Heart Failure - Treatment Flashcards

1
Q

What is chronic heart failure characterised by?

A

Progressive cardiac dysfunction

Breathlessness

Tiredness

Neurohormonal disturbances

Sudden death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is heart failure?

A

State at 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the state at 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 pressure?

A

Heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the different kinds of heart failure?

A

Systolic heart failure

Diastolic (or relaxation) heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is systolic heart failure?

A

Decreases pumping function of the heart, which results in fluid back up in the lungs and heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Where does fluid backup to in systolic heart failure?

A

Lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is diastolic heart failure?

A

Thickened and stiff heart muscle causes it to not fill with blood properly, fluid will backup into venous system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Where does fluid backup to in diastolic heart failure?

A

Venous system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the prevalence of chronic heart failure?

A

2-10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How does the incidence of chronic heart failure change with age?

A

Increases with age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the prognosis of heart failure like?

A

Poor

5 year mortality of 50% rising to 80% in a year for some patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are some risk factors for heart failure?

A

Coronary artery disease

Hypertension

Valvular heart disease

Alcoholism

Infection (viral)

Diabetes

Congenital heart defects

Other (obesity, age, smoking)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the process of the pathological progression of cardiovascular disease?

A

1) Myocardial injury
2) Pathologic remodelling
3) Low ejection fraction
4) Death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the process of systolic dysfunction?

A

1) In a failing or damaging heart the Frank-Sarling relationship is lost
2) Circulatory volume increase and the heart dilates, the force of contraction weakens and cardiac output drops further
3) Cardiac output then activates renin-angiotensin-aldosterone system (RAAS) further
4) Results in cycle in which RAAS is activated, circulatory volume increases and cardiac performance deteriorates further
5) As the heart starts to dilate the cardiac myocytes undergo hypertrophy and then fibrosis and the heart is further weakened

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the Frank-Sarling law?

A

If the muscle of a healthy heart is stretched it will contract with greater forcves and pump out more blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What does RAAS stand for?

A

Renin-angiotensin-aldosterone system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What does heart failure usually occur following?

A

Sustained hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What does RAAS cause the release of?

A

Angiotensin and aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What does angiotensin and aldosterone (RAAS) cause?

A

Salt and water retention

Vasoconstriction

Hypertrophy

Fibrosis of cardiac myocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What does activation of the sympathetic system cause the release of?

A

Noradrenaline and adrenaline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What does noradrenaline and adrenaline (sympathetic system) cause?

A

Vasocontriction

Stimulate renin release

Myocyte hypertrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is salt and water excretion caused by?

A

Natriuretic peptide system

EDRF

Atrial and brain natriuretic peptides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the final result of the processes occuring in a failing heart?

A

Failing heart that cannot pump out sufficient blood

Progressive retention of salt and water resulting in oedema and pulmonary oedema

Progressive myocyte death and fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the aims of treatment for heart failure?

