Heart Failure Pathology Flashcards
What does heart failure usually result from and what are the mechanisms that often cause it?
usually results from slowly developing intrinsic deficit in contraction (but occasionally occurs acutely)
- mechanisms:
-
Abnormal load presented to heart
- acute: fluid overload, MI, valve dysfunction
- chronically: ischemic heart disease, dilated cardiomyopathy, HTN
-
Impaired ventricular filling
- acute: pericarditis or tamponade
- chronically: restrictive cardiomyopathy, severe left ventricular hypertrphy
-
obstruction due to valve stenosis
- chronically: rheumatic valve disease (usually mitral valve)
what are the 2 characterizations of heart failure (not left and right) and what are some examples of each characterization?
- Systolic dysfunction: progressive deterioration of cardiac (contractile) force
- ischemic heart disease
- pressure or volume overload
- dilated cardiomyopathy
- diastolic dysfunction: inability of heart to relx, expand, and fill sufficiently during diastole
- massive ventricular hypertrophy
- amyloidosis
- myocardial fibrosis
- constrictive pericarditis
When the heart is understress it uses 3 compensatory mechanisms. WHat are they?
- Frank-Starling (rapidly occuring)
- increased preload dilation (increased EDV) helps sustain cardiac performance by enhancing contractility
- results in increased wall tension and increased oxygen requirements
- Neurohormonal systems (rapidly occuring) release of NE by cardiac nerves: increase HR, contractility, vascular resistance
- activate renin-angiotensin-aldosterone system: increased Na and water reabsorption, increases cardiac output and increased vasoconstriction
- release of ANP: secreted from atrial mycytes when atrium is dilated, causing vasodilation, diuresis
- Hypertrophy
- compensatory response to increased load occrs over weeks to months,increase number of sarcomeres, no hyperplasia
- 600g: pulmonary HTN and IHD
- 800g: systemic HTN, aortic stenosis, mitral regurgitation, dilated cardiomyopathy
- aortic regurgitation, hypertrophic cardiomyopathy
- compensatory response to increased load occrs over weeks to months,increase number of sarcomeres, no hyperplasia
How does hypertrophy reflect the nature of the stimulus?
Pressure overload=concentric hypertrophy (HTN, aortic stenosis)
VOlume overload= hypertrophy accompanied by dilation (mitral or aortic regurgitation
What does sustained hypertrophy lead to?
- Cardiac hypertrophy often evolves to cardiac failure
- increased myocyte size leads to decreased capillary density, increased intercapillary distance and icnreased fibrous tissue
- higher cardiac oxygen consumption
- altered gene expression and proteins
- loss of myocytes due to apoptosis
- ALSO LV Hypertrophy is an independent risk factor for sudden death
Effects of left sided heart failure are primarily due to progressive damming of blood within the pulmonary circulation and diminshed peripheral blood pressure and flow (IHD, HTN, Aortic and Mitral valve diseases, non=ischemic myocardial diseases)
WHat are the effects of left-sided heart failure on the heart and what are the secondary effects of that?
Left ventricular hypertrophy and often diltion, often resultng in mitral valve insufficiency
secondary enlargement of left atrium leads to atrial fibrilation leads to stagnant blood in atrium leads to thrombus and embolic stroke
Whats up with the nuclei on the right?
they are hypertrophied
What are the effects of left sided- heart failure on the lungs?
increased pulmonary pressure in pulmonary veins which is transmitted to capillaries and arteries
leads to pulmonary congestion/edema, heart failure cells, dyspnea, orthopnea, and paroxysmal nocturnal dyspnea (when supine venous return increases and diaphragms elevate
rales on exam
wht are these brown cells? what is the light purple?
The brown are hemosiderin-laden macrophages aka heart failure cells
the light purple is fluid in the air space
what are the effects of left sided heart failure on the kidneys? how about on the brain?
- decreased renal perfusion activates renin-angiotensin-aldosterone system which leads to increased blood volume
- if perfusion deficit is severe it leads to prerenal azotemia (impaired kidney function due to low perfusion)
brain: cerebral hypoxia and encephalopathy
what are the effects of right sided heart failure usually due to?
effects are primarily due to engorgement of systemic and portal venous systems (secondary to LHF, pulmonary HTN, primary myocardial disease, tricuspid or pulmonary valvular disease)
What does right heart failure do to the heart, liver/portal system, kidneys, brain, pleural space, periphery
heart: right ventricle responds to the increased workload with hypertrophy and often dilation
liver and portal system: elevated pressure in the portal vein leads to congestive hepatosplenomegaly, cardiac cirrhosis, ascites
kidneys: congestion, fluid retention, peripheral edema, azotemia (more marked with right heart failure than left)
brain: venous congestion and hypoxic encephalopathy
Pleural and pericardial effusion, atelectasis (collapse of lungs)
peripheral edema: at ankle, presacral
eventual anasarca (generalized massive edema)
What is up with this liver?
“nut meg” appearance. liver with centrilobular congestion due to right sided heart failure
Left heart failure:
- pulmonary
- kidneys
- brain
right heart failure:
- systemic and portal veins
- kidenys
- brain
Left heart failure:
- pulmonary: pulmonary congestion and edema prominent
- kidneys: reduced perfusion, fluid retention, azotemia less prominent
- brain: reduced perfusion, cerebral hypoxia and encephalopathy
right heart failure:
- systemic and portal venous congestion
- hepatosplenomegaly, peripheral edema, pleural effusion, ascites
- kidenys: congestion, fluid retention and azotemia more prominent
- brain: venous congestion, hypoxemia and encephalopathy
