Microvascular volume increases, most strikingly in dependent areas, ie, the bases in upright posture. Careful examination of the cardiac silhouette, evaluation of chamber enlargement, and a search for cardiac calcifications may reveal important etiologic clues.
Echocardiography can help evaluate chamber dimensions, valve function, ejection fraction, wall motion abnormalities, and LV hypertrophy. Doppler or color Doppler echocardiography accurately detects pericardial effusion, intracardiac thrombi, and tumors and recognizes calcifications within the cardiac valves, mitral annulus, and the wall of the aorta. Underlying coronary artery disease is strongly suggested by localized or segmental wall motion abnormalities. Doppler studies of mitral and pulmonary venous inflow are often useful in identifying and quantitating LV diastolic dysfunction.
Other important investigations include a full blood count to in order to exclude anaemia, urea and electrolytes, thyroid function tests, liver function tests and cardiac enzymes if recent infarction is suspected.
Vascular failure.
Circulatory failure of vascular origin occurs in disorder of normal ratio between vascular bed capacity and circulating blood volume. It develops in blood volume decrease (blood loss, dehydration), or in vascular tonus drop. The latter frequently depends on:
1)reflex disturbance of vascular vasomotor innervation in traumas, serous tunic irritation, myocardial infarction, pulmonary artery embolism etc;
2)vascular vasomotor innervation disturbance of cerebral origin (in hypercapnia, acute hypoxia of oliencephalon, psychogenic reactions);
З) vascular paresis of toxic origin, which is observed in plural infections and intoxications.
Vascular tonus drop leads to disorder of body blood distribution: deposited blood volume increases, particularly in vessels of abdominal viscera, and circulating blood volume decreases. Circulating blood volume decrease involves decrease of the heart venous return, decrease of stroke volume, decrease of arterial and venous pressures. Vascular circulatory failure may be acute and in this case is called collapse. Circulating blood volume decrease and arterial pressure fall leads to cerebral ischemia, hence such symptoms as dizziness (vertigo), blackout, ringing in patient‘s ears are characteristic for
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acute vascular failure; loss of consciousness is frequently observed. On physical examination pallor, diaphoresis, extremity coldness, quick hypopnoe, weak, sometimes thready pulse, blood pressure fall are noticed.
Syncope refers to acute vascular failure manifestations, it is transitory loss of consciousness due to insufficient cerebral blood supply. Syncope may appear in over fatigue, frightened condition, stuffy rooms. It is caused by central nervous regulation disorder of vascular tonus, leading to blood accumulation in abdominal vessels. In syncope pallor, diaphoresis, extremity coldness, weak or thready pulse are noticed.
In some people inclination to syncope is observed in change of supine position to vertical, especially in young asthenics, more frequently in women. Over fatigue, anemia, carried-out infectious disease are predisposing factors. Such syncope is called orthostatic collapse. It is explained by insufficiently fast reaction of vasomotor apparatus, owing to that in patient‘s position change the blood rushes from upper body half into lower extremities and abdominal cavity vessels.
HYPERTENSION
Arterial hypertension is elevation of systolic (systolic BP >= 140 mm Hg) and/or diastolic BP (>= 90 mm Hg,), either primary or secondary, which can damage the walls of arteries, arterioles and the left ventricle of the heart with serious consequences, chiefly affecting the brain, heart, kidneys and eyes.
Prevalence
It is one of the most common disorders in the Western world, with a prevalence of about 15%.
It is estimated that there are nearly 50 million hypertensives in the USA and about 27 % of all patients with cardiovascular disease in Russia. Hypertension occurs more often in black adults (32%) than in white (23%) adults, and morbidity and mortality are greater in blacks. Diastolic BP increases with age until age 55 or 60.
Prevalence of isolated systolic hypertension (ISH-- >= 140 mm Hg systolic, < 90 mm Hg diastolic) increases with age until at least age 80. If persons with ISH and diastolic hypertension are considered, > 50% of black and white men and > 60% of women over age 65 have hypertension. ISH is more prevalent among women than men in
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both races. Between 85 and 90% of cases are primary (essential); in 5 or 10%, hypertension is secondary to bilateral renal parenchymal disease or endocrinopathy , and only 1 or 2% of cases are due to a potentially curable condition.
Etiology and Pathogenesis
Primary hypertension: Primary (essential) hypertension is of unknown etiology; its diverse hemodynamic and pathophysiologic derangements are unlikely to result from a single cause. The term ―hypertensive disease is used in Russia.
Heredity is a predisposing factor, as shown by the relevance of a family history of hypertension and by racial variations in prevalence. but the exact mechanism is unclear. Environmental factors (eg, dietary Na, obesity, stress) seem to act only in genetically susceptible persons.
The pathogenic mechanisms must lead to increased total peripheral vascular resistance (TPR) by inducing vasoconstriction, to increased cardiac output (CO), or to both because BP equals CO (flow) times resistance. Although expansion of intravascular and extravascular fluid volume is widely claimed to be important, such expansion can only raise BP by increasing CO (by increasing venous return to the heart), by increasing TPR (by causing vasoconstriction), or by both; it frequently does neither.
