You are currently viewing Hypertension “A Silent Killer”

Hypertension “A Silent Killer”

HYPERTENSION OR “THE SILENT KILLER“

Hypertension or high blood pressure is a very common and serious condition that can lead to or complicate many health problems. The risk of cardiovascular morbidity and mortality is directly correlated with blood pressure. Risks of stroke, MI, angina, heart failure, kidney failure, or early death from a cardiovascular cause are directly correlated with BP.

Hypertension is often called “the silent killer” because it generally has no symptoms until serious complications develop. There are three general types of hypertension. Essential or primary hypertension occurs when the condition has no known cause. This form of hypertension cannot be cured, but it can be controlled. More than 90% of individuals with hypertension have essential hypertension. Genetic factors may play an important role in the development of essential hypertension. When hypertension is caused by another condition or disease process, it is called secondary hypertension. Fewer than 10% of patients have secondary hypertension; where either a co-morbid disease or drug is responsible for elevated BP. In most of these cases, renal dysfunction resulting from severe chronic kidney disease or renovascular disease is the most common secondary cause.

Hypertension has a variety of causes. Blood pressure generally tends to rise with age. Hypertension can also be caused by other medical conditions, such as thyroid disease or chronic kidney disease. Hypertension may also be a side effect of certain medications, such as over-the-counter cold medications and oral contraceptives, and other hormone drugs.

Obesity, heredity, and lifestyle also play a role in the development of hypertension. When symptoms do occur, they can differ between individuals depending on such factors as the level of blood pressure, age, underlying cause, medical history, the presence of complications, and general health. For more information on symptoms and complications, refer to symptoms of hypertension.

Diagnosis of hypertension includes performing a complete evaluation that includes a medical history and physical examination and a series of blood pressure readings. Systolic blood pressure is a stronger predictor of cardiovascular diseases than diastolic blood pressure in adults ≥ 50 years of age and is the most important clinical blood pressure parameter for most patients. Patients with diastolic blood pressure value less than 90 mmHg and systolic blood pressure values ≥ 140 mmHg have isolated systolic hypertension. Many people think of a reading of 120/80mmHg as “normal”. There are many variations of normal that are dependent on a variety of factors. As a very general guide, adults should keep their blood pressure below 140/90mmHg. Also, current guidelines consider consistent readings over 120/80mmHg as a condition called pre-hypertension, which should be monitored and addressed to ensure that blood pressure does not rise higher over time. It is very possible that a diagnosis of hypertension can be missed or delayed because there are generally no symptoms in the early stages. Patient compliance with a good treatment plan generally results in a normalization of blood pressure and also minimizes complications.

The heart is relatively small, roughly the same size as your closed fist. Heart rest on the diaphragm, near the midline of the thoracic cavity. It lies in the mediastinum, a mass of tissue that extends from the sternum to the vertebral column between the lungs. The human heart is covered by a double-walled covering called the pericardium. The membrane that surrounds and protects the heart is the pericardium. It confines the heart to its position in the mediastinum while allowing sufficient freedom of movement for vigorous and rapid contraction. The pericardium consists of two parts; the fibrous pericardium and the serous pericardium. The superficial fibrous pericardium is composed of tough, inelastic dense irregular connective tissue. The fibrous pericardium prevent overstretching of the heart, provide protection

BLOOD PRESSURE (BP)

Blood pressure (BP) is defined as lateral pressure exerted by the blood on the walls of the blood vessels while flowing through them. Blood pressure in a blood vessel depends upon two things.

1) Distance from the heart.

2) Nature of the blood vessel.

Blood pressure is more in blood vessels close to the heart. Blood pressure is more in the arterial system than in the venous system. This is because the walls of arteries are thicker and less elastic; the walls of the veins are thinner and more elastic.

Normal blood pressure is 120/80 mmHg, Systolic BP (SBP) is the maximum BP during the ventricular systole- 120 mmHg. Range: 110-130 mmHg

Diastolic BP (DBP) is the minimum pressure during the ventricular diastole. It is 80 mmHg. Range: 70-90 mmHg

Plus pressure (PP) means the difference between systolic BP and diastolic BP. ie, 40 mmHg., SBP: DBP: PP = 3:2:1

Mean arterial blood pressure

It is not the arithmetic mean but it is less than that. It is because most of the time BP is closer to diastolic value than systolic value. It because the duration of ventricular diastole is longer than the duration of systole.

