1. Hydralazine
    Vasodilator (esp arterioles) Stimulation of guanylyl cyclase. Tx of mild/mod htn. Side effects COMMON (headache, nausea, dizziness, sweating, angina/arrythmias w ischemic heart disease, lupus)
  2. Minoxidil
    Vasodilator (esp arterioles). Activates k channels for hyperpolarization. Reflex increase in cardiac func also fluid retention. Tx of mild/mod htn. Sfx: chf, tamponade, reflex tacycardia, hair growth (ROGAINE)
  3. Diazoxide
    Vasodilator ( esp arterioles). Activates k channels. Salt and water retention. Tachycardia and increased CO. Tx of htn emergencies and malignant htn). Sfx: fluid retention and hyperglycemia, hyperuricemia
  4. Nitroprusside
    Vasodilator. Generates NO which activates guanylyl cyclase. Acts on arteries and veins to reduce preload and afterload. Use to produce hypotension in surg and htn emergencies (IV in hospital) RAPID decr in MAP
  5. Nitroglycerin
    Vasodilator( esp veins). Generates NO which activates guanylyl cyclase. Use for hypotension in surg and htn emergencies. Sfx: headache, short action, tolerance
  6. Epoprostenol
    Vasodilator. Prostacyclin (PGI2). Uses cAMP. Counteracts thromboxane A2. Use as potent antihypertensive but administer continuously thru IV ( use for pulmonary htn).
  7. Bosentan
    Non-selective endothelin receptor blocker. Use for pulmonary htn. Sfx: edema, headache, inhibition spermatogenesis, resp tract infection, decrease hematocrit, hepatic effects
  8. What is the initial approach to tx htn?
    Thiazide diuretic. Then use combos. Secondary approach is ACEI, ARBs, Ca channel blockers, or other vasodilators
  9. Implications of anti-htn meds in dentistry?
    Sedation w centrally acting drugs, NSAIDs antagonize anti-htns, orthostatic hypotension, sensitivity to catecholamines (adrenergic blockers), dry mouth, gingival hyperplasia (ca channel blockers), angioedema and cough (ACEI)
  10. What are the major determinants of myocardial oxygen consumption?
    Heart rate, contractility, wall stress
  11. Coronary blood flow is mainly regulated by what?
    • Myocardial oxygen consumption (MVO2)
    • But also by autoregulation (arterioles constricting/relaxing)
    • Wall tension
    • Nueral regulation (affect heart rate and contractility)
    • Humoral regulation
    • Myogenic tone
  12. 3 types of acute coronary syndrome?
    • Stable (occurs w exercise etc), unstable, acute
    • Also variant (aka Prinzmetals) with vasospasm wo stenosis and microvascular angina which occurs in females more and has no stenosis
  13. Drug classes to treat ACS and mechanisms?
    • Nitrovasodilators (increase supply and decrrease demand)
    • B receptor antagonists (decrase demand)
    • Ca channel blockers (increase supply and decrease demand)
    • Misc drugs ( alleviate causes)
  14. Determinants of oxygen supply to the heart?
    Coronary blood flow and oxyfen extraction
  15. As MVO2 increases, what happens to coronary blood flow?
    Also increases (myocytes tell arterioles to dilate)
  16. cAMP, cGMP, and hyperpolarization of k channels all do what to VSM?
  17. What is the effect of reactive oxygen species on VSM?
    • Prevents activation of cGMP. No relaxation. Can occur with
    • Atherosclerosis
    • Diabetes
    • Htn
    • Ang II
    • Inflammation
  18. What types of vessels does atherosclerosis occur within?
    Large arteries
  19. Signs of ACS
    • Chest pain (substernal vise-like)
    • Arm pain
    • Back pain
    • Dyspnea
    • Lasts 5-30 min
    • Can have no signs!
    • Arm pain
  20. What is the most important drug type used for ACS?
    • Nitrovasodilators
    • They release NO like normal endothelium
    • Reduce O2 demand:
    • Venodilator, arterial dilator, reduce wall stress, but have indirect reflex increase in hrart rate and contractility
    • Increase O2 supply: dilate conduit arteries at stenosis, increase subendocardial blood flow, increase collateral blood flow, decreased platelet activation
  21. Why does GTN (nitroglycerin) relax large coronary arteries much more than small ones?
    Bc of enzymatic (mtALDH) release of NO. Other nitrovasodilators have similar effect on all size arteries
  22. Nitroglycerin (GTN)
    First pass hepatic metab, short duration
  23. What is the benefit of a sublingual tablet or spray of GTN?
    Avoid first pass effect. Rapid onset. (but only ladts 30-60min)
  24. In what forms amyl nitrite used?
    Inhalant (limited use)
  25. Isosorbide dinitrate (ISDN)
    3-5 hr duration. Administer 3-4 times/ d
  26. Isosorbide mononitrate (ISMN)
    Longer action than ISDN. Dose 2 times/d. Minimal first pass effect.
