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Cardio Exam 2 > 26 - Congestive Heart Failure > Flashcards

26 - Congestive Heart Failure Flashcards

1
Q

What is heart failure?

A

Inadequate blood flow for metabolic needs

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2
Q

What are the primary and secondary causes of heart failure?

A

Primary

  • This is what we will talk about in this course
  • Cardiac origin, periphery affected

Secondary

  • Peripheral cause, cardiac affected
  • Sepsis, anemia, toxins, etc.
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3
Q

Describe systolic heart failure

A

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

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4
Q

Descrie diastolic heart failure

A

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
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5
Q

Describe the pathophysiology of heart failure

A
  • Begins with decreased cardiac output
  • Compensated by increased volume (retention of Na+ and water)
  • Cardiac response
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6
Q

How does the heart respond to heart failure?

A
  • Increased filling volume (LVEDV)
  • Increased fiber length, which allows increased force of contraction
  • Starling law
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7
Q

Describe the Starling law curves

A
  • 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.
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8
Q

What does the body do in HF when senses a drop in tissue perfusion and interprets it as ischemia?

A
  • 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
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9
Q

What are the “upstream” consequences in HF?

A
  • Left ventricular failure leads to pulmonary congestion and dyspnea
  • Right ventricular failure leads to systemic congestion and edema
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10
Q

What are the “downstream” consequences in HF?

A
  • 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)
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11
Q

What is the most common cause of R ventricular failure?

A

Left ventricular failure

  • Pulmonary vascular congestion from left ventricular failure increases the workload on the right ventricle
  • Eventually the right ventricle will fail
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12
Q

What are symptoms of L ventricular failure?

A
  • Dyspnea: exertion, recumbent, nocturnal, resting
  • Diminished exercise capacity (output down)
  • Nocturia (recumbent diuresis)
  • CNS impairment (memory, insomnia, etc; end organ)
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13
Q

What are symptoms of R ventricular failure?

A
  • Peripheral edema (Includes hepatosplenomegaly, legs up to back!)
  • Edema of bowel wall can impair med absorption
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14
Q

What is the NYHA functional classification of HF?

A

Classes I-IV to determine level of heart failure

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15
Q

Describe class I

A
  • No functional limitation
  • Ordinary physical activity does not cause undue fatigue, dyspnea or palpitations
  • Normal life expectancy for comorbidities
  • At-risk population
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16
Q

Describe class II

A
  • Slight limitation of activity
  • Ordinary activity precipitates dyspnea, fatigue, palpitations or angina
  • 25% risk in 1 year
17
Q

Describe class III

A
  • 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
18
Q

Describe class IV

A
  • Symptoms at rest
  • Unable to carry on any physical activity without discomfort
  • 50% risk in 1 year
19
Q

What would you see on physical examination in left HF?

A
  • 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.

20
Q

What would you see on physical examination in right HF?

A
  • Hepatojugular reflux
  • Kussmaul’s sign
  • – Paradoxical JVD from increased R chest pressures
  • – Inhalation normally increases blood return.
  • Congestive hepatomegaly (Ascites)
  • Edema – symmetrical, pitting, dependent
21
Q

What would you see in a cardiac exam?

A
  • 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)
22
Q

What would you see in laboratory test?

A
  • Electrolyte abnormalities (GFR, lytes)
  • Liver enzyme elevations (stasis)
  • Findings related to precipitating causes (e.g. TSH)
23
Q

What would you see in an x-ray?

A
  • Cardiomegaly
  • Pulmonary congestion
  • Pleural effusion
  • Kerley lines
24
Q

What is the prognosis of HF patients?

A
  • Overall US mortality is 50% in 5 yr; one year 30-40%

- Most die of 1) pump failure or 2) tachyarrhythmias

25
Q

What makes the prognosis worse?

A 
Male gender
CAD
S3
Low/narrow pulse pressure
High number NYHA functional class
Reduced exercise capacity
26
Q

What are the therapy goals?

A
  • 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
27
Q

What does HF therapy depend on?

A

The stage of HF

28
Q

What are the two most beneficial therapies of HF?

A
  • ACEi

- Beta-blockers

29
Q

Describe stage A therapy

A

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
30
Q

Describe stage B therapy

A

Cardiac structure changes without symptoms

Drugs of choice

  • ACEi
  • Beta blockers
  • Diuretics
  • Digoxin (?)

Goal is to prevent worsening dysfunction, reduce hospitalizations, etc.

31
Q

Describe stage C therapy

A

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

32
Q

Describe stage D therapy

A

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
33
Q

How important are ACEi?

A

VERY

- ACEIs are now mandatory agents for treating HF

34
Q

How do ACEi work?

A

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
35
Q

Should you use ARBs instead of ACEi?

A

Angiotensin Receptor Blockers

  • No, generally stick with ACEi
  • May be useful in combination
36
Q

When should vasodilators be used?

A

When ACEi are not tolerated

37
Q

What are two beta blockers

A

Metoprolol
- Beta-1 antagonist

Carvediolol
- Beta-1 antagonist with vasodilator properties

38
Q

What do you do when a patient responds poorly to therapy?

A

Strategies for improvement

  • Patient education (compliance)
  • Review diagnoses, retest
  • Modify therapy
39
Q

Why do patients sometimes respond poorly?

A
  • Poor compliance
  • Advanced myocardial dysfunction
  • Co-existing diseases (e.g. renal, liver)

Cardio Exam 2 (12 decks)

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