Mean arterial BP=Diastolic BP+1/3 of pulse pressure i.e., 80+13=93 mmHg.

Physiological Variations

Age: BP more in adults than in children.

Sex: BP more in males than females.

Pregnancy: During the later stages of pregnancy BP usually increases.

Altitude: BP is higher in people living at higher altitudes.

Exercise: Systolic BP increases during exercise.

Emotion: BP rises during emotional expressions.

Sleep: BP falls during sleep

Factor Affecting Blood Pressure

1) Volume of blood.

2) Force of contraction of the heart.

3) Heart rate and BP are inversely proportional.

4) Viscosity of blood.

5) Nature of the blood.

6) Elasticity of blood vessel

REGULATION OF BLOOD PRESSURE

It means maintaining constant blood pressure within a narrow variation. Both increases in blood pressure (hypertension) and a decrease in blood pressure(hypotension) are harmful in the body.

The mechanism of regulation of BP is divided into two groups.

1) Rapidly acting mechanism

2) Slow acting mechanism

1. Rapidly acting mechanism

This includes both nervous regulations as well as endocrine or hormonal regulation.

2. Nervous Regulation of BP

The smooth muscles of blood vessels will always remain in a state of contraction. Because of this, the blood vessels remain in a state of constriction-vasoconstriction. The degree of vasoconstriction depends upon the sympathetic tone. When sympathetic tone increases the degree of vasoconstriction will also increase. When vasoconstriction increases total peripheral resistance (TPR) wills increases which will in turn increase BP. Suppose the BP increases that will be detected by the baroreceptors situated at the aortic arch and carotid sinus. These baroreceptors will send impulses to the medulla oblongata. In the medulla oblongata, there is a group of nervous concerned with the control of BP. It is known as the vasomotor center. There are two different areas, the pressor area, and the Depressor area. These impulses coming from baroreceptors will inhibit the pressor area; this will decrease the sympathetic tone. This will increase vasodilatation. TPR decreases so BP decreases to a normal level. This mechanism operated very fast. It corrects BP within a few seconds.

HYPERTENSION

Hypertension is defined as abnormally high blood pressure (more than 120/80 mm Hg) in the arteries. A persistent increase in systemic arterial blood pressure is known as hypertension. Usually, a mean arterial pressure greater than 110mm Hg under resting conditions is considered to be hypertensive; this level normally occurs when the diastolic blood pressure is greater than 90 mm Hg and the systolic pressure is greater than about 135-140 mm Hg. Hypertension is generally symptomless but increases the risk of various other cardiovascular diseases like stroke, heart attack, and non-cardiovascular diseases like renal damage, end-stage renal failure, etc.

Although hypertension is a common health problem with sometimes devastating consequences, it often remains asymptomatic until late in its course. A sustained diastolic pressure greater than 90 mm Hg, or a sustained systolic pressure above 140 mm Hg, is considered to constitute hypertension90-95% of hypertension is idiopathic (essential hypertension), which is compatible with long life, unless a myocardial infarction, cerebrovascular accident, or other complication supervenes. Most of the remainder of “benign hypertension” secondary to renal disease or, less often to narrowing of the renal artery, usually by an atheromatous plaque (renovascular hypertension). Infrequently, hypertension is secondary to diseases of the adrenal glands, such as primary aldosteronism, Cushing syndrome, pheochromocytoma, or other disorders. Various determinants play an important role in hypertensive conditions and causation of premature cardiovascular risk over and beyond hypertension.

THE COMMON DETERMINANTS

  1. Age and sex: BP generally rises with age in both males and females. The rise is steeper in middle age and thereafter. In the initial phase, the pressure is more in men while in the later phase rise is more in women.
  2. Weight: the rise in BP with respect to weight is found to be directly proportional.
  3. Alcohol consumption: it is also reported that alcohol intake positively increase BP, but the reason is not clear
  4. Geographic variation: geographical variation can affect BP via variable contributing factors like TPR, hypoxia, primitive condition, etc.
  5. Smoking: tobacco combustion results in nicotine and carbon monoxide production, a potent vasoconstrictor leading to the development of hypertension.
  6. Salt consumption: Salt intake can promote rigidity to vascular smooth muscle and therefore excessive salt intake (more than 8 -10 gm per day) may result in hypertension.
  7. Genetic predisposition: Based upon the survey it is now believed that hypertension may be the result of typical genetic makeup.