  27. Adverse effects of nitrates?
    • Tolerance (interrupt therapy 8-12 hrs)
    • Headache
    • Orthostatic hypotension
    • Reflex tachycardia
    • Gi distress (oral) or skin irritation (patch)
    • Contraind w PDE5 inhibitors
  28. Why are nitrates contraindicated w PDE5 inhibitors?
    PDE5 inhibtors increase cGMP too (inhibit breakdown to GMP) so result is hypotension (drop of over 25mm hg)
  29. Sildenafil, tadalafil, vardenafil
    PDE5 inhibitors used to treat ED
  30. Propranolol metoprolol atenolol nadolol
    • B-adrenergic blockers
    • Blocking B1 effects: decrease heart rate and contractility and decrease renin release
    • Blocking B2 effects: potentiate a-adrenergic effects (vasoconstriction) and may exacerbate vasospasm
    • Use for ACS in combo w nitrates
    • Adverse fx: bronchospasm, hypoglycemia, hyperlipidemia, myocardial depression, bradycardia, reduced exercise tolerance, sleep disturbances, cold extremities, impotence, rebound w discontinuation ( bc upregulation of receptors)
  31. Verapamil, diltiazem
    Cardioselective ca channel blockers. decrease contractility, decrease heart rate, decrease arterial pressure (decr O2 demand) and vasodilate arteries and prevent coronary and cerebral vasospasm (increase O2 supply)
  32. What are the uses of ca channel blockers?
    ACS, HTN, supraventricular arrythmias, cerebral hemmorhage or vasospasm
  33. What are the adverse effects of ca channel blockers?
    Dizziness, nausea, headache, flushing, hypotension, edema, arrythmias, reflex tachycardia, gingival hyperplasia
  34. Nifedipine, amlodipine, felodipine, nicardipine, nimodipine
    Dihydropyridine ca channel blockers. Decrease art pressure, decrease heart rate (reduce O2 demand) and vasodilate epicardial arteries and stenoses and prevent coronary and cerebral vasospasm (increase O2 supply)
  35. Ranolazine
    New class of antianginal. Piperazine derivative (partial fatty acid ox inhibitor). Shifts ATP production to that from glycolysis. Inhibits late na channel to decrease na and ca inside ischemic myocytes). Minimal effect on heart rate and bp (use w other drugs in refractory pts). Improves exercise tolerance. Works better in males.
  36. How would you treat chronic stable angina?
    B blockers and aspirin (81mg). If contraindiacted to use bb (reynauds, asthma, depression, diabetes, some arrythmias) use ca channel blockers. Nitrates are cheap and safe but tolerance and side fx limit monotherapy (so use in combo). Also, STATINS to reduce high cholesterol
  37. What is the chronic treatment of unstable angina?
    Reduce demand and prevent vasoconstriction with nitrates, b-blockers, ca channel blockers (prevent vasospasm). Stabilize plaques with statins. Prevent platelet aggregation/activation w aspirin, clopidogrel, glycoprotein IIb/IIa blockers. Limit thrombus formation w heparin and THROMBIN INHIBITORS (hirudin, hirulog)
  38. Prasugrel, clopidogrel (Plavix)
    Thienopyridines. Req hepatic biotransformation. Noncomp irreversible ADP antagonist at P2 receptors. Blocks ADP mediated activation of glycoprotein GP IIa/IIb. INHIBITS PLATELET AGGREGATION. Use w aspirin. ACS (esp stents!) MI and sroke. Side fx: neutropenia
  39. What is the treatment of acute angina/ MI?
    MONA. also b blockers blunt increase in heart rate from GTN
  40. Implications for dentistry and pts with angina?
    Meds should be near (GTN in office), sit before stand, pts taking b-blockers should avoid other cardio depressants and LA w NE, gingival hyperplasia w ca channel blockers
  41. What 3 categories of drugs provide mortality benefit in HF when used alone?
    B-blockers, ARBs, ACEIs
  42. What types of treatment exist for HF?
    • Drugs that: decrease preload (loop diuretics/ thiazides/ spironolactone)
    • Decrease afterload (ACEIs, ARBs, vasodilators), improve contractility (adrenergic agonists, phosphodiesterase inhibitors, cardiac glycosides) and interrupting compensatory responses (various)
  43. Define HF
    Complex syndrome where ventricle cannot fill or eject blood properly. Can be structural or functional problem. 80 percent of ppl w HF are over 65.
