Cardiovascular Pharmacology

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jknell
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209626
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Cardiovascular Pharmacology
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2013-03-26 16:58:53
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  1. Antihypertensive Therapy
    • 1. Essential HTN
    • 2. CHF
    • 3. DM
  2. Antihypertensive Therapy: Essential HTN
    • -Diuretics
    • -ACEIs
    • -ARBs
    • -CCBs
  3. Antihypertensive Therapy: CHF
    • -Diuretics
    • -ACEIs/ARBs
    • -β-Blocker (compensated CHF)
    • -K+ Sparing diuretics

    **β-Blockers must be used cautiously in decompensated CHF and are CI in cardiogenic shock
  4. Antihypertensive Therapy: Diabetes Mellitus
    • -ACEIs/ARBs
    • -CCB
    • -Diuretics
    • -β-Blockers
    • -α-Blockers

    ACEIs: protective against diabetic nephropathy
  5. Calcium Channel Blockers
    • DHP:
    • -Nifedipine
    • -Amlodipine

    • Non-DHP:
    • -Verapamil
    • -Diltiazem

    • Mechanism:
    • -block voltage gated L-type calcium channels
    • -reduces contractility
    • -DHP: effect predominantly vascular smooth muscle
    • -Non-DHP: effect vascular smooth muscle and cardiac muscle

    • Vascular smooth muscle:
    • amlodipine = nifedipine > diltiazem > verapamil

    • Heart:
    • verapamil > diltiazem > amlodipine = nifedipine
    • "Verapamil = Ventricle"

    • Clinical Use:
    • -HTN-angina
    • -arrhythmias (NOT nifedipine)
    • -Prinzmetal's angina
    • -Raynaud's

    • Toxicity:
    • -Cardiac depression
    • -AV block
    • -peripheral edema
    • -flushing
    • -dizziness
    • -constipation
  6. Hydralazine
    • Mechanism:
    • -increase cGMP → smooth muscle relaxation
    • -vasodilates arterioles > veins
    • -afterload reduction

    • Clinical Use:
    • -severe HTN
    • -CHF
    • -First line for HTN in pregnancy (with methyldopa)
    • -frequently given with β-blocker to prevent reflex tachycardia

    • Toxicity:
    • -compensatory tachycardia (CI: angina/CAD)
    • -fluid retention
    • -nausea
    • -HA-angina
    • -Lupus-like syndrome
  7. Malignant HTN Treatment
    • Commonly used drugs:
    • -Nitroprusside
    • -Nicardipine
    • -Clevdipine
    • -Labetolol
    • -Fenoldopam
  8. Nitroprusside
    • Mechanism:
    • -short acting
    • -increase cGMP via direct release of NO

    • Clinical Use:
    • -Malignant hypertension

    • Toxicity:
    • -can cause cyanide toxicity (releases cyanide)
  9. Fenoldopam
    • Mechanism:
    • -dopamine D1 receptor agonist
    • -causes coronary, peripheral, renal and splanchnic vasodilation
    • -decreases BP and increases natriuresis
  10. Nitroglycerin, Isosorbide Dinitrate
    • Mechanism:
    • -vasodilate by releasing NO in smooth muscle
    • -causing increase cGMP and smooth muscle relaxation
    • -dilate veins >> arteries
    • -decreases preload

    • Clinical Use:
    • -angina
    • -pulmonary edema

    • Toxicity:
    • -reflex tachycardia
    • -hypotension
    • -flushing
    • -HA

    • "Monday Disease"
    • -in industrial exposure
    • -development of tolerance for the vasodilating action during work week and loss of tolerance over the weekend
    • -results in tachycardia, dizziness, and HA upon re-exposure
  11. Antianginal Therapy
    • Goal:
    • -reduction of MVO2 by decreasing 1 or more of the determinants: EDV, BP, HR, contractility, ejection time

    • Nitrates
    • -affect preload

    • β-Blockers
    • -affect afterload

    • Calcium Channel Blockers
    • -Nifedipine is similar to Nitrates in effect
    • -Verapamil is similar to β-Blockers in effect

    • Pindolol and acebutolol
    • -partial β-Blockers that are CI in angina
  12. Antianginal Therapy: Effects of Nitrates
    • End-diastolic volume
    • BP
    • Contractility (reflex response)
    • Heart Rate (reflex response)
    • Ejection time
    • MVO2
  13. Antianginal Therapy: Effects of β-Blockers
    • End-diastolic volume
    • BP
    • Contractility
    • Heart Rate
    • Ejection Time
    • MVO2
  14. Antianginal Therapy: Effects of Nitrates + β-Blockers
    • No effect or End-diastolic volume
    • Blood Pressure
    • Little/No effect on Contractility
    • Heart Rate
    • Little/no Effect on Ejection Time
    • ↓↓ MVO2
  15. Lipid Lowering Agents
    • 1. HMG-CoA Reductase Inhibitors
    • 2. Niacin (B3)
    • 3. Bile Acid Resins
    • 4. Cholesterol Absorption Blockers
    • 5. Fibrates



