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CV Pharmacology 2 Flashcards

(46 cards)

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1
Q

Arrhythmia

A

Heart condition with disturbances in

  • Pacemaker impulse formation
  • Contraction impulse conduction
  • Combo of those 2

-Insufficient rate/timing of heart contraction to maintain normal CO

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2
Q

Ventricular Arrythmia

A

Most common cause of sudden death

-Meds that decrease incidence of VA, don’t decrease risk of sudden death

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3
Q

Electrophysiology-Resting Potential

A

Interior is more negative compared to outside

Na and Ca are higher outside the cell, K+ is higher inside the cell

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4
Q

Cardiac Action Potential Phases

A
  • Phase 4: Resting phase, diastole
  • Phase 0: Opening of Na+ channels/rapid depolarization
  • Phase 1: Initial rapid depolarization, close of fast Na channels. R and S waves
  • Phase 2: Plateau: balance between inward Ca and outward K. ST segment
  • Phase 3: repolarization. T wave
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5
Q

Mechanisms of Cardiac Arrhythmias

A

Disorders of impulse formation/conduction

-Causes include: ischemia, excess discharge to transmitters, toxic substance exposure (includes drugs), unknown

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6
Q

Disorder of Impulse formation

A
  • No signal from pacemaker site
  • ectopic pacemaker
  • Oscillatory after-depolarizations: spontaneous activity in non-pacemaker tissues, can be due to drugs used to treat other cardio pathologies

Can result in Bradycardia (AV Block), Tachycardia (reentrant circuit)

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7
Q

Types of Arrhythmias (locations)

A

Sinus, Supraventricular, AV Junctions, Conduction, Ventricular

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8
Q

Anti-arrhythmic Drugs

A

These drugs can cause arrhythmias.

  • Sodium Channel Block
  • Beta-adrenergic receptor block
  • prolong repolarization
  • Calcium channel block
  • Adenosine and Digitalis
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9
Q

Classification of Anti-arrhythmics

A

Based on MOA

  • Class 1: Blocks fast Sodium Channels
  • -Subclass 1a: Quinidine
  • -Subclass 1b: Lidocaine, Phenytoin
  • -Subclass 1c: Flecainide, propefenone
  • Class 2: B-adrenergic blockers: Propanalol, the other “-lols”
  • Class 3: K+ Channel Blockers: developed because people died from Na channel blockers; Amiodarone, Ibultide, Bretylium
  • Class 4: Calcium Channel Blockers: Verapamil; S/E: excessive bradycardia, peripheral vasodilation-> dizzy, headache
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10
Q

Pacemakers

A

Surgical implantation of electrical leads to a pulse generator. Generator can sense electrical activity generated by heart and delivers impulses when needed. Only speeds up heart for bradycardia, can’t do anything for tachycardia.

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11
Q

Rehab considerations for anti-arrythmics

A

S/E of agents: change in nature of arrhythmias/increased potential for them,

Monitor ECG, Presence of faintness/dizziness

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12
Q

CHF

A
  • Heart cannot provide adequate perfusion of peripheral organs to meet metabolic requirement.
  • Fluid accumulates in peripheral tissues since heart can’t maintain proper circulation.
  • Peripheral edema, decreased tolerance for physical activity, dyspnea/SOB

Classification: 1= asymptomatic, 2= mild, 3= moderate, 4= severe

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13
Q

Factors contributing to CHF

A

Ischemic heart disease, CAD (less blood flow to heart), MI, Hypertension, Diabetes, Lung Disease, Cardiomyopathies (Dilated, Hypertrophic), Abnormal heart valves, congenital heart defects, severe anemia, hyperthyroidism, cardiac arrhythmia

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14
Q

Types of Heart Failure

A

Left Ventricular: Most common, systolic: can’t contract, diastolic: can’t relax

Right Ventricular: Occurs after LV failure, less blood received causes damage, less pumping by right, venous pooling in legs

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15
Q

Onset of Disease for CHF

A

Chronic: can take years

Endogenous Compensatory Mechanisms: size enlargement, increase muscle mass, increased heart rate, narrow blood vessels/increase BP, blood flow diversion, increase SNS output

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16
Q

CHF Symptoms

A

SOB: blood pooling in pulmonary veins, fluid in lungs, occurs during rest, activity, sleep.