  44. Cardinal signs of HF
    Dyspnea, fatigue (leads to exercise intolerance), and sometimes fluid retention (may lead to pulmonary congestionand edema)
  45. Describe starling relationship
    Increase filling pressure leads to increase stretch and increase SV
  46. What 3 factors influence myocardial performance (SV)?
    Preload, afterload, ionotropic state ( which is influenced by contractile properties of the muscle, autonomic nerves, circulating catecholomines)
  47. What 4 things can cause cardiac remodeling?
    Direct sympathetic nervous stimulation, elevated cardiac filing pressures, Ang II, and aldosterone
  48. Signs and symptoms of HF
    • Compensatory hemodynamic abnormalities
    • Dysreg of Ca homeostasis which impairs contraction and rekaxation (uptake of Ca by Na/Ca exchanger)
    • Dysreg of contractile proteins
    • Desensitization of B-adrenergic receptors leads to reduced Ca uptakr into SR
  49. Describe the sequelae of HF
    • Decrease in CO activates neurohumoral sysrem
    • Compensation maintains perfusion to organs
    • Increase in volume leads to wall stress and hypertrophic remodeling
    • Nuerohumoral activation directly induces apoptosis of myocytes
  50. What are the 5 cardiovascular adaptation mechanism associated with HF?
    • Abnormal baroreflex control (interpret high bp as normal)
    • Cardiac hypertrophy (at lower ionotropic state)
    • Altered renal function (SNS induces constriction of glomeruli and stimulatesrenin release)
    • Vasoconstriction (SNS, RAAS, ADH)
    • Edema
  51. What is the most useful test to evaluate pts with HF?
    • Echocardiogram and Doppler flow to see abnormalities of myocardium, heart valves, or pericardium. See whether
    • L ventricular ejection fraction is preserved or reduced?
    • L ventricle is normal or abnormal?
    • Other structural changes of valves, pericardium, or rt ventricle?
  52. What are causes of high cardiac output HF?
    Anemias and thyrotoxicosis
  53. Describe the stages of HF
    • A: risk for HF but no structural abnormalities
    • B: structural heart disease but no signs of HF
    • C: structural heart disease w prior or current symptoms
    • D: refractory HF
  54. Treatment of stage A HF?
    • Treat HTN, dyslipidemia, cease drugs and alcohol.
    • Drugs: ACEIs, ARBs
  55. Treatment of stage B HF?
    • Treat HTN, dyslipidemia, cease drugs and alcohol.
    • Drugs: ACEIs, ARBs, B-blockers
  56. Treatment of stage C HF?
    • Same as stage A and B but restrict salt intake.
    • Drugs: diruretics, ACEIs, B-blockers
    • Some pts may take aldosterone antagonists, digitalis, hydralazine/nitrates
  57. Treatment of stage D HF?
    • End of life care.
    • Heart transplant, mechanical support, experimental surgery/drugs
  58. Where does renin come from?
    Juxtaglomerular cells of the kidney
  59. How do ACE inhibitors work?
    Potent arterial dilators to reduce afterload and increase SV and CO
  60. What is the first line of therapy for HF?
    ACEIs. (Esp for all pts with reduced LVEF). Often combined with a B-blocker.
  61. What are contraindications of the use of ACEIs?
    Adverse reactions (angioedema) or impaired renal function (AngII helps perfuse kidney)
  62. Side effects of ACEIs?
    Hypotension, hyperkalemia, kidney failure in pts with impaired renal function, angioedema, cough
  63. Captopril, enalapril, ramipril, lisinopril, quinapril, fosinipril
    ACE inhibitors. Stop conversion of Ang I to Ang II. Inhibit breakdown of bradykinin (a vasodilator)
  64. What is the mechanism of AT1 angiotensin receptor blockers (ARBs)?
    Block actions of Ang II/III: cardiac remodeling, vasoconstriction, release of aldosterone. do NOT prevent brsdykinin breakdown
  65. What 3 types of bb reduce risk of death from HF?
    • Metoprolol
    • Carvedilol
    • Bisoprolol
  66. Who should take cardiac glycosides? (digoxin, digitoxin, ouabain)
    • HF pts in atrial fibrillation or severe HF ( also should be on ACEIs or ARBs, bb, and diuretics.
