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Hypertension Exercise Program

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Hypertension Exercise Program Summary


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Section I Hypertension

Arterial Hypertension 705 Importance of the Arterioles in Hypertension Enhanced Sensitivity of Arterioles to Vasoconstrictor Stimuli in Hypertension Impaired Relaxation of Arterioles to Vasodilator Stimuli Structural Alterations in Arterioles during Hypertension Arteriolar Rarefaction Oxidative Stress and Arteriolar Function in Hypertension Dietary Salt Intake and Arteriolar Function Influence of Gender on Arteriolar Function in Hypertension Capillary and Venular Responses to Arterial Hypertension 713

Initial diagnostic evaluation of hypertension

Only 1-2 of all hypertensive patients will prove to have a secondary cause of hypertension. Age of onset greater than 60 years, age of onset less than 20 in African-American patients, or less than 30 in white patients suggests a secondary cause. Blood pressure that is does not respond to a three-drug regimen or a sudden acceleration of blood pressure suggests secondary hypertension. Evaluation of Secondary Hypertension Renovascular Hypertension IV. Non-pharmacologic treatment of hypertension A. Lifestyle modification 1. The mean drop in blood pressure with lifestyle modification is 9 mm Hg. Weight loss, in the range of 10 pounds, can lead to a significant reduction in blood pressure. Exercise should consist of a minimum of 30 minutes of brisk walking, 3 times per week. Limitation of liquor to 2 oz a day has been shown to reduce blood pressure.

Pseudomalignant hypertension

Elderly patients with diabetes or renal failure and diffuse vascular disease can occasionally develop a condition called 'pseudomalignant hypertension' ( Messerii.,. 1985). As a result of advanced atherosclerosis, their blood vessels become relatively non-compressible. This makes it very difficult, and sometimes impossible, to measure an accurate cuff blood pressure and can result in artefactually elevated blood pressure measurements. There are numerous case reports of such patients receiving unnecessarily aggressive antihypertensive agents in efforts to control their artefactual hypertension, which even result in shock or cardiac arrest of the patient. In such cases, intra-arterial catheter monitoring shows the true pressure to be much lower than that measured by sphygmomanometry. These patients can

Perioperative hypertension

Intraoperative and immediate postoperative severe hypertension is usually associated with systemic vasoconstriction with relative intravascular hypovolemia. It is generally best treated with a vasodilator ( Ha. p.ern.199.5). In patients with ischemic heart disease, it is important to limit heart rate to avoid increased myocardial ischemia. Nitrovasodilators are generally first-line therapy for perioperative hypertension. Intravenous b-blockers can be cautiously used to control heart rate, recognizing that they can also depress myocardial contractility. Other options include dihydropyridine or calcium-channel blockers such as nicardipine or isradipine.

Uncomplicated severe hypertension

Many more patients are seen with transient asymptomatic hypertension than with a hypertensive emergency or urgency. The hypertension is generally related to other conditions such as pain, anxiety, withdrawal symptoms, or as a compensatory response to mild intravascular volume loss. If the patients are asymptomatic, not perioperative, and without active bleeding, the prognosis is stable and the underlying disorder is the focus of care. Such patients are at greater risk from excessive hypotension resulting from the unnecessary use of antihypertensive agents than from the hypertension itself ( F.ag. 0 1989). The approach is to treat the patient, not the blood pressure. Close follow-up is important, rather than the immediate initiation of antihypertensive therapy. Antihypertensive agents Table 3 and Table 4 list by category agents most commonly used to treat severe hypertension. Table 2 gives medical conditions for which each agent is mainly used. Table 3 Parenteral agents for severe...

Etiology and classification of pulmonary hypertension

Pulmonary hypertension is the consequence of either acute or chronic athological mechanisms resulting in a loss of the independence of pulmonary artery pressure and cardiac output. Although pulmonary hypertension can be characterized by more or less arbitrary pulmonary artery pressure limits under static conditions, it is Table 1 Definition of pulmonary hypertension Pulmonary hypertension can be differentiated by (a) its underlying pathophysiological mechanism ( Table.2), (b) clinically by its pulmonary or extrapulmonary origin (Table 3), or (c) its anatomical location (i.e. pre- or postcapillary). Many pathological conditions can eventually result in pulmonary hypertension, but in the intensive care unit (ICU) most patients develop pulmonary hypertension in relation to the acuteness of the underlying disease. Other patients, in whom pulmonary hypertension is either latent or develops subacutely, are clinically asymptomatic unless severe structural changes in pulmonary vasculature...

