Heart Failure

Med school notes.

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>1/100 people over 65.

Risk Factors
Refer individual underlying cause cards.

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Heart failure has an underlying cause and a precipitating reason for admission.
Underlying cause usually long-standing, whereas precipitating causes are critical, and an urgent priority for intervention and prognostic benefit.

Underlying causes
- think of preload, intrinsic heart function and afterload.

Conditions affecting preload

Fluid overload
Tamponade / pneumothorax

Conditions affecting myocardial function

Endocardium / Valves
Valvular heart disease.
Congenital heart disease.
Hypertensive heart disease.
Cor Pulmonale.
Blood supply

Tamponade / pneumothorax

Conditions affecting afterload
Aortic stenosis
Tamponade / pneumothorax

High Output heart failure
 (see card)

Precipitating causes

Infection (esp pulmonary, endocarditis).
PE (HF pts at risk).
Arrythmia (tachy or brady, AV dissociation, loss of synchronicity).
Subacute systemic hypertension.
Fluid overload - eg renal failure.
Drugs (negative inotropes eg Ca antagonists, antiarrhythmics; fluid retaining drugs eg licorice, NSAIDs, steroids).
Withdrawl of therapy / non compliance / social issues with tx.
Surgery, anaesthesia.
- most common cause post-op is fluid overload
--> may be acute load or 'fluid creep'
--> stopping epidurals can acutely raise afterload, and increase preload as fluid returns.

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Distinction useful early; differences are often blurred later in the course.

Systolic vs Diastolic
Systolic if cannot contract and expel blood.
Diastolic if cannot relax and fill.

High output vs Low output.

Low output if low CO.
High output if high CO.

Acute vs Chronic

In acute forms, the underlying cause is very relevant.

Right vs Left Sided
A rigid distinction is artificial in chronic disease due to:
i) secondary right sided failure from chronic pulmonary hypertension in left sided failure;
ii) retention of salt and water being characteristic of all forms of failure.

See also:
Heart Failure (LVSD)
for left ventricular systolic dysfunction (most common).
Heart Failure (diastolic) for diastolic dysfunction.
Heart Failure (high output) for high output failure.

Compensations Preceeding Failure
When failing, the heart tries to increase contractility via:
i) hypertrophy +/- dilation : mass of contractile tissue is augmented to try to aid pumping. 
ii) Frank-Starling mechanism
iii) Neurohumoral activation

Backward vs Forward Failure
The end result both systolic and diastolic uncompensated failure.
Backward Failure
Failure to circulate blood leads to a rise in central venous pressure.
Resultant transudation causes salt and water retention.
Forward Failure
Low CO causes low renal perfusion, causes salt and water retention.

Salt and Fluid Retention
Adrenergic, RAAS, and ADH systems all contribute to retention.
Hence untreated CHF pts have increased blood volume, sodium and interstitial fluid.
 - Acute pts have less fluid, but higher central venous pressures.
Retention provides an important compensatory mechanism to maintain CO.
However it leads to many of the disease manifestations.
ANP/BNP partly opposes retention.

Related to increased CVP and fluid/salt retention.
Increased hydrostatic pressure in capillary beds causes transudation.
Symptoms also due to hypoperfusion of bodily tissues.

Pulmonary Oedema
Pressures increase to push fluid into alveolar spaces.
See card.

Pleural Effusion
Pleural veins drain into both systemic and pulmonary veins.
Most common if pressure from both veinous systems, can be seen if very high pressure in just one.
More frequently right than left.
Ascitis is also possible in R heart failure.

Cardiogenic Shock
See shock card.

Vicious Cycle
Catecholamines are released to stimulate output
--> unfortunately failing heart is on a 'flat' curve.
--> SV does not increases, but rate does
--> less diastolic time worsens filling
--> ischaemia and worsening failure.

Natural history
Natural history is to deteriorate, through further damage, heart stress, neurohormonal factors, or MI.
Best outlook when cause can be found and treated.
Asymptomatic - <5% die/year.
Mild 10%/year.
Moderate 20-30%.
Severe 30-80%.
40% die suddenly - ?VF, but no evidence that this can be treated with antiarrythmics.
Others die of exacerbations (40%).

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Left HF / Salt and Fluid Retention.

Dyspnoea, orthopnoea, PND, 'cardiac asthma'.
Acute pulmonary oedema.
Refer Heart Failure (LVSD) card for details.

Left HF / Systemic Hypoperfusion

Fatigue, dyspnoea, weakness, exercise intolerance.
Confusion, memory dysfx, headache, anxiety.

Right HF / Salt and Fluid Retention

Anorexia and nausea (portal congestion).
Leg / sacral, abdominal / scrotal swelling.


General examination
Patient sits upright.
Uncomfortable lying flat for few minutes.
Cardiac cachexia (TNF circulation, metabolic rate up, work of breathing up, anorexia, intestinal vein distension, rarely protein-losing enteropathy).
Cheyne-Stokes respiration (severe).

