EXAM 3: heart + meds Flashcards

1
Q

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.

A

-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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the cardiac conduction system, including the five phases of cardiac action potential.

A

-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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Identify the characteristics of normal sinus rhythm.

A

-P waves are upright & uniform in appearance.
-One P wave for each QRS complex.
-One P wave precedes each QRS complex.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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.

A

-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!!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Aortic Regurgitation

A

-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).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Mitral Valve Stenosis

A

-Narrowing of mitral valve

Cause: rheumatic heart disease

-Manifestations: A-fib, L atrium hypertrophy & dilation, R vent. failure, Reduced CO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Aortic Stenosis

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Systolic HF

A

-Weak pump, reduced ejection faction <40%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Diastolic HF

A

-Poor filling, normal ejection faction (55-70%)

-Inadequate relaxation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

L Sided HF

A

-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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

R Sided HF

A

-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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe the therapeutic actions, indications, pharmacokinetics, contraindications, most common adverse reactions, and important drug-drug interactions associated with drugs used of cardiotonic agents.

A

-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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Pericarditis (Peri)

A

-Inflammation of pericardium

-Causes: viruses, bacteria, trauma, drugs

-Symptoms: Chest rub, pericardial friction rub

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Pericardial Effusion (Peri)

A

-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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Cardiac Tamponade (Peri)

A

-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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Dilated (Cardiomyopathy) (Myo)

A

-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.

17
Q

Hypertrophic Obstructive (Cardiomyopathy) (Myo)

A

-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.

18
Q

Restrictive

A

-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

19
Q

Endocarditis

A

-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

20
Q

Cardiogenic shock

A

-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.

21
Q

Describe the complications of shock related to the lungs, kidneys, gastrointestinal tract, and blood clotting.

A

-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.

22
Q

Class I – Lidocaine

A

-decrease depolarization

-decrease automaticity of ventricular cells

-manages acute ventricular arrhythmias (MI)

23
Q

Class II – Propranolol

A

-beta blocker: decrease contractility; decrease SA node power

-treat cardiac arrhythmias

-treat suprventricular tachycardias

-oral & IV

24
Q

Class III – Amiodarone

A

-treatment for life-threatening ventricular arrhythmias

-acts directly on heart muscle to prolong repolarization

-given oral and IV

25
Q

Class IV – Diltiazem

A

-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

26
Q

Cardiac glycoside: Digoxin

A

-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