Primary pulmonary hypertension

This diagnosis is established when no evidence of a secondary cause can be established. The pulmonary artery wedge pressure should be normal ( TabieJ,). Although etiology cannot be attributed to any single disorder, the predominant target group, young women of childbearing age, is rather homogenous with a mostly fatal outcome. The pulmonary arteriopathy with plexiform lesions, pronounced intimal proliferation, and medial hypertrophy are not exclusive to primary pulmonary hypertension but can also be found in chronic thromboembolism. Evidence exists that a reduced fibrinolytic activity promotes thrombosis leading to vascular obstruction. Deposits of immune complexes, fibrin deposits, and lymphocytic infiltration are demonstrable. In the etiology of primary pulmonary hypertension, a familial predisposition has been demonstrated in some cases, as well as an association with certain drugs (e.g. oral contraceptives, sulfonamides, and antiarrhythmic drugs). Primary pulmonary hypertension...

Secondary causes of chronic pulmonary hypertension

Chronic pulmonary hypertension develops when the underlying disease is not diagnosed because the pathophysiological changes are mild and do not result in clinical symptomatology (e.g. congenital heart diseases, thromboembolic disease), or when the primary disease becomes chronic despite adequate therapy (e.g. inflammatory or infectious diseases). The pathophysiological alterations of the pulmonary circulation are progressive and are mainly determined by the time course of vascular remodeling. All entities except primary pulmonary hypertension result in pulmonary hypertension secondary to an underlying disease ( Table.3).

Pathophysiological consequences of pulmonary hypertension

Exertional shortness of breath may represent the first discrete clinical symptom of pulmonary hypertension. Dyspnea at rest and pathologic heart sounds, particularly a loud secondary pulmonary sound, indicate advanced-stage pulmonary hypertension. Under experimental conditions, pulmonary artery pressures increase when more than two-thirds of the vascular bed is occluded. In patients with a thromboembolic episode, a 70 per cent obstruction of the vascular bed is still compatible with life. When pulmonary hypertension results from increased pulmonary blood flow or pulmonary venous congestion, such as with a ventricular septal defect, the right heart slowly adapts to the slow rise in vascular resistance and responds by hypertrophy. When pulmonary artery and systemic pressures eventually equalize, the left-to-right direction of blood flow through the shunt reverses (Eisenmenger syndrome) and a further increase in vascular resistance due to hypoxemia results in right ventricular failure....

Essential Hypertension

Approximately 50 of patients with essential hypertension are insulin resistant hyperinsulinemic 75 , and it is this subset of patients with essential hypertension that have the atherogenic lipoprotein phenotype characteristic of individuals with the IRS high TG and low HDL-C concentrations, smaller and denser LDL-particles, and an exaggerated degree of postprandial lipemia 69 . Furthermore, there is evidence that it is these patients in whom essential hypertension is present as a component of the IRS that are at the greatest CVD risk 76-79 . The importance of the link between the dyslipidemia present in insulin-resistant hyperinsulinemic patients with essential hypertension and CVD has received considerable support from results of the Copenhagen Male Study. In one publication 78 , Jeppesen and colleagues demonstrated that blood pressure, per se, was less predictive of CVD in individuals with the characteristic dyslipidemia of the IRS - a high TG and a low HDL-C concentration - than in...

Types And Causes Of Hypertension

Essential or primary hypertension is defined as a medical condition denoted by consecutive high (above 140 90 mmHg) blood pressure readings in the absence of a known causal disease.14 It is the result of elevated arterial pressure associated with increased cardiac output, total peripheral resistance, or both.15 Unfortunately, mystery exists about the causes and treatment of this form, even though 95 of all hypertensive patients have essential hypertension.9 Primary hypertension affects approximately one-third of the world's adult population.4 Secondary hypertension is the sudden onset of high blood pressure in children or people over the age of 50.9 A mere 5 of those with hypertension have the secondary type.9 Systemic arterial hypertension is one of the most common cardiovascular diseases of industrialized populations. It affects approximately 20 of adults in these societies, and the percentage is higher among the elderly and blacks.15 Males were at higher risk to develop...

The Importance of Medullary Blood Flow and Nitric Oxide in Hypertension

Renal medullary NOS activity and NO production exceeds that in the cortex. NO acts in autocrine and paracrine fashion to modulate both vasoconstriction and epithelial NaCl reabsorption. NOS isoforms have specific effects 18 . NOS1 inhibition reduces NO levels in the medulla and induces salt-sensitive hypertension without altering medullary perfusion. Global inhibition of NOS1, NOS2, and NOS3 isoforms decreases medullary NO levels, medullary blood flow, and tissue oxygen tension and leads to salt-dependent hypertension 19 . NO generation may be important to abrogate tissue hypoxia that would otherwise arise from release of vasoconstrictors. Angll, norepineph-rine, and vasopressin stimulate release of NO in the medulla. Subpressor infusion of N(w)-nitro-L-arginine methyl ester (LNAME) into the renal interstitium does not affect medullary blood flow or pO2 but enables otherwise ineffective doses of Angll, norepinephrine, or vasopressin to reduce perfusion. Data broadly support the...

