Cardio Pharm

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  1. Conductance in cardiac slow response tissue is dependent on what three things?
    • 1. Rate of phase 0 depolarization
    • 2. Threshold potential
    • 3. Resting Membran Potential
  2. Increase in cAMP on the heart tissue will:
    • Increase upstroke velocity in pacemakers by increase of Ca influx
    • Shorten the AP duration by increasing K efflux
    • Increase HR by increasing Na funny channel influx (increasing slope of phase 4)
  3. Saved By Pharm Class
    • Sodium
    • Beta blockers
    • Potassium
    • Calcium
  4. Antiarrhythmic Drug: Class Ia General
    • Drugs: Quinidine, Procainimide, Disopyramid
    • Block fast Na channels
    • prefer to be open or activated "state dependent" blockage
    • increases AP duration & ERP
    • Also blocks K channels (prolongs depolarization ... slows phase 4)
    • Increase QT interval
  5. Antiarrhythmic Drug: Class Ia - Quinidine
    • Mechanism: blocks fast Na channels, K channels, muscarinic receptors (increases HR), alpha blockade (decreases BP, reflexive tachy)
    • Administration: PO
    • Clinical use: a fib, need to combine with digoxin to slow AV conduction, both atrial and ventricular dysrhythmias, reentrant, ectopic SVT and ventricular tachy
    • Adverse effects: cinchonism (tinnitis, blurred vision, CNS excitation, GI disturbance), QT interval increased (may lead to torsades), thrombocytopenia, hypotension
    • Drug interactions: hyperK, displaces digoxin from tissue binding sites
  6. Antiarrhythmic Drug: Class Ia- Procainamide
    • Mechanism: blocks fast Na channels, K channels, less muscarinic block, NO alpha block (less likely to cause a dysrhythmia)
    • Clinical use: atrial and ventricular dyshrhythmias, reentrant and ectopic SVT, ventricular tachy, a fib (with digoxin)
    • Metabolism: N-acetylation (genotypic variation) into N-acetyl procainamide & active metabolite (which can block K channels, prolongs repolarization, can cause Torsades)
    • Adverse effects: SLE-like syndrome in slow acetylators, hematoxicity (thrombocytopenia, agranulocytosis), Torsades
  7. Antiarrhythmic Drug: Class Ib- General
    • Drugs: Lidocaine Mexiletine
    • Mechanism: blocks inactivated channels: prefers the tissues to be partially depolarized (slow conduction in hypoxic & ischemic tissues), increases threshold for excitation & less excitation of hypoxic tissue (accelerated phase 3)
    • decreases APD: due to block of slow Na "window" currents but increases diastole & extends their time to recover
    • Clinical use: acute ventricular dysrhythmias (post MI) and digitalis-induced dysrhythmias
    • IB is Best for MI
  8. Antiarrhythmic Drug: Class Ib- Lidocaine
    • Uses: tx for: post MI, open heart surgery, digoxin therapy
    • Side Effects: CNS toxicity (seizures), less cardiotoxic than conventional anti-arrhythmias
    • Administration: IV (to prevent 1st pass effects)
    • 'li don't know what to do, so I'll work on good and bad tissue' :)
  9. Antiarrhythmic Drug: Class Ib- Mexiletine
    • Clinical use: same as lidocaine
    • Administration: PO
  10. Antiarrhythmic Drug: Class Ic- General
    • Drugs: Flecainimide, Encainide, Propafenone
    • Mechanism: blocks fast Na channels (espeically Purkinje tissue), no effect on APD, no ANS effects
    • Toxicity: contraindicated post-MI, prodysrhythmic if used in prophylactic VT tx,significantly prolongs the refractory period in AV node
    • IC is Contraindicated in MI, flee from using it after an MI
  11. Antiarrhythmic Drug: Class II - Beta Blockers (general)
    • Drugs: Propranolol, esmolol, metoprolol, atenolol, timolol
    • Mechanism: decreases cAMP, decreases Ca++ currents (indirect Ca channel blocker), suppresses abnormal pacemakers by decreasing the slope of phase 4
    • AV node is parcticularly sensitive - increases PR interval
    • Clinical use: Vtach, SVT, slows ventricular rate during afib, migraines, ST thyrotoxicosis, essential, perioperative htn
    • Toxicity: impotence, exacerbation of asthma, CV (bradycardia, AV block, CHF), CNS (sedation, sleep alterations), may mask signs of hypoglycemia
    • OD tx: glucagon
  12. Antiarrhythmic Drug: Class II - Beta
