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PH-CV12

Hypertensive heart disease

How a ventricle pumping against high pressure thickens (Laplace), why the thick wall fills poorly, enlarges the atrium and runs short of oxygen, how it can finally dilate, and how lung disease does the same to the right ventricle.

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  • 5 steps · 10 questions
  • 3D normal anatomy

By the end, you can

  • Use the law of Laplace to explain why a pressure load produces concentric hypertrophy and a dilated ventricle has a high wall stress.
  • Explain how hypertrophy and fibrosis impair relaxation and filling, and why this enlarges the left atrium and favours atrial fibrillation.
  • Explain why hypertrophied muscle becomes ischaemic even with normal coronary arteries.
  • Describe how compensated concentric hypertrophy can progress to a dilated, failing ventricle, and relate cor pulmonale to the same process on the right.
  • Recognise the morphology, ECG and echocardiographic criteria and differentials of hypertensive heart disease, and explain how treatment acts on its mechanism.

What it is

Hypertensive heart disease is the change in the heart caused by long-standing systemic hypertension: left ventricular hypertrophy, usually concentric, with impaired filling, left atrial enlargement, ischaemia of the thickened muscle and, in some people, later dilatation and heart failure. It is diagnosed when hypertrophy accompanies hypertension and no other cause explains it. Cor pulmonale is the right-sided counterpart: right ventricular hypertrophy or dilatation from pulmonary hypertension caused by disease of the lungs or their vessels.

4 types to tell apart
Compensated concentric hypertrophy
A thick wall round a normal or small cavity, with normal wall stress and ejection fraction; often silent, apart from impaired relaxation.
Heart failure with preserved ejection fraction
The stiff, thick ventricle fills only at a high pressure, congesting the lungs although it empties normally.
Dilated (decompensated) hypertensive heart
After years of overload, muscle loss and fibrosis let the ventricle dilate and its contraction weaken (heart failure with reduced ejection fraction).
Cor pulmonale
Chronic (hypertrophy from slowly rising pulmonary pressure, usually lung disease) or acute (sudden dilatation, as after a large pulmonary embolus).

US spelling: ischaemia → ischemia, fibre → fiber.

Normal function

How the left ventricle carries its load

The ejects against the systemic arterial pressure, about five times the pressure the meets in the lungs, and its wall is about three times thicker. That pressure, the afterload, is the main load it carries in systole.

How hard each muscle fibre must pull is set by the wall stress, described by the law of Laplace: stress is roughly pressure × cavity radius ÷ (2 × wall thickness). A higher pressure or a larger cavity raises the stress on every fibre; a thicker wall shares it among more muscle. Wall stress is a main driver of the muscle’s oxygen demand.

Filling needs different properties: in diastole the muscle must relax actively, pumping calcium back into its stores, and the wall must be compliant so that the ventricle fills at a low pressure. The belongs to both ventricles and moves with whichever side has the higher pressure.

Point to it on the model