Persistent cough/wheeze

Edema

Tiredness/fatigue (lack of O2)

Lack of appetite/nausea

Confusion/impaired thinking

increased heart rate

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17
Q

Therapeutic Overview for CHF

A

Problems include:

  • reduced contractionf roce
  • decreased CO
  • Increased TPR
  • inadequate organ perfusion
  • edema
  • decreased exercise tolerance
  • ischemic heart disease
  • sudden death
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18
Q

Drug Therapies for CHF

A

Chronic:
-ACE inhibitors, Beta Blockers, ATII antagonists, aldosterone antagonists, digoxin, diuretics

Acute:
-Diuretics, PDE inhibitors, Vasodilators

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19
Q

Cardiac Glycosides: MOA, Electrophysiology, Overall Effect, Therapeutic Uses, PK

Study These Flashcards
A

From Plants

  • increase force of myocardial contraction, has toxic S/Es
  • Digoxin most common

MOA: Inhibits Na-K Pump

Electrophysio effects: Spontaneous Depolarization of atrial cells

Overall Effect: Increase CO, increase efficiency, decrease HR, decrease cardiac size

Therapeutic Uses: oral inotropic agent, doesn’t stop disease progression

PK: long 1/2 life, metabolized in liver, excreted in kidneys

20
Q

Cardiac Glycosides Side effects

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A

Low therapeutic index, effects caused by Na-K pump inhibition.

CNS: Malaise, confusion, depression, vertigo

GI: anorexia, nausea, cramping, diarrhea

Cardia: bradycardia. arrhythmias

Hypercalcemia= increase toxicity

K+: Hypokalemia: increase toxicity, Contraindicated for patients using K+ depleting diuretics

Vision: Yellow Tinted vision

21
Q

PDE Inhibitors MOA, Therapeutic Use

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A

used for management of acute heart failure

+ inotropy, increase rate of myocardial relaxation, decrease TPR and afterload

MOA: increased cardiac contraction, relaxes vascular smooth muscle

Therapeutic Uses: Amrinone/Milrinone: doesn’t stop disease progression/prolong life, prescribed when other therapies don’t work

22
Q

PDE Inhibitors Side Effects

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A

Sudden death secondary to ventricular arrhythmias

Hypotension, thrombocytopenia

23
Q

Beta Blockers MOA, Therapeutic Use

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A

Standard therapy for CHF, cheap, reduce sudden death caused by other drugs

Propranolol, Carvedilol

MOA: unclear, prevents development of arrhythmias

Therapeutic Use: Oral, given with other therapies (ACE, digoxin), effective for Class 2/3

24
Q

Beta Blockers Side Effects

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A

Cardiac decomp, bradycardia, hypoglycemia, cold extremities, fluid retention, fatigue

