Blood pressure normal control

A 40-year-old man, who had taken stavudine 30 mg bd, lamivudine 150 mg bd, and indinavir 800 mg qds, developed an occipital headache, nausea, and vomiting. His blood pressure was 220/140 mmHg and he had bilateral papilledema. His blood pressure was controlled and his symptoms disappeared. An MRI scan of the brain showed lesions in the periventricular white matter the nuclei semiovale and occipital asta were most severely affected. Indinavir was withdrawn and replaced by nel-finavir his blood pressure returned to normal and the MRI white matter lesions disappeared. 

If the bicarbonate level is low, give bicarbonate if the urine output is low, administer a diuretic if the bleeding patient has a sinking blood pressure, make the blood pressure normal. Unfortunately, such interventions are commonly ineffective and even harmful. For example, sepsis—which is a common predecessor of MODS—is often accompanied by hypocalcaemia. In controlled experimental conditions, administering calcium to normalize the laboratory value increases mortality. 

Mean arterial pressure and cardiac output, an expression of the amount of blood that the heart pumps each minute, are the key Indicators of the normal functioning of the cardiovascular system. Mean arterial pressure is strictly controlled, but by changing the cardiac output, a person can adapt, e.g., to increased oxygen requirement due to increased workload. Blood flow in vital organs may vary for many reasons, but is usually due to decreased cardiac output. However, there can be very dramatic changes in blood pressure, e.g., blood pressure plummets during an anaphylactic allergic reaction. Also cytotoxic chemicals, such as heavy metals, may decrease the blood pressure. 

Although blood pressure control follows Ohm s law and seems to be simple, it underlies a complex circuit of interrelated systems. Hence, numerous physiologic systems that have pleiotropic effects and interact in complex fashion have been found to modulate blood pressure. Because of their number and complexity it is beyond the scope of the current account to cover all mechanisms and feedback circuits involved in blood pressure control. Rather, an overview of the clinically most relevant ones is presented. These systems include the heart, the blood vessels, the extracellular volume, the kidneys, the nervous system, a variety of humoral factors, and molecular events at the cellular level. They are intertwined to maintain adequate tissue perfusion and nutrition. Normal blood pressure control can be related to cardiac output and the total peripheral resistance. The stroke volume and the heart rate determine cardiac output. Each cycle of cardiac contraction propels a bolus of about 70 ml blood into the systemic arterial system. As one example of the interaction of these multiple systems, the stroke volume is dependent in part on intravascular volume regulated by the kidneys as well as on myocardial contractility. The latter is, in turn, a complex function involving sympathetic and parasympathetic control of heart rate intrinsic activity of the cardiac conduction system complex membrane transport and cellular events requiring influx of calcium, which lead to myocardial fibre shortening and relaxation and affects the humoral substances (e.g., catecholamines) in stimulation heart rate and myocardial fibre tension. 

Lawton W J, DiBona (2000) Normal blood pressure control and the evaluation of hypertension. In Johnson RJ, Feehally J (eds) Comprehensive clinical nephrology. Mosby, London, pp 37.1-37.11... 

In addition to excess sodium intake, abnormal renal sodium retention may be the primary event in the development of hypertension, and it includes abnormalities in the pressure-natriuresis mechanism. In hypertensive individuals, this theory proposes a shift in the control mechanism preventing the normalization of blood pressure. The mechanisms behind the resetting of the pressure-natriuresis curve may include afferent arteriolar vasoconstriction, decreased glomerular ultrafiltration, or an increase in tubular sodium reabsorption.4 Other theories supporting abnormal renal sodium retention suggest a congenital reduction in the number of nephrons, enhanced renin secretion from nephrons that are ischemic, or an acquired compensatory mechanism for renal sodium retention.9... 

An example of this type of reflex is the baroreceptor reflex (see Figure 1.2). Baroreceptors located in some of the major systemic arteries are sensory receptors that monitor blood pressure. If blood pressure decreases, the number of sensory impulses sent from the baroreceptors to the cardiovascular control center in the brainstem also decreases. As a result of this change in baroreceptor stimulation and sensory input to the brainstem, ANS discharge to the heart and blood vessels is adjusted to increase heart rate and vascular resistance so that blood pressure increases to its normal value. 