Idiopathic Intracranial Hypertension

This condition has previously been termed benign intracranial hypertension (BIH) or pseudotumor cerebri. The intracranial pressure is raised however, there are no localising signs, no alteration in level of consciousness, the cere-brospinal fluid composition is normal and there is no evidence of hydrocephalus or other cause of raised ICP on neuroimaging. It is thus a diagnosis of exclusion. Chronic meningitis, venous sinus thrombosis and indeed spinal cord tumors may produce a similar clinical picture. An association with various drugs, metabolic and endocrinological disorders is recognized and this needs to be considered during the clinical evaluation of these patients.

Pulmonary hypertension

Pulmonary hypertension has been described in up to 15 per cent of patients with SLE, although usually it is not clinically significant. The pathology of pulmonary hypertension is not well understood, since vasculitis of the pulmonary vasculature is rarely seen. The role of recurrent pulmonary thromboembolism and antiphospholipid antibody syndrome should be considered among the major etiologies of pulmonary hypertension. Other potential mechanisms responsible include a chronic hypoxic state due to interstitial fibrosis and the chronic alveolar hemorrhage syndrome. Clinically, pulmonary hypertension in SLE is analogous to primary (idiopathic) pulmonary hypertension. Raynaud's phenomenon is common. The secondary form of pulmonary hypertension caused by chronic and recurrent pulmonary emboli can be treated by pulmonary thromboembolectomy. Thus diagnostic tests including pulmonary angiography should be considered. The prognosis in those with persistent pulmonary hypertension is grave....

Influence of Gender on Arteriolar Function in Hypertension

Females prior to menopause are much less susceptible to hypertension and other cardiovascular diseases than males, indicating that gender has a protective effect in these disorders and that female sex hormones can offset some of the alterations in arteriolar function that may occur with hypertension in males. For example, flow-induced arteriolar dilation is significantly reduced in male spontaneously hypertensive rats compared to females, because of the loss of the nitric oxide (NO)-mediated portion of the response. This impairment of the NO-mediated component of flow induced dilation results in a maintained elevation of wall shear stress in the male rats, suggesting that female sex hormones play an important role in maintaining NO-dependent vasodilator responses and in preserving the regulation of arteriolar shear stress by nitric oxide. Arteriolar dilation in response to increases in perfusate flow is also impaired in isolated gracilis muscle arterioles of ovariectomized female...

Fetal Growth and Hypertension

Barker et al. published in 1989 an inverse relation independent of gestational age between systolic blood pressure and birth weight among a British sample of 9921 10-year-olds and 3259 adults aged 36 years.174 They also showed that 10-year-olds living in areas with high cardiovascular mortality in England and Wales were shorter and had higher resting pulse rates than those living in other areas. Their mothers were also shorter and had higher diastolic blood pressures. The authors suggested that besides intrauterine environment, persisting geographical differences in childhood environment may contribute to the observed risk from hypertension. Another report from Barker's team in 1992 showed a strong trend of higher blood pressure in adult life with lower birth weight, lower ponderal index, and greater placental weight.175 through 71 years decreased by 5.2 mmHg for every kilogram increase in birth weight. They concluded that essential hypertension was initiated in fetal life, and...

Review Of Important Factors Relating To Hypertension

Essential hypertension is a process of variable course and severity. Several options are open to the physician depending upon the severity of the drug therapy. Condition weight reduction and diet control may be adequate treatment however, drug therapy is sometimes needed. When drug therapy is required, it usually begins with a diuretic followed by the addition of the other agents based on the patient's response. However, certain classes of drugs may be more advantageous (fewer side effects) when patients have other diseases. It is not unreasonable to see patients treated by the same provider on different drugs. The effectiveness of diuretics in the treatment of essential hypertension arises from the fact that diuretic agents decrease tubular reabsorption of sodium, which caused a reduction in blood pressure. Some of the common diuretics include hydrochlorothiazide, spironolactone (Aldactone ), furosemide (Lasix ), and triamterene (Dyrenium ). These agents will be discussed in detail...

Combining Antihypertensive Drugs

An antihypertensive drug can be used alone or in combination with one or more drugs that fall into one of five categories. Diuretics promote sodium depletion, which decreases extracellular fluid volume. It is the first-line drug for treating mild hypertension. Hydrochlorothiazide (HydroDIURIL), a thiazide, is the most frequently prescribed diuretic to control mild hypertension. Diuretics are not used if hypertension is the result of renal-angiotensin-aldosterone involvement because these drugs tend to elevate the serum renin level. Hydrochlorothiazides are combined with beta blockers, and angiotensin-converting enzyme (ACE) inhibitors. ACE inhibitors tend to increase serum potassium (K) levels. When they are combined with the thiazide diuretic, serum potassium loss is minimized. A list of drugs utilized in the treatment of hypertension is provided in the Appendix. Detailed tables show doses, recommendations, expectations, side effects, contraindications, and more available on the...

