Heart Failure: Treatment Flashcards
1
Q
What is chronic heart failure characterised by?
A
- Progressive cardiac dysfunction
- Dyspnoea
- Tiredness
- Neurohormonal disturbances
- Sudden death
2
Q
Heart failure
A
Heart failure is the state in which the heart is unable to pump blood at a rate commensurate with the requirements of the tissues or can do so only from high pressures
3
Q
What are the types of heart failure?
A
- Systolic heart failure (HFrEF)
- Diastolic (or relaxation) heart failure (HFpEF)
4
Q
What does HFrEF involve?
A
Decreased pumping function of the heart which results in fluid back up in the lungs and heart failure
5
Q
What does HFpEF involve?
A
- Involves a thickened and stiff heart muscle
- As a result heart does not fill with blood properly
- This results in fluid backup in the lungs and heart failure
6
Q
What is the prevalence of chronic heart failure?
A
2-10%
7
Q
What does incidence of chronic heart failure increase with?
A
Age
8
Q
What is the prognosis of chronic heart failure?
A
-Poor with 5 year mortality of 50% rising to 80% with 1 year
9
Q
What are the risk factors for heart failure?
A
- CAD
- Hypertension
- Valvular heart disease
- Alcoholism
- Viral infection
- Diabetes
- CHD
- Obesity
- Age
- Smoking
- High/low haematocrit
- OSAS
10
Q
What is the number 1 risk factor for HF?
A
Hypertension
11
Q
What is Frank Starling Law?
A
If the muscle of a healthy heart is stretched it will contract with greater force and pump out more blood
12
Q
How is Frank Starling Law affected with systolic dysfunction?
A
- In the failing or damages heart this relationship is lodt
- As circulatory volume increases the heart dilates, the force of contraction weakens and CO drops further
- Decreased CO activates the RAAS further
13
Q
What does activation of the RAAS by decreased CO result in?
A
-A vicious cycle in which the RAAS is activated, circulatory volume increases and cardiac performance deteriorates further
14
Q
What happens to the cardiac myocytes as the heart starts to dilate?
A
They undergo hypertrophy and then fibrosis and thus the heart is further weakened
15
Q
When does HF usually occur?
A
- Following sustained hypertension
- Following myocardial damage
16
Q
Why does HF occur following systolic/diastolic dysfunction?
A
- CO falls
- Body registers this as a loss in circulatory volume
- Vasoconstrictor system activation
- Salt and water retaining system activation
17
Q
What does RAAS cause the release of?
A
- Angiotensin II
- Aldosterone
18
Q
What is the result of the RAAS?
A
- Salt and water retention
- Vasoconstriction
- Hypertrophy and fibrosis of cardiac myocytes
19
Q
What does the release of noradrenaline and adrenaline by the SNS cause?
A
- Vasoconstriction
- Stimulates renin release
- Myocyte hypertrophy
20
Q
What is responsible for salt and water excretion and vasodilation?
A
- Natriuretic peptide system ANP/BNP
- EDRF
21
Q
What are ANP and BNP?
A
-Potent vasodilators and natriuretic peptides with short half lives
22
Q
What is the final result of all these systems?
A
- A failing heart that can not pump out sufficient blood to supply the needs of the body
- Progressive retention of salt and water which results in oedema, pulmonary oedema
- Progressive myocyte death and fibrosis
23
Q
What are the 2 main aims of treatment?
A
- Improve symptoms
- Improve survival
24
Q
What drugs improve symptoms?
A
- Diuretics
- Digoxin
25
What drugs improve survival?
- B blockers
| - Ivabradine
26
What drugs improve symptoms and survival?
- ACE inhibitors/ARBs
- Spironolactone
- Valsartan-sacubitril
27
What is the outcome of symptomatic treatement?
- Inhibition of detrimental neurohormonal adaptations
- Enhancement od beneficial neurohormonal adaptations
- Enhancement of cardiac function
28
What is the mainstay of symptomatic treatment?
Loop diuretics
29
Give 2 examples of loop diuretics.
- Furosemide
| - Bumetanide
30
Give examples of B blockers used
- Carvedilol
- Bisoprolol
- Metoprolol
31
What are the groups of drug available to block the effects of angiotensin II?
- ACE inhibitors (Ramipril)
| - Angiotensin antagonists (Valsartan, Losartan)
32
What blocks the effects of aldosterone?
Spironolactone
33
How are beneficial hormonal changes enhanced?
Natriuretic peptide systems
34
What metabolises ANP/BNP/
Neutral endopeptidase
35
What prevents metabolism and enhances ANP/BNP actions?
Neprolysin
36
What enhances cardiac function?
- Positive inotropes
| - Vasodilators
37
What is the only positive inotrope in use?
-Digoxin
38
What do positive inotropes do?
Improve the ability of the heart to pump and so improve cardiac status
39
How do nitrovasodilators improve cardiac function?
Reduce preload and afterload
40
What is hydralazine?
Arterial dilator whown to improve cardiac function
41
What does furosemide do?
-Removes excess salt and water
42
What do loop diuretics do?
- Induce profound diuresis
- Inhibit the Na-K-Cl transporter in the loop of Henle
- Work at very low glomerular filtration rates
- Prevent the reabsorption of 20% of filtered sodium and water
43
What can be used in diuretic resistant patients?
