Heart failure and cardiomyopathies Flashcards
What is HF
Inability to adequately fill or empty the ventricle
Cause of HF
CAD Cardiomyopathy Valve problems HTN Diseased pericardium Pulmonary HTN (cor pulmonale)
What are two examples of high-output HF
Pregnancy and anemia
HF patho
Pressure overload Volume overload Ischemia/Infarct Myocardial inflammatory disease Restricted diastolic filling
HF adaptive responses
Frank-Starling relationship
SNS activation
Alterations in contractility, HR, afterload
Humorally mediated responses
Eventually these responses become maladaptive and myocardial remodeling takes place
Frank-Starling curve basics
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)
SNS activation does 4 basic things for HF
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
Other adaptive responses
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.
Myocardial remodeling
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
Clinical features of HF
Dyspnea, orthopnea, paroxysmal nocturnal dyspnea
Fatigue, weakness at rest
Tachycardia, A-fib, S3 gallop (indicates filling problem)
Oliguria, edema, JVD, lung rales, tachypnea
HF Dx
CXR
Elevated BNP
Echo
MRI
HF management
ACE/ARBs Aldosterone blockers Diuretics Digoxin Inotropes BB Vasodilators Bivent pacing Nesiritide Assist devices
**4 Things to remember about anesthetic management in HF **
- HR- Normal to high (very rate dependent)
- Preload- Normal to high
- Afterload- Low to normal
- Contractility- Increase it
Be very careful of high MAC anesthesia
Other management considerations in HF
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
Give a run down of HF
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
Some cardiomyopathy examples
Hypertrophic
Myocarditis
Peripartum
Toxic myopathies (ETOH, cocaine)
Hypertrophic CM patho
Enlarged heart
LV outflow tract obstruction (asymmetric septal hypertrophy)
Diastolic dysfunction (heart unable to relax)
Myocardial ischemia
Dysrhythmias
What is thought to be the root cause of hypertrophic CM? Who does it typically occur in?
Ca++ channel abnormalities
Typically seen in young children during exertion. Often leads to sudden death.
S/s of hypertrophic CM
Angina Fatigue Syncope Tachydysrhythmias HF Sudden death- usually this happens without any s/s
Tx for hypertrophic CM
Beta Blockers
Calcium channel blockers
Treat underlying cause if possible
What worsens outflow in hypertrophic CM
Hypovolemia
Vasodilators
Tachycardia
Positive pressure ventilation
Hypotension
What improves outflow in hypertrophic CM
Decreased contractility, increase preload, increase afterload
BB Volatile anesthetics Ca channel blockers Hypervolemia Bradycardia Hypertension Alpha-adrenergic stimulation
Anesthetic management in hypertrophic CM
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
Dilated cardiomyopathy
LV or biventricular dilation, systemic dysfunction, and normal LV thickness
ETOH’ers almost always have some degree of this
Cor pulmonale
RV enlargement with either hypertrophy and/or dilation that may progress to right HF
Typically caused by pulm HTN from chronic alveolar hypoxia
