EXAM 3: heart + meds Flashcards
Describe the therapeutic actions, indications, pharmacokinetics, contraindications, most common adverse reactions, and important drug-drug interactions associated with drugs used for the treatment of arrhythmias and heart failure.
-Diuretics - remove extra fluids
-ACE inhibitors or ARBs - reduce afterload & prevent/help reverse cardiac remodeling
-Beta Blockers - decrease pre-load & prevent/help reverse cardiac remodeling
-Inotropic agents-cardiac glycoside (digoxin) - Increase contractility; doesn’t make heart pump faster, but slows it down.
-Vasodilators - decrease preload (through vasodilation); reduce afterload (through A dilaton).
-Oxygen - increase O2 content of blood.
Describe the cardiac conduction system, including the five phases of cardiac action potential.
-Phase 0: depolarization - rapid upstroke of action potential - influx of sodium - (sodium channel blockers work here).
-Phase 1: early repolarization (no drugs).
-Phase 2: plateau (straight) - calcium enters and promotes A & V contraction! - (calcium channel blockers- reduce contractility; beta-blockers - slow conduction).
-Phase 3: final repolarization period - (potassium channel blockers).
-Phase 4: diastolic repolarization period - (beta blockers & calcium channel blockers)
Identify the characteristics of normal sinus rhythm.
-P waves are upright & uniform in appearance.
-One P wave for each QRS complex.
-One P wave precedes each QRS complex.
Describe the characteristics of premature atrial contractions, premature ventricular contractions, atrial fibrillation, first-, second-, and third-degree heart block, ventricular tachycardia, ventricular fibrillation, bundle branch blocks, and long QT syndrome.
-Heart block: slowed conduction from P wave to QRS (3 degrees of severity).
-Atrial flutter: sawtooth P wave pattern - atrium rate LESS than 300.
-Atrial fibrillation: no distinct P wave - atrium rate MORE than 300.
-V tachycardia & V fibrillation: CPR needed stat!!!
Aortic Regurgitation
-Incomplete closure during diastole - backflow into the left ventricle
-Cause: Congenital, Aging, Infective Endocarditis
-Treatment: Vasodilator to decrease resistance, valve replacement, Inotropic Agents (improve pumping action).
Mitral Valve Stenosis
-Narrowing of mitral valve
Cause: rheumatic heart disease
-Manifestations: A-fib, L atrium hypertrophy & dilation, R vent. failure, Reduced CO
Aortic Stenosis
Cause: Congenital; Age degeneration, Rheumatic heart disease; Smoking
Patho:
*Resistance to blood flow from L ventricle,
-L vent hypertrophy,
-Increased O2 demand of the heart.
-In aortic stenosis, this door becomes narrowed, making it harder for blood to flow out of the heart and into the rest of your body.
Manifestations: L-sided H failure symptoms, Decreased stroke vol & CO, Murmur.
Treatment: Vasodilators, valve replacement.
Systolic HF
-Weak pump, reduced ejection faction <40%
Diastolic HF
-Poor filling, normal ejection faction (55-70%)
-Inadequate relaxation
L Sided HF
-Impaired pumping of O2 blood FROM pulmonary system to systemic circulation.
-Blood pools in heart and pulmonary circ.
-Causes pulmonary edema.
-Causes: damage to myocardial muscle, HTN, CAD, angina, etc.
-Systolic and Diastolic failure.
-Manifestations: crackles, dyspnea, orthopnea, cough & frothy sputum, fatigue, altered mental state, S3 sound.
R Sided HF
-Blood from peripheral venous return doesn’t get pushed forward to pulm circ.
-Thus -> backup/stagnation of systemic venous return.
-Causes: HTN, COPD, Valvular disease, Pulmonary HTN.
-Manifestations: Weight gain, edema in lower ex, abdominal distention, valvular disease
Describe the therapeutic actions, indications, pharmacokinetics, contraindications, most common adverse reactions, and important drug-drug interactions associated with drugs used of cardiotonic agents.