    • Also used for arrythmias
  67. Mechanisms of glycosides?
    • Inhibition of na/k ATPase to increase intracellular Ca andincrease force of contraction
    • Sensitizebaroreceptors to decrease SNS
    • Inhibit na/k ATPase inkidney which lowers na resorption so lower renin secreted
  68. Toxicity of glycosides?
    • Electrical: arrythmias, heart block, etc
    • Increased tox w hypokalemia, hypercalcemia, hypothyroidism
    • Clarithromycin, quinidine, verapamil increase tox
  69. Spironolactone and eplerenone
    Aldosterone antag: used in pts w severe HF or L vent dysfunc after MI. Class C or D HF- low dose with ACEI reduces mortaliy. USE W DIRURETICS. Risk of life-threatening hyperkalemia.
  70. How do vasodilators allow the heart to function more effectively?
    • Reduce preload
    • Reduce afterload
    • Both
    • (decrease filling pressures and volume)
  71. T or F: arterial dilators increase CO and promote diuresis
  72. T or F: venous dilators decrease preload and also increase coronary art flow which may increase ventricular func.
  73. T or F: hydralazine decreases renal blood floe
    F. Its used in pts who cant tolerate ACEIs
  74. What is treatment for pts w refractory HF in the hospital?
    Ionotropic agents: dobutamine, dopamine, milrinone. SHORT TERM USE
  75. Dopamine
    Stimulates b adrenergic feceptors on heart. Increases contractility. Stimulates a2 receptors at high doses to venoconstriction (makes HF worse). Tachycardia can provoke ischemia in pts w CAD
  76. Dobutamine
    B agonist. For pts w systolic dysfunc. Stimulates b1 and b2 receptors (ionotropy dominates)
  77. Side effects of dobutamine
    Tachycardia and arrythmias
  78. cAMP phosphodiesterase inhibitors
    • Inamrinone, milrinone
    • Used for advanced HF. Accelerate relaxation so more time for ca to enter cells and increase contraction
  79. Define pacemaker potential
    Slow inward movement of calcium and na. Change it to alter rate of depolarization.
  80. Most common sustained arrythmias
    Atrial fibrillation
  81. Artificial pacemaker
    Connects signal bt SA node and AV
  82. What dental devices shouldn't be used near a pt w a cardio dryer defibrillator or pacemaker?
    Ultrasonic scalers, composite curing lights, electrosurgical units (anything emitting electromagnetic waves)
  83. Types of drugs for arrythmias
    • Na blockers (1): slow upstroke of AP and block spontaneous depolarization
    • K blockers (3): increase duration of AP
    • Ca blockers (4): slowing spontsneous depolarization
    • B blockers (2): prolonging AV conduction
  84. Where do thrombi develop in atrial fib?
    Left atria. Risk for brain infarcts.
  85. Treatment of a fib
    Warfarin and aspirin to decrease clot risk
  86. Atrial based arrythmias
    Sinus tach, sinus bradycardia, atrial flutter
  87. Ventricular arrythmias
    Premature ventricular contraction (PVCs), ventricular tach, ventricular fib
  88. Impaired av transmission
    • First degree: PR interval increased
    • 2nd degree: ventricular rate irregular
    • 3rd degree: ventricular rate slow but regular
  89. Wolf Parkinson white syndrome
    Tachycardia with accessory path
  90. Torsades
    Dangerous. May progress to v-fib. Electrical loops in ventricle. Risk of quinidine and disopyramide
  91. A-fib
    • Electrical loops in atria.
    • Causes: HTN, age, HF, autonomic imbalance, channelopathies, atrial stretch, reduced atrial contraction, ca overload
  92. disopyramide, flecainide, lidocaine, mexiletine, moricizine, procainamide, propafenone, quinidine
    Na channel blockers to treat HF. Oral meds except lido which is given after ischemia through IV. slows upstroke of AP. RISK OF OTHER ARRYTHMIAS, WORSEN HF, and AV BLOCK. cimetidine reduces clearance
  93. Amiodarone, dofetilide, sotalol
    K channel blockers. Inhibit repolarization (prolong AP). WARFARIN increases effectiveness. Amiodarone also acts on na channeks. Sotalol is also a bb.
  94. Bepridil, diltiazem, verapamil
    • Ca channel blockers. Decrease conduction thru AV node, decrease firing in the SA node, reduce slope of pacemaker potential.
    • Sfx: hypotension (esp w inhlational anesthetics), AV block, bradycardia, gingival enlargment
  95. Adenosine
    Slows AV conduction. Inhibitory on nerves (caffeine/theophylline reduce effects) Given IV. short lived side effects are dyspnea, bronchospasm, hypotension. Dipyridamole amplifies.
  96. Propranolol, metoprolol, atenolol, timolol, Esmolol
    Bb used in arrythmias. Decrease conduction thru AV node (reduce slope ofpacemaker potential). Side effects are fatigue, worsening of HF, hypotension, ED, bronchospasm
  97. Magnesium
    IV for torsades des pointes
Card Set
pharmacolgy heart drugs