Hypertension Lecture Notes-BSC Clinical Medicine

Causes, Management and Dangers Associated With Hypertension

INTRODUCTION

Arterial blood pressure is defined as the lateral pressure exerted by the column of blood on wall of arteries. The pressure is exerted when blood flows through the arteries. Generally, the term ‘bloodpressure’ refers to arterial blood pressure.

ARTERIAL BLOOD PRESSURE

Arterial blood pressure is expressed in four different terms:

  1. Systolic blood pressure
  2. Diastolic blood pressure
  3. Pulse pressure
  4. Mean arterial blood pressure.

SYSTOLIC BLOOD PRESSURE

Systolic blood pressure (systolic pressure) is defined as the maximum pressure exerted in the arteries during systole of heart.

Normal systolic pressure: 120 mm Hg (110 mm Hg to 140 mm Hg).

DIASTOLIC BLOOD PRESSURE

Diastolic blood pressure (diastolic pressure) is defined as the minimum pressure exerted in the arteries during diastole of heart.

Normal diastolic pressure: 80 mm Hg (60 mm Hg to 80 mm Hg).

PULSE PRESSURE

Pulse pressure is the difference between the systolic pressure and diastolic pressure.

Normal pulse pressure: 40 mm Hg (120 – 80 = 40).

MEAN ARTERIAL BLOOD PRESSURE

Mean arterial blood pressure is the average pressure existing in the arteries. It is not the arithmetic mean of systolic and diastolic pressures.

It is the diastolic pressure plus one third of pulse pressure.

To determine the mean pressure, diastolic pressure is considered than the systolic

pressure. It is because, the diastolic period of cardiac cycle is longer (0.53 second) than the systolic period (0.27 second).

Normal mean arterial pressure: 93 mm Hg (80 + 13 = 93).

Formula to calculate mean arterial blood pressure:

Mean arterial blood pressure

=Diastolic pressure + 1/3 of pulse pressure

= 80 + 40/3= 93.3 mm Hg SYSTEMIC HYPERTENSION

Systemic arterial hypertension is one of the most common maladies of mankind, affecting

about 20% of the population globally.

Though it was considered to be a disease related to affluence, it is no longer so.

All sections of the population in India suffer from the disease, the prevalence in urban

population is higher compared to that of the rural population.

Diabetes and hypertension coexist in affects the long-term prognosis mutually.

Hypertension about 30-40% of cases and the combination adversely leads to damage of

the target organs – heart, brain, optic fundi, kidneys and blood vessels both acutely and

on a long-term basis. This is not always so since other factors such as hyperlipidemias and tobacco smoking may also influence the final outcome.

MEASUREMENT OF BP

This is ideally done using a mercury sphygmomanometer. The patient should be seated in a quiet room for 15 minutes before recording BP. BP may also be recorded in the supine and standing position. At all postures, the arm should be supported at heart level.

The BP cuff for adults should have a bladder 13-15 cm wide and 30-35 cm long.

In about a third the SBP is greater than 140 mm Hg while the DBP is 90 mm Hg or less (Isolated systolic hypertension)

Obesity: In adults obesity may confer a two-fold risk to develop hypertension. Central

obesity is the stronger predictor of risk.

Dietary sodium and potassium intake: The SBP and DBP are related directly with sodium intake and urinary sodium loss. Reduction of dietary sodium by 100 mmol/daydefinitely leads to lowering of SBP on long-term follow up.

Potassium intake bears an inverse relation to blood pressure. Higher potassium intake lowers blood pressure.

Other factors: Alcohol intake, tobacco smoking, sedentary life style and noise pollution

markedly elevate the BP level. Modification of life style helps to lower the BP

considerably.

PATHOLOGY

Main pathological process occurs in the heart and several parts of the arterial tree.

Cardiac changes: The left ventricle hypertrophies in 20- 50% of mild to moderate hypertensives.

The muscle fibres hypertrophy and this process is reversible with antihypertensive therapy.

At autopsy, left ventricular hypertrophy is diagnosed if it weighs above 131 g/m2 body surface in men and 100 g/m2 body surface in women. Unlike physiological hypertrophy occurring as a result of exercise, in hypertension left ventricular hypertrophy leads to diastolic dysfunction, arrhythmias, acceleration of coronary atherosclerosis and left ventricular failure.

Cardiac failure is caused by degeneration and lysis of myofibrils. The extent of hypertrophy and levels of blood pressure do not correlate in all cases buthypertrophy is more pronounced in those with early onset hypertension.

Arterial changes: Arteries and arterioles show thickening (arteriolosclerosis). Arteriolar changes are well seen in the kidneys. Renal vessels show medial hypertrophy and intimal fibrosis.

Progressive occlusion of arterial lumen leads to scarring of glomeruli and tubular atrophy

Many develop symptoms after knowing that they are hypertensives. The symptoms are vague and non-specific in such patients.

These symptoms include fatigue, dizziness, palpitation, headache and anxiety. Though many types of headache have been described, throbbing headache, felt in suboccipital region on waking up after sleep is suggestive of hypertension The cerebral arteries go into spasm in response to a rapid rise in blood pressure. Edema and ischemia of the brain develop.

Clinically it is characterized by intense headache, visual disturbances, convulsions, loss of consciousness and varying degrees of focal neurological deficits. Prompt reduction of blood pressure completely reverts the attacks and restores the normal state.

This feature distinguishes hypertensive encephalopathy from cerebral infarction or hemorrhage in which the neurological deficit persists.

3.Kidneys:

Atheroma of the renal arteries results in reduction of blood supply to the kidney and progressive loss of renal function.

In malignant hypertension renal function deteriorates rapidly, ending in renal failure.

  1. Retina:

The retinal arterioles undergo changes. These have been graded. The retinal changes give an indication of the progress of hypertension and help to determine the prognosis.

Grades I and II are seen in the early phases of hypertension. Grade III is suggestive of the accelerated phase and grade IV indicates transition to the malignant phase.

Grade I : Arteriolar narrowing and increase in light reflex over the arterioles.

Grade II : Marked arteriolar narrowing and arteriovenous nicking.

Grade III: Grade II + flame-shaped hemorrhages and fluffy (soft) exudates.

Grade IV: Grade III + papilledema.

Once the malignant phase sets in, death occurs within two years as a result of cardiac

failure, renal failure, or cerebral hemorrhage. Prompt treatment arrests the malignant phase and its complications. The retinal changes also regress and revert to Grade II

Hypertensive patients can be classified into risk group A, B and C based on the presence or absence of major risk factors, target organ damage and clinical cardiovascular disease.

Major Risk Factors

  • Smoking
  • Dyslipidemia
  • Diabetes mellitus
  • Age older than 60 years
  • Sex (men and postmenopausal women)
  • Family history of cardiovascular disease.

Life Style Modifications

Lose weight, if overweight

Moderation of alcohol intake to less than 30 ml spirits per day

Increase aerobic physical activity (30-45 minutes on most days of the week, at least five sessions)

Reduce sodium intake to less than 100 mmol per day.

Maintain adequate intake of dietary potassium (90 mmol/day)

Maintain adequate intake of dietary calcium and magnesium for general health.

Stop smoking and reduce intake of dietary saturated fat to below 7% of total calorie intake for overall cardiovascular health.

Relaxation and biofeedback technique– transcendental medication, yoga exercise such as Savasana.

Lifestyle modification brings down blood pressure and also helps to reduce the dosage of drugs needed