Article Text

Cardiac and vascular pathophysiology in hypertension
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1. Jamil Mayet,
2. Alun Hughes
1. International Centre for Circulatory Health, 10th Floor QEQM Wing, St Mary’s Hospital, and Imperial College Paddington and Clinical Pharmacology, NHLI, Imperial College of Science, Technology & Medicine, London, UK
1. Correspondence to:
Professor Alun Hughes, International Centre for Circulatory Health, 10th Floor, QEQM Wing, St Mary’s Hospital and Imperial College, Paddington, London W2 1NY, UK;
a.hughes{at}imperial.ac.uk

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Hypertension is one the earliest recorded medical conditions (Nei Jin by Huang Ti around 2600BC); it has shaped the course of modern history1 and the consequences of hypertension (myocardial infarction, strokes, and heart failure) will soon be the leading global cause of death. Nevertheless, despite intensive research, the aetiology of hypertension remains obscure; only around 5% of cases have an identifiable cause.2 Indeed, primary or essential hypertension is perhaps better not considered a disease at all,w1 rather (as suggested by Sir Geoffrey Rose) a level of blood pressure above which treatment does more good than harm. An individual’s blood pressure depends on the complex interplay of heart and blood vessels and understanding this relation is the key to understanding the pathophysiology of hypertension.

## NORMAL CARDIAC AND VASCULAR PHYSIOLOGY

### Relation between mean pressure and mean flow in the human circulation

The role of the circulation is to deliver blood to the tissues and flow occurs because of the pressure difference established by the pumping action of the heart. The relation between the pressure difference and flow can be described by a relation that is analogous to Ohm’s Law for electrical current (box 1) and sometimes termed Darcy’s Law.

$Math$

(where ΔP = pressure difference. Q = bulk flow, R = resistance)

This relation can be restated for the whole circulation in terms of mean arterial pressure, cardiac output, and peripheral resistance (box 2).

$Math$

(where MAP = mean arterial pressure, CO = cardiac output (= stroke volume × heart rate), PVR = total peripheral vascular resistance)

Although a simplification, this emphasises that an elevation of mean blood pressure can only come about as a result of an increase in cardiac output (CO), an increase in total peripheral vascular resistance (PVR), or a combination of both.

CO is a consequence of left ventricular pump function, which in turn depends on a number of factors (fig 1) including …

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