Cardio Pharm

Card Set Information

Author:
Boards
ID:
74764
Filename:
Cardio Pharm
Updated:
2011-03-24 17:18:53
Tags:
Cardio Pharm
Folders:

Description:
Cardio Pharm
Show Answers:

Home > Flashcards > Print Preview

The flashcards below were created by user Boards on FreezingBlue Flashcards. What would you like to do?


  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!

What would you like to do?

Home > Flashcards > Print Preview