35 Heart failure Flashcards
Give 4 reasons of decreased SV.
- Weakened myocardial contractility (genetic, drug-induced, infections, infarction)
- Increase afterload e.g. hypertension
- increased plasma volume leading to increased preload, causing overstretching of cardiomyocytes
- Decrease compliance of myocardial wall (>reduced EDV)
1-3 systolic dysfunctions
4 diastolic dysfunction
Diastolic dysfunction
A. often co-exist with systolic dysfunction
B. may be due to wall thickening, alterations in protein organisation, energy metabolism and Ca2+ removal
C. EDV can be unchanged
D. End diastolic pressure is much lower
all except D
EDV is decreased or unchanged but EDV is significantly increased
Systolic dysfunction
A. may be a result of myocardial injury, loss of cardiomyocytes
B. may be a result of decreased Ca2+ influx
C. may be a result of increased Ca2+-troponin affinity
D. may be a result of decreased b-receptor expression or sensitivity
All except C
should be decreased
A
B and D are results of abnormal
excitation-contraction coupling function
Ventricular hypertrophy is a feature of A. Systolic dysfunction B. Diastolic dysfunction C. Both D. None
C
What are the changes in P-V loop in systolic dysfunction?
Contractility and SV decreased,
length of xaxis will decrease
slope of contractility will decrease (slide 7)
What is the ejection fraction in systolic dysfunction?
lower than 0.4
normal: 0.55
What are the compensatory processes of systolic dysfunction?
decrease CO and MAP triggers baroreceptor reflex and RAAS
- increased sympathetic activity on the heart, arterioles > partially restored CO
- CVP increases, due to sympathetic stimulation on RAAS, but CO is still below normal
- CO becomes normal at the new steady state, but the CVP is very high
slide 8
Renin release due to decrease in CO output triggers Ang II to increase and in the long term, will cause structural remodelling in the heart.
T/F?
T
Ventricular hypertrophy
How do pressure and volume overload cause ventricular hypertrophy respectively?
Pressure:
wider, thicker muscles
Volume:
longer muscle cells
#concentric hypertrophy also stiffens the ventricular wall, making it less compliant and less able to relax fully – as in diastolic dysfunction
In heart failure, Ang II aldosterone levels increases.
What will usually compensate the effect brought by these vasoconstrictors?
Is it seen in heart failure patients?
ANP
protective function of natriuretic peptide is lost in heart failure so there is no opposing to RAAS
What can be indicative of endothelial dysfunction?
What is the effect of this on heart and vessels and thus MAP?
Increased release on endothelin 1 and decreased NO;
promotes hypertrophy of the heart and vessels
> increasing resistance, increase MAP
Suggest 6 ways of heart failure management.
- decrease plasma volume -reduce congestion and edema
- decrease resistance to blood flow - reduce congestion and pressures in arterial and venous sides
(decrease afterload by reducing arteriolar constriction
and decrease preload by reducing venoconstriction and cardiac filling pressure)
- increase stroke volume - increase CO
- increase Ca2+ sensitivity to troponin - increase CO
- inhibit structural alterations in myocardial tissues
- inhibit b-receptors downregulation and desensitization
What is the effect of cardiac glycoside - e.g. digoxin?
inhibits Na+/K+ ATPase, raise intracellular Na+ concentration
> less Ca2+ is extruded via NCX (3Na+ in, 1 Ca2+ out)
> increase contractility of the heart
What substance(s) are responsible for structural changes in myocardial and vascular walls as heart failure progresses?
Endothelin 1 and Ang II
What are the main aims for treating heart failure?
- increase heart contractility
- prevent structural of receptor changes
- decrease cardiac load