  16. HMG-CoA Reductase Inhibitors
    • Lovastatin
    • Pravastatin
    • Simvastatin
    • Atorvastatin
    • Rosuvastatin

    • Mechanism:
    • -inhibit conversion of HMG-CoA to mevalonate, a XOL precursor

    • Effect on LDL: ↓↓↓
    • Effect on HDL:
    • Effect on TGs:

    • Side Effects:
    • -hepatotoxicity (increased LFTs)
    • -rhabdomyolysis
  17. Niacin (B3)
    • Mechanism:
    • -inhibits lipolysis in adipose tissue
    • -reduces hepatic vLDL secretion into circulation

    • Effect on LDL: ↓↓
    • Effect on HDL: ↑↑
    • Effect on TGs: 

    • Side Effects:
    • -red, flushed face (decreased by aspirin or long term use)
    • -hyperglycemia (acanthosis nigricans)
    • -hyperuricemia (exacerbates gout)
  18. Bile Acid Resins
    • Cholestyramine
    • Colestipol
    • Colesevelam

    • Mechanism:
    • -prevent intestinal reabsorption of bile acids
    • -liver must use XOL to make more

    • Effect on LDL: ↓↓
    • Effect on HDL: slighty ↑
    • Effect on TGs: slightly ↑

    • Side Effects:
    • -patients hate it
    • -tastes bad
    • -causes GI discomfort
    • -decreased absorption of fat soluble vitamins
    • -cholesterol gall stones
  19. Cholesterol Absorption Blockers
    Ezetimibe

    • Mechanism:
    • -Prevent XOL reabsorption at small intestine brush border

    • Effect on LDL: ↓↓
    • Effect on HDL: --
    • Effect on TGs: --

    • Side Effects:
    • -rare increase in LFTs
    • -diarrhea
  20. Fibrates
    • Gemfibrozil
    • Clofibrate
    • Bezafibrate
    • Fenofibrate

    • Mechanism:
    • -upregulate LPL → increased TG clearance

    • Effect on LDL:
    • Effect on HDL:
    • Effect on TGs: ↓↓↓

    • Side Effects:
    • -myositis
    • -hepatotoxicity (increased LFTs)
    • -XOL gallstones
  21. Cardiac Glycosides
    Digoxin

    • Pharm:
    • -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
    • -decreases intracellular Ca2+ concentration → positive ionotropy
    • -stimulates vagus nerve → decreased HR

    • Clinical Use :
    • -CHF (increase contractility)
    • -A Fib (decrease conduction at AV node and depression of SA node)

    • Toxicity:
    • 1. Cholinergic:
    • -nausea/vomiting
    • -diarrhea
    • -blurry yellow vision (think Van Gogh)

    • 2. EKG:
    • -↑ PR
    • -↓ QT
    • -ST scooping
    • -T wave inversion
    • -arrhythmia
    • -AV block

    • 3. Hypokalemia
    • -poor prognostic indicator

    • Factors Predisposing to Toxicity:
    • -renal failure (decreased excretion)
    • -hypokalemia (permissive for digoxin binding at K+ binding site on Na+/K+ ATPase)
    • -Quinidine (decreased digoxin clearance, displaces digoxin from tissue-binding sites)

    • Antidote:
    • -slowly normalize K+
    • -lidocaine
    • -cardiac pacer
    • -anti-digoxin Fab fragments
    • -Mg2+
  22. Antiarrhythmics: Na+ Channel Blockers (Class I)
    Local anesthetics

    • Mechanism:
    • -slow or block conduction (especially in depolarized cells)
    • -decrease phase 0 slope and increased threshold for firing in abnormal pacemaker cells



    Are state dependent: selectively depress tissue that is frequently depolarized (eg: tachycardia)

    Hyperkalemia causes increased toxicity for all Class I drugs

    • Class IA:
    • -Quinidine
    • -Procainamide
    • -Disopyramide
    • "The Queen Proclaims Diso's pyramid"

    • Class IB
    • -Lidocaine
    • -Mexiletine
    • -Tocainide
    • "I'd Buy Lidy's Mexican Tacos"

    • Class IC
    • -Flecainide
    • -Propafenone
  23. Class IA Antiarrhythmics
    • Quinindine
    • Procainamide
    • Disopyramide

    "The Queen Proclaims Diso's pyramid"

    • Mechanism:
    • -↑ AP duration
    • -↑ effective refractory period (ERP)
    • -↑ QT interval

    • Clinical Uses:
    • -affect both atrial and ventricular arrhythmias
    • -especially reentrant and ectopic supraventricular and ventricular tachycardia