TYPES OF HYPERTENSION

Category pressure Systolic pressure mm Hg Diastolic pressure mm Hg

Normal 90–119 60-79

Pre-hypertension 120–139 80–89

Stage 1 140–159 90–99

Stage 2 ≥160 ≥100

Isolated systolic Hypertension ≥140 <90

 

It is divided into two types

1) Primary hypertension (Essential hypertension)

2) Secondary hypertension (Non-essential hypertension)

PRIMARY HYPERTENSION

It results when arterial blood pressure is increased due to increased peripheral resistance. It is further divided into two types namely: benign and malignant hypertension

 Benign hypertension

Here, there is a moderate increase in blood pressure with systolic pressure of 200 mm Hg and a diastolic pressure of above 100 mm Hg. However, in resting condition and sleep, the blood pressure returns to a normal level. Later, if there is an increase in blood pressure it will not come back to normal level in resting conditions.

 Malignant hypertension

Here, the blood pressure elevated to a great extends of about 250 mm Hg of systolic pressure and 150 mm Hg of diastolic pressure. It produces severe symptoms like renal disease, retinal disease, and is a fatal disease, it causes death within a few years.

Some of the characteristics of primary or essential hypertension are,

1) The mean arterial pressure is increased by 40-60 %.

2) The renal blood flow in the later stages is decreased about one-half of normal.

3) The resistance to blood flow through the kidney is increased 2-4 fold.

4) The kidneys will not excrete adequate amounts of salt and water unless the arterial pressure is high.

SECONDARY HYPERTENSION

The different forms of secondary hypertension are:

Cardiovascular hypertension

It is produced due to

  1. Atherosclerosis- hardening and narrowing of blood vessels
  2. Coarctation of the aorta- narrowing of the aorta.

 Renal hypertension

It is produced due to

  1. Stenosis renal arteries- narrowing of one or both renal arteries, so that the renal function is impaired.
  2. Glomerulonephritis- nephritis with inflammation of the capillary loops in the renal glomeruli.

 Endocrine hypertension

It occurs due to

  1. Pheochromocytoma- tumor in adrenal medulla
  2. Hyperaldosteronism- excess secretion of aldosterone from adrenal cortex Conn’s syndrome.
  3. Cushing’s syndrome- excess secretion of cortisone.
  4. Gigantism or Acromegaly- excess secretion of growth hormone.

 Neurogenic hypertension

Acute hypertension can be caused by strong stimulation of the sympathetic nervous system.

  1. Section of the baroreceptors nerves.
  2. Lesions in tractus solitarius
  3. Increased intracranial pressure

EFFECT OF HYPERTENSION

The common organ damage by long-standing hypertension is the heart, blood vessels, retina, and central nervous system.

  1. CVS: Increased myocardial work leads to concentric hypertrophy of the left ventricle, angina pectoris, and accelerated coronary artery diseases. There is systolic as well as diastolic dysfunction.
  1. Kidneys: Progressive arteriosclerosis involves both the efferent and afferent renal arterioles and capillaries of the glomerular tuft. This leads to compromise in renal function, shrinkage of kidneys, proteinuria.
  2. CNS: Hypertension may cause microaneurysms, which may rupture and cause cerebral hemorrhage.

Accelerated atherosclerosis may cause cerebral thrombosis, embolism, and infection. Cerebral arteriolar spasm may cause hypertensive encephalopathy.

  1. Fundus: The following changes may occur:
  • Grade I: Arteriolar narrowing leading to copper wire and silver wire appearance.
  • Grade II: Arteriovenous nipping where arteries cross the vein.
  • Grade III: In addition to Grade II changes, superficial flame-shaped and deep dot-like hemorrhages and cotton wool exudates.
  • Grade IV: Grade III change with papilledema.

SYMPTOMS [17,18]

The clinical features may be due to the elevated BP itself, target organ involvement, or due to underlying diseases, as in secondary hypertension.

 Symptoms due to hypertension:

  1. Headache: This occurs usually in the morning hours. It is throbbing and usually frontal.
  2. Dizziness: The patients feel unsteady.
  3. Epistaxis: This occurs due to increased pressure, causing rupture of the capillaries of the nose. The bleeding reduces circulating volume and lowers the BP

Symptoms due to the affection of organs

  1. CVS:
  2. Dyspnea on exertion (insipient LVF)
  3. Anginal chest pain (IHD)
  4. Palpitation
  5. Kidneys: Hematuria, nocturia, polyuria
  6. CNS:
  7. Transient ischemic attacks (TIA or stroke) with focal neurological deficit.
  8. Hypertensive encephalopathy (headache, vomiting, convulsion, unconsciousness, focal neurological deficit).
  9. Dizziness, tinnitus, and syncope.
  10. Retina: Blurred vision or sudden blindness.

