Heart Failure

Question 1

Heart failure classification

Answer 1

Class I -

Question 2

Investigations and management

Answer 2

1. Does the patient have heart failure?
   Would need to perform a History and clinical examination?
   Differential diagnosis? - could be anaemic from breathlessness
2. What sort of heart failure does the patient have?
   Heart Failure with a reduced Ejection Fraction (HRrEF)
   Heart Failure with a preserved Ejection Fraction (HRpEF)
   Valvular / structural (e.g. VSD) heart failure
   Right ventricular failure
   High output cardiac failure
3. What is causing heart failure?
   Ischaemic heart disease? Hypertension? Viral? Alcohol?

Management

Question 3

Investigations for case study

35 year old male 
Married with 3 kids 
Progressive SOB 1 month 
Sudden onset severe SOB 
No peripheral oedema
No significant PMH (past medical history)
No medications
Temp 36.8, Pulse 130, BP 170/70mmHg, Loud heart murmur, RR 40, pO2 91% and Profuse bilateral
crepitations

Answer 3

Recognise that this is an emergency
ABCDE
Immediate treatment:
i.v. Furosemide 80mg stat
O2
Highly likely to require respiratory support
Second line i.v. nitrates, i.v. morphine

Investigations:
ECG - Fast Atrial fibrillation
May have caused decompensation
Tachycardia may be due to pulmonary oedema, priority is to treat this.
Rate control is challenging, as some drugs e.g. beta blockers may make acute heart failure worse
Anticoagulate

Chest X-ray - shows cardiomegaly
Upper lobe diversion 
Fluid in the fissure 
Pleural effusions 
Kelley B lines 

Trans thoracic Echocardiogram - shows potential aortic stenosis
May need surgery

i.v. Furosemide
Venodilatory (dilation of veins) effect immediate.
Onset diuretic (increase the flow of urine) action 30minutes peaking 60- 90minutes

Helps as reduces hydrostatic pressure in lungs and decreases burden on heart - wont solve problem but will buy time to allow breathing to return back to normal and prevent immediate HF and lack of O2 to brain - to further treat patient

Higher doses required in renal failure 
Monitoring key:
	HR, BP, RR, pO2%, CXR 
	Fluid balance, hourly urine output 
	Daily weights (aim for 1kg weight loss per day)

Question 4

Information for case study 2

65 year old female
NYHA III for 2 weeks
Orthopnoea and PND
Baseline NYHA I
Myocardial infarction 5 years ago
She’s on Aspirin 75mg od and Atorvastatin 80mg od
Apyrexial (without fever (normal body temp))
Pulse 70, BP 100/60 mmHg, Normal heart sounds and bibasal crepitations (crackles at base of both lungs)

Answer 4

Investigations:
ECG - showed LBBB
CXR - chest x ray - mild congestion in lungs

Blood tests:
FBC
Patients with heart failure are often anaemic
Anaemia might explain symptoms

U&Es
Renal function often deteriorates in heart failure
Na / K levels important for medications
LFTs - May be elevated due to hepatic congestion
Clotting - Important if considering anticoagulation
Thyroid function, vitamin D level - Alternative explanation for symptoms
CRP - Look for infection / inflammation
CHECK BNP (brain naturetic peptide) - this is a hormone released in response to atrial/ventricular stretch due to fluid overflow

Atrial fibrillation can triple BNP levels
Has a negative predictive value of 97%

They found BNP levels to be at 2000 - treatment = furosemide (treats fluid build up) and urgent referral to specialist

Question 5

Naturetic peptides

Answer 5

Can be both good and bad

Good as during increased ventricular loading conditions - can increase diuresis and vasodilation and decrease RAAS activity

Bad as during an Afib - the heart is put under strain release in BNP, therefore stimulating natriuresis, diuresis vasodilation and decreased RAAS activity - therefore decreasing blood pressure

Question 6

Sympathetic activation in heart failure

Answer 6

Activation of SNS causes:
activation of RAAS —> increased fluid retention —> increased wall stress —> myocardial hypertrophy (and potentially decreased contractility)

Vasoconstriction —> increased wall stress —> myocardial hypertrophy and decreased contractility

Increased HR and contractility —> increased myocardial oxygen demand —> decreased contractility

Baroreceptor-mediated response 
Early compensatory mechanism to improve CO:
	Cardiac contractility
	Arterial and venous vasoconstriction
	Tachycardia 
However long-term deleterious effects:
	ß

Question 7

ß blockers - physiological effects

Answer 7

1. Reduce heart rate (cardiac beta receptor)

2. Reduce BP

Question 8

RAAS in heart failure

Answer 8

Angiotensin 2 will cause vasoconstriction and enhanced SNS activity and increased salt and water retention

Treating the Renin-angiotensin Aldosterone system:
Using -
ACE inhibitors to prevent Angiotensin converting enzyme from converting angiotensin 1 to angiotensin 2
Angiotensin receptor blocker to prevent vasoconstriction at peripheries and increased SNS activity, as well as preventing angiotensin 2 being converted to aldosterone

Role of Aldosterone Receptor Antagonists SPIRONOLACTONE
In spite of ACE inhibitor / ARB therapy sometimes, aldosterone concentration can return to normal
Aldosterone