Heart Failure (LVSD)
DEFINITION
Heart failure (see card) in which the principle abnormality is left ventricular systolic dysfunction, meaning that the left ventricle is cannot contract normally to expel sufficient blood to supply tissue requirements.

D I A B M I M

INCIDENCE
See Heart Failure card.

D I A B M I M

AETIOLOGY
See Heart Failure card.

D I A B M I M

BIOLOGICAL BEHAVIOUR
Pathophysiology
Normal Physiology
Typical CO is 5 L/min, increasing to max 25 L/min on exertion, a five-fold increase.
CO = SV x HR.
Heart Rate can double CO (beyond 140bpm, diastolic filling period reduced at expense of output).
Inotropic state may increase SV (and CO) by 15%.
But Starlings Curve is major mechanism for increasing CO (via SV):
 -  as preload increases, CO increases.
 - up to 5L of pooled blood (mostly in abdomen) returns to heart when needed, eg on exercise / catecholamine release.

Failing Heart
When heart can't increase systolic output, heart failure results.
Starling's curve compensates until right shifted so heart sits on flat part.
The crucial (prognostic) indicator is systolic ejection fraction (should be 70% ie 70mls/min)

Complications
Dilation
Occurs aften all other methods of compensation fail.
Dilation allows greater ejection fraction through increased SV.
However, very inefficient,  as myocardial O2 consumption is proportional to diameter of heart.
Also may lead to functional valve ring dilation and regurgitation.


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MANIFESTATIONS
Symptoms
Systemic
Salt and Fluid Retention - Lungs
Exertional dyspnoea- main feature and a marker of severity, eventually apparent at rest
- Is due to reduced lung compliance and increased work of breathing.
- Increases resp drive.
- Demands more O2 consumption.
Orthopnoea - later feature.
- When supine, fluid redistribution increases pulmonary hydrostatic pressure.
- When supine the diaphragm is relatively elevated.
- Classically releived by sitting up and opening window.
Paroxysmal Nocturnal Dyspnoea.
- Resp centre and adrenergic drive depressed at night.
- Drops O2 tension further in pts with oedema, reduced compliance.
- Severe SOB awakens pt, frightening.
- Cough and wheeze continues upright.
'Cardiac Asthma'
- Wheezy bronchospasm, due to lung oedema.
Acute Pulmonary Oedema
- Marked increase in pulmonary capillary pressure.
- High enough to acutely cause alveolar oedema.
- Extreme SOB, blood-tinged expectoration.
Salt and Fluid Retention - Systemic
Anorexia and nausea (portal congestion).
Systemic Hypoperfusion
Fatigue.
Exacerbates dyspnoea through resp muscle fatigue
Muscular weakness.
Reduced exercise capacity.
Cerebral hypoxia - confusion, memory dysfx, headache, anxiety.

Signs
See Heart Failure card.

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INVESTIGATIONS
See Heart Failure card.

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MANAGEMENT
See Heart Failure card.

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