    Blocker - Propranolol
    • Mechanism: non-selective
    • Clinical use: Vtach, SVT, slows ventricular rate during afib, migraines, ST thyrotoxicosis, essential, perioperative htnToxicity: impotence, exacerbation of asthma, CV (bradycardia, AV block, CHF), CNS (sedation, sleep alterations), may mask signs of hypoglycemiaOD tx: glucagon
  13. Antiarrhythmic Drug: Class II- Beta Blocker - Esmolol
    • Mechanism: Short acting
    • Clinical use: acute SVTClinical use: Vtach, SVT, slows ventricular rate during afib, migraines, ST thyrotoxicosis, essential, perioperative htnToxicity: impotence, exacerbation of asthma, CV (bradycardia, AV block, CHF), CNS (sedation, sleep alterations), may mask signs of hypoglycemia OD tx: glucagon
    • Administration: IV only
  14. Antiarrhythmic Drug: Class II- Beta Blocker- Metoprolol
    • Side effect: can cause dyslipidemia
    • Clinical use: Vtach, SVT, slows ventricular rate during afib, migraines, ST thyrotoxicosis, essential, perioperative htnToxicity: impotence, exacerbation of asthma, CV (bradycardia, AV block, CHF), CNS (sedation, sleep alterations), may mask signs of hypoglycemia OD tx: glucagon
    • B1 selective: I met a guy, who liked B1 better than B2.... do, do, do, do
  15. Antiarrhythmic Drug: Class III- K Channel Blocker (general)
    • Drugs: Amiodarone, Sotalol, ibutilide, bretylium, dofetidilide
    • Mechanism: Increases AP duraction, increases ERP, last resort drugs, increases QT (torsades...except for in amiodarone)
  16. Antiarrhythmic Drug: Class III- Amiodarone
    • Characteristics: dirty drug (all classes), effects in all cardiac tissue, long t1/2 (80 days), binds excessively to tissues (large Vd), alters lipid mb
    • Clinical use: all dysrhythmias
    • Side effects: caused by iodine in the drug: pulmonary fibrosis, smurf skin, phototoxicity, corneal deposits, hepatic necrosis, thyroid dysfn, constipation, CV (heart block, bradycardia, CHF)
    • Better replacement: Dronaderone
    • Check labs: PFTs (pulmonary), LFTs (liver), TFTs (thyroid)
  17. Antiarrhythmic Drug: Class III: Sotalol
    • Characteristics: decreases K conductance, slows phase III, Beta1 blockade (decrease HR & AV conduction)
    • Clinical use: life threatening ventricular dysrrhythmia
    • Side effects: torsades de points,excessive AV block
  18. Antiarrythmic Drug: Class III: Ibutilide and Bretylium side effects:
    • Ibutilide: Torsades
    • Bretylium: new dysrrhythmia
  19. Antiarrhythmic Drug: Class IV: Ca Channel Blockers
    • Drugs: Verapamil, diltiazem
    • Mechanism: moslty effects V nodes, decreases conduction velocity, increases ERP and PR interval
    • Clinical use: prevention of nodal, Raynauds syndrome, dysrhythmias, SVT
    • Toxicity: constipation, flushing, edema, CV effects (CHF, heart block, sinus node depression)
    • Drug interaction: additive AV block w/ B blockers & digoxin, verapamil displaces digoxin from tissue binding sites
  20. Antiarrhythmic Drugs: Unclassified: Adenosine
    • Activates the adenosine receptors in heart & kidneys
    • Gi coupled decrease in cAMP
    • SHORT t1/2 (<10s)
    • Clinical use: drug of choice for SVT, and AV nodal dysrrhythmias
    • Administration: IV
    • Antagonist: methylxanthine (theophylline and caffiene)
    • Side effects: flushing, sedation, dyspnea
  21. Antiarrhythmic Drugs that displace digoxin are:
    • quinidine
    • verapamil
  22. Drugs that cause long QT Syndrome (possibly Torsades) are:
    • class Ia: Quinidine
    • all class III (except for amiodarone)
  23. Viscerosomatics:
    Cardiac
    Atria
    Ventricles
    Anterior MI
    Posterior/Inferior MI
    Sympathetic Ganglion
    Vagus
    Occiput
    • Cardiac: T1-T5L
    • Atria: T4-T6L
    • Ventricles: C8-T3L]
    • Ant. MI: T1-T4L
    • Post/Inf. MI: C2/OA/cranial base
    • Sympathetic Ganglion: C2,5,7
    • Vaguse: C1 & C2
    • Occiput: PNS
  24. Sympathetic Innervation of Heart
    Left Sympathetic Chain:
    Right Sympathetic Chain:
    • Left Sympathetic Chain: AV nodes, ectopic foci & ventricular fibrillation
    • Right Sympathetic Chain: SA nodes (SVT)
  25. Parasympathetic Innervation of Heart
    Left Vagus Nerve:
    Right Vagus Nerve:

