CV Pharmacology 2 Flashcards
Arrhythmia
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
Ventricular Arrythmia
Most common cause of sudden death
-Meds that decrease incidence of VA, don’t decrease risk of sudden death
Electrophysiology-Resting Potential
Interior is more negative compared to outside
Na and Ca are higher outside the cell, K+ is higher inside the cell
Cardiac Action Potential Phases
- 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
Mechanisms of Cardiac Arrhythmias
Disorders of impulse formation/conduction
-Causes include: ischemia, excess discharge to transmitters, toxic substance exposure (includes drugs), unknown
Disorder of Impulse formation
- 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)
Types of Arrhythmias (locations)
Sinus, Supraventricular, AV Junctions, Conduction, Ventricular
Anti-arrhythmic Drugs
These drugs can cause arrhythmias.
- Sodium Channel Block
- Beta-adrenergic receptor block
- prolong repolarization
- Calcium channel block
- Adenosine and Digitalis
Classification of Anti-arrhythmics
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
Pacemakers
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.
Rehab considerations for anti-arrythmics
S/E of agents: change in nature of arrhythmias/increased potential for them,
Monitor ECG, Presence of faintness/dizziness
CHF
- 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
Factors contributing to CHF
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
Types of Heart Failure
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
Onset of Disease for CHF
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
CHF Symptoms
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
Therapeutic Overview for CHF
Problems include:
- reduced contractionf roce
- decreased CO
- Increased TPR
- inadequate organ perfusion
- edema
- decreased exercise tolerance
- ischemic heart disease
- sudden death
Drug Therapies for CHF
Chronic:
-ACE inhibitors, Beta Blockers, ATII antagonists, aldosterone antagonists, digoxin, diuretics
Acute:
-Diuretics, PDE inhibitors, Vasodilators
Cardiac Glycosides: MOA, Electrophysiology, Overall Effect, Therapeutic Uses, PK
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
Cardiac Glycosides Side effects
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
PDE Inhibitors MOA, Therapeutic Use
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
PDE Inhibitors Side Effects
Sudden death secondary to ventricular arrhythmias
Hypotension, thrombocytopenia
Beta Blockers MOA, Therapeutic Use
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
Beta Blockers Side Effects
Cardiac decomp, bradycardia, hypoglycemia, cold extremities, fluid retention, fatigue
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
Direct acting sympathomimetics Side Effects
Restlessness, tremor, headache, cerebral hemorrhage, cardiac arrhythmias, caution in patients with beta blockers, can develop dobutamine tolerance
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
ACE/AT1 Side Effects
ACE: Cough, angioneurotic edema, hypotension, hyperkalemia
Both ACE and AT1 are teratogenic
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
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
Aldosterone Antagonists
Aldosterone promotes: Sodium retention, Magnesium and Potassium loss, increase SNS, decrease PSNS, myocardial fibrosis
Aldosterone Antagonists Side effects
Hyperkalemia, agranulocytosis, anaphylaxis, hepatotoxicity, renal failure
Spironolactone (alactone)= gynecomastia, sexual dysfunction
Eplerenone (inspra)= arrhythmia, MI
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
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
Anticoagulants
Inhibit clot formation, prevent new blots
Venous: DVT and Pulmonary Embolism
Arterial: Coronary Thrombosis (MI), Artificial Heart Valves, CVA
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
Heparin Side Effects
Decreased Platelet Count= Thrombocytopenia
Hemorrhage
Drug Interactions: Increased effect with ASA, NSAIDs, thrombolytics; decreased effect with NTG
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
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.
Dabigatran
Prophylaxis and treatment of venous thromboembolism and PE
No specific antidote: use activated prothrombin complex concentrate, activated charcoal
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
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
Edoxaban
Prophylaxis for nonvalvular atrial fib, CVA, embolism, Treats DVT and PE
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
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
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