Loop diuretics in combination with thiazide diuretics
44
What can a combination of loop diuretics and thiazide diuretics induce?
Diuresis of 5-10 litres per day
45
What are the adverse drug reactions of loop and thiazide diuretics combination?
- Dehydration
- Hypokalaemia
- Hyponatraemia
- Gout
- Impaired glucose tolerance, diabetes
46
What drugs does furosemide interact with?
- Aminoglycosides
- Lithium
- NSAIDs
- Antihypertensives
- Vancomycin
47
Furosemide and aminoglycosides
Aural and renal toxicity
48
Furosemide and lithium
Renal toxicity
49
Furosemide and NSAIDs
Renal toxicity
50
Furosemide and antihypertensives
Profound hypotension
51
Furosemide and vancomycin
Renal toxicity
52
How is mortality reduced/
- Angiotensin blockade
- B receptor blockade
- Aldosterone blockade
- ANP/BNP enhancement
53
What do ACEI not block?
The conversion of angiotensin I to angiotensin II by alternative enzymes such as chymase
54
What organs can angiotensin II damage?
- Brain
- Blood vessels
- Heart
- Kidneys
55
What effect can Ang II have on the kidney?
- Decrease GFR
- Increased proteinuria
- Increased aldosterone release
- Glomerular sclerosis
- Renal failure
56
What effect can Ang II have on the heart?
- LV hypertrophy
- Fibrosis
- Remodelling
- Apoptosis
- Heart failure
- MI
57
What effect can Ang II have on the blood vessels?
- Atherosclerosis
- Vasoconstriction
- Vascular hypertrophy
- Endothelial dysfunction
- Hypertension
58
What effect can Ang II have on the brain?
Stroke
59
Give 3 examples of ACE inhibitors.
- Ramipril
- Enalapril
- Lisinopril
60
What do ACEI do?
- Competitively block angiotensin converting enzyme
- Prevent the conversion of angiotensin I to angiotensin II
- Reduce preload and afterload on the heart
61
What do ACEI reduce in CHF patients?
- Morbidity
| - Mortality
62
What do ACEI reduce in post MI patients?
- Morbidity
- Mortality
- Onset of HF
63
What are the adverse drug reactions of ACEI?
- First dose hypotension
- Cough
- Angioedema
- Renal impairment
- Renal failure
- Hyperkalaemia
64
What drugs do ACEI interact with?
- NSAIDs
- Potassium supplements
- Potassium sparing diuretics
65
ACEI and NSAIDs
Acute renal failure
66
ACEI and potassium supplements
Hyperkalaemia
67
ACEI and potassium sparing diuretics
Hyperkalaemia
68
What do ARBs do?
- Selectively block the angiotensin II, AT1 receptor
| - Effective but not as effective as ACEI
69
What are patients given if they are intolerant of ACEI?
ARBs
70
What effect does Ang II have on AT1?
- Vasoconstriction
- Vascular proliferation
- Aldosterone secretion
- Cardiac myocyte proliferation
- Increased sympathetic tone
71
What effect does angiontensin II have on AT2?
- Vasodilation
- Antiproliferation
- Apoptosis
72
What is valsartan-sacubitril (ARNI)
Combined valsartan and ARB and neprilysin
73
How does valsartan-sacubitril work?
- ARB blcoks AT1 receptor
| - Neprilysin stops bread down of ANP and BNP by neutral endopeptidases
74
Give an example of an aldosterone antagonist
Spironolactone
75
What does spironolactone do?
- Potassium sparing diuretic
- Inhibits the actions of aldosterone
- Acts in the distal tubule
76
What is spironolactone used in combination with?
Loop diuretics
77
What is spironolactone particularly useful in?
Resistant oedema
78
When has spironolactone be proven to reduce mortality?
In combination with ACEI
79
What do B blockers do?
-Block the actions of the sympathetic system
80
What may B blockers precipitate?
Severe deterioration in CHF
81
When should B blockers be used in the treatment of HF?
Only when the patient has been stabilised and not during acute presentation
82
What is ivabradine?
Specific inhibitor of the If current in the SA node
83
What does ivabradine not do?
- No action on other channels in the heart or vascular system
- Does not modify myocardial contractility and intracardiac conduction, even in patients with impaired systolic function
84
What is the recommendation for the use of ivabradine?
Ivabradine can be beneficial to reduce HF hospitalization for patients with symptomatic (NYHA class II-III) stable chronic HFrEF (LVEF ≤35%) who are receiving standard therapy, including a beta blocker at maximum tolerated dose, and who are in sinus rhythm with a heart rate of 70 bpm or greater at rest.
85
What does digoxin do?
Increases the availability of calcium in the myocyte
86
What are the side effects of digoxin?
- Narrow therapeutic index
- Arrhythmias
- Nausea
- Confusion
87
What is warfarin?
Anticoagulant
88
Why is warfarin used in HF?
Dilated ventricle gives rise to thrombus formation and thrombo-embolic events
89
What is the therapeutic regime for HF?
- Furosemide +/- thiazide
- Furosemide + pulsed metolazone
- ACEI
- ARB
- B blocker +/- ivabradine
- MRA-spironolactone (25mg)
- Digoxin
- Warfarin
90
How is the benefit of drug therapies monitored?
- Symptomatic relief (SOB, tiredness, lethargy)
- Clinical relief (peripheral oedema, ascites, weight)
- Monitor weight regularly
- Patient education
