26 - Congestive Heart Failure Flashcards
What is heart failure?
Inadequate blood flow for metabolic needs
What are the primary and secondary causes of heart failure?
Primary
- This is what we will talk about in this course
- Cardiac origin, periphery affected
Secondary
- Peripheral cause, cardiac affected
- Sepsis, anemia, toxins, etc.
Describe systolic heart failure
Remember systolic = contraction, so systolic heart failure is when the heart cannot contract enough (weakened contractility) and the heart can’t empty
- Ejection fraction will be
Descrie diastolic heart failure
Remember diastolic = relaxation, so diastolic heart failure is when muscular hypertrophy prevents the heart from filling properly
- Ejection fraction will be >50%
- Hypertension will occur without ischemia
Describe the pathophysiology of heart failure
- Begins with decreased cardiac output
- Compensated by increased volume (retention of Na+ and water)
- Cardiac response
How does the heart respond to heart failure?
- Increased filling volume (LVEDV)
- Increased fiber length, which allows increased force of contraction
- Starling law
Describe the Starling law curves
- Up to a limit, stroke volume and LVEDV increase in tandem.
- In HF, the LVEDV is up but the stroke volume (LVEDV-LVESV) is down.
- Less is pumped out per cycle.
What does the body do in HF when senses a drop in tissue perfusion and interprets it as ischemia?
- Increases contractility, rate, peripheral resistance (Epinephrine, norepinephrine)
- Increases ischemia (systolic) or hypertrophy (diastolic) (Increased O2 demand, increased work load)
- Renin/angiotensin activated as if hypovolemic
What are the “upstream” consequences in HF?
- Left ventricular failure leads to pulmonary congestion and dyspnea
- Right ventricular failure leads to systemic congestion and edema
What are the “downstream” consequences in HF?
- Left ventricular failure leads to poor organ perfusion and therefore decreased function (renal, cerebral, cardiac –> Na+/H2O retention, confusion, ischemia)
- Right ventricular failure leads to lower filling pressures, creating diastolic failure (can’t fill)
What is the most common cause of R ventricular failure?
Left ventricular failure
- Pulmonary vascular congestion from left ventricular failure increases the workload on the right ventricle
- Eventually the right ventricle will fail
What are symptoms of L ventricular failure?
- Dyspnea: exertion, recumbent, nocturnal, resting
- Diminished exercise capacity (output down)
- Nocturia (recumbent diuresis)
- CNS impairment (memory, insomnia, etc; end organ)
What are symptoms of R ventricular failure?
- Peripheral edema (Includes hepatosplenomegaly, legs up to back!)
- Edema of bowel wall can impair med absorption
What is the NYHA functional classification of HF?
Classes I-IV to determine level of heart failure
Describe class I
- No functional limitation
- Ordinary physical activity does not cause undue fatigue, dyspnea or palpitations
- Normal life expectancy for comorbidities
- At-risk population
Describe class II
- Slight limitation of activity
- Ordinary activity precipitates dyspnea, fatigue, palpitations or angina
- 25% risk in 1 year
Describe class III
- Market limitation
- Less than normal activity precipitates symptoms
- Marked limitation of physical activity
- Less than ordinary physical activity leads to symptoms
- 50% risk in 1 year
Describe class IV
- Symptoms at rest
- Unable to carry on any physical activity without discomfort
- 50% risk in 1 year
What would you see on physical examination in left HF?
- Pallor, cool extremities
- Anxiety, dyspnea at rest
- Pulses normal to rapid, weak
- Blood pressure varies
- Pulmonary rales, pleural effusion
Remember: usually not “pure” Left HF.
What would you see on physical examination in right HF?
- Hepatojugular reflux
- Kussmaul’s sign
- – Paradoxical JVD from increased R chest pressures
- – Inhalation normally increases blood return.
- Congestive hepatomegaly (Ascites)
- Edema – symmetrical, pitting, dependent
What would you see in a cardiac exam?
- Kussmaul’s sign
- Cardiomegaly
- S3 almost universal (LV or RV)
- S4 rare; absent in A fib.
- Pulsus alternans
- Murmurs
- – Systolic: MR, AS, TR
- – Diastolic: AI
- Cardiac cachexia (late)
What would you see in laboratory test?
- Electrolyte abnormalities (GFR, lytes)
- Liver enzyme elevations (stasis)
- Findings related to precipitating causes (e.g. TSH)
What would you see in an x-ray?
- Cardiomegaly
- Pulmonary congestion
- Pleural effusion
- Kerley lines
What is the prognosis of HF patients?
- Overall US mortality is 50% in 5 yr; one year 30-40%
- Most die of 1) pump failure or 2) tachyarrhythmias
What makes the prognosis worse?
Male gender CAD S3 Low/narrow pulse pressure High number NYHA functional class Reduced exercise capacity
What are the therapy goals?
- Relieve symptoms – make the patient feel better
- Improve NYHA functional class (Challenging once patient has progressed to class 3 or 4)
- Decrease frequency and intensity of treatment (might reduce cost; inconsistent finding)
- Delay progression of myocardial dysfunction
- Reduce premature HF mortality
What does HF therapy depend on?
The stage of HF
What are the two most beneficial therapies of HF?
- ACEi
- Beta-blockers
Describe stage A therapy
Pre-symptoms, at risk but heart is okay
- ACE inhibitors are drug of choice
- Beta blockers may be beneficial
- Aim to prevent dysfunction and HF or any irreversible damage
Describe stage B therapy
Cardiac structure changes without symptoms
Drugs of choice
- ACEi
- Beta blockers
- Diuretics
- Digoxin (?)
Goal is to prevent worsening dysfunction, reduce hospitalizations, etc.
Describe stage C therapy
Cardiac structure changes with symptoms
Drugs of choice
- ACEi
- Spironolactone
- Diuretics
- Beta blockers
Goal is to reduce premature HF mortality, reduce disability and hospitalization and reduce symptoms
Describe stage D therapy
Advanced disease with continued symptoms
Drugs cannot salvage the patient!
- ACEi will improve symptoms and reduce premature HF mortality
Goals
- Palliation
- Reduce hospitalizations
- Bridge patient to transplant
How important are ACEi?
VERY
- ACEIs are now mandatory agents for treating HF
How do ACEi work?
Adverse effects of angiotensin II in HF—mediated by AT-1 receptors:
- Myocyte hypertrophy
- Myocyte apoptosis
- Presynaptic facilitation of norepinephrine release
- Direct myocyte toxicity
- Proliferation of fibroblasts
Should you use ARBs instead of ACEi?
Angiotensin Receptor Blockers
- No, generally stick with ACEi
- May be useful in combination
When should vasodilators be used?
When ACEi are not tolerated
What are two beta blockers
Metoprolol
- Beta-1 antagonist
Carvediolol
- Beta-1 antagonist with vasodilator properties
What do you do when a patient responds poorly to therapy?
Strategies for improvement
- Patient education (compliance)
- Review diagnoses, retest
- Modify therapy
Why do patients sometimes respond poorly?
- Poor compliance
- Advanced myocardial dysfunction
- Co-existing diseases (e.g. renal, liver)
