Heart Failure Flashcards
________ ________ is the FINAL common pathway of many cardiac diseases
Heart Failure
Early compensatory mechanisms to myocardial insults include……….. and are initially protective but become maladaptive with time
Inc. preload and wall thickness (SNS and RAAS)
clinical syndrome characterized largely by fluid retention leading to pathologically elevated filling pressure; worsened by physiologic compensation with SNS and RAAS; decreased contractility, stroke volume, and increased preload
Heart Failure
Heart failure can be caused by… (4 total)
Impaired contractility (ischemia, dilation)
Inc. afterload (HTN, AS)
Inc. volume (valve insufficiency)
Impaired ventricular filling (hypertrophy)
Most common cause of heart failure
Myocardial infarction
Two main physiologic adaptations to decreased stroke volume are…….
Inc. preload (Frank-Starling)
Inc. wall thickness
When contractility is impaired, a higher _________ is required to increase stroke volume
preload
Increased preload leads to increased stroke volume up to a point (True or False)
True. (plateaus to where no increase in pressure affects stroke volume)
Increased left atrial pressure can result in…
pulmonary edema
How is preload regulated (3 total)
Venous tone (sympathetic activity via baroreceptors) Blood volume (Sympathetic, RAAS, ADH) Body position
Norepinephrine application to the kidney causes…
Renin release Fluid retention (inc. preload)
Cardiovascular response to chronic beta-adrenergic receptor stimulation
Downregulation of receptors Energy starvation Cardiomyocyte death Ventricular arrhythmias Fibrosis
Dec. perfusion stimulates sympathetic outflow, causing……. which worsens disease progression
Cardiac activity–> myocardial toxicity and arrhythmias
Renal activity–> vasoconstriction and fluid retention
Renal response to reduced stroke volume
Reduced stroke volume—> reduced effective arterial blood volume—> increased renin and aldosterone—> increased blood volume and vasoconstriction
How does heart failure disrupt the negative feedback loop of the renin-angiotensin system?
Gradual decrease in cardiac output, and thus renal perfusion, perpetually stimulates renin release (as futile as a dog chasing it’s own tail)
How does the SNS and RAAS increase preload?
Inc. circulating volume
Inc. venous return
Natriuretic peptides that counteract maladaptive neurohormones (help reduce blood volume and promotes vasodilation)
ANP (atrial natriuretic peptide)
BNP (brain natriuretic peptide)
Determinants of afterload (3 total)
Systemic vascular resistance
Aortic compliance
Aortic valve resistance
Concentric hypertrophy (pathologic) will progress to what over years of chronic stressors
Eccentric hypertrophy (dilation)
Most common phenotype for heart failure
Cardiac dilation (eccentric hypertrophy)
Two main modes of heart failure
Ischemia
Hypertrophic (concentric to eccentric)
Fibrosis impairs the heart’s ability to (contract/relax/both)
Both
Morphologic features of ventricular remodeling
Hypertrophic myocytes
Dead myocytes
Fibrosis
When stroke volume decreases, ______ will increase in an attempt to preserve MAP
Systemic vascular resistance
The increase in __________ due to SNS and RAAs can further impair cardiac performance by decreasing stroke volume, beginning the maladaptive cycle
afterload (due to increased SVR)
Medications to _______ ________ are central to treating heart failure (opposed SNS and RAAS effects)
reduce afterload
You can have good systolic activity with diastolic dysfunction (True or False)
True
Dec. Contractility
Dec. Stroke Volume
Inc. stiffness
Systolic Dysfunction
Normal contractility
Dec. stroke volume
Inc. stiffness
Diastolic Dysfunction
Diastolic Dysfunction
Why does the RAAS contribute to the worsening of heart failure?
The kidneys cannot tell the difference between poor perfusion due to dehydration vs. low cardiac output
Mean survival after a diagnosis of heart failure is…
5 years
Classification system for Heart Failure
NYHA Functional Class (I-IV)