NURS 165 Study Guide - Final Guide: Pulmonary Circulation, Viscosity, Splenomegaly
Heart Failure Pathophysiology Study Guide
• Cardiac output = heart rate * stroke volume
o HR determined by symp. & parasymp. nervous systems
o SV determined by preload & afterload (also SNS)
▪ Preload depends on blood volume & ability of ventricle to relax
during diastole
▪ Stroke volume increases when end diastolic ventricular
volume increases (w/in normal ranges) –Starling’s Law
• Leads to increased stretch & better crossbridge
formation in cardiac contraction
• Starling’s Law details relationship between EDV and
stroke volume
o Contractility also affects Frank-Starling curve
▪ Inc. contractility = inc. stroke volume and inc. preload
▪ When heart can’t function, contractility increases as
compensation mechanism
• This is okay in short term, but very bad long term!
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• Determinants of Blood Volume
o Extracellular fluid
o Sodium intake (water follows sodium)
▪ Retention/excretion of sodium & water also a factor
(controlled by hormones)
▪ Aldosterone inc. sodium/water retention
▪ Vasopressin/ADH inc. water retention
• Alcohol suppresses vasopressin → inc. urination
▪ ANP, BNP inc. sodium excretion
• Epidemiology of HF
o Affects 5.7 million Americans
o 20% of US adults will develop in lifetime
▪ Chance inc. with age
o Most common cause of hospitalization for patients younger than 65
o Higher incidence in men, but women make up more cases (longer life
expectancy)
o Half die within 5 years of diagnosis
• Concepts & Definitions
o Heart failure is NOT a single disease, it is a syndrome with common
findings
o Defined as inability of heart to produce enough cardiac output to meet
needs of body (see Genius)
o Left HF more common; but is most common cause of right HF
o Isolated right HF is often complication of lung disease
o See Genius for more definitions
• Systolic Heart Failure
o Impaired ability of ventricle to contract; reducing stroke volume and
ejection fraction to less than 40%
o Occurs due to weakened heart wall
o Heart wall not being used for blood pumping function → remodeling
(ventricle wall thins, chamber enlarges) → no longer suitable for
function
o Causes
▪ Coronary artery disease
▪ Myocardial infarction
▪ Hypertension
▪ Valve disorders (ex. Aortic stenosis)
▪ Family history
• Dilated cardiomyopathy (see pic below)
▪ Toxic damage to heart
▪ Idiopathic (mystery causes) – may be postpartum related
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• Diastolic Heart Failure
o Impaired ability of ventricle to relax → decreased filling and EDV
o Ventricle wall very stiff
o Causes
▪ Ventricular hypertrophy (in turn due to hypertension)
▪ Ischemic fibrosis (makes ventricle stiff)
▪ Hypertrophic cardiomyopathy
• Genetic condition – thickening or enlargement of
ventricular walls, blood flow obstruction @ LV outflow
• Often presents as heart failure
• Leading cause of sudden death in young athletes
• High Output Heart Failure (HOHF)
o HF is defined as state when cardiac output is insufficient to meet
needs of body
o When needs of body inc. but CO doesn’t raise to meet them →
HOHF
▪ Ex. Hyperthyroidism in elderly, anemia, some kidney failures
o Treatment is in treatment of underlying cause
• Systolic vs. Diastolic HF
o Systolic: ventricles enlarged, walls thinner
o Diastolic: ventricles smaller, walls thicker
o Systolic: less blood pumped out of ventricles
▪ Can’t contract as well
o Diastolic: less blood fills ventricles
▪ Can’t relax as well
• Classification
o New York Heart Association (NYHA)
▪ Class I: Functional capacity not limited enough to produce
symptoms
▪ Class II: Slight limitation, comfortable at rest and with mild
exertion. Symptoms with strenuous activity
▪ Class III: Patient only comfortable at rest; symptoms with even
slight exertion
▪ Class IV: Symptoms even at rest
o American College of Cardiology/American Heart Association
(ACC/AHA)
▪ Stage A: Patient at high risk for heart failure, but no heart
disease or symptoms of HF
▪ Stage B: Patient with structural heart disease, but no HF signs
▪ Stage C: Patient with structural heart disease; prior or current
heart disease symptoms
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