Chronic Heart Failure CUE CARDS

Question 1

What is Chronic Heart Failure?

What is it characterised by?

Answer 1

A complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood and that is characterised by specific symptoms (fatigue and shortness of breath) and signs (fluid retention)

Question 2

What are the presentations of CHF?

Answer 2

> Decreased exercise tolerance: due to dyspnoea and/or fatigue (may be attributed to ageing/deconditioning or pulmonary disease)

> Fluid Retention: leg or abdominal swelling, orthopnea, frequent coughing (produce mucous or pink, blood-tinged sputum)

Question 3

What is the difference between systolic and diastolic heart failure?

Answer 3

> Systolic heart failure are seen in those patients who have had MI, which has led to scarring of the ventricular tissue, causing the ventricle to not contract properly, therefore they don’t eject as much blood
Diastolic heart failure - ventricle doesn’t relax properly (usually due to long standing hypertension) - too much pressure - ventricle doesn’t fill very well - what gets in gets pumped out - not enough blood getting intro ventricle

Question 4

What is the first half of the process of cardiac remodelling?

Answer 4

> Ventricular dysfunction (in patients who have had STEMI)
Scarring on ventricle because of ischaemic damage (doesn’t function properly)
Body’s normal response to that is to try to dilate muscle and cause hypertrophy of the muscle (try to make wall grow and ventricle get bigger)
Driven off neurohormonal pathways (sympathetic nervous system and renin-angiotensin-aldosterone system)

Question 5

What is the second half of the process of cardiac remodelling?

Answer 5

> Activation of neurohormonal pathways is a compensatory mechanism to poor ventricular function that was caused by a STEMI
There changes are ok in the short term, they help to compensate initially, but in the end, they end up detrimental - cause problems
Ventricles get too big, they become floppy and don’t really work very well

Question 6

Discuss CHF Disease Trajectory

Answer 6

> In CHF, see pattern where there’s a continued decline over a period of time
Remodelling driving process forward leading to worsening function
Amongst pattern discussed above, we have acute exacerbations where HF becomes less stable, accelerated period of disease activity, recover, stable and have another exacerbation

Question 7

How is HF diagnosed?

Answer 7

> Clinical signs and symptoms
> ECG
> Echocardiogram
> JVP
> ANP
> BNP

Question 8

What are the treatment aims of CHF?

Answer 8

> Slow disease progression: cardiac remodelling, intefere with n/h pathways, reduction of CV risk, prevent further ischaemic episodes

> Improve Quality of Life: improve symptoms, prevent hospitalisation

Question 9

What are the non-pharmacological options of CHF?

Answer 9

> Patient education
> Regular physical activity
> Weight reduction
> Oxygen therapy
> Reduce salt intake (fluid retention)
> Fluid restriction (severe cases: 1.5L per day)
> Other lifestyle advice, as appropriate

Question 10

Discuss the role of ACEi to slow disease progression in CHF?

Discuss the dose used in CHF

When are they initiated?

Answer 10

> Increase ejection fraction
Reduction in enlargement of ventricles initially - some symptomatic relief but using predominantly to stop remodelling process
Dose is pushed as high as patient can tolerate or to maximum because we want to block pathway as best we can to prevent remodelling
Can be initiated anytime and uptitrate quite actively

Question 11

Discuss the use of ACEi and ATII antagonists in CHF?

Can ATII antagonists be substituted in place of ACEi?

Answer 11

> ACEi and ATII antagonists can be combined in CHF, however, there is an increased risk of adverse renal effects
However, in some patients who can’t take some of the other medications - need to block that pathway properly
If patient cannot tolerate ACEi (cough, angioedema), can use ATII antagonists

Question 12

Discuss Beta Blockers dosing in CHF

Answer 12

> In someone with HF, starting beta blocker - risk of making symptoms worse
Cardiac output being increased by sympathetic activity - forcing heart to beat a bit faster and harder
Start beta blocker when relatively stable (not in period of acute exacerbation) - start low and actively uptitrate but slowly

Question 13

Why can’t non dihydropyridine CCB be substituted for a beta blocker?

Answer 13

> Don’t have the same benefits in HF than what a beta blocker does
Actually contraindicated in CHF (make worse)
No alternative to a beta blocker in CHF

Question 14

What beta blockers are used in Heart Failure?