Pulmonary hypertension unrelated to sepsis and acute respiratory distress syndrome

Epoprostenol and PGE1 allow treatment of pulmonary hypertension of primary or secondary etiology (mitral stenosis, congestive heart failure, and chronic lung disease). and Radermacher _199_Z). In patients with primary pulmonary hypertension, epoprostenol is a fundamental element of therapeutic strategy which improves quality of (Barst .eta 1996), aerosolization of epoprostenol or its stable analog iloprost offers a new strategy for treatment of patients with primary pulmonary hypertension

Secondary pulmonary arterial hypertension

Secondary pulmonary arterial hypertension may occur after major surgery and during chronic obstructive lung disease, pulmonary thromboembolism, acute respiratory distress syndrome, and septic shock. Occasionally, endstage cystic fibrosis or interstitial lung disease is responsible for decompensation of a cor pulmonale. In selected cases, pulmonary hypertension during decompensated chronic obstructive lung disease and acute respiratory failure may limit the circulatory changes adaptive for hypoxemia. In fact, hypoxic vasoconstriction in the lung is a mechanism for maintaining arterial oxygenation in poorly ventilated areas of diseased lungs. Nevertheless, this may lead to right ventricular afterload mismatch and a limitation of cardiac output reserve, whereas, in contrast, a rise in cardiac output may be necessary to maintain tissue O2 delivery in face of hypoxemia. Hence vasodilators, including nitrates, phosphodiesterase inhibitors, prostaglandins, hydralazine, ketanserin, calcium...

Enhanced Sensitivity of Arterioles to Vasoconstrictor Stimuli in Hypertension

One of the primary functional alterations that has been reported in arterioles during hypertension is an increase in their sensitivity to a variety of vasoconstrictor stimuli including the adrenergic neurotransmitter norepinephrine and other vasoconstrictor agonists, elevations in intravascu-lar pressure (myogenic response), and an enhanced constriction in response to physiological stimuli such as increased oxygen availability. The increase in the sensitivity of arteri-oles to vasoconstrictor stimuli in hypertension may have a number of underlying causes, including intrinsic alterations in the electrophysiological responses of the vascular smooth muscle (VSM) cell membrane, changes in the nature and or production of chemical modulators of vascular tone produced by the endothelium or by the vascular smooth muscle cells themselves, alterations in intracellular Ca2+ homeo-stasis or in other second-messenger systems regulating contractile function, and the potential effects of increased...

Other Treatments For Hypertension

Most Cam Therapies 2018

The disappointing results of some hypertensive therapies have caused doubts about traditional approaches to management of hypertension.36 Rates of successful blood pressure control remain low among treated patients.4 Only 47 of patients with hypertension achieve optimal blood pressures below 140 90 mmHg.37 Hypertension treatments that will help patients establish healthy lifestyle changes and have fewer and less severe side effects would probably lead to more optimum results and higher rates of patient compliance with treatment programs. In fact, the most common reason patients seek complementary alternative medicine (CAM) is dissatisfaction with the ability of conventional medicine to treat chronic diseases. Interestingly, those most likely to utilize CAM have higher educational levels, poorer health, and holistic philosophies.38 A number of herbs are recommended for the treatment of hypertension. Some have dangerous side effects and can be toxic. The list includes aconite...

Thirsty Genes Putative Thrifty Genes that May Have Been Selected to Counter Water Stress but Now Lead to Hypertension

Intestine Cholesterol Absorption Gene

Humans have a physiological requirement for salt and mineral sodium. Indeed, one of our most basic senses of taste is for saltiness. This taste is not unpleasant, and it is perhaps unsurprising that in the West, our salt intake far exceeds our physiologic needs. Even the U.S. Food and Drug Administration recommendation of 6 g day for a low-salt diet is estimated to be 3.5x that of the typical Paleolithic diet. Some people are sensitive to salt and possess a genetic predisposition toward developing life-threatening hypertension (high blood pressure). Ten percent of people are affected by salt sensitivity in this way. It has been suggested that our early hunter-gatherer ancestors survived on little salt. However, the agricultural revolution and urbanization led to an increase in salt usage with genetically predisposed individuals developing age-related hypertension (64). Lev-Ran and Porta (64) hypothesize that selection pressures may have favored the emergence of a salt-sensitive,...

Importance of the Arterioles in Hypertension

Arterioles and the small arteries that are located immediately upstream from the arterioles are the major sites of vascular resistance in the peripheral circulation. Thus, changes in the structure and function of these vessels can play a crucial role in the development and maintenance of hypertension, since an elevation in peripheral vascular resistance is a common denominator in virtually all forms of this disease. In addition to controlling the resistance to blood flow in peripheral vascular beds, arterioles play a crucial role in determining the distribution of blood flow within the tissues. Therefore, changes in arteriolar structure, function, and microvessel density can have important implications for the supply of oxygen and nutrients to the tissues in hypertensive individuals. A variety of alterations in arteriolar structure and function can lead to an elevated vascular resistance in hypertension (Figure 1). These include increases in active resting tone an enhanced response to...