    • Left Vagus nerve: AV node block
    • Right Vagus nerve: SA node block (sinuse bradycardia)
  26. What are the 4 MC used classes of antihypertensive drugs?
    • ACEI, ARBs
    • Beta Blockers
    • CCB
    • Diuretics (#1 drug used) / Dilators

    these are the ABCDs of hypertension
  27. Antihypertensive Drug: ACEI
    • Drug: Captopril (all other '-pril' drugs)
    • Mechanism: Block formation of AngioII which prevents AT1-receptor stimulation, decreases aldosterone and VD, inhibit degredation of bradykinin (cough)
    • Clinical use: mild to moderate htn, protective of diabetic nephropathy, CHF
    • Side effects: dry cough, hyperK, acute renal failure in renal stenosis, angioedema
    • CONTRAINDICATED IN PREGNANCY
  28. Antihypertensive Drug: ARBs
    • Drug: Losartan (all other '-sartan' drugs)
    • Mechanism: blocks AT1 receptors with the same results as ACEIs on BP but the ARBs don't interfere with bradykinin degredation (don't get the cough)
    • Clinical use: mild to moderate htn, protective of diabetic nephropathy, CHF
    • Aliskiren does not interfere with bradykinin degredation
    • Side effects: hyperK, acute renal failure in renal artery stenosis, angioedema
    • CONTRAINIDCATED IN PREGNANCY
  29. Antihypertensive Drug (alter sympathetic activity): Beta blockers
    • Side effects: CV depression, fatigue, sexual dysfunction, increased LDL & TG
    • Caution use with: asthma, vasospastic disorder, DM (alteration of glycemia and maksing of tachycardia when hypoglycemic)
  30. Antihypertensive Drug (alter sympathetic activity): Alpha 1 Blockers
    • Drugs: Prazosin, doxazosin, terazosin
    • Mechanism: decreases arteriolar and venous resistance (non selective), reflexive tachy
    • Use: htn, BPH (decreases urinary sphincter tone)
    • Side effects: first dose syncope (VD for the first time), orthostatic hypotension (venodilation), urinary incontinence
    • Advantage: good effect on lipid profile (increase HDL and decreases LDL)
    • start low and go slow
  31. Antihypertensive Drug (alters sympathetic activity): Alpha 2 Agonists
    • Drugs: clonidine, methyldopa (prodrug)
    • Mechanism: decreases SNS outflow, decreases TPR and HR
  32. Antihypertensive Drug (alters sympathetic activity): Alpha 2 Agonist: Clonidine
    • Mechanism: decreases SNS outflow, decreases TPR and HR
    • Use: mild/moderate htn, opiate w/drawal
    • Side effects: CNS depression, edema
    • Drug interactions: TCA decrease alpha 2 agonist effets
  33. Antihypertensive Drug (alters sympathetic activity): Alpha 2 Agonist: Methyl dopa
    • Mechanism: decreases SNS outflow, decreases TPR and HR
    • Use: mild/moderate htn, hypertensive management in pregnancy
    • side effects: +ve COOMBs, CNS depression, edema
    • Drug interactions: TCA decreased the effectiveness
  34. Antihypertensive Drug (alters sympathetic activity): Interfering w/ storage vesicles: Reserpine
    • Destroys vesicles: decreases CO and TPR (decreases NEp in periphery) reserpinze the neuron!, decreased DA, and serotonin in CNS
    • Side effects: depression (severe), edema, increased GI secretions
  35. Antihypertensive Drug (alters sympathetic activity): Interfering with storage vesicles: Guanethidine
    • Accumulated into nerve endes by reuptake
    • binds vesicles
    • inhibits NEp release
    • Side effects: diarrhea, edema
    • Drug interactions: TCA block the reuptake and action
  36. Antihypertensive Drug: CCB
    • Drugs: verapamil, diltiazem, dihydropyridines: prototype: nifedipine (fed up with the Ca channel blockers already)
    • Mechanism: blocks L-type Ca channels in heart and blood vessels,CO (diltiazem and verapamil) and all others decrease TPR
    • Vascular SM: nifedipine > diltiazem > verapamil (Verapamil = ventricles)
    • Heart: Verapamil > diltiazem > nifedipine
    • use: hypertension (all), angina (all), antiarrhythmia (verapamil and diltiazem)
    • Side effects: reflex tachy ('-dipines'), gingival hyperplasia ('-dipines'), constipation (verapamil), hypertension, angina, arrhythmias, agina, arrhythmias (not nifedipine), Prinzmetal's angina,, Raynaud's, CV depression, AV block, peripheral edema, flushing, dizziness
  37. Drugs that cause gingival hyperplasia
    • CCBs (-dipines)
    • phenytoin
    • cyclosporin (organ transplant tx)
  38. Antihypertensive Drug: Vasodilators: Direct acting thru NO: Hydralazine
    • Mechanism: decrease TPR arteriolar dilation (NOT VENOUS)= aferload reduction, increases cGMP = SM relaxation
    • Clinical Use: moderate/severe htn, first line in PREGNANCY w/ methyldopa
