2 Heart Failure Flashcards
Heart failure
Common syndrome may caused by any structural or functional cardiac disorder that impairs the ability of the ventricle to fill or eject blood
HF clinical significance
Heart insufficient pumping causes:
Blood and fluid to backup in lungs
Buildup of fluid in feet, ankles and legs (edema)
Tiredness/shortness of breath
Common end stage of many forms of chronic heart disease
Progressive condition
Precipitates of HF
- Uncontrolled HT - increase BP - too much pressure on heart - pump fails
- Myocardial ischemia -muscle not getting good perfusion - cannot function as pump
- Sever emotional/physical stress
Types of HF
Systolic - contractile function abnormality (HFrEF)
Diastolic - relaxation abnormal due to stiffness/filling (HFpEF)
HFpEF
Abnormal diastolic function with LV hypertrophy
Preserved ejection fraction - Refers to signs and symptoms of clinical HF in a patient with a normal LVEF and LV diastolic dysfunction
LVEF greater then or equal to 50%
Relaxation is compromised due to stiffness of ventricles/fibrosis - less blood fills the heart so when EF is calculated the proportion is still the same
EF= SV/EDV
HFrEF
Reduced EF (restricted) systolic dysfunction
Progressive chamber dilation
LVEF less than or equal to 40%
Decrease SV and decrease CO
Pressure-volume relationships in systolic dysfunction in HF
Systolic- decrease in myocardial contractility, decrease SV, decrease CO
Compensations:
Increase SNS
Renal/salt water retention = increase EDV and increase pressure (activated in low BP)
Left ventricle hypertrophy = decrease wall stress, decrease afterload, increase contractility
Pressure-volume relationships in diastolic dysfunction in HF
Relaxation - stiff ventricles
LVEDV and SV preserved
Abnormal increase in left ventricular diastolic pressure - decrease in L ventricular dispensability
Clinical consequences of an increased LV diastolic pressure
LV diastolic pressure depends on: ventricular blood volume and stretch of ventricular muscle
During diastolic:
When the mitral valve is open - LV, LA and pulmonary vein form a “common chamber” continuous with the pulmonary capillary bed = back flow into lungs and increase pressure on L ventricle
Increase in LV diastolic pressure - increases pulmonary vein/capillary pressure - causing dyspnea, exercise limitation and pulmonary congestion!!
Compensatory mechanisms
Signs and symptoms of HF caused in part by compensatory mechanisms
Frank-starling mechanism: increase EDV increase CO
Activation of nuerohumoral systems:
SNS = increase HR, myocardial contractility and vascular resistance - too much contractility heart fails as pump
Activation of renin-Angiotensin-aldosterone system = systemic and renal vasoconstriction - response to low BP and vasoconstriction to increase BP
ADH = increases systemic vascular resistance, potent vasoconstrictor = HT = organ/heart failure
Myocardial adaptation: cardiac hypertrophy is compensatory response of myocardium to an increase in mechanical work
Consequences of compensatory hypertrophy
Increase protein synthesis and oxygen demand
As a result of ischemia and chronic workload increase other pathologic changes occur:
Cardiomyocyte loss by apoptosis
Accumulation of excess ECM - fibrosis (HFpEF)
Hypertrophied heart is vulnerable to ischemia related injury = cardiac failure