Muscle Pump Failure (Heart Failure) Flashcards
1
Q
What is the equation for cardiac output?
A
CO = heart rate x stroke volume
2
Q
What is the equation for cardiac reserve?
A
maximal cardiac output - cardiac output at rest
3
Q
What is preload?
A
The level of stretch that a cardiomyocyte is exposed to before ventricular ejection
4
Q
What is preload equivalent to?
A
left ventricular end-diastolic volume
5
Q
What is left ventricular end-diastolic volume?
A
The volume within the ventricle at the end of diastole, just before it contracts
6
Q
What is afterload?
A
The pressure against which the heart is contracting when it ejects blood
7
Q
During which conditions is afterload increased?
A
- hypertension
2. increased peripheral vasoconstriction
8
Q
In cardiac muscle, how does sarcomere length affect tension?
A
small increases in sarcomere length cause a rapid increase in tension
9
Q
Using the Frank-Starling curve, what happens when a physiological limit is reached?
A
There is a decompensation which leads to a sudden and rapid decrease in tension
10
Q
What is described by the Bowditch phenomenon?
A
As the heart rate increases, cardiac output increases
Increasing heart rate to an extreme can lead to a reduction in cardiac performance
11
Q
What is on the x and y axis of the Bowditch curve?
A
Cardiac performance - y
Heart rate - x
12
Q
What is described by the Anrep effect?
A
Increasing the afterload, through increasing systemic vascular resistance, increases cardiac performance up until a limit
13
Q
What is on the x and y axis of the Anrep curve?
A
cardiac performance - y
afterload - x
14
Q
what is the consequence of reducing cardiac output?
A
reduced organ perfusion
15
Q
What is the role of the baroreceptor reflex?
A
It is an autonomic reflex that helps to detect changes in pressure of the blood
16
Q
What do baroreceptors detect?
A
Arterial stretch
This determines whether the blood pressure is high or low
17
Q
What does the afferent end of the baroreceptor end in?
A
The nucleus tractus solitarius and rostral ventrolateral medulla
18
Q
How do the baroreceptors augment vagal tone?
What is the result of this?
A
They activate the vagus nerve which:
- reduces the heart rate
- reduces stroke volume
- causes vasodilation
19
Q
What is the baroreceptor reflex pathway when blood pressure is too high?
A
- The parasympathetic NS innervates the SAN and AVN via the vagus nerve
- This decreases the heart rate
- This leads to reduced cardiac output
20
Q
What is the baroreceptor reflex pathway when blood pressure is too low?
How does it affect the heart?
A
- The sympathetic NS innervated the SAN, AVN, conducting tissue and myocytes of the atria and ventricles
- This increases heart rate and contractility
- This increases cardiac output
21
Q
How does the sympathetic nervous system in the baroreceptor reflex affect the blood vessels?
A
It causes constriction of blood vessels
This increases systemic vascular resistance
This acts to increase blood pressure
22
Q
What happens when blood pressure is too high?
A
- baroreceptors detect increased arterial stretch
2. they activate the parasympathetic nervous system to increase vagal tone
23
Q
What happens when vagal tone is increased?
A
The heart rate is lowered and cardiac output is reduced
24
Q
What is the result of increasing systemic vascular resistance?
A
It leads to an increase in afterload
This causes a temporary increase in cardiac output
25
What does the juxtoglomerular apparatus detect?
1. renal perfusion pressure at the glomerulus
| 2. sodium concentration in the fluid surrounding the distal convoluted tubule
26
What is the role of the juxtoglomerular apparatus?
If either renal perfusion or sodium concentration is reduced, it releases renin
27
What is the process in the kidney that occurs in order for renin to be produced?
Inactive prorenin is converted to renin and active prorenin
28
Where is angiotensinogen released from?
The liver
29
How does angiotensinogen interact with renin?
It is cleaved by renin to form angiotensin I
This is inactive
30
what is the main role of angiotensin converting enzyme (ACE)?
Where is it released from?
The lungs release ACE
It converts angiotensin I to active angiotensin II
31
What is the secondary role of angiotensin converting enzyme (ACE)?
It breaks down bradykinin (vasodilator)
This prevents vasodilation
32
What are the actions and effects of angiotensin II?