    • Coadministered: with beta blocker to prevent reflexive tachycardia
    • Side effects: SLE-like syndrome in slow acetylators, edema, reflex tach, headache, angina
    • Metabolism: phase II involving trasferases
  39. Antihypertensive Drug: Vasodilators: Direct acting thru NO: Nitroprusside
    • Mechanism: decreases TPR via dilation of both arterioles & venules
    • Use: hypertensive emergencies, malignant htn
    • Administration: IV
    • Side effect: cyanide poisioning (which is why coadministration w/ nitrites and thiosulfate is needed)
  40. Antihypertensive Drug: Vasodilator: Direct acting thru NO: Nitroglycerin, Isosorbide dinitrate
    • Mechanism: VD by releasing NO in SM = increase cGMP and SM relaxation, dilates veins >> arteries, lowers preload
    • Clinical Use: angina, pulmonary edema, aprhodisiac & erection enhancer
    • Toxicity: reflex tachy, hypotension, flushing, "Monday Disease" in industrial exposure - dev't of tolerance for VD action during work week and loss of tolerance over weekend = tachy, dizziness & headache on reexposure
  41. Antihypertensive Drug: Vasodilators: Direct acting thru K channels: Minoxidil
    • Mechanism: K channel opener = hyperpolarizes and relaxes vascular SM
    • Clinical use: severe htn
    • Toxicity: hypertrichosis (hirsuitism), pericardial effusion, reflex tachy, angina, Na retension, T wave changes on EKG
  42. What is the drug of choice for methemoglobinemia?
    • Methylene blue
    • Mechanism: causes the met-Hbg to form free Hbg again)
  43. Pulmonary Hypertension:
    Bosentan
    • Note: Endothelin (ET1) is a powerful VC thru ET-A and ET-B receptor
    • Mechanism: Bosentan is an ETA receptor
    • antagonist
    • Administration: PO
    • Side effects: anything associated with VD (headache, flushing, hypotension, etc.)
    • CONTRAINDICATED IN PREGNANCY
  44. Pulmonary Hypertension: Epoprostenol
    • Mechanism: is a prostacylcine that causes VD
    • Administration: infusion pumps
  45. Pulmonary Hypertension: Sildenafil *
    Mechanism: inhibits type V phosphodiesterase (PDE5 = increases cGMP = relaxes arteries) to reduce the hypertension
  46. What are the suitable antihypertensive drugs for a pt with angina?
    • beta blockers
    • CCB
  47. What are the suitable antihypertensive drugs for diabetic patients?
    • ACEI (protective against diabetic nephropathy)
    • ARB
    • CCB
    • diuretics (thiazides first line)
    • Beta blockers
    • Alpha blockers
  48. What are the suitable antihypertensive drugs for pts w/ heart failure?
    • ACEI
    • ARB
    • Beta blockers (for compensated CHF but contraindicated in decompensated CHF)
    • diuretics (K sparing)
  49. What are the suitable antihypertensive drugs post-MI?
    Beta blockers
  50. What are the most suitable antihypertensive drugs for pts w/ BPH?
    Alpha blockers
  51. What are the most suitable antihypertensive drugs for pts with dyslipidemia?
    • Alpha blockers
    • CCB
    • ACEI
    • ARBs
  52. What is the most suitable antihypertensive drug for pts with essential hypertension?
    • Diuretics (thiazide unless contraindicated)
    • ACE
    • ARB
    • CCB
  53. Malignant hypertension treatment includes:
    • 1. Nitroprusside: short acting, increases cGMP = direct release of NO, CN toxicity
    • 2. Fenoldopam: D1 receptor agonist - relaxes vascular SM
    • 3. Diazoxide: K channel opener: hyperpolarizes and relaxes vascular SM, can cause hyperglycemia by reducing insulin release
  54. Inotropic Drug: Cardiac Glycoside: Digoxin
    • Characteristics: 75% bioavailability, 20-40% protein bound, t1/2=40 hours (thus need loading dose), urinary excretion
    • Mechanism: direct inhibition of Na/K ATPase = inhibition of Na/Ca exchanger/antiport = increases Ca = + inotropy, also stimulates the vagus nerve
    • Clinical use: CHF (increases contractility), atrial fib (decreases conduction at AV node & depression of SA node), SVT (except Wolff-Parkinson-White sydnrome)
    • Toxicity:
    • Cholinergic - n/v/d, blurry yellow vision (think Van Gogh)
    • ECG - increase PR, decreased QT, scooping (hockey stick) depression of ST segment, T wave inversion, dysrhythmia, hyperK
    • Kidneys - worsens renal failure (decreases excretion)
    • Quinidine - decreases clearance, displaces digoxin from tissue binding (so does verapamil)
    • Antidote: slowly normalize K, lidocaine, cardiac pacer, anti-dig Fab fragments, Mg
  55. What are the most common Heart Failure drug classes?
    • 1. ACE/ARBs
    • 2. Beta Blockers
    • 3. Diuretics

