
    • Really really decreased
  • Effect on HDL (“good cholesterol”)
    • Increased
  • Effect on triglycerides
    • Decreased
  • Mechanisms of action
    • Inhibit conversion of HMG-CoA to mevalonate, a cholesterol precursor
  • Side effects / problems
    • Hepatotoxicity (increased LFTs), rhabdomyolysis (esp. when used with fibrates and niacin)
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9
Q

Lipid-lowering agents:
Niacin (vitamin B3)

  • Effect on LDL
  • Effect on HDL
  • Effect on triglycerides
  • Mechanisms of action
  • Side effects / problems
A
  • Effect on LDL (“bad cholesterol”)
    • Really decreased
  • Effect on HDL (“good cholesterol”)
    • Really increased
  • Effect on triglycerides
    • Decreased
  • Mechanisms of action
    • Inhibits lipolysis in adipose tissue
    • Reduces hepatic VLDL synthesis
  • Side effects / problems
    • Red, flushed face, which is decreased by aspirin or long-term use
    • Hyperglycemia (acanthosis nigricans)
    • Hyperuricemia (exacerbates gout)
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10
Q

Lipid-lowering agents:
Bile acid resins (cholestyramine, colestipol, colesevelam)

  • Effect on LDL
  • Effect on HDL
  • Effect on triglycerides
  • Mechanisms of action
  • Side effects / problems
A
  • Effect on LDL (“bad cholesterol”)
    • Really decreased
  • Effect on HDL (“good cholesterol”)
    • Slightly increased
  • Effect on triglycerides
    • Slightly increased
  • Mechanisms of action
    • Prevent intestinal reabsorption of bile acids
    • Liver must use cholesterol to make more
  • Side effects / problems
    • Patients hate it—tastes bad and causes GI discomfort, decreased absorption of fat-soluble vitamins
    • Cholesterol gallstones
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11
Q

Lipid-lowering agents:
Cholesterol absorption blockers (ezetimibe)

  • Effect on LDL
  • Effect on HDL
  • Effect on triglycerides
  • Mechanisms of action
  • Side effects / problems
A
  • Effect on LDL (“bad cholesterol”)
    • Really decreased
  • Effect on HDL (“good cholesterol”)
    • No effect
  • Effect on triglycerides
    • No effect
  • Mechanisms of action
    • Prevent cholesterol absorption at small intestine brush border
  • Side effects / problems
    • Rare increased LFTs, diarrhea
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12
Q

Lipid-lowering agents:
Fibrates (gemfibrozil, clofibrate, bezafibrate, fenofibrate)

  • Effect on LDL
  • Effect on HDL
  • Effect on triglycerides
  • Mechanisms of action
  • Side effects / problems
A
  • Effect on LDL (“bad cholesterol”)
    • Decreased
  • Effect on HDL (“good cholesterol”)
    • Increased
  • Effect on triglycerides
    • Really really decreased
  • Mechanisms of action
    • Upregulate LPL –> increased TG clearance
    • Activates PPAR-α to induce HDL synthesis
  • Side effects / problems
    • Myositis (increased risk with concurrent statins), hepatotoxicity (increased LFTs), cholesterol gallstones (esp. with concurrent bile acid resins)
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13
Q

Cardiac glycosides

  • Examples
  • Mechanism
  • Clinical use
  • Toxicity
  • Antidote
A
  • Examples
    • Digoxin
      • 75% bioavailability
      • 20–40% protein bound
      • t1/2 = 40 hours
      • Urinary excretion.
  • Mechanism
    • Direct inhibition of Na+/K+ ATPase leads to indirect inhibition of Na+/Ca2+ exchanger/antiport.
    • Increased [Ca2+]i –>Ž positive inotropy.
    • Stimulates vagus nerve –>Ž decreased HR.
  • Clinical use
    • CHF (increased contractility)
    • Atrial fibrillation (decreased conduction at AV node and depression of SA node).
  • Toxicity
    • Cholinergic—nausea, vomiting, diarrhea, blurry yellow vision (think Van Gogh).
    • ECG—increased PR, decreased QT, ST scooping, T-wave inversion, arrhythmia, AV block.
    • Can lead to hyperkalemia, which indicates poor prognosis.
    • Factors predisposing to toxicity—renal failure (decreased excretion), hypokalemia (permissive for digoxin binding at K+-binding site on Na+/K+ ATPase), verapamil, amiodarone, quinidine (decreased digoxin clearance; displaces digoxin from tissue-binding sites).
  • Antidote
    • Slowly normalize K+, cardiac pacer, anti-digoxin Fab fragments, Mg2+.
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14
Q

Antiarrhythmics—Na+ channel blockers (class I)

A
  • Slow or block (decrease) conduction (especially in depolarized cells). 
  • Decrease slope of phase 0 depolarization and increase threshold for firing in abnormal pacemaker cells.
  • Are state dependent (selectively depress tissue that is frequently depolarized [e.g., tachycardia]).
  • Hyperkalemia causes increased toxicity for all class I drugs.
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15
Q

Antiarrhythmics—Na+ channel blockers (class IA)