25
Direct acting sympathomimetics (Dopamine,dobutamine, Nor/Epi) MOA, therapeutic Uses
causes immediate increase in inotropy, used for acute CHF, goal to increase CO w/o affecting TPR MOA: - Nor/Epi: increase CO/TPR - Dopamine: vasodilation (dopamine receptors) and increase CO (beta receptors) - Dobutamine: peripheral vasodilation Therapeutic Uses Given IV -Dopamine: used in cardiogenic, traumatic,hypovolemic shock -Dobutamine: used for patients with low CO, don't use in hypotensive patients
26
Direct acting sympathomimetics Side Effects
Restlessness, tremor, headache, cerebral hemorrhage, cardiac arrhythmias, caution in patients with beta blockers, can develop dobutamine tolerance
27
ACE Inhibitors/AT1 receptor antag. Drug names, Therapeutic Uses
Goal: reduce afterload/preload, reduce workload Positive cardiac inotropy, used for chronic CHF ACE: Captopril, Enalopril AT1: Losartan, Valsartan Therapeutic Uses: drug of choice in heart failure, increase survival in long-term CHF -ACE: slow progression Left Vent. Dyfunction -AT1 antag: More effective than ACE, used in conjunction with ACE for increased effectiveness
28
ACE/AT1 Side Effects
ACE: Cough, angioneurotic edema, hypotension, hyperkalemia Both ACE and AT1 are teratogenic
29
Vasodilators
Reduce TPR without large decrease in BP Reduce Preload/afterload, relieve symptoms, increase exercise tolerance Drugs: -Nitroglycerin: acute iscemia/heart fialure, orally active, quick onset for relief - Isosorbide dintrate/hydralizine: chronic admin for long-term relief, IV - Nesiritide/Natrecor: recomb brain-natriuretic peptide (BNP), vasodilator, inhibit remodeling, suppresses aldosterone secretion. Adverse effects= hypotension, renal failure
30
Diuretics
Used in CHF to reduce ECF Volume, used for acute CHF with volume overload Goal= reduce preload/afterload OD= excessive reduction in preload/overreduction in stroke volume Thiazide/loop diuretics (furesomide) used as adjunct therapies
31
Aldosterone Antagonists
Aldosterone promotes: Sodium retention, Magnesium and Potassium loss, increase SNS, decrease PSNS, myocardial fibrosis
32
Aldosterone Antagonists Side effects
Hyperkalemia, agranulocytosis, anaphylaxis, hepatotoxicity, renal failure Spironolactone (alactone)= gynecomastia, sexual dysfunction Eplerenone (inspra)= arrhythmia, MI
33
Rehab Considerations for CHF drugs
Be alert to signs of CHF like dyspnea, rales, cough, Digitalis toxicity signs- dizziness, confusion, nausea, arrhythmias Patients on diuretics sometimes exhibit fatigue/weakness due to fluid/electrolyte depletion Vasodilators: hypotension, postural hypotension
34
Coagulation/Circulatory Disorders
Drugs are used to maintain/preserve/restore circulation Anti-coagulants: prevent clot formation that inhibit circulation Anti-platelets: prevent platelet aggregation Thrombolytics: Clot busters Antilipemics: decrease lipid concentration Peripheral Vasodilators: promote dilation of vessels
35
Anticoagulants
Inhibit clot formation, prevent new blots Venous: DVT and Pulmonary Embolism Arterial: Coronary Thrombosis (MI), Artificial Heart Valves, CVA
36
Heparin
Natural substance in liver that prevents clot formation Primary use is to prevent venous thrombosis that can lead to pulm embolism/stroke. Poor absorption through GI, Given SQ/IV Prolongs Clotting time: partial thromboplastin time, and activated partial thromboplastin time. Used for DVT, PE, CVA, heart valved prosthesis, DV surgery, post op, hemodialysis. Low dose: prophylaxis Full dose: treat thromboembolism, promote neutralization of activated clotting factors= prevention of emboli formation
37
Heparin Side Effects
Decreased Platelet Count= Thrombocytopenia Hemorrhage Drug Interactions: Increased effect with ASA, NSAIDs, thrombolytics; decreased effect with NTG
38
Low Molecular Weight Heparin (LMWH)
prevent venous thromboembolism Enoxaprin/Lovenox and Dalteparin Sodium (Fragmin) -more stable, lower risk of bleeding Use: prevent DVT after hip/knee replacement surgery, abd. surgery Can be given at home, SW, BID Given in abdomen RX is 7 to 14 days Dont take antiplatelet drugs during therapy
39
Warfarin/Coumadin
Inhibits activity of vitamin K required for activation of clotting factors. Use: prophylactically to precent venous thrombosis, A. Fib, PE, coronary occlusion, thrombophlebitis. Prolongs clotting time, and monitored by Prothrombin time and INR INR is 1.3-2.0, therapeutic levels on coumadin = 2-3 INR replaces prothrombin time, INR is more accurate. well absorbed through GI tract, food decreases absorption. Long 1/2 life, watch for petetchiae, ecchymosis, tarry stool. hematemesis. Vit. K= antagonist for Warfarin.
40
Dabigatran
Prophylaxis and treatment of venous thromboembolism and PE No specific antidote: use activated prothrombin complex concentrate, activated charcoal
41
Rivaroxaban
Stroke prevention in patients with non-valvular atrial fib. Acute treatment of DVT/PE, secondary prevention of DVT/PE NO specific antidote, Prothrombin complex concentrate
42
Apixaban
Prophylaxis in patients with non-valvular atrial fib, CVA, Embolism Treatment/prophylaxis for recurrent DVT and PE Prophylaxis for post-op DVT for total hip replacement No specific antidote: use Prothrombin complex concentrate, activated charcoal
43
Edoxaban
Prophylaxis for nonvalvular atrial fib, CVA, embolism, Treats DVT and PE
44
Anti-platelet Drugs
Aspirin, Dipyridamole, Ticlopidine, Abciximab, Tirofiban Prevents thrombosis in arteries by suppressing platelet aggregation. Prevention of MI/Stroke for clients with family history Prevention of repeat stroke, stroke in clients having TIAs
45
Thrombolytics
Thromboembolism: occlusion of an artery or vein caused by thrombus or embolus; results in ischemia that causes necrosis of the tissue distal to obstructed area Thrombolytics promote fibrinolytic mechanism (plasminogen into plasmin and destroy fibrin in clot) Use for acute MI; w/in 4 hours to dissolve clot/unblock artery Also pulmonary embolism, DVT, Non-coronary occlusion Streptokinase, urokinase, tissue plasminogen activator, anisoylated plasminogen streptokinase activator complex
46
Thrombolytics Side effects/misc
Hemorrhage, allergic rxns, vascular collapse Onset/peak rapid, duration 12 hours tPa most expensive Aminocaproic acid used to stop bleeding by inhibiting plasminogen activation

Pharmacology (12 decks)

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