8. Heart Failure Flashcards
Heart failure may be acute, chronic, acute exacerbation of chronic HF, systolic or diastolic HF, or right-sided or left-sided HF. The most extreme HF occurs when
all compensatory mechanisms have failed, and the result is cardiogenic shock.
An understanding of these concepts and the mgmt of each, as well as an understanding of heart failure classifications is needed.
Heart failure
is a clinical syndrome that is characterized by signs and symptoms associated with high intracardiac pressures and decreased cardiac output.
Acute decompensated heart failure
is the abrupt onset of symptoms that are severe enough to merit hospitalization.
~ 75% of pts with acute decompensated HF have a hx of chronic HF.
Heart failure with SYSTOLIC DYSFUNCTION
(ie. left ventricular systolic dysfunction –LVSD): ejection fraction (EF) is 40% or less, problem with ejection
Heart failure with DIASTOLIC DYSFUNCTION:
EF is > 50%, problem with filling, ejection is OK
What is BNP?
B-type natriuretic peptide (BNP) is released by the ventricle when the ventricle is under wall stress in attempts to dilate and decrease ventricular pressure.
BNP elevates when the LV is under stress (LV failure) or, to a lesser degree, BNP elevates when the RV is under stress (pulmonary hypertension, pulmonary embolism).
Pathophysiology of Acute Decompensated Systolic Dysfunction
CAD, cardiomyopathy, acute arrhythmia, valvular dysfunction
|
V
Wall motion abnormality, LV unable to eject normally
|
V
EF < 40%
LVEDP increases
|
V
Pulmonary edema, hypoxemia
|
V
Catecholamine release, increased systemic vascular resistance (SVR).
If EF continues to drop
CO (cardiac output) will drop
|
V
BP
Further increasing SVR
(cycle continues, making it harder for LV to eject normally)
When systolic dysfunction is prolonged and becomes chronic
compensatory HORMONES lead to ventricular remodeling over time.
Drugs are used to decrease neurohormonal effects
Progressive (chronic) systolic dysfunction (compensatory mechanisms)
Persistent systolic dysfunction
|
V
Activation of endogenous neurohormonal systems, Norepinephrine, vasopressin, angiotensin I
| | |
V V V
Vasoconstriction angiotensin II + aldosterone
| | |
| V |
| vasoconstriction V
| | Na + H2O rtn
V V |
V
VENTRICULAR REMODELING
(hypertrophy, chamber dilation, apoptosis)
|
V
Further worsening of ventricular performance
[But beta-adrenergic blockers prevent effects of norepinephrine]
[ACE inhibitors prevent effects of angiotensin I & ARBs prevent effects of angiotensin II]
[Aldosterone antagonists prevent effects of aldosterone]
Pathophysiology of HF with Diastolic Dysfunction
Chronic hypertension, valvular disease, restrictive or hypertrophic cardiomyopathy
|
V
Stiff LV due to inability of myofibrils to relax. Impaired LV filling (empties OK, EF normal)
–>ncreased LVEDP
|
V
Pulmonary Edema
Know the differences between systolic and diastolic HF
Primary problem, signs, trmt, what’s contraindicated, and cardiomyopathy types
*Primary problem of Systolic HF
Ejection problem, dilated chamber
-can fill OK
*Primary problem of Distolic HF
Filling problem, hypertrophied chamber or septum
-can eject OK
*Signs of Systolic HF
-Dilated LV
-PMI shifted to left
-Valvular insufficiency (dilation causes mitral valve insufficiency)
-EF less-than-or-equal to 40%
-Pulmonary edema due to poor ventricular emptying
-S3 heart sound
-BP is normal or low (usually)
-BNP is elevated.
*Signs of Diastolic HF
-Normal ventricular size
-Thick ventricular walls and/or thick septum
-Normal contractile function
-Normal EF
-Pulmonary edema due to high ventricular pressure
-S4 heart sound with hypertension
-BP is often high
-BNP is elevated.