    the ABDs of heart failure
  56. Pharmacotherapy in heart failure is aimed at:
    • Decreasing preload: diuretics, ACEI, ARB, venodilators
    • Decreasing afterload: ACEI, ARB, arteriodilators
    • Increasing contractility: digoxin (cardiac glycoside), beta agonist
    • Decreasing remodeling: ACEI, ARB, sprinolactone
  57. What are the 2 things that cause cardiac remodeling?
    • Aldosterone
    • Beta blockers (ie metoprolol, carvedilol)
  58. Common Inotropic Drugs
    (drugs that increase contractility)
    • Digoxin
    • Phosphodiesterase inhibitors: milrinone, inarinone
  59. Inotropic Drug: Phosphodiesterase Inhibitors
    • Drugs: Milranone, inamrinone
    • Mechanism: increases cAMP in heart muscle = increased inotropy, increases cAMP in SM = decreased TPR
    • Clinical use: only acutely beneficial (increased mortality LT use)
  60. Inotropic Drug: DA / Dobutamine
    Acute use only in heart failure
  61. Miscellaneous Drugs used in Heart Failure:
    • Diuretics: Loops (backward failure), spironolactone + ACEI (to reduce remodeling)
    • Metoprolol & carvedilol (decreases remodeling)
    • Nesiritide: acutely
    • recombinant form of human B-type nautriuretic peptide (rh BNP)
    • binds to natriuretic peptide receptors = increases cGMP = VD = acutely decompensated CHF
  62. What are the three main classes of drugs used in treating classic angina?
    • Nitrates
    • Beta blockers
    • CCB

