Heart Failure Flashcards

1
Q

What is heart failure?

A

A clinical syndrome, comprising of dyspnoea, fatigue, or fluid retention - due to cardiac dysfunction (structural/functional abnormalities) - at rest or on exertion, with accompanying neurohormonal activation.

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2
Q

What is the prevalence and prognosis of heart failure?

A

Prevalence is increasing - more cases of hypertension, obesity, diabetes and CHD.
Prognosis - 1YS rate is worse than breast, uterus, prostate, and bladder cancer.

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3
Q

What is the burden of heart disease?

A

~2wk avg hospital admission length.
Longer than breast and lung cancer.
High readmission rates (often within 1wk).

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4
Q

What are the symptoms of heart failure?

A

SOB and fatigue (non-specific).
Reduced exercise capacity.

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5
Q

What are the signs of heart failure?

A

Crackles, oedema, tachycardia (non-specific).
HS3, raised JV, displaced/abnormal apex beat (insensitive).

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6
Q

What is the diagnosis of heart failure?

A

Incorrect in 50% of cases.
Considers symptoms and signs.
Objective evidence of cardiac dysfunction (ECHO, RNVG/MUGA, MRI).

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7
Q

What is the interpretation of an ECG of heart failure?

A

If entirely normal - LVSD is unlikely.
Problem - interpretation confidence.

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8
Q

What is the interpretation of BNP of heart failure?

A

Low - excludes HF/LVSD.
High - indicates ECHO or cardiac assessment.
Recommended first-line test in suspected HF.
A predictor or mortality and morbidity.
Can test at bedside; cheap.

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9
Q

How is heart failure classified?

A

NYHA:
I - no exercise limit or symptoms.
II - mild exercise limit, symptoms on exertion.
III - moderate exercise limit, only comfortable at rest.
IV - severe exercise limit, discomfort at rest.

Also considers LV impairment and BNP elevation.

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10
Q

What is the neurohormonal hypothesis of heart failure?

A

RAAS - LV hypertrophy/remodelling and fibrosis; hypokalaemia and hypomagnesaemia.
SNS - arrhythmogenic.

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11
Q

What are the causes of LVSD?

A

MI, severe aortic valve disease or MR.
Dilated cardiomyopathy - not due to IHD/VSD (inherited, toxins, acute myocarditis, HIV, hypertension).

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12
Q

What is the diagnosis of LVSD?

A

PMH - MI, DM, hypertension, post-partum.
FH - familial DCM.
SH - IVDU, alcohol abuse.
Exclude renal failure and anaemia.
Consider sarcoidosis and muscular dystrophy.

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13
Q

What is always done to investigate LVSD?

A

ECHO - for valvular/diastolic dysfunction, pericardial effusion, cardiac tamponade, LVH, CHD, hypertension (atrial dilatation).
May not identify constriction or shunts.

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14
Q

What are the investigations for LVSD?

A

ECG and CXR.
Coronary angiography or CT coronary angiogram - if chest pain or <70yrs old.
Revascularisation - if ischaemic.
Cardiac MRI - for infarction, inflammation, fibrosis.
Assessment from a cardiologist.

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15
Q

What is LVEF?

A

Changed by disease or physiology.
Analogous to Hb/anaemia.
Difficult to quantify accurately by ECHO.

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16
Q

What is Simpson’s Biplane?

A

The LV cavity is divided into multiple slices of known thickness and diameter (thinner slices equals more accurate volume).
The endocardial border is traced.

17
Q

What are the advantages and disadvantages to Simpson’s Biplane?

A

Accurate and easy - the gold standard.
Has major technical difficulties and is time consuming. Depends on the quality of imaging, the operator, the calculation method, and contrast agents.

18
Q

What is a MUGA scan?

A

Easier to obtain an accurate LVEF; reproducible.
Uses radiation; gives no additional structural information.

19
Q

What is a cardiac MRI?

A

More accurate than ECHO; additional information on tissue characteristics.
Expensive; time-consuming; requires breath-holding; cannot be done at bedside; claustrophobia issues.

20
Q

What is the LV function assessment?

A

Normal - 55-70%.
Mild - 40-55%.
Moderate - 30-40%.
Severe - <30%.

LV systolic function is a potent predictor of death in hospitalised HF patients.