    • Toxicity:
    • -thrombocytopenia
    • -torsades de pointes due to ↑ QT interval
    • -Quinidine (cinchonism: HA, tinnitus)
    • -Procainamide (reversible SLE-like syndrome)
    • -Disopyramide (HF)
  24. Class IB Antiarrhythmics
    • Lidocaine
    • Mexiletine
    • Tocainide

    "I'd Buy Lidy's Mexican Tacos"

    **Phenytoin can also fall into the IB category

    • Mechanism:
    • -↓ AP duration
    • -preferentially affect ischemic or depolarized Purkinje and ventricular tissue

    • Clinical Use:
    • -acute ventricular arrhythmias (esp post-MI)
    • -digitalis induced arrhythmias

    "IB is Best post-MI"

    • Toxicity:
    • -local anesthetic
    • -CNS stimulation/depression
    • -CV depression
  25. Class IC Antiarrhythmics
    • Flecainide
    • Propafenone

    • Mechanism:
    • -no effect on AP duration

    • Clinical Use:
    • -Useful in ventricular tachycardias that progress to VF and in intractable SVT
    • -usually used only as last resort in tachyarrhythmias
    • -for patients without structural abnormalities

    • Toxicity:
    • -proarrhythmic, especially post-MI (Contraindicated!!!)
    • -significantly prolongs the refractory period at the AV node

    "IC is Contraindicated in structural heart disease and post-MI"
  26. Antiarrhythmics: β-Blockers (Class II)
    • Metoprolol
    • Propanolol
    • Esmolol
    • Atenolol
    • Timolol
  27. Class II Antiarrhythmics
    • Metoprolol
    • Propanolol
    • Esmolol
    • Atenolol
    • Timolol

    • Mechanism:
    • -decrease SA and AV node activity by decrease cAMP and decreasing Ca2+ currents
    • -suppresses abnormal pacemakers by decreasing phase 4 slope
    • -AV node is particularly sensitive (increased PR interval)
    • *esmolol is very short acting

    • Clinical Use:
    • -ventricular tachycardia
    • -SVT
    • -slowing ventricular rate during Afib and A flutter

    • Toxicity:
    • -impotence
    • -exacerbation of asthma
    • -CV effects (bradycardia, AV block, CHF)
    • -CNS effects (sedation, sleep alterations)
    • -may mask signs of hypoglycemia
    • -Metoprolol: may cause dyslipidemia
    • -Propanolol: can exacerbate vasospasm in Prinzmetal's angina

    • Overdose:
    • -tx with glucagon
  28. Antiarrhythmics: K+ Channel blockers (Class III)
    • Amiodarone
    • Ibutilide
    • Dofetilide
    • Sotalol

    "AIDS"
  29. Class III Antiarrhythmics
    • Amiodarone
    • Ibutilide
    • Dofetilide
    • Sotalol

    "AIDS"

    • Mechanism:
    • -increase AP duration
    • -increase ERP
    • -increase QT interval

    • Clinical Use:
    • -when other antiarrhythmics fail

    • Toxicity:
    • 1. Sotalol:
    • -torsades de pointes
    • -excessive β block

    • 2. Amiodarone:
    • -pulmonary fibrosis
    • -hepatotoxicity
    • -hypo/hyperthyroidism (amiodarone is 40% iodine)
    • -corneal deposits
    • -skin deposits (blue/gray) resulting in photodermatitis
    • -neurologic effects
    • -constipation
    • -CV effects (bradycardia, heart block, CHF)

    **Amiodarone has class I, II, III and IV effects b/c it alters the lipid membrane

    Remember to check PFTs, LFTs and TFTs when using amiodarone
  30. Antiarrhythmics: Ca2+ Channel blockers (Class IV)
    • Verapamil
    • Diltiazem
  31. Class IV Antiarrhythmics
    • Verapamil
    • Diltiazem

    • Mechanism:
    • -decrease conduction velocity
    • -increase ERP
    • -increase PR interval

    • Clinical Use:
    • -prevention of nodal arrhythmias (SVT)

    • Toxicity:
    • -constipation
    • -flushing
    • -edema
    • -CV effects (CHF, AV block, SA depression)
  32. Other Antiarrhythmics
    • Adenosine
    • Mg2+
  33. Adenosine
    • Mechanism:
    • -increase K+ out of cells → hyperpolarizing cell and decrease ICa
    • -very short acting (~15 sec)

    • Clinical Use:
    • -drug of choice in diagnosing/abolishing supraventricular tachycardia

    • Toxicity:
    • -flushing
    • -hypotension
    • -chest pain

    Effects blocked by theophyline and caffeine
  34. Mg2+
    • Effective in:
    • -Torsades de pointes
    • -digoxin toxicity

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