Acute Heart Failure Flashcards
1
Q
What is heart failure?
A
Inability to provide adequate CO to support the needs of the tissues (or can do so at the expense of a raised filling pressure)
2
Q
What is acute heart failure?
A
Cardiogenic shock
3
Q
What type of heart failure evolves over months, years and decades?
A
Chronic heart failure
4
Q
How is aortic pressure kept constant, even if the system is failing around it ?
A
By the activity of the baroreceptors in the aortic arch
5
Q
At what pressure is aortic pressure kept constant?
A
100mmHg
6
Q
What happens to CO in right HF?
A
- Impaired pumping causes the output of both ventricles to be reduced so that the CO falls to 6L/min (from 8)
- The left and right circulations are in series so that fall in the right CO must cause a fall in the left CO
7
Q
What impacts on the progression of the disease?
A
How the baroreceptor reflex achieves constant aortic pressure
8
Q
How does RHF affect blood pressure?
A
- Systemic venous pressure rises bc RV EDP is increased i.e. the RH backs up
- However, circulatory reflexes tend to maintain mean pulmonary artery pressure, LV EDP and aortic pressure at virtually normal levels
9
Q
How does LHF affect CO?
A
- Impairing pumping causes the output of both ventricles to be reduced so that CO falls
10
Q
How does LHF affect BP?
A
- Pulmonary venous pressure rises bc LV EDP is increased i.e. the LH backs up
- However circulatory reflexes tend to maintain mean aortic pressure at virtually normal levels
- The elevated pulmonary venous pressure is transmitted through the lungs bc they are low resistance, causing a slight rise in pulmonary artery pressure to 40mmHg
- Pressures elevated on both sides of the pulmonary circulation
11
Q
What type of heart failure occurs in most patients?
A
Congestive heart failure
12
Q
What causes congestive heart failure?
A
Heart failure is principally due to failure of LV which in turn affects the performance of the RV
13
Q
What are the effects of congestive heart failure?
A
When moderately severe, HF is accompanied by:
- Fall in CO
- Significant elevation of pulmonary venous pressure to 16mmHg bc left EDP is increased (i.e. the LH backs up)
- Modest elevation fo mean pulmonary artery to 40mmHg (bc lungs back up)
- Systemic venous pressures (bc RV also backs up)
14
Q
What are the 3 primary causes of heart failure?
A
1) Pressure overload
2) Volume overload
3) Contractile dysfunction
15
Q
How does pressure overload lead to HF?
A
Hypertension, aortic stenosis
16
Q
How does volume overload lead to HF?
A
Aortic or mitral valve regurgitation, causing the volume to be higher than normal
17
Q
What are causes of contractile dysfunction leading to heart failure?
A
1) Ischaemic heart disease
2) Myocardial disease
3) Pregnancy (pregnancy-induced HF)
4) Congenital cardiomyopathies (protein, heart muscle is compromised)
18
Q
What is LaPlace’s Law?
A
- For a fixed wall stress (i.e. muscular effort) a small ventricle can generate higher pressures than a large ventricle
- For the same pressure, a smaller radius can tolerate a higher pressure
19
Q
How does LaPlace’s Law apply to heart failure?
A
- In a heart, wall stress is the force needed from the muscle
- So when the heart gets bigger, to maintain the same BP, it must either increase the amount of work done in the fibres in the wall of the heart or increase wall thickness
20
Q
How does the heart contract?
A
The fibres in the walls generate tension or ‘wall stress’
21
Q
What happens to the heart wall in the early stages of heart failure?
A
The disease is in its compensated phase → it maintains pressures (and output) by increasing wall thickness
22
Q
Why is increasing the wall thickness of the heart a problem?
A
It exacerbates the underlying problem with the compromised ventricular muscle → eventually the heart dilates i.e. the lumen gets bigger without an associated increase in wall thickness
23
Q
How does heart dilation lead to decompensated heart failure?
A
If the lumen gets bigger (R increases) without an increase in width, then the pressure must drop otherwise the myofibrils will have to work even harder to maintain wall stress → this will push the heart into the viscous spiral of the decompensated phase of failure
24
Q
Why does compensated heart failure eventually fail?
A
- In compensated heart failure, wall stress is normalised by concentric hypertrophy
- However, as this muscle is not normal heart muscle, it will fail
- This leads to an increase in radius (heart dilation) and wall stress
25
What happens during severe aortic stenosis or hypertension?