Current Medical Treatments For Hypertension

Hypertensive drugs are normally taken on a continuous basis.9 In diseases such as hypertension, diabetes, and asthma, a relapse following cessation of treatment is considered evidence of the effectiveness of the treatment and the need to continue monitoring the patient.32 The six main drug treatments for hypertension are diuretics, beta-blockers, calcium antagonists, angiotensin-converting enzyme (ACE) inhibitors, angiotensin II antagonists, and alpha-adrenergic blockers, although no reliable data support the last two regimens.23 Keeping in mind the terrible risks the disease involves, some people with high blood pressure do not feel any warning signs and thus fail to realize they have a major illness.9 They feel fine and the treatments are expensive and cause uncomfortable side effects. Thus, only 24 of patients with hypertension in the U.S. are adequately treated.7 Discontinuation of treatments and switching therapies increase the costs of patient care.4 In the U.S., nearly 75 of...

Management Of Hypertension

Hypertension results from an intense sympathetic storm . Increased circulating catecholamines associated with rises in intracranial pressure produce marked hypertension as well as tachycardia and pronounced vasoconstriction. Electrocardiographic and enzyme changes indicative of myocardial ischemia have been documented during this phase. Acute left ventricular failure and pulmonary edema may result. Fortunately this period is usually self-limiting and requires no treatment. If treatment is considered necessary, use of sodium nitroprusside, an agent with rapid onset and offset of action is recommended. In experimental studies, beta-blockers have also been used to abolish the hypertension seen during brain herniation. In the clinical setting, the short acting beta-blocker esmolol (Brevibloc) can be considered. The negative inotropic effects of esmolol are short-lived due to its short half-life and rapid disappearance from the circulation when the infusion is discontinued. A loading dose...

Intracranial hypertension and cerebral edema

How Correct Intracranial Pressure

The development of cerebral edema which underlies the rise in intracranial pressure probably depends on a variety of causative events. Increased permeability of the blood-brain barrier will result in leakage of protein-rich fluid into the extracellular space of the brain. The efficacy of mannitol in lowering intracranial pressure suggests that an intracellular cytotoxic mechanism is also important. The clinical signs of cerebral edema, namely systemic hypertension, decerebrate posturing, and abnormal pupillary reflexes, are generally attributed to brainstem compression. In an early series, cerebellar or uncal herniation was found at autopsy in 25 per cent of patients with cerebral edema. More recent experience shows that this is comparatively rare and that cerebral ischemia is the more likely underlying cause ( Fig 3).

Structural Alterations in Arterioles during Hypertension

In addition to the changes in functional arteriolar control mechanisms in hypertension, structural alterations of arteri-oles and small arteries can contribute to the elevated vascular resistance in this disease. These changes include structural narrowing of the lumen, thickening of the vascular wall leading to an increased wall lumen ratio, and altered mechanical properties of the vessel, such as increased stiffness and reduced distensibility of the vessel wall. These structural alterations of the vascular wall may be caused, at least in part, by alterations in the composition of the wall, such as changes in collagen and elastin content in the vessel wall, or by alterations in the specific types of collagen present in the vascular wall. Most reports indicate that wall thickening is not a common response to elevated blood pressure in the smaller arte-rioles however, wall thickening is prominent in the larger arteries that lie upstream from the microcirculation. There is evidence that...

Hypertension High Blood Pressure

When pressure exerted by blood on the walls of the arteries is greater than normal, blood pressure rises. Usually, blood pressure falls when at rest. It rises in response to strenuous physical activity, stress, or a perceived danger in which the sympathetic nervous system dominates, arteries constrict, and more blood is sent to the brain increasing blood pressure. This heightened state of the sympathetic system does not seem to retreat in individuals with hypertension and damage to the heart, kidney, arteries, and other organs becomes inevitable. Blood pressure is considered high at a reading of 140 90. There are no symptoms of the illness and it is recommended individuals over 40 be checked. Hypertension can be controlled by permanent diet and lifestyle changes this includes reducing stress, maintaining proper weight (not more than 5 lb overweight), and eating foods containing compounds that reduce blood pressure such as celery, garlic, and fresh fruits and vegetables. Having a home...

