Lecture 8: Heart Failure Flashcards
Cause of increased jugular venous pressure (jugular vein distention):
- increased blood volume (CHF)
- increased right atrial pressure
What does a diminished S1 heart sound indicate?
- stiff left ventricle
- problem with contractility
The two types of heart failure:
- systolic
- diastolic
Systolic heart failure:
- impaired contractility.
- ejection fraction reduced.
- decreased cardiac output.
Diastolic heart failure:
- impaired filling (stiff ventricle; diminished S1).
- same ejection fraction.
- decreased cardiac output.
Draw ESPVR curve of heart failure with preserved EF:
diastolic dysfunction
- increased EDP
- decreased EDV
- same ESV and EF
Draw ESPVR curve of heart failure with reduced EF:
systolic dysfunction
- reduced inotropy (NEW ESPVR LINE)
- reduced ESV
- increased preload and EDP
Both systolic and diastolic heart failure have high demand for:
- oxygen
- Both have increased EDP; increased wall stress
Cause of systolic heart failure:
- hypertension/ischemia
- unfavorable remodeling
- necrosis
- fibrosis
- reduced ejection fraction
- reduced cardiac output
- reduced perfusion pressure
- compensatory mechanisms (SNS; fluid retention)
Draw cardiac function curve for non-compensated heart failure:
- decreased cardiac output leads to a decrease in MAP and an increase in RAP.
What form of heart failure exhibits increased preload?
systolic heart failure
Once the SNS becomes active in heart failure, what are its compensatory effects?
-
vasoconstriction (alpha-1)
- increased TPR
-
splanchnic bed vasoconstriction (alpha-1)
- increased venous volume/return/RAP
-
sodium and fluid retention (kidneys)
- increased intravascular volume
What is the effect of SNS splanchnic bed vasoconstriction in heart failure?
- shift of blood volume from arterial to venous
- increases venous return
- increased RAP
Draw cardiac function curve for compensated heart failure:
- SNS causes increased RAP, MAP, and intravascular volume.
Mechanism of peripheral edema in heart failure:
- increased RAP leads to decrease in venous return.
- increase in capillary pressures leads to edema.
Mechanism of pulmonary edema in heart failure:
- Impaired filling/ejection of LV increases LVP.
- LAP increases, backs up into the pulmonary veins.
- Increased pulmonary venous pressure leads to increase in pulmonary capillary hydrostatic pressure.
- Pulmonary edema occurs.
Heart failure treatment:
Decrease fluids, decrease heart rate, increase contractile force.
- loop diuretic (furosemide)
- beta-blocker (metoprolol; atenolol)
- positive inotropic (digoxin)
Draw the following cardiac function curves overlayed:
A: healthy
C: compensated HF
D: HF plus digoxin and furosemide
How does total intravascular volume increase in euvolemic patients with congestive heart failure?
- low pressure baroreceptors interpret decreased MAP due to decreased CO.
- baroreceptors activate SNS, kidneys become activated.
- fluid becomes retained on top of already normal fluid levels.
What are the benefits and costs of having increased intravascular volume in congestive heart failure?
- benefit: increased preload and slightly increased CO.
- cost: peripheral and pulmonary edema.
Mechanism of and hormonal response to heart failure:
- high pressure baroreceptors fire at slower rate due to decreased MAP.
- SNS activated (norepinephrine/epinephrine).
- SNS stimulates arginine-vasopression secretion from hypothalamus.
- Low renal BP stimulates AII secretion from kidney.
- AII stimulates aldosterone secretion from adrenal cortex.