- The acute effect is an increase in wall stress
- The heart responds by thickening its wall so that, during the compensated phase, wall stress is normalised by concentric hypertrophy
- However, when dilation develops, radius increases and wall stress rises
- This has a number of deleterious consequences
26
What conditions lead to volume overload?
Aortic/mitral valve regurgitation
27
What occurs in volume overload?
- Initially leads to ventricular dilation → increased radius
- Some hypertrophy can then normalise wall stress (but not normal muscle)
- However, when failure sets in, the degree of dilation exceeds the degree of hypertrophy and wall stress increases
28
What are two types of contractile dysfunction?
1) Hypertrophic cardiomyopathy
| 2) Dilated cardiomyopathy
29
What happens in the two stages of hypertrophic cardiomyopathy?
1) Compensated concentric hypertrophy leads to a normal relation between wall thickness and wall stress
2) The development of dilation leads to myocardial failure (inadequate hypertrophy, failing)
30
What happens in the two stages of dilated cardiomyopathy?
1) Initial compensated phase → hypertrophy is proportional to the degree of chamber enlargement
2) Excessive chamber enlargement and inadequate hypertrophy (hypertrophy + dilation, failing)
31
How can you tell the difference between LV and congestive heart failure?
In congestive heart failure, the RV is also hypertrophied
32
How much does a normal heart weigh (male and female)?
<450g (male), <400g (female)
33
How much might a hypertrophied heart weigh?
850g
34
What is the normal ratio of LV weight to body height?
< 36 g/m2
35
What are cardiac compensatory mechanisms?
Myocyte growth (hypertrophy)
36
When do cardiac myocytes lose their ability to divide?
Soon after birth
37
How does heart growth (normal and pathological occur?
Through an increase in cell size (hypertrophy) rather than cell number (proliferation)
38
Why does the heart grow pathologically?
- The heart responds to the increase in wall stress and that the stretch of cardiac myocytes is somehow detected
- This is transduced into a stimulus for protein synthesis and cellular enlargement
39
What else can stresses of the growth stimulus for cardiac myocytes cause?
A small number of cells to become disorganised and even enter into apoptosis (programmed cell death)
40
What type of cell growth occurs during normal neonatal growth?
Physiological hypertrophy
41
What type of cell growth occurs in heart failure?
1) Concentric hypertrophy → the cells principally get fatter
| 2) Eccentric hypertrophy → cells are elongated as a result of dilation
42
What happens in concentric and eccentric hypertrophy genetically?
- The adult hear cells revert back to the genetic programme that allowed them to grow during embryonic and neonatal development
- Hence these pathologically growing adult heart cells re-express embryonic genes that had previously been switched off
43
What are the 3 phases of heart failure?
1) Short term acute failure
2) Compensated hypertrophy
3) Chronic failure
44
What happens in short term acute failure?
Functional reserves are overwhelmed by overload
45
What happens in compensated hypertrophy?
Heart enlarges and adapts → can last years/decades
46
What happens in chronic failure?
- Exhaustion, cell death and necrosis
- Law of LaPlace → viscous spiral downwards
- 50% of patients die within 2 years
47
What reflex mediates the response of the circulatory system to decrease CO during HF?
Baroreceptor reflex
48
What is the action of the baroreceptor reflex as CO falls?
1) The fall in BP stimulates the baroreceptors to increase sympathetic outflow
2) Increased sympathetic stimulation causes peripheral vasoconstriction, increased HR and contractility
3) This returns BP to noraml
49
Why does constriction of the renal arteries occur as part of the baroreceptor reflex?
To try and retain salt and water and hence maintain BP
50
Why is the baroreceptor reflex essential for survival in the acute phase of heart failure e.g. following cardiogenic shock?
To divert blood to the brain and essential organs to maintain BP
51
What is the bad thing about the baroreceptor reflex in the long term?
It is deleterious in the longer term
52
What is the principal hormonal response to the fall in CO?
The stimulation of the RAA system
53
Why does renin secretion increase?
In response to hypoperfusion and sympathetic stimulation
54
What cells secrete renin?
Juxtaglomerular cells
55
What are the effects of renin (RAA system)?