A

Improve symptoms

Improve symptoms and survival

Improve survival

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What drugs are used to improve the symptoms of heart failure?
Diuretics Digoxin
26
What drugs are used to improve symptoms and survival of heart failure?
ACE inhibitors/ARBs Spirolactone Vaslartan-sububitril
27
What drugs are used to improve survival of heart failure?
Beta blockers Ivabradine
28
What are some different treatment regimens for heart failure?
Inhibition of detrimental neurohormonal adaptations Enhancement of beneficial neurohormonal adaptations Enhancement of cardiac function
29
30
How is inhibition of detrimental neurohormonal adaptations achieved?
Beta blockers (such as carvedilol, bisoprolol and metoprolol) ``` Stopping RAAS activation: ACE inhibitors (such as ramipril or angiotensin antagonists such as valsartan or losartan to stop angiotensin II) Aldosterone blocked by spironolactone ``` Loop diuretics
31
How is enhancement of beneficial neurohormonal adaptations achieved?
Natriuretic peptid system ANP/BNP (which are potent natriuretic agents and vasodilators) Neprolysin (prevents metabolism and enhances ANP/BNP actions
32
What does ANP stand for?
Atrial natriuretic peptides
33
What does BNP stand for?
Brain natriuretic peptides
34
How is enhancement of cardiac function achieved?
Positive inotropes (such as digoxin, improved hearts ability to pump) Vasodilators: Nitrovasodilators reduce preload and after load improve cardiac function Hydralazine is an arterial dilator
35
How is mortality of heart failure with treatment?
Still high
36
What is an example of a loop diuretic?
Furosemide
37
What does a loop diuretic do?
Removes excess salt and water by inducing profound diuresis by inhibiting Na-K-Cl transporter in the loop of Henle
38
What can loop diuretics be used in combination with?
Thiazide diuretics
39
What are potential adverse reactions from loop diuretics?
Dehydration Hypotension Hypokaemia Hyponatraemia Gout Impaired glucose tolerance
40
What are potential drug-drug interactions of loop diuretics (furosemide)?
Aminoglycosides (renal toxicity) Lithium (renal toxicity) NSAIDs (renal toxicity) Antihypertensives (profound hypotension) Vancomycin (renal toxicity)
41
How is mortality of heart failure reduced?
Angiotensin blockage Beta receptor blockage Aldosterone blockage ANP/BNP enhancement
42
What does ACEI stand for?
Angiotensin converting enzyme inhibitors
43
What are examples of angiotensin converting enzyme inhibitors?
Ramipril Enalapril Lisonopril
44
How do angiotensin converting enzyme inhibitors work?
Competitively block angiotensin converting enzyme, preventing the conversion of angiotensin I into angiotenin II Reduces preload and afterload on the heart
45
What are potential adverse drug reactions of angiotensin converting enzyme inhibitors?
First dose hypotension Cough Angioedema Renal impairment Renal failure Hyperkalaemia
46
What are potential drug-drug interactions of angiotensin converting enzyme inhibitors?
NSAIDS (acute renal failure) Potassium supplements (hyperkalaemia) Potassium sparing diuretics (hyperkalaemia)
47
What does ARBs stand for?
Angiotensin receptor blockers
48
How do angiotensin receptor blockers work?
Selectively block angiotensin II AT1 receptor
49
What is more effective for heart block out of ACEI and ARBs?
ARBs
50
When is ARBs recommended to be used in heart failure?
In ACEI intolerance
51
What does ARNI stand for?
Valsartan-sucubiril
52
How does valsartan-sacubitril (ARNI) work?
ARB blocks AT1 receptor and Neprilysin stops breakdown of ANP and BNP by neural endopeptidases
53
What is valsartan-sacubitril (ARNI) a combination of?
Valsartan and ARB and Neprilysin
54
What receptor do ARBs block?
AT1 receptor
55
What is an example of an aldosterone antagonist?
Spironolactone
56
What is spironolactone and where does it act?
Potassium sparring diuretic that acts in the distal tubule
57
When are aldosterone antagonists proven to reduce mortality?
When used in combination with ACEIs
58
What are examples of beta blockers?
Carvedilol Bisoprolol Metoprolol
59
Why must patients treated with beta blockers be selected carefully?
Beta blockers are potentially hazardous in chronic heart failure
60
How do beta blockers work?
Block the actions of the sympathetic system
61
When should beta blockers only be used?
When patient has been stabilised and not during an acute presentation
62
How does ivabradine work?
Inhibitor of the If current in the sinoatrial node Does not modify myocardial contractility and intracardiac conduction even in patients with impaired systolic function
63
What is an example of a positive inotrope?
Digoxin
64
How do positive inotropes (digoxin) work?
Increases availability of calcium in the myocyte
65
What is a complication with digoxin?
Narrow therapeutic index
66
What are potential side effects of digoxin?
Arrhythmias Nausea Confustion
67
What is an example of an anticoagulant?
Warfarin
68
Why is warfarin sometimes used in heart failure?
Dilated ventricle gives rise to thrombus formation and thrombo-embolic events, which warfarin prevents
69
What are different therapeutic regimes for heart failure?
70
How is the benefit of treatment monitored?
Symptomatic relief (shortness of breath, tiredness, lethargy) Clinical relief (peripheral oedema, ascites, weight) Monitor weight regularly (increase medication according to symptoms or weight) Patient education