Heart failure and cardiomyopathies Flashcards

1
Q

What is HF

A

Inability to adequately fill or empty the ventricle

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2
Q

Cause of HF

A
CAD
Cardiomyopathy
Valve problems
HTN
Diseased pericardium
Pulmonary HTN (cor pulmonale)
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3
Q

What are two examples of high-output HF

A

Pregnancy and anemia

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4
Q

HF patho

A
Pressure overload 
Volume overload
Ischemia/Infarct
Myocardial inflammatory disease
Restricted diastolic filling
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5
Q

HF adaptive responses

A

Frank-Starling relationship
SNS activation
Alterations in contractility, HR, afterload
Humorally mediated responses

Eventually these responses become maladaptive and myocardial remodeling takes place

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6
Q

Frank-Starling curve basics

A

Up/Left- Good, more stretch, more contractility (early, acute, compensated HF)

Down/Right- Bad, too much/too little stretch leads to decreased contractility (later, decompensated HF)

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7
Q

SNS activation does 4 basic things for HF

A

Arteriolar constriction: Maintains BP despite decrease in CO. Blood flow is redirected to coronary/cerebral circulation.

Venous constriction: Increases preload–> CO maintained according to FS relationship (more stretch–> greater contractility)

RAAS: Decrease in renal BF activates RAAS (Na+ H2O retention)–> increased volume–> increased CO

Increased HR: HRxSV=CO

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8
Q

Other adaptive responses

A

CO increased: Contraction velocity increased, afterload decreased, HR increased

B-type natriuretic peptide- feedback to protect against too much volume/pressure. Weak in humans, but levels can tell you about the state of HF.

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9
Q

Myocardial remodeling

A

Bad. Big, hypertrophied heart (pressure load) results from long term activation of compensatory mechanisms for HF.

Myocardial dilation, wall thinning (volume load)

Interstitial collagen deposition increased (inflammation)–> leads to fibrosis/scarring and stiffening of the heart

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10
Q

Clinical features of HF

A

Dyspnea, orthopnea, paroxysmal nocturnal dyspnea

Fatigue, weakness at rest

Tachycardia, A-fib, S3 gallop (indicates filling problem)

Oliguria, edema, JVD, lung rales, tachypnea

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11
Q

HF Dx

A

CXR

Elevated BNP

Echo

MRI

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12
Q

HF management

A
ACE/ARBs
Aldosterone blockers
Diuretics
Digoxin
Inotropes
BB
Vasodilators
Bivent pacing
Nesiritide
Assist devices
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13
Q

**4 Things to remember about anesthetic management in HF **

A
  1. HR- Normal to high (very rate dependent)
  2. Preload- Normal to high
  3. Afterload- Low to normal
  4. Contractility- Increase it

Be very careful of high MAC anesthesia

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14
Q

Other management considerations in HF

A

Maintain medication regime (esp. BB) unless contraindicated (ACE inhibitors)

Treat hypotension judiciously- ephedrine, phenylephrine, vasopressin are all good

May need to decrease general anesthetic doses, balanced approach is advised

Positive pressure ventilation beneficial

Regional is ok

Avoid fluid overload, keep track of fluids

+/- A-line

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15
Q

Give a run down of HF

A

Decreased contractility–> ventricle stretches, dilates–> increased ventricle radius increases work–> increased work means increased O2 consumption–> Cardiac output falls–> SNS outflow to increase HR, SVR–> Stroke volume falls

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16
Q

Some cardiomyopathy examples

A

Hypertrophic

Myocarditis

Peripartum

Toxic myopathies (ETOH, cocaine)

17
Q

Hypertrophic CM patho

A

Enlarged heart

LV outflow tract obstruction (asymmetric septal hypertrophy)

Diastolic dysfunction (heart unable to relax)

Myocardial ischemia

Dysrhythmias

18
Q

What is thought to be the root cause of hypertrophic CM? Who does it typically occur in?

A

Ca++ channel abnormalities

Typically seen in young children during exertion. Often leads to sudden death.

19
Q

S/s of hypertrophic CM

A
Angina
Fatigue
Syncope
Tachydysrhythmias
HF
Sudden death- usually this happens without any s/s
20
Q

Tx for hypertrophic CM

A

Beta Blockers

Calcium channel blockers

Treat underlying cause if possible

21
Q

What worsens outflow in hypertrophic CM

A

Hypovolemia

Vasodilators

Tachycardia

Positive pressure ventilation

Hypotension

22
Q

What improves outflow in hypertrophic CM

A

Decreased contractility, increase preload, increase afterload

BB
Volatile anesthetics
Ca channel blockers
Hypervolemia
Bradycardia
Hypertension
Alpha-adrenergic stimulation
23
Q

Anesthetic management in hypertrophic CM

A

Mild decrease in contractility
Minimize effects on preload and afterload

Treat hypotension with phenylephrine and VOLUME
Replace blood/fluids promptly
AVOID beta agonists
AVOID vasodilators
Maintain NSR
24
Q

Dilated cardiomyopathy

A

LV or biventricular dilation, systemic dysfunction, and normal LV thickness

ETOH’ers almost always have some degree of this

25
Q

Cor pulmonale

A

RV enlargement with either hypertrophy and/or dilation that may progress to right HF

Typically caused by pulm HTN from chronic alveolar hypoxia