INVESTIGATIONS

To assess target organ damage

X-ray of a chest for heart size, ECG for LV hypertrophy and evidence of IHD., Echocardiogram for LV systolic and diastolic functions., Urinalysis- proteinuria > 200 mg/ day and hematuria suggest renal involvement.

To detect the cause of hypertension

  1. X-ray chest-

Rib notching suggests coarctation of the aorta. , Mediastinal widening suggests aortic dissection.

  1. Imaging of the abdomen

3.Angiography

TREATMENT [31, 32, 33, 38, 41] FOR HYPERTENSION

ANTIHYPERTENSIVE DRUGS

As arterial pressure is a product of cardiac output and peripheral vascular resistance, it can be lowered by the action of a drug on either the peripheral resistance or cardiac output, or both. Drugs may be reduced cardiac output by either inhibiting myocardial contractility or decreasing ventricular filling pressure. Reduction in ventricular filling pressure may be achieved by action on the venous tone or blood volume via renal effect. Drugs can reduce peripheral resistance by acting on smooth muscle to relax of resistance vessel or by interfering with the activity of systems that produced constriction of the resistance vessel (e.g., the sympathetic nervous system)  The simultaneous use of a drug with a similar mechanism of action and hemodynamic effects often produces little additional benefit. However, concurrent use of a drug from different classes is a strategy for achieving effective control of blood pressure while minimizing the dose-related adverse effects.

NON-PHARMACOLOGICAL MANAGEMENT OF HYPERTENSION

In the initial phase of hypertension (high, normal, or mild hypertension), the non-pharmacological measures can lower the B.P. in most individuals. in some patients, who do not show any reduction even after 04-06 months need drug therapy. it is a harmless treatment and helpful either to eliminate the requirement of drug or reduce the dose as well as dose regiment. Non pharmacological approaches to the reduction of blood pressure generally are advisable as the initial approach to the treatment of patients with diastolic blood pressure in the range of 90 to 95 mmHg. Further, these approaches will augment the effectiveness of pharmacological therapy in patients with higher-level blood pressure. Non-pharmacological methods to lower blood pressure allow the patient to participate actively in the management of his or her disease. Reduction of weight, restriction of salt, and moderation in the use of alcohol may be reduced blood pressure and improve the effectiveness of drug treatment. In addition, regular isotonic exercise also lowers blood pressure in hypertensive patients.

Smoking per se does not cause hypertension. However, smokers do have a higher incidence of malignant hypertension, and smoking is a major risk factor for coronary heart disease. Hypertensive patients have an exceptionally great incentive to stop smoking. Consumption of caffeine can raise blood pressure and elevate plasma concentrations of norepinephrine, but long-term consumption of caffeine causes tolerance to these effects and has not been associated with the development of hypertension.

Reduction of Body Weight Obesity and hypertension are closely associated, and the degree of obesity is positively correlated with the incidence of hypertension. Obese hypertensives may lower their blood pressure by losing weight regardless of a change in salt consumption. The mechanism by which obesity causes hypertension is unclear but increases the secretion of insulin in obesity could result in insulin-mediated enhancement of renal tubular reabsorption of Na+ and an expansion of extracellular volume. Obesity is also associated with increased activity of the sympathetic nervous system. A combination of aerobic physical exercise and dietary counseling may enhance compliance.

Sodium Restriction

Severe restriction of salt will lower the blood pressure in most hospitalized hypertensive patients; this treatment method was advocated before the development of effective antihypertensive drugs. However severe salt restriction is not practical from a standpoint of compliance. Several studies have shown that moderate restriction of salt intake to approximately 5 g per day (2 g Na+) will, on average, lower blood pressure by 12 mm Hg systolic and 6 mm Hg diastolic. An additional benefit of salt restriction is improved responsiveness to some antihypertensive drugs.

Alcohol Restriction

Consumption of alcohol can raise blood pressure, but it is unclear how much alcohol must be consumed to observe this effect. Heavy consumption of alcohol increases the risk of cerebrovascular accidents but not coronary heart disease. In the fact, a small amount of ethanol has been found to protect against the development of coronary artery disease. The mechanism by which alcohol raises blood pressure is unknown, but it may involve increased transport of Ca2+ into vascular smooth muscle cells. Excessive intake of alcohol also may result in poor compliance with antihypertensive regimens. All hypertensive patients should be advised to restrict consumption of ethanol to more than 30 ml per day.

