26 Flashcards
Define HF
- Inadequate blood flow for metabolic needs
Primary HF
- Cause: cardiac origin, peripherally affected
- Can’t empty –> systolic
–> weakened contractility (low ejection fraction)
- Can’t fill –> diastolic
–> muscular hypertrophy (low volume)
describe the pathophsiology of HF
- Begins with decreased cardiac output
- compensate by increased volume (retain Na+ and H20)
- Heart response limited to:
–> increase volume (filling) - increase left ventricular end diastolic volume
–> increased fiber length (spilling) - increase force of contraction
–> starlings law (SV and LVEDV increase together)
describe the bodies response to tissue ischemia
- increases contractility, rate, peripheral resistance (epinephrine, norepinephrine)
- Increase ischemia (systolic) or hypertorphy (diastolic) (increased O2 demand, increased work load)
- renen/angiotensin activated as if hypovolemic
describe symptoms of LV Failure
- Dyspnea (exertion, recumbent, nocturnal, resting)
- Diminished exercise capacity (output down)
- nocturia (recombent diuresis)
describe sysmptoms of RV failrue
- peripheral edema
- Edema of bowel wall can impair med absorption
describe NYHA functional classification
- Class 1 - no limitation
- Class 2 - slight limitation of activity (ordinary activity precipitates dyspnea, fatigue, angina)
- Class 3 = makred limitation (less than normal activity)
- Class 4 - symptoms at rest
describeing physical exams of LEFT HF
- Pallor, cool extremities
- anxiety, dyspnea at rest
- pulses normal to rapid, weak
- blood pressure varies
- Pulmonary rales, pleural effusion
physical exam of Right HF
- Hepatojugular reflux
- kassmauls sign
–> paradoxical JVD from increased R chest pressure (inhallation normally increases blood return (rise in JVD)
- congestive hepatomegally (ascites)
- Edema (symmetrical, pitting, dependent)
describe goals of therapy for HF
- relieve symptoms
- improve NYHA functional class
- decrease frequency and intesnity of tx
- delay progression of myocardial dysfunction
- reduce premature HF mortality
therapy at Stage A
- Stage A = pre-symptoms, at risk, heart ok
- ACE inhibitors
- beta blockers may be benefit
therapy at stage B
- Stage B = no symptoms, cardiac structure changes)
- Goals
–> prevent worsening dysfunction
–> improve symptoms
–> reduce disability and hospitalizations
- Drugs = ACEIs, beta blockers, diuretics, digoxin (?)
Therapy at stage C
- Stage C = structural changes and symptoms present)
- Goals:
–> reduce premature HF mortality
–> reduce diability and hospitalization
–> improve symptoms and functional capacity
- Drugs = ACEI, spironolactone, diuretics, beta blockers
therapy at stage D
- Stage D = advnaced disease, continued symptoms, require aggressive therapy)
- goals:
–> palliation (feel better)
–> reduce hospitalizations
- Drugs = improve symptoms (cannot salvage the patient)
Describe adverse effects of angiotensin II in HF
- mediated by AT-1 receptors
- Myocyte hypertrophy
- myocyte apoptosis
- proliferation of fibroblasts
**ACEI are now MANDATORY agents for tx of HF**