Postoperative Hypertension

Consider the following four factors in the management of hypertension etiology, LV function, renal function, age. In most cases, restart the preoperative antihypertensive medications unless there have been postoperative changes in LV and or renal function. Table 40.2 summarizes current treatment of patients with postoperative hypertension at TGH. Table 40.2. Management of postoperative hypertension Table 40.2. Management of postoperative hypertension

Pulmonary Arterial Hypertension

A major disorder involving the pulmonary microvasculature and eicosanoids is pulmonary arterial hypertension (PAH). PAH primarily affects the small pulmonary arteries with a diameter of less than 100 microns. Pathological changes include medial hypertrophy, intimal proliferation, in situ thrombosis, and plexiform lesions, the latter likely a disordered attempt at neovascularization. PAH may occur without an associated disorder, primary pulmonary hypertension (PPH), or in association with connective tissue disease, congenital heart disease, portal hypertension, HIV infection, or use of appetite suppressants. Disruption of the endothelial lining of the microvasculature in PAH is associated with changes in the local milieu of protein and lipid mediators. Whether these changes are causative or secondary to the pathological changes is uncertain. It is noteworthy that similar pathological changes have been found in the microvasculature of patients undergoing thromboen-darterectomy for...

Stage I prevention of intracranial hypertension general medical and nursing care avoidable factors

This section lists simple preventive measures and interventions that should be used in all patients who are either at risk of developing intracranial hypertension or have raised ICP (Box 7.4).965 salt wasting, defined as the loss of sodium during intracranial disease leading to hyponatraemia and volume depletion, is the alternative cause of hyponatraemia. Possible mechanisms leading to this syndrome are secretion of atrial and brain natriuretic peptides as well as ouabain-like compounds. The two syndromes are differentiated by the volume status of the patient. Cerebral salt wasting is treated with fluid and sodium substitution (for a detailed review see Harrigan81). Overenthusiastic hypertensive-hypervolaemic therapy remains very controversial, especially in the context of head injury with its multiple pathology and uncertainty over the integrity of the blood-brain barrier.82-84 It carries the risk of development of vasogenic oedema but also of adult respiratory distress syndrome85...

Antihypertensive Agents

Exposure-response information plays an important role in the development of drugs for the treatment of many cardiovascular illnesses, including hypertension. The surrogate markers measured as response for antihypertensive drugs include changes in blood pressure. Exposure-response data are usually collected in Phase II trials that are double-blind, randomized, placebo-controlled, and parallel-group in design. In the development of antihypertensive drugs such as the angiotensin-converting enzyme (ACE) inhibitors or beta blockers, it is important that exposure-response information be obtained across several orders of magnitude of doses in order to be able to determine the optimum dose for patients. In October 2000, the FDA convened an advisory committee meeting to discuss the importance of obtaining appropriate dose-response information during antihypertensive drug development. The committee concluded that elucidating the full range of dose-response relationships for antihypertensive...

Hypertension And Cerebrovascular Disease

Next to age, the most important factor predisposing to cerebral infarction or haemorrhage is hypertension. The risk is equal in males and females and is proportional to the height of blood pressure (diastolic and systolic). In hypertension, a shift of this curve results in relative protection from hypertensive encephalopathy The pathological effects of sustained hypertension are An acute, usually transient, cerebral syndrome precipitated by sudden severe hypertension. The excessive blood pressure may be due to malignant hypertension from any cause, or uncontrolled hypertension in glomerulonephritis, pregnancy (eclampsia) or phaeochromocytoma.


Investigating clinical records from a fairly large population during 1960-1974, Kokmen and collaborators (Kokmen et al., 1991) have shown that out of the 20 risk factors studied, hypertension along with episodic depression and personality disorders were the only risk factors to have statistically significant associations for potential clinical risk factor to develop AD. Since then, there have been a number of extensive studies largely supporting the notion that hypertension is an important risk factor for AD. However, the mechanistic interactions between hypertension and the AD neuropathology are far from clear. For a discussion on these interactions, the reader could consult a recent review by Skoog and Gustafson (Skoog & Gustafson, 2006). There is no antihypertensive therapeutic strategy for the prevention of AD at the present time. Furthermore, hypertension as a target is complicated by the observation that blood pressure often falls when AD is clinically diagnosed (Birkenhager &...

Pathophysiology of heart failure

Impaired ventricular filling, or diastolic dysfunction, is common, especially in elderly hypertensive patients, and may be seen in 30 of patients who have clinical evidence of HF. It is characterized by ventricular hypertrophy, with preserved cardiac contractility. Impaired diastolic filling leads to a reduction in stroke volume and a corresponding reduction in cardiac output. Routine echocardiography is required in any patient with new-onset HF, since measurement of left ventricular function helps differentiate systolic from diastolic dysfunction.

Epidemiological aspects

Sudden unexpected cardiac arrest in adults has an incidence of 0.1 to 0.2 per cent in the general population, with 80 per cent of cases due to coronary heart disease. The incidence of cardiac arrest increases exponentially with age, reflecting the escalating frequency of coronary heart disease, but at all ages men are at greater risk than women. For coronary heart disease populations, hereditary factors producing hypertension, diabetes, lipid abnormalities, and male-pattern baldness predispose to cardiac arrest. Racial characteristics are important, with increased risks in colored populations, although the reasons for this are unclear. Cigarette smoking is the major acquired (and preventable) risk factor, although sedentary occupation and diet also play significant roles.