-Digoxin: Increase the force of heart contractions & slows heart rate
-Dobutamine: Increases heart rate & contractility (stim beta adrenergic receptors)
-Dopamine: Increases heart rate & contractility
-Epinephren: increases heart rate, contractility, & blood pressure
Pericarditis (Peri)
-Inflammation of pericardium
-Causes: viruses, bacteria, trauma, drugs
-Symptoms: Chest rub, pericardial friction rub
Pericardial Effusion (Peri)
-Accumulation of fluid in the pericardial cavity (serous, purulent, or sanguineous)
-Causes: infections, neoplasms, surgery, trauma
-Can lead to cardiac tamponade
-Drugs: NSAIDs, colchicine, corticosteroids
Cardiac Tamponade (Peri)
-Compression of heart from fluid, pus, or blood.
-Cause: P. Effusion
-Increased intracardiac pressure, limits diastolic filling.
-Decrease stroke volume & CO
-Widening of blood pressure - what does this mean?
-Increase HR; lower BP; jugular vein distention; muffled heart sounds.
-Treat: NSAID, Corticosteroids, Pericardiocentesis - most important thing
Dilated (Cardiomyopathy) (Myo)
-Distended thin cardiac muscle.
-Causes: drugs & toxins, infection, renal disease, ischemia.
-Patho: impaired systolic function leads to systolic heart failure.
-Manifestations: dyspnea, fatigue, pedal edema, jugular vein distention.
-Treatment: Reduce volume & increase contractility.
Hypertrophic Obstructive (Cardiomyopathy) (Myo)
-Enlarged, thick cardiac muscle.
-Cause: inherited/response to increased cardiac workload.
-Left atrium dilated b/c of poor diastolic relaxation.
-Manifestation: Decrease outflow to left vent, vent dysrhythmia, sudden death.
Restrictive
-Stiff hard muscle.
-Filling resistance.
-Increased resting pressure.
-Causes: inherited or other issues
-Patho: resistance to filling both ventricles; increase in resting pressures.
-Myocardium is rigid & non-compliant.
-Manifestations - R-sided heart failure
-Treatment - the underlying cause
Endocarditis
-Infection of the heart valves & endocardium.
-Causes: staph infection & surgeries (prosthetic valves, pacemakers, contaminated needles).
-Risk factors: The immunocompromised.
-Endo damage leads to collagen buildup, microorganisms adhering to damaged areas, and ineffective vegetation adhering to heart valves.
-Manifestations: fever, chills, anorexia, malaise, cough, dyspnea
-Treatment: NSAIDs, Colchicine,
Corticosteroids and if the above doesn’t work -> Antibiotics
Cardiogenic shock
-Failure of the heart to pump effectively & maintain cardiac output due to cardiac cause.
-Extra strain on the heart causes decreased tissue perfusion.
-Manifestations: Decreased CO (extremely low), Hypotension, LOC decrease, edema, etc.
-Treat: Vasopressors (dopamine & epi) -> increases cardiac contraction; increase CO; increase kidney perfusion.
-Epi -> increase HR and CO
-Inotropic agent (Dobutamine) -> strengthens cardiac contraction; increase CO.
Describe the complications of shock related to the lungs, kidneys, gastrointestinal tract, and blood clotting.
-Lungs - Hypoxia which leads to dyspnea & tachypnea.
-Kidneys - Oliguria - decreased urine output & acute kidney injury.
-GI - ileus (intestines stop working properly) b/c they don’t receive enough blood flow.
-Blood clotting - DIC (disseminated intravascular coagulation) - condition where body’s blood clotting system becomes overactivated.
Class I – Lidocaine
-decrease depolarization
-decrease automaticity of ventricular cells
-manages acute ventricular arrhythmias (MI)
Class II – Propranolol
-beta blocker: decrease contractility; decrease SA node power
-treat cardiac arrhythmias
-treat suprventricular tachycardias
-oral & IV
Class III – Amiodarone
-treatment for life-threatening ventricular arrhythmias
-acts directly on heart muscle to prolong repolarization
-given oral and IV
Class IV – Diltiazem
-ca+ channel blocker: reduces contractility; slows SA node automation; decreases AV power
-blocks movement of calcium ions across the cell membrane
-also treats HTN and angina in adults
Cardiac glycoside: Digoxin
-Increases contractility -> helps ventricles empty more completely
-Decrease heart rate
-low therapeutic index - watch for toxicity
-Side effects: Dig tox - can be caused by low vitamin K/diutetics that lower vit K
-High K leads to low therapeutic effect of vit K as well
-Other S/E = N/V/D; visual disturbances - blurred vision, YG halos, diplopia