Answer 14

> Selective beta 1 blocking: metoprolol, nebivolol, bisoprolol

> Non selective beta blocker a1 blocking activity: carvedilol which may be reserved for patients with slightly more severe HF

Question 15

What is the role of aldosterone antagonists in CHF to slow disease progression?

Answer 15

> Spironolactone typically used except for group of STEMI patients, in hospital and have poor ejection fraction at that time (eplerenone)
Low dose of spionolactone is used: 12.5-50mg/day

Question 16

When is Ivabradine used in CHF?

Answer 16

> Predominantly in those who have a high baseline heart rate
Doesn’t have the same effect as a beta blocker in blocking the sympathetic pathways that drive ventricular remodelling
Ivabradine should only be considered in those who cannot tolerate a beta-block (when appropriately initiated) or have a high heart rate despite maximum tolerated beta blocker

Question 17

Why are neprilysin inhibitors such as sacubitril, combined with ATII antagonists such as valsartan rather than an ACEi?

What is its place in therapy? Why are these combined?

Answer 17

> ACEi and Neprilysin inhibitors block breakdown of bradykinin = leads to angioedema

> Stop/prevent combination with ACEi
Used in patients who are not sufficiently controlled with a beta-blocker and ACEi
May benefit from addition of sacubitril = STOP ACEi

Question 18

What is the role of managing fluid balance in CHF?

How do patients manage this?

Answer 18

> Fluid management is a key component of symptom control
Determines a persons ‘ dry’ or ‘euvolaemic’ weight
Patients should weigh themselves every morning after going to the toilet and before getting dressed or eating breakfast (steady weight gains over a period of days indicates fluid retention)

Question 19

What does ‘dry’ weight mean?

Answer 19

Weight at which a patient, who has been fluid overloaded and treated with a diuretic, reaches a steady weight with no remaining signs of overload

Question 20

What should a patients fluid intake be?

Answer 20

> Intake of more than 2L of fluid per day should be avoided

> Reduce to 1.5L during episodes of fluid retention

Question 21

What are important points when counselling a patient in CHF?

Answer 21

> Weigh yourself everyday and keep track of your weight
Restrict your fluid intake and salt intake adb
Call Dr. or HF nurse ASAP if: you gain or lose more than 2kg over 2 days, there’s increased swelling in your ankles, legs or abdomen, you are coughing a lot, especially at night

Question 22

What is the role of Loop Diuretics such as Furosemide to improve quality of life in patients with CHF?

Answer 22

> Key element in the symptomatic treatment of HF

> Particularly breathlessness and peripheral oedema

Question 23

What is the dosing of Furosemide in CHF?

Answer 23

> Dose may be fixed in some patients or adaptive to how much fluid they’ve retained
If they have more fluid, need to get rid of more fluid (bigger dose of diuretic)
Dose titrated according to patients weight (increase dose during fluid retention episodes until dry weight achieved)
May be in combination with thiazide diuretic to produce a more profound diuresis

Question 24

If there is weight gain (>2kg in 24-48hrs) what should treatment options follow?

Answer 24

> Is there an acute precipitant? yes = address underlying course
No or uncertain = institute flexible diuretic regimen (20mg furosemide for each kg of weight gain)

Question 25

Loop Diuretics:

When is bumetanide used?

When is ethacrynic acid use?

Answer 25

> Bumetamide: used when people have a lot of fluid around GI tract (fluid barrier to drug absorption)

> Ethacrynic acid doesn’t have a sulfonamide (used in patients with sulfonamide allergy)

Question 26

How do NSAIDs contribute to triple whammy?

Answer 26

> NSAIDs cause fluid retention
Patients with CHF are likely to be taking diuretics and ACEi
If the patient accidentally became a little dehydrated, they can enter acute renal failure

Question 27

Discuss the role of digoxin in improving quality of life in CHF

Answer 27

Provides symptomatic relief and reduces hospital admissions

Question 28

How is Systolic HF managed?

Answer 28

1. Start with ACEi (consider ARB if not tolerated)
2. When stable, add beta blocker
3. If still symptomatic: add aldosterone antagonist
4. If still symptomatic: replace ACEi or ARB by sacubitril w/ valsartan OR add digoxin or ivabradine
5. Fluid overload = treat with loop diuretic, consider adding thiazide diuretic