2

Click here to load reader

Chf pathp physio

Embed Size (px)

Citation preview

Page 1: Chf pathp physio

Depressed ejection fraction (<40%)-coronary heart dse-hypertention-chronic volume overload.

Pulmonary heart disease-cor pulmonale-pulmonary vascular dis

Ant-lat portion of upper medula

Vasoconstriction of blood vessels

Converts angiotensinogen to angiotensin I

Preserved ejection fraction (>40-50%)-aging-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

Renal hypoperfusion

Release of rennin

ACE converts angiotensin I to angiotensin II

Stimulate cardiac regulatory center in the pons & medulla

arginine vasopressin (ADH) from posterior pituitary

Vasoconstriction

Inc the permeability of the renal collecting ducts

Vasoconstriction of the peripheral vasculature

Page 2: Chf pathp physio

Reabsorbtion of water& electrolyte

aldosterone

Inc cardiac output(via compensation)

Inc force of contractilityInc preload (20-25mmHg)

Remodeling of LV

Inc heart rates/sx: tachycardia

Transcriptional and posttranscriptional changes in the genes and proteins

Excessive beta activation

Leakage of Ca

Inc in pulmonary capillary pressure

Pulmonary congestion(s/sx: DOB)

Stiffning of the ventricles

(s/sx: arrhythmias)

Dec diastolic filling

Inc wall stress of LV

LV wall thining

From prolate ellipsoid to

spherical shape

Papillary msc r pulled apart

Further dec SV

Incomp of mitral valve

Afterload mismatch

Mitral regurgitation

Dec CO

Inc afterload,

HEART FAILURE

LV End systolic vol inc

dyspnea

1

1