Near-normal glycemia reduces the risk of microvascular disease complications, but aggressive management of traditional cardiovascular risk factors (i.e., smoking cessation, treatment of dyslipidemia, intensive blood pressure control, antiplatelet therapy) is needed to reduce macrovascular disease risk. 

As shown in double-blind, placebo-controlled, randomized studies with healthy subjects, both infused [145] and oral [146] L-arg significantly inhibited (by =40%) ADP-induced platelet aggregation in vitro and potentiated platelet cGMP content. The effect, though, was weak the plasma concentration of L-arg required to produce an anti-platelet effect was some 2-fold above normal, steady-state levels, and the oral anti-aggregatory L-arg dose was 4-fold greater than the usual daily L-arg intake in humans. The infused L-arg dose that effectively inhibited platelet activity (30 g total) was hypotensive and increased heart rate, whereas the oral anti-platelet dose (7 g per day over 3 days) did not affect blood pressure, suggestive of oral L-arg platelet selectivity. 

A normal diet contains a sufficient amount of both sodium and potassium. The body has specific mechanisms for regulating the Na ion concentration, which is important in the control of blood pressure (Chapter 22). However, there is less potassium in the normal diet and it may not always be sufficient (e.g. if the sweating rate is high). Fruit and fruit juices are good natural sources of this electrolyte. 

Hypertension is both a cause and a result of CRF. Most dialysis patients are salt and water sensitive. Thus, if one removes salt and water with the dialysis procedure and minimizes weight gain between dialysis with strict dietary control of salt and water intake, normal blood pressure can be achieved. The availability of newer and effective antihypertensive agents has largely replaced the use of bilateral nephrectomy to control the blood pressure. 

Few studies have examined noradrenergic function in patients with phobic disorders. In patients with specific phobias, increases in subjective anxiety and increased heart rate, blood pressure, plasma NE, and epinephrine have been associated with exposure to the phobic stimulus (Nesse et al. 1985). This finding may be of interest from the standpoint of the model of conditioned fear, reviewed above, in which a potentiated release of NE occurs in response to a reexposure to the original stressful stimulus. Patients with social phobia have been found to have greater increases in plasma NE in comparison to healthy controls and patients with panic disorder (Stein et al. 1992). In contrast to panic disorder patients, the density of lymphocyte a-adrenoceptors is normal in social phobic patients (Stein et al. 1993). The growth hormone response to intravenous clonidine (a marker of central a2-receptor function) is blunted in social phobia patients (Tancer et al. 1990). 

Given orally at normal therapeutic doses BDZs have little effect on cardiovascular, respiratory or autonomic function. Respiratory depression and reduced systolic blood pressure may occur but this is seen principally with intravenous administration or overdose. Leucopenia and eosinophilia are rare. There was a suggestion in the early 1980s of increased risk of breast cancer but a subsequent large case-control study refuted this. 

Physiologically, in both normal and hypertensive individuals, blood pressure is maintained by moment-to-moment regulation of cardiac output and peripheral vascular resistance, exerted at three anatomic sites (Figure 11-1) arterioles, postcapillary venules (capacitance vessels), and heart. A fourth anatomic control site, the kidney, contributes to maintenance of blood pressure by regulating the volume of intravascular fluid. Baroreflexes, mediated by autonomic nerves, act in combination with humoral mechanisms, including the renin-angiotensin-aldosterone system, to coordinate function at these four control sites and to maintain normal blood pressure. Finally, local release of vasoactive substances from vascular endothelium may also be involved in the regulation of vascular resistance. For example, endothelin-1 (see Chapter 17) constricts and nitric oxide (see Chapter 19) dilates blood vessels. 

Blood pressure in a hypertensive patient is controlled by the same mechanisms that are operative in normotensive subjects. Regulation of blood pressure in hypertensive patients differs from healthy patients in that the baroreceptors and the renal blood volume-pressure control systems appear to be "set" at a higher level of blood pressure. All antihypertensive drugs act by interfering with these normal... 

All antihypertensive agents act at one or more of the four anatomic control sites depicted in Figure 11-1 and produce their effects by interfering with normal mechanisms of blood pressure regulation. A useful classification of these agents categorizes them according to... 

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