The document discusses the pathophysiology of heart failure, including causes such as coronary heart disease, hypertension, and pulmonary heart disease. It describes how injury to the heart muscle leads to a loss of cardiac myocyte function and decreased contractility, stroke volume, and cardiac output. As a compensatory response, the sympathetic nervous system is stimulated to increase heart rate, vasoconstriction, and fluid retention in an attempt to increase cardiac preload and output. However, over time the increased stress on the heart leads to remodeling of the left ventricle and further decreases in stroke volume and cardiac output, resulting in heart failure.

1. Depressed ejection
fraction (<40%)
-coronary heart dse
-hypertention
-chronic volume
overload.
Preserved ejection fraction
(>40-50%)
-aging
Pulmonary heart
disease
-cor pulmonale
-pulmonary vascular dis
-pathologic hypertrophy
-restrictive cardiomyopathy
-fibrosis
High-output states
-thyrotoxicosis
-beri-beri
-chronic anemia
-systemic arteriovenous
Injury to the heart muscle
Loss of function of cardiac myocytes
Dec. ability of the myocardium to Generate force
Dec cardiac contractility
Dec SV
Dec CO (s/sx: dec exercise tolerance)
“Unloading” of high pressure baroreceptors in carotid sinus & aortic arch
Efferent sympathetic nervous system
Ant-lat portion of upper medula
Stimulate cardiac regulatory center in the pons & medulla
arginine vasopressin (ADH) from posterior pituitary
Vasoconstriction of blood vessels
Vasoconstriction
Inc the permeability of the renal collecting ducts
Renal hypoperfusion
Release of rennin
Converts angiotensinogen to angiotensin I
ACE converts angiotensin I to angiotensin II
Vasoconstriction of the peripheral vasculature

2. aldosterone
Reabsorbtion of water& electrolyte
Transcriptional and
posttranscriptional changes in the
genes and proteins
Inc afterload,
Excessive beta activation
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Inc force of contractility
Inc preload (2025mmHg)
Inc cardiac output
(via compensation)
Inc heart rate
s/sx: tachycardia
LV End
systolic vol inc
Inc in pulmonary
capillary pressure
Pulmonary
congestion
(s/sx: DOB)
From prolate
ellipsoid to
spherical shape
Remodeling of LV
Leakage of Ca
Dec diastolic filling
Papillary msc r
pulled apart
dyspnea
Incomp of
mitral valve
Inc wall stress of LV
Mitral
regurgitation
LV wall thining
Afterload mismatch
Further dec SV
Dec CO
HEART FAILURE
Stiffning of the
ventricles
(s/sx:
arrhythmias)
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