Special cerebral resuscitation measures

In over 50 per cent of cases of sudden death outside hospital, standard external cardiopulmonary resuscitation with advanced life support has failed to achieve restoration of spontaneous circulation. In such cases, restoration of spontaneous circulation and promotion of cerebral blood flow, during and after reperfusion from prolonged cardiac arrest, might be achieved with open-chest cardiopulmonary resuscitation or (portable) emergency (closed-chest) cardiopulmonary bypass and a combination of early postcardiac arrest induced hypertension, mild hemodilution, and PaCO2 control. Cerebral blood flow promotion can be achieved by creating the above-mentioned initial hypertensive bout followed by controlled mild hypertension for a few hours, mild hemodilution with colloid plasma substitute to a hematocrit of about 30 per cent, and PaCO2 control. After admission to the intensive care unit (ICU), these measures to promote cerebral blood flow could be titrated against mixed cerebral venous PO2...

A pAdrenergic receptor blockers

P-blockers are recommended first-line agents in uncomplicated hypertension, or in hypertensive patients with angina pectoris, cardiac arrhythmias, mitral valve prolapse, a history of myocardial infarction (MI), diastolic dysfunction, or migraine headaches. p-blockers are preferred in young Caucasian hypertensive patients (younger than 40-50). African-Americans tend to respond less well to p-blockers.

Ethnic Considerations

Likewise, a genetic factor in African-Americans makes them less responsive to beta-blocking agents used in cardiac and antihypertensive medications. Asians have a genetic factor that causes undesirable side effects when given the typical dose of benzodiazepines (diazepam Valium ) alprazolam Xanax , tricyclic antidepressants, atropine, and propranol Inderal . Therefore, a lower dose must be given.

Obesity as a Chronic Disease

Along with genetics, except for certain medical conditions, most patients' obesity is the result of an unhealthy lifestyle of overeating and lack of physical activity. Fortunately, improved medical management has lowered the prevalence of some cardiac risk factors, especially among obese patients. From 1962 to 2000, hypercholesterolemia was reduced among obese patients 21-percentage-points (39 vs 18 ), and hypertension by an 18-percentage-point reduction (42 vs 24 ) 5 . Yet even with improved medical management of comorbidi-ties associated with obesity, the estimated number of excess deaths in 2000 associated with oesity was 111,909 6 .

Reflex control of respiratory activity

Other sensory inputs (e.g. information of hyperinflation or deflation of the lungs from pulmonary stretch receptors) activate a variety of respiratory and non-respiratory NTS neurons for rapid adaptation (physiological mechanisms to turn off inspiration). Other NTS neurons also receive afferent inputs from arterial chemoreceptors and baroreceptors which can modulate the central respiratory network (e.g. respiratory depression during arterial hypertension).

Energy Balance And Body Weight

Obesity is recognised as a leading cause of insulin resistance (21). It therefore contributes to the development of Type 2 diabetes. This is particularly true for a central distribution of body fat, associated with a range of metabolic disturbances. Weight management is crucial in controlling blood glucose levels in people with Type 2 diabetes, although from UKPDS there is evidence that to normalise glucose tolerance usually requires major weight loss. Studies suggest that at least 80 of newly diagnosed patients with Type 2 diabetes are overweight and weight loss in people with Type 2 diabetes who are overweight increases life expectancy. Obesity is an additional risk factor for coronary heart disease and stroke. All cardiac risk factors (glycaemia, hypertension, lipids) are improved with weight management (22). This is true for individuals with Type 1 diabetes as well as Type 2 diabetes. However, it is also important to make sure that energy requirements are adequate in children and...

Cardiovascular disease

Acute unexplained dyspnea may be a clinical sign of pulmonary embolism. Because of mismatching in the ventilation-to-perfusion ratio, even a low degree of obstruction produces hypoxemia which is responsible for the breathlessness. Greater obstruction may provoke pulmonary hypertension or cardiogenic shock, which also cause breathlessness.

The Obesity Epedemic in America

The significance of overweight or obese BMI is that it correlates with an increased relative risk for developing chronic diseases and cancers. The data from a 10-year follow-up of the combined Nurses' Health Study and the Physician's Health Professionals Follow-Up Study show men and women who are overweight, compared to a normal BMI of 18 to 24.9, are more likely to develop gallstones, hypertension, high cholesterol, and heart disease. The relative risk (RR) for developing diabetes of an individual with a BMI 35 or greater is 20 times greater than for someone with a normal BMI 18 . The American Heart Association's scientific statement on obesity as an independent risk factor for heart disease states obesity not only relates to but independently predicts coronary atherosclerosis 19 . The relative risk (RR) of cardiovascular death increases with BMI. A BMI of 19 to 21.9 has an RR of 1, and a BMI 32 has a RR over 3 20 .