  • Examples
  • Mechanism
  • Clinical use
  • Toxicity
A
  • Examples
    • Quinidine, Procainamide, Disopyramide.
    • “The Queen Proclaims Diso’s pyramid.”
  • Mechanism
    • Increased AP duration, increased effective refractory period (ERP), increased QT interval.
  • Clinical use
    • Both atrial and ventricular arrhythmias, especially re-entrant and ectopic SVT and VT.
  • Toxicity
    • Cinchonism (headache, tinnitus with quinidine), reversible SLE-like syndrome (procainamide), heart failure (disopyramide), thrombocytopenia, torsades de pointes due to increased QT interval.
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16
Q

Antiarrhythmics—Na+ channel blockers (class IB)

  • Examples
  • Mechanism
  • Clinical use
  • Toxicity
A
  • Examples
    • Lidocaine, Mexiletine.
  • Mechanism
    • Decrease AP duration.
    • Preferentially affect ischemic or depolarized Purkinje and ventricular tissue.
    • Phenytoin can also fall into the IB category.
  • Clinical use
    • Acute ventricular arrhythmias (especially post-MI), digitalis-induced arrhythmias.
    • IB** is Best post-MI.**
  • Toxicity
    • CNS stimulation/depression, cardiovascular depression.
17
Q

Antiarrhythmics—Na+ channel blockers (class IC)

  • Examples
  • Mechanism
  • Clinical use
  • Toxicity
A
  • Examples
    • Flecainide, Propafenone.
    • “Can I have Fries, Please.”
  • Mechanism
    • Significantly prolongs refractory period in AV node.
    • Minimal effect on AP duration.
  • Clinical use
    • SVTs, including atrial fibrillation.
    • Only as a last resort in refractory VT.
  • Toxicity
    • Proarrhythmic, especially post-MI (contraindicated).
    • IC** is Contraindicated in structural and ischemic heart disease.**
18
Q

Antiarrhythmics—β-blockers (class II)

  • Examples
  • Mechanism
  • Clinical use
  • Toxicity
A
  • Examples
    • Metoprolol, propranolol, esmolol, atenolol, timolol, carvedilol.
  • Mechanism
    • Decrease SA and AV nodal activity by decreasing cAMP, decreasing Ca2+ currents.
    • Suppress abnormal pacemakers by decreasing slope of phase 4.
    • AV node particularly sensitive—increased PR interval.
    • Esmolol very short acting.
  • Clinical use
    • SVT, slowing ventricular rate during atrial fibrillation and atrial flutter.
  • Toxicity
    • Impotence, exacerbation of COPD and asthma, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alterations).
    • May mask the signs of hypoglycemia.
    • Metoprolol can cause dyslipidemia.
    • Propranolol can exacerbate vasospasm in Prinzmetal angina.
    • Contraindicated in cocaine users (risk of unopposed α-adrenergic receptor agonist activity).
    • Treat overdose with glucagon.
19
Q

Antiarrhythmics—K+ channel blockers (class III)

  • Examples
  • Mechanism
  • Clinical use
  • Toxicity
A
  • Examples
    • Amiodarone, Ibutilide, Dofetilide, Sotalol.
    • “AIDS.”
  • Mechanism
    • Increase AP duration, increase ERP.
    • Used when other antiarrhythmics fail. 
    • Increase QT interval.
  • Clinical use
    • Atrial fibrillation, atrial flutter
    • Ventricular tachycardia (amiodarone, sotalol).
  • Toxicity
    • Sotalol—torsades de pointes, excessive β blockade.
    • Ibutilide—torsades de pointes.
    • Amiodarone—pulmonary fibrosis, hepatotoxicity, hypothyroidism/ hyperthyroidism (amiodarone is 40% iodine by weight), corneal deposits, skin deposits (blue/gray) resulting in photodermatitis, neurologic effects, constipation, cardiovascular effects (bradycardia, heart block, CHF).
    • Remember to check PFTs, LFTs, and TFTs when using amiodarone.
    • Amiodarone has class I, II, III, and IV effects and alters the lipid membrane.
20
Q

Antiarrhythmics—Ca2+ channel blockers (class IV)

  • Examples
  • Mechanism
  • Clinical use
  • Toxicity
A
  • Examples
    • Verapamil, diltiazem.
  • Mechanism
    • Decrease conduction velocity, increase ERP, increase PR interval.
  • Clinical use
    • Prevention of nodal arrhythmias (e.g., SVT), rate control in atrial fibrillation.
  • Toxicity
    • Constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression).
21
Q

Other antiarrhythmics

  • Adenosine
  • Mg2+
A
  • Adenosine 
    • Increasing K+ out of cells Ž–> hyperpolarizing the cell and decreasing ICa.
    • Drug of choice in diagnosing/abolishing supraventricular tachycardia.
    • Very short acting (~ 15 sec).
    • Adverse effects include flushing, hypotension, chest pain.
    • Effects blocked by theophylline and caffeine.
  • Mg2+
    • Effective in torsades de pointes and digoxin toxicity.

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