1. increases water retention
2. increases sodium reabsorption
3. causes vasoconstriction
These act to increase systemic vascular resistance
33
What group of chemicals does angiotensin II cause the release of?
Catecholamines
These increase cardiac output and systemic vascular resistance
34
What main chemical does angiotensin II cause the release of, and what is the consequence?
Aldosterone release from adrenal glands
It increases plasma volume, which increases preload and consequently cardiac output
35
What is aldosterone and where is it released from?
A mineralocorticoid
It is released from the zona glomerulosa in the adrenal cortex
36
Where does aldosterone act on?
Why is it released?
Released in response to angiotensin II
It has effects on the distal convoluted tubule and collecting duct
37
What is meant by aldosterone being 'internalised'?
It binds to an intracellular aldosterone receptor
38
What is the main consequence of aldosterone binding to an aldosterone receptor?
It increases transcription of the gene for epithelial sodium ion channels
This leads to increased sodium, and consequently water, reabsorption
39
What are the other consequences of aldosterone binding to the aldosterone receptor?
1. excretion of potassium ions
| 2. increases the amount of angiotensin II receptors
40
What are the 2 types of myocardial dysfunction?
Systolic or diastolic
41
What is systolic dysfunction (heart failure)
There is a reduction/dysfunction in how the heart contracts
42
What is ejection fraction like in systolic heart failure?
There is a reduced ejection fraction of 25%
The amount of blood pumped around the body with each systolic impulse is reduced
43
How is preload affected in systolic heart failure?
Over time, the preload increases
This increases the extent to which the left ventricle is stretched
44
How is the left ventricle affected by systolic heart failure?
What is the long-term consequence of this?
The increased preload leads to thinning of the ventricle walls over time
The ventricle cannot pump blood with enough force to push it throughout the body
45
What is involved in diastolic dysfunction (heart failure)?
There is a reduction/dysfunction in how the heart relaxes
This is due to the left ventricle being stiffer than normal
46
What is ejection fraction like in diastolic dysfunction?
It is normal - over 55%
47
What does a reduction in relaxation of the heart lead to?
Although ejection fraction is the same, there is less blood filling the LV
Less blood is being ejected
48
What is the usual cause of diastolic dysfunction?
Left ventricular hypertrophy
49
What are the 3 main consequences of a failed ejection fraction?
1. reduced cardiac output leads to a reduction in systolic blood pressure
2. reduced arterial stretch
(activation of baroreceptors)
3. reduced renal perfusion
(activation of the RAAS)
50
what is the consequence of myocardial infarction?
There is a reduction in systolic function as part of the heart dies and can no longer pump blood
51
What happens in an anterolateral infarct?
The anterior wall of the LV is completely blocked off
This leads to death of heart muscle in the left ventricle
52
What happens in a posteroinferior infarct?
There is death of a small portion of the right ventricle
53
What are the 4 main risk factors for myocardial infarction?
1. excessive alcohol consumption
2. idiopathic cardiomyopathy due to genetic disorder
3. viral cardiomyopathy
4. tachycardic cardiomyopathy
54
What is the initial reaction to a reduction in cardiac output?
Activation of the renin-angiotensin-aldosterone system and baroreceptors
55
What is the response of the RAAS to a decreased cardiac output?
Increase in plasma volume
This increases preload, which lengthens the sarcomeres
56
How does a raised preload affect the LV and stroke volume?
End-diastolic pressure is raised in the LV
This leads to an increase in cardiac output, which also augments stroke volume
57
what is the name for the action of the RAAS increasing the cardiac output?
What is the problem with this?
This is compensation
It can work for a while, but is not maintained for very long
58
What process happens as a result of the compensation effects not being able to be maintained?
Decompensation
59
What process precedes decompensation?
The left ventricle stretch exceeds physiological levels
60
What happens to sarcomere tension during decompensation?
1. sarcomeres stretched beyond their physiological barrier
2. this leads to movement to the descending limb of the sarcomere tension curve
3. there is a sudden drop off in sarcomere tension
61
How can small rises in preload affect sarcomere tension in decompensation?
Small rises in preload cause large drops in sarcomere tension
This affects LV contractility and stroke volume
62
what is the result of large drops in sarcomere tension?
Reduced cardiac output
This has further effects on the autonomic nervous system and RAAS
63
What curve can be used to describe how decompensation leads to reduced cardiac output?