Abnormal Na transport across the cell wall due to a defect in or inhibition of the Na-K pump (Na+,K+-ATPase) or due to increased permeability to Na+ has been described in some cases of hypertension. The net result is increased intracellular Na, which makes the cell more sensitive to sympathetic stimulation. Because Ca follows Na, it is postulated that the accumulation of intracellular Ca (and not Na per se) is responsible for the increased sensitivity. Na+,K+-ATPase may also be responsible for pumping norepinephrine back into the sympathetic neurons to inactivate this neurotransmitter. Thus, inhibition of this mechanism could conceivably enhance the effect of norepinephrine. Defects in Na transport have been described in normotensive children of hypertensive parents.
Stimulation of the sympathetic nervous system raises BP, usually more in hypertensive or prehypertensive patients than in normotensive patients. Whether this hyperresponsiveness resides in the sympathetic nervous system itself or in the
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myocardium and vascular smooth muscle that it innervates is unknown, but it can often be detected before sustained hypertension develops. A high resting pulse rate, which can be a manifestation of increased sympathetic nervous activity, is a well-known predictor of subsequent hypertension. Some hypertensive patients have a higher-than-normal circulating plasma catecholamine level at rest, especially early in clinical development.
In the renin-angiotensin-aldosterone system, the juxtaglomerular apparatus helps regulate volume and pressure. Renin, a proteolytic enzyme formed in the granules of the juxtaglomerular apparatus cells, catalyzes conversion of the protein angiotensinogen to angiotensin I. This inactive product is cleaved by a converting enzyme, mainly in the lung but also in the kidney and brain, to angiotensin II, which is a potent vasoconstrictor that also stimulates release of aldosterone. Also found in the circulation, the angiotensin III is as active as angiotensin II in stimulating aldosterone release but has much less pressor activity.
Renin secretion is controlled by at least four mechanisms that are not mutually exclusive: A renal vascular receptor responds to changes in tension in the afferent arteriolar wall; a macula densa receptor detects changes in the delivery rate or concentration of NaCl in the distal tubule; circulating angiotensin has a negative feedback effect on renin secretion; and the sympathetic nervous system stimulates renin secretion via the renal nerve mediated by receptors.
The mosaic theory states that multiple factors sustain elevated BP even though an aberration of only one was initially responsible; eg, the interaction between the sympathetic nervous system and the renin-angiotensin-aldosterone system. Sympathetic innervation of the juxtaglomerular apparatus in the kidney releases renin; angiotensin stimulates autonomic centers in the brain to increase sympathetic discharge. Angiotensin also stimulates production of aldosterone, which leads to Na retention; excessive intracellular Na enhances the reactivity of vascular smooth muscle to sympathetic stimulation.
Hypertension leads to more hypertension. Other mechanisms become involved when hypertension due to an identifiable cause (eg, catecholamine release from a pheochromocytoma, renin and angiotensin from renal artery stenosis, aldosterone from an
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adrenal cortical adenoma) has existed for some time. Smooth muscle cell hypertrophy and hyperplasia in the arterioles resulting from prolonged hypertension reduce the caliber of the lumen, thus increasing TPR. In addition, trivial shortening of hypertrophied smooth muscle in the thickened wall of an arteriole will reduce the radius of an already narrowed lumen to a much greater extent than if the muscle and lumen were normal. This may be why the longer hypertension has existed, the less likely surgery for secondary causes will restore BP to normal.
Deficiency of a vasodilator substance rather than excess of a vasoconstrictor (eg, angiotensin, norepinephrine) may cause hypertension. The kallikrein system, which produces the potent vasodilator bradykinin, is beginning to be studied. Extracts of renal medulla contain vasodilators, including a neutral lipid and a prostaglandin; absence of these vasodilators due to renal parenchymal disease or bilateral nephrectomy would permit BP to rise. Modest hypertension sensitive to Na and water balance is characteristic for anephric persons (renoprival hypertension).
Endothelial cells produce potent vasodilators (nitric oxide, prostacyclin) and the most potent vasoconstrictor, endothelin. Therefore, dysfunction of the endothelium could have a profound effect on BP. The endothelium's role in hypertension is being investigated. Evidence that hypertensive persons have decreased activity of nitric oxide is preliminary.
Secondary hypertension: Secondary hypertension is associated with renal parenchymal disease (eg, chronic glomerulonephritis or pyelonephritis, polycystic renal disease, collagen disease of the kidney, obstructive uropathy) or pheochromocytoma, Cushing's syndrome, primary aldosteronism, hyperthyroidism, myxedema, coarctation of the aorta, or renovascular disease. It may also be associated with the use of excessive alcohol, oral contraceptives, sympathomimetics, corticosteroids, cocaine, or licorice.
Hypertension associated with chronic renal parenchymal disease results from combination of a renin-dependent mechanism and a volume-dependent mechanism. In most cases, increased renin activity cannot be demonstrated in peripheral blood, and careful attention to fluid balance usually controls BP.
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