Physical Exercise

Increased physical activity lowers rates of cardiovascular disease in men. It is not known if this beneficial effect is secondary to an antihypertensive response to exercise. Lake of physical activity is associated with a higher incidence of hypertension. Regular isotonic exercise reduces blood volume and plasma catecholamines and elevates plasma concentration of atrial natriuretic factor. The beneficial effect of exercise can occur in subjects who demonstrate no change0 in body weight or salt intake during the training period.

Relaxation and Biofeedback therapy

The fact that long term stressful stimuli can cause sustained hypertension in animals has given credence to the possibility that relaxation therapy will lower blood pressure in some hypertensive patients. Only those few patients with mild hypertension who wish to use this method should be encouraged to try, and these patients should be closely followed and receive pharmacological treatment if necessary.

Diet Lacto vegetarian diet and high intake of polyunsaturated fish oils lower BP due to the high content of potassium and vegetable diet high content of fiber. Natural vegetables containing high levels of potassium, which lower the BP by:

  1. Increased sodium excretion.
  2. Decreased sympathetic activity.
  3. Decreased renin-angiotensin secretion and direct dilation of renal arteries.

References

  1. Robbins Basic Pathology, 7th Edition, 338-341, 704,705.
  2. Pathophysiology, Dr. S.L. Bodhankar, and Dr.N.S.Vyawahare, 2.17-2.22.
  3. Lippincott’s Illustrated Reviews, Pharmacology, 2nd Edition, 179-192,227.
  4. Text Book of Physiology, Dr. A.P.Krishna, 61-92.
  5. Goodman and Gillman’s- The Pharmacological Basis of Therapeutics, 10th edition, 871,872,895,896.
  6. Text Book of Pathology, Harshmohan, 5th edition, 708,709.
  7. Pharmacotherapy, a Pathophysiological Approach, Joseph. J. Dippiro, 7th edition149-169,280-283,1031,1032,
  8. Principles of Anatomy and Physiology, Gerard. J. Tortora and Bryan Derrickson,696-703,750-756,798,799.
  9. Harrison’s Principles of Internal Medicine, 17th edition, volume-II, 1365-1387.
  10. Roger Walker, Clive Edward, Clinical Pharmacy and Therapeutics, 3rd edition, 265-275.
  11. Ross and Wilson, Anatomy and Physiology in Health and Illness, 10th edition, 80-92.
  12. Essentials of medical pharmacology, K.D.Tripathi, 6th edition, 135,142,486,489,539-553,564,566,570.
  13. Pharmacology and Pharmacotherapeutics, R.S. Sathoskar, 20th edition, 402-431.
  14. Modern Patient Counseling, Dr. R.S. Gaud, and Prof. P.Toke, 24.1-24.7.
  15. Pathophysiology, Dr. Prakash Ghadi, 188-195.
  16. Concise Medical Physiology, Sujit. K.Chaudhuri, 177-180.
  17. Devin K. Binder etal ‘Idiopathic Intracranial Hypertension’, Neurosurgery; Volume-54, Number 3, March 2004; 538-552.
  18. Martin Thomas, ‘Hypertension- clinical features and investigation’, Hospital Pharmacist (Special features), Volume-14, April 2007; 111-116.
  1. S.Y. Hsiao etal ‘Prevalence, awareness, treatment, and control of hypertension in Taiwan’, Journal of human hypertension; Volume- 15, March 2001, 793-798.
  1. Amira Peco-Antic etal ‘Severe renovascular hypertension in an infant with congenital solitary pelvic kidney’

This Post Has 12 Comments

  1. Mahnoor Khalid

    Highly informative👍

    1. Faheem

      Thank you

  2. Anonymous

    👍👍

  3. Dr waheed

    Great job

  4. Dr waheed

    Great job indeed, it is so informative nd simple to understand

    1. Faheem

      Thanks alot Dr Waheed

  5. Namra Sohail.

    Good job.. Great information

    1. Faheem Zaman

      Thank you

  6. Anonymous

    Friutfull…masha allah keep it up bro..

  7. Anonymous

    Very informative

    1. Anonymous

      Thanks alot Doc

Leave a Reply