Bowditch effect
| cardiac output - y - heart rate - x
64
In heart failure, what does back pressure in the left ventricle cause?
Raised pressure in the pulmonary circulation
65
What is the consequence to the lungs of heart failure?
Why does it happen?
Increased hydrostatic pressure in PC forces fluid outside of the vascular compartment
The interstitial space in the lungs fills with fluid
This leads to pulmonary oedema and/or pleural effusion
66
What signs of heart failure are exhibited by the patient?
They become breathless and their oxygen saturation drops
67
What is meant by orthopnoea?
Why does it occur?
How lying flat worsens the symptoms in the patient
Lying flat causes fluid to enter a large proportion of the lungs
68
What are the first steps leading to heart failure affecting the right ventricle?
1. Back pressure in the lungs goes back on the RV
2. The back pressure is transmitted to the venae cavae
3. The pressure in the internal jugular vein rises
69
what can usually be detected as a result of raised pressure in the internal jugular vein?
Jugular venous pulse is raised
Pulsing in the neck can often be detected
70
What causes peripheral oedema in heart failure?
Gravity and raised orthostatic pressures will force fluid from vascular compartments to the peripheral tissues
71
What does peripheral oedema in heart failure often occur alongside of?
1. swelling of the ankles/sacrum
| 2. hepatomegaly/ascites
72
What are the acute therapy options for heart failure?
1. oxygen therapy
2. non-invasive ventilation
3. invasive ventilation
73
Why is oxygen given to heart failure patients?
Why is it often not sufficient as a standalone treatment?
To optimise alveolar ventilation
Often there is a need to increase the pressure in the airways to oxygenate blood
74
What is non-invasive ventilation?
What is the most common type of way to use this treatment?
Oxygen masks e.g. CPAP
This involves constant pressure through the mask that forces oxygen into the lungs and forces fluid out of the alveoli
75
What does morphine do to help treat heart failure?
It causes pulmonary vasodilation
This relaxes the pulmonary vessels and reduces the pressure within them
It also helps with breathing and pain
76
What is the consequence to the heart of taking morphine?
It helps to reduce the preload
It takes the strain off the left ventricle
77
What are diuretics used for in treating heart failure?
They limit the reabsorption of fluid
78
What is the consequence to the heart of taking diuretics?
Reduced plasma volume works to decrease the preload
This offloads the ventricles and maximises left ventricular contractility
79
What are the side effects of taking diuretics?
1. renal dysfunction
2. reduction in Na+, K+ and Mg2+ levels
3. Thiazides can induce diabetes
80
what are beta receptors involved in?
Myocardial and renal responses to reduced cardiac output
81
How do beta blockers affect the heart?
Blocking the beta receptors reduces heart rate
Reducing the heart rate gives more time for the LV to relax
This gives it more time to fill with blood, improving stroke volume
82
How do beta blockers affect the kidneys?
They prevent RAAS overactivation which prevents fluid retention
It also causes bradykinin accumulation, which causes dry coughs
83
Which types of patients should not receive beta blockers?
1. asthma patients
2. patients with heart blocks
3. patients with low heart rate
84
What is the role of spironolactone/eplerenone?
They block aldosterone as they are mineralocorticoid receptor antagonists
85
Why are spironolactone/eplerenone known as 'potassium sparing diuretics'?
Too much aldosterone causes excessive loss of potassium
86
Why are potassium sparing diuretics often used alongside furosemide?
They prevent furosemide from getting rid of too much potassium
87
what is the role of ACE inhibitors?
They block the conversion of angiotensin I to angiotensin II
This reduces the effects of angiotensin II on vasculature
88
What are the effects of ACE inhibitors?
1. diminish release of aldosterone
| 2. cause bradykinin accumulation (dry cough)
89
What type of patients are given Ivabradine?
Asthma patients
90
How does Ivabradine work?
It acts on funny ion channels in the SA node to reduce the heart rate
91
When is Digoxin used to reduce the heart rate?
In elderly patients with low blood pressure
or
In patients with atrial fibrillation
92
What is valsartan?
Angiotensin II receptor blocker
93
What is sacubitril?
A neprilysin inhibitor
It enhances the action of natriuretic peptides, which promote sodium and water excretion
94
What 2 drugs used in combination are more effective than ACEi/ARBs?
Sacubitril and valsartan