1) Circulating renin stimulates a plasma substrate to convert circling angiotensinogen to angiotensin I which is converted at the tissues to angiotensin II by the action fo ACE
2) Angiotensin II causes vasoconstriction at the tissues and hence raises BP
3) Angiotensin II also causes the release of aldosterone which causes salt and water retention which helps maintain BP and renal perfusion
56
How does the baroreceptor reflex increase CO?
- The peripheral vasoconstriction and salt and water retention raise CVP and hence preload
- This helps maintain CO (via Starling mechanism) but at the cost of a raised LVEDP
57
What else is released by the increase BP?
ANP
58
How is ANP released?
- The increase in CVP causes the atria to stretch
| - This in turn stimulates the production and release of ANP
59
What are the actions of ANP?
1) Diuretic action → directly vasodilators and inhibits aldosterone secretion
2) Inhibits the release of NA from terminal neurones which further promotes the vasodilating action
3) It is an endogenous antagonist for angiotensin II
4) In the heart increases directly in proportion to the extent of congestive heart failure
60
Why do the beneficial effects of ANP not dominate?
- The increase in ANP is overwhelmed by the vasoconstriction and salt and water retention induced by the activation of the RAA system
- ANP secretion becomes down-regulated and the vascular ANP receptors are desensitised
61
What keeps you alive in the short term (but kills you in the long term and have medication to prevent it)?
1) Sympathetic activation
2) Increased RAA system
3) Increased aldosterone secretion
4) Increased myocardial hypertrophy
62
What are the consequences of of heart failure?
1) Cardiac changes
2) Capillary filtration
3) Pulmonary congestion
63
What is the main cardiac change?
Cardiac hypertrophy
64
What is cardiac hypertrophy negative?
1) It increases susceptibility of ischaemia
2) Increases incidence of arrhythmias and sudden death
3) Pushes the heart down slippery slope towards failure
4) The hypertrophied heart not only consumes more oxygen but the growth of heart muscle also outstrips the growth of its arteries and capillaries
65
What else is compromised due to cardiac hypertrophy and what is the effect of this?
Coronary vascular reserve
- The heart cannot respond to the demands made upon it (i.e. during exercise) and blood flow can be limiting
- This creates a supply/demand imbalance which can lead to focal ischaemia, fibrosis and collagen deposition
66
What is the effect of focal fibroses and the substantial increase in interstitial collagen?
1) They make the heart stiffer and therefore it is harder for the myofibrils to generate force
2) Therefore it decreases contractility
3) This decline in contractility and increase in stiffness exacerbates the dilation and failure which in turn increases wall stress via LaPlace's Law
4) This sets in motion a vicious cycle which, if unchecked, will lead to death
67
What is different in pulmonary circulation compared to normal circulation?
- The colloidal osmotic pressure is higher than the hydrostatic pressure throughout the capillary network
- This leads to a net loss of fluid from the lung
- This is not a problem as we constantly breathing in humidified air and the lungs are therefore kept from accumulating this fluid by this constant fluid transport
68
What happens to the pulmonary circulation in heart failure (high LEDP)?
1) In heart failure, the fluid movement in the lung is reversed
2) The hydrostatic pressure is raised in the pulmonary circulation and hence the hydrostatic pressure is higher than the colloidal osmotic pressure on the arterial side of the capillary bed
3) This leads to a net gain of fluid in the lung which is a major problem in heart failure
69
How does pulmonary congestion occur?
1) Accumulation of fluid in the lungs makes it harder to breathe
2) As heart failure progresses this fluid not only accumulates in the interstitium but also fills the alveoli and reduces the area for gas exchange
3) This leads to dyspnoea
70
What does mild heart failure lead to in the lungs?
Pleural effusion
71
What happens in pleural effusion?
- Fluid accumulation in interstitium and pleural spaces
- Lungs stiffer, more difficult to breathe
- Increased pulmonary vascular resistance and pulmonary artery pressure
72
What does severe heart failure lead to in the lungs?
Pulmonary oedema
73
What happens in pulmonary oedema?
- Fluid accumulation in alveoli
- Reduced volume for gas exchange (patient can drown)
- Severe pulmonary congestion
- Really increased pulmonary artery pressure
- Increased RA pressure
- RH failure
- Increased systemic venous pressure
- Oedema (and peripheral if it is really bad)
74
What happens in normal circulation?
There is no net movement of fluid