Peripheral Exam
Cyanosis of lips and nail beds (severe).
Cold extremities, pale, urine output down (severe).
Reduced pulse pressure (severe).
Pulsus alternans (severe).
Occasionally diastolic BP high (vasoconstriction).
Hypotension (if severe and acute)
Postural hypotension (Rx related).
JVP distended (reflects CVP).
Dependent oedema - both legs / sacrum (rarely involves arms and face unless end-stage).
Hepatomegaly, possibly pulsatile if TR (may cause jaundice, esp if acute).
Congesitve splenomegaly if longstanding hepatomegaly.
Features of underlying cause - eg hypertension, atheromatous disease.

Displaced sustained apex.


Reduced pulse pressure.
Displaced sustained apex.


Dullness to percussion over lung bases.
Stony dull if pleural effusion.


3rd / 4th heart sounds (not specific).
Moist inspiratory creps in lung bases (elevated CVP).
Widespread coarse crepitations with exp wheeze (acute alveolar oedema).

Classification - Functional

New York Heart Assoc Guidelines
I - disease, but asymptomatic.
II - angina/dyspnoea on moderate exertion.
III - angina/dyspnoea on mild exertion.
IV - angina/dyspnoea at rest.

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Directed at detecting underlying cause in acute, precipitating cause in known chronic patients.
Delay while initial therapy instigated.
Important features:


Us + Es (baselines, ?arrhythmia).
LFTs - transaminases up if hepatic congestion, perhaps strikingly if acute.
Others as clinically indicated.


FBC - ?precipitant eg anaemia, unsuspected sepsis.


As appropriate

Low sodium (retained).
May contain protein, with high specific gravity.


CXR shows pulmonary venous congestion/oedema (dilation of upper lobe veins, Kerley B lines, Bat's wing hilar shadowing) +/- cardiomegaly +/- infection.
ECG - ?arrythmia, ischaemia recent or old, LVH.
Echo - urgent if acute valve/tamponade cause suspected.
Else baseline echo for fx assessment and prognosis (LV ejection fraction prognostic).


TFT on all pts.
Others as per suspicion, eg hamachromatosis, amyloid.

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Target appropriate risk factors, aggressively.
Light low-salt meals.

1.  Correct precipitating cause.
2.  Correct underlying cause (if possible).
3.  Control CHF state.

Acute Management
Correct any precipitating factors.
Pulmonary oedema - see card.
Cardiogenic shock
--> Poor prognosis.
- occasionally a failing heart can have a high preload requirement
--> reducing preload by diuresis may worsen cardiac output.

Further Diuresis
Measure urine output for first 24 hrs to monitor diuresis.
Identify a target weight if pt reliable, or visit old notes.
Weigh daily.
Monitor K+ and Mg2+, supplements only usually needed if high dose diuretics.
Patients are switched to oral to early in Auckland - be aggressive.

Controlling the CHF state
There are no complete rules (beside ACEis), as pts vary in many respects.
1.  Reduce work of heart (preload and afterload).
2.  Control excess Na+, H2O retention.
3.  Enhance myocardial contractility.

Prognostic Therapies
Only 25% of people are on correct therapy.
ACE inhibitor
Prevents fibrosis, improves remodelling via inhibiting Ang II growth-inducing property on collagen.
Improves LV function.
Angiotensin II antagonists
Future hope, not proven yet (NEJM 2002 (347):1795-7).
(26 trials) - NNT 23 (13 mnths), RRR 34%.
(RALES trial) - NNT 9 (2 yrs), RRR 30%.
Also increases ejection fraction by 6-7%.
Needs 2-3 mo to work.
Saves lives by preventing the rising K+.
Control any Hypertension and arrhythmia.
BNP Guided Treatment
RRR ~30% for CV event, ~35% for HF or death.
Not in common practice yet.

Symptomatic Therapies
Reduces afterload, improves LV fx.
Ongoing diuresis.
(Helps ~ 1 in 4, not routine).
Core principle - reduces work of heart.
Emotional rest - institute diazepam 2-5mg tid if not achieved.
Limit DVT/PE risk (!).
Na+ restriction
Reduces hypervolaemia.

Which Therapy for Which Pt?
Stepwise increase in therapies, as py NYHA class.
Class I
ACEi, even if asymptomatic
Class II
Restrict exercise somewhat.
Low Na+ diet.
Beta blocker - start low dose if stable (eg 12.5mg metoprolol).
Class III
Further exercise restriction
Add diuretic as gets towards class III.
Add digoxin as above.
Class IV
No Na+ in diet.
Restrict exertion (not absolute).
Once dose up around 80mg frusemide, add other diuretics as you increase the frusemide further.
Thiazide boluses IV, (eg bendrofluazide) and spironolactone 25 mg (ie target all aspects of the tubule, effectively pulling out the plug).

Amiodarone first choice - least negative inotropic effect for severe HF.<br>

Consider if pt has marked LV impairment.
Or AF.

Consider if pt has chronic AF.

If Non-responding
Repeat CXR.

Underlying Cause
Is underlying cause confirmed?
Exclude aggravating factors and intervene in selected cases.

Follow Up
Repeat CXR prior to discharge.

Depends on underlying cause.
Surgeons may consider transplants.

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