    Angina: stable/classic: occurs from xcise/effort due to coronary atherosclerotic occulsion

    Goal in tx: decrease oxygen requirement by lowering TPR, CO or both

    NBC for angina
  63. What are the two main classes of drugs used in treating vasospastic (Prinzmetal) angina?
    • Nitrates
    • CCB


    Vasospastic angina: due to reversible decrease in coronary BF (vasospam)

    Goal in tx: increase oxygen delivery by reducing the spasm, no beta blockers used!
  64. Nitrates: Classical and Vasospastic Angina treatment
    • Drugs:
    • isosorbide: extended release for chronic use
    • Nitroglycerin: sublingual (rapidly acting, little 1st pass), transdermal (slow action), IV
    • Nitrates are prodrugs of NO
    • Mechanism: decreases preload = decreases cardiac work = decreases oxgen requirement, decrease the infarct size and post-MI mortality
    • Side effects: flushing, headache (MC), orthostatic hypotension, reflex tachycardia, fluid retention
    • Cautions/contraindications: tachyphylaxis, CV toxicity w/ sildenafil
  65. Nitrate & phosphodiesterase drug: Sildenafil (viagra)
    • Mechanism: inhibits PDE5 = increases cGMP = VD = increases BF = increases erectile response
    • Contraindication: cocomitant use of nitrates or other VD can cause sudden death, MI
  66. Antianginal Drug: Beta Blockers + Carvedilol
    • Use: angina of effort (classical angina), contraindicated in vasospastic angina
    • Drugs: carvedilol equivalent clinically to isosorbide
  67. Antianginal Drug: CCB
    • Use: vasospastic angina
    • Drugs: nifedipine
    • note: recurring COMLEX question: nifedipine is vasular selective- DOC for Raynauds, vasospam, cyanotic extremity
  68. Treatment for an MI (acute and chronically)
    Acute: MONA: Morphine, Oxygen, Nitro, ASA

    Chronically: Beta blocker, ACEI, statins
  69. "Have I not commanded you? Be strong and courageous, do not be terrified, do not be discouraged, for the Lord God is with you wherever you go" Joshua 1:9
    aka He'll be there even as we go through this journey of board craziness!

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Boards
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74764
Filename:
Cardio Pharm
Updated:
2011-03-24 21:18:53
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Cardio Pharm
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