Congestive Heart Failure Flashcards
Congestive heart failure is not a _______
disease it is a complication of other diseases A SYNDROME
Congestive Heart failure is due to
serious heart disease (endpoint of serious heart disease)
Congestive heart failure results in
cardiac, pulmonary & systemic congestion
Etiology of congestive heart failure (major ones)
- CAD
- uncontrolled hypertension
- cardiomyopathy
- valvular disease
- MI
- excessive cardiac workload
- volume overload
Most important risk factors to target for prevention of congestive heart failure
- Ischemic heart disease
- Hyperlipidemia
- smoking
- low ejection fraction
normal healthy heart can increase CO apporx
5x @ resting level (this is called cardiac reserve)
When in heart failure
cardiac reserve used at rest
Patho of left sided heart failure
- Left ventricle fails to eject sufficient volume
- Residual volume develops in left ventricle
- Left atrium pumps harder to empty blood into left ventricle
- fails to empty full
- residual volume in Left atrium
- Left atrium unable to receive full pulmonary return
- pulmonary congestion & edema
- Right ventricle workload increases
- Right ventricle hypertrophy (to meet demand)
left sided heart failure
- failure to eject into systemic circuit
- results in inadequate cardiac output
- pooling into pulmonary circuit
- leads to pulmonary congestion & pulmonary edema
with left sided heart failure the heart fails to eject into
systemic circuit
left sided heart failure leads to
pulmonary congestion & pulmonary edema
Right sided heart failure
- Failure to eject into pulmonary circuit
- pooling in systemic circuit
- causes peripheral edema & abdominal distention
with right sided heart failure heart fails to eject into
pulmonary circuit
right sided heart failure causes
-peripheral edema & abdominal distention
right sided heart failure normally follows
left sided failure
Manifestations of Right sided heart failure
Congestion of peripheral tissues:
- Dependent edema & ascites
- GI tract congestion (anorexia, wt loss, GI distress)
- Liver congestion (signs related to impaired liver function)
Manifestations of Left sided heart failure
Decreased cardiac output:
-leads to activity intolerance & signs of decreased tissue perfusion
Pulmonary congestion:
-leads to impaired gas change (cyanosis & signs of hypoxia) and pulmonary edema (cough w frothy sputum, orthopnea, paroxysmal nocturnal dyspnea)
What is ascites
accumulation of fluid in peritoneal cavity, causing abdominal swelling
Compensated heart failure
- body trying to repair, minimize compensate, if can’t fails
- compensation before heart failure
- compensatory mechanisms conceal extent of damage
- clinically asymptomatic
Compensatory mechanisms for heart failure
- Ventricle Dilation (Frank-Starling Law)
- Sympathetic nervous system
- Renin angiotensin adlosterone system
- Naturiuetic peptides (ANP & BNP)
- Endothelins
- Cardiac hypertrophy & remodeling
Ventricle dilation (compensatory mechanism)
(also known as Frank-Starling Law)
- increase EDV (end diastolic volume), leads to muscle stretch, increases preload, increases cardiac ouput
- cannot do this on a long term basis
what 3 compensatory mechanisms start working in minutes to hours
- Ventricle Dilation (Frank-Starling Law)
- Sympathetic nervous system
- Renin angiotensin adlosterone system
What is the end diastolic volume
volume of blood in the right and/or left ventricle at end load or filling in (diastole) or amount of blood in ventricles just before systole
what is the preload
preload is the end diastolic volume that stretches the right or left ventricle of the heart to its greatest dimensions
Sympathetic nervous system (compensatory mechanism)
Activated by a decrease in C02, aims to Increase Cardiac output, causes:
-Vasoconstriction (increase pressure in vessels, Increase venous return)
-Tachycardia
-Increases contractility
(all of these increase cardiac output)
RAAS (compensatory mechanism)
approx 25% of cardiac output goes to kidneys
- decrease in cardiac output leads to decrease in renal perfusion
- RAAS triggered
- Angiotensin II
- Aldosterone & ADH (aldosterone also causes vasoconstriction)
- Hypervolemia
- Increases preload
- increases cardiac output
natriuretic peptides (ANP & BNP) (compensatory mechanism)
- both produced by heart (ANP in atrium & BNP in ventricles)
- Both potent causes diuresis & naturesis (sodium loss through kidney, decreasing blood volume)
- affects vascular smooth muscle (vasoconstriction & dilation)
- Oppose action of SNS & RAAS
Endothelins (compensatory mechanism)
- secreted chemicals by endothelium & cardiac muscle
- Vasoconstrictors
- cause vascular & cardiac & smooth muscle hypertrophy
Endothelins (compensatory mechanism)
- secreted chemicals by endothelium & cardiac muscle
- Vasoconstrictors
- cause vascular & cardiac & smooth muscle hypertrophy – occurs in cardiac muscle so more forceful contractions can occur
- needs more resources so demand can’t be met long term
Cardiac hypertrophy & remodeling (compensatory mechanism)
- hypertrophy d/t increased workload
- eventually decreases contractility
- requires more oxygen– cardiac dysfunction
Manifestations of congestive heart failure
- various
- decrease CO (effects of impaired pumping)
- decreased renal perfusion
- SNS responses: increase BP, tachycardia, vasoconstriction
Diagnosing congestive heart failure
- History & physical exam (risk factors present)
- Lab tests (renal fx, fluid electrolutes, liver fx, CBC, Hct, ABGs)
- ECG & echocardiogram
Treatment for acute congestive heart failure
Stabilize & correct cause (see MI)
Treatment for chronic congestive heart failure
Symptomatic (relive mnfts), decrease risks and increase function
