Heart Failure

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-Pathophysiology
-Treatment
-Anesthetic Management

PATHOPHYSIOLOGY

-systolic dysfunction
-diastolic dysfunction

SYSTOLIC DYSFUNCTION

-heart is unable to pump enough blood to meet the body’s oxygen demand (metabolic requirements)

Common causes of systolic dysfunction:
-coronary artery disease
-valvular dysfunction
-cardiac dysrhythmias
-pericardial disease

Clinical manifestations of systolic heart failure may include:
-system venous congestion
-pulmonary venous congestion leading to pulmonary edema
-fatigue
-acidosis due to oxygen debt at the tissue level

DIASTOLIC DYSFUNCTION
-decreased compliance of the heart resulting in inadequate LV filling leading to decreased cardiac output

Common causes of diastolic heart failure:
-hypertension
-coronary heart disease
-hypertrophic cardiomyopathy
-pericardial disease

Diagnostic studies for heart failure:
-chest radiograph
-electrocardiogram
-mixed venous saturation (SV02) ex. low Sv02 indicating inadequate oxygen delivery to peripheral tissues
-ABG: increased (A-a) gradient indicates inadequate delivery or increased utilization of oxygen by tissues

COMPENSATORY MECHANISMS OF HEART FAILURE
-increased preload
-increased sympathetic tone
-activation of RAAS
-stimulation of AVP
-ventricular hypertrophy

Increased Preload
-increase in preload is an attempt to maintain cardiac output
-increased preload attempts to maximize the stroke volume based on Frank Starling Law
preload increased beyond the LV ability to contract (worsening ejection fraction) leads to:
-worsening venous congestion
-increased vascular congestion leads to transudation of fluid into the pulmonary interstitium
-pulmonary edema occurs as fluid continues to engorge the alveoli
-increased volume within the LV leads to dilation of the AV annulus resulting in valvular regurgitation
-aortic regurgitation further reduces LV cardiac output and results in an increased LVEDP
-as the LVEDP increases subendocardial coronary arteries become more compressed
-compressed subendocardial coronary arteries leads to decreased coronary blood flow…ischemia
-myocardial ischemia amidst increased myocardial work (ex. increased wall tension due to inc LVEDP)
-viscious cycle of myocardial deterioration and pump failure

Increased Sympathetic Tone
-failing heart subjected to increased wall tension (ex. inc LVEDP) stimulates SNS
-increased SNS increases the release of NE at the nerve endings leading to the cardiac receptors
-increased SNS increase the release of Epi from the adrenal medulla
-initial stimulation of SNS assist in cardiac contractility to overcome the LV wall tension despite inc SVR
-continual SNS stimulation overburdens to failing heart to which the increased SVR leads to decreased CO
-decreasing CO in a failing heart with increased SVR leads to the viscious myocardial cycle

Ventricular Hypertrophy
-ventricular hypertrophy as a result of either pressure or volume overload
-increased sarcomere length allows to actin and myosin filaments to overlap for optimal contraction
-volume overloaded ventricle results from diastolic wall stress leading to eccentric LVH
-pressure overloaded ventricle results from systolic wall stress leading to concentric LVH
-progression of LVH often leads to decreased diastolic compliance and eventual diastolic heart failure