Initiatives To Increase Donation

One fairly successful approach to increasing the organ supply has been to broaden the criteria for donor acceptance, but only to the extent that donation can occur without negatively impacting transplant outcomes. As transplantation technology has evolved, transplant physicians have discovered that donor organs that had previously been considered unacceptable are often quite suitable for transplantation. It is not surprising that as donor management and post-transplant care of the recipient have improved, so has the ability to use organs from expanded donors a term coined by transplant professionals in the mid 1990s. There are many examples of expanded donors, and undoubtedly the list will continue to grow. Acceptance of organs from older donors, donors with some degree of hypertension, non-heartbeating donors, Hepatitis C positive donors, and other expanded donors all have been used effectively given the appropriate donor patient circumstances. Some disagreement remains regarding...

Pharmacological support

Attempts to modify the inflammatory process in ARDS with pharmacological agents have met with only limited success. Agents used have included non-steroidal anti-inflammatory drugs (e.g. ibuprofen), prostaglandins (alprostadil), thromboxane synthetase inhibitors (ketoconazole), antioxidants ( -acetylcysteine), and neutrophil activator inhibitors (e.g. pentoxifylline). Corticosteroids are beneficial in animal models, but clinical trials have been disappointing. High-dose steroids have a place in the treatment of patients with significant fibroproliferation or high bronchoalveolar eosinophil counts, where sepsis is excluded. Most progress has been made in the area of inhaled vasodilators used in an attempt to improve ventilation-perfusion relationships and decrease intrapulmonary shunting. This is achieved by increasing blood flow to ventilated lung units. Reducing pulmonary vascular resistance may also decrease pulmonary edema formation and therefore increase arterial oxygenation....

Supplemental Reading

Lee Drew, MD, has been invited by Modern Pharmaceutical Company to participate in a new drug trial for hypertension. For every patient Dr. Drew recruits through his small private practice, he will receive 1,000 to help defray the costs of quarterly blood draws and the additional paperwork required by the study. In addition, Modern Pharmaceuticals will replace Dr. Drew's computer system to enable better patient tracking. Given the declining reimbursement rates from third-party payers, Dr. Drew could really use the financial support but wonders what benefits this drug offers to patients. Is it simply a me-too or copycat drug, designed primarily to make money for the drug company And, if so, can Dr. Drew be justified in asking patients to enroll in the study Still, Dr. Drew finds the financial incentives tempting and knows the risk to patients is low. How should Dr. Drew resolve the ethical dilemma Answer Dr. Drew faces many ethical questions in deciding whether or not to participate in...

Anesthesia for Posterior Fossa Surgery

Interference with the cardiorespiratory centers in the brainstem can result in cardiovascular instability during surgery and in airway and breathing problems post-operatively. Pressure on the nucleus of the vagus results in profound bradycardia, even cardiac standstill, and other cardiac arrhythmias and hypertension can be caused by brainstem manipulation. Vigilance by the anesthesiologist and close cooperation between surgeon and anesthesiologist are essential.

Cardiovascular failure

Acute respiratory failure further damages cardiac function by additional mechanisms. First, hypoxemia increases pulmonary hypertension by enhancing the hypoxic vasoconstrictive effect. Second, when hyperinflation develops, some pulmonary vessels collapse, leading to a reduction in the vascular cross-sectional area that also impairs right ventricular impedance. Third, pleural pressure becomes more negative during inspiration and even positive during active expiration, translating these pressure swings to the transmural ventricular pressure. As a result, both right ventricular preload and afterload increase.

Management of Elevated Intracranial Pressure

Intracranial hypertension is defined as an ICP 15 mmHg. A progressive rise from this level, or sustained ICP 20 mmHg, should prompt investigation and treatment. A progressive rise in ICP may indicate the development of hemorrhage hematoma, edema, hydrocephalus or a combination of these causes, and an immediate CT scan is indicated. A sustained elevated ICP increases the risk of secondary injury from ischemia and or herniation.

Preface To The Third Edition

Furthei the changes of the written parts of the MRCP exam, notably the removal of negative marking in Part 1 and the change to MCQ ('Best of Five') based questions in Part 2A, there has also been a change in the content of the MRCP 2A papers. The exam is increasingly orientated around evidence based medicine, up-to-date patient management and current guidelines. This is a move away from the esoteric questions seen in the past and it makes a more useful exam. Candidates have said that a large proportion of questions could now be answered with adequate clinical experience. That does however mean that preparation for Part 2A needs to inc lude the British Medical Journal, the journal of the Royal College of Physicians and the Drugs and Therapeutics Bulletin. The candidates need to be aware of the latest guidelines regarding the treatment of bread and butter entities such as hypertension, diabetes and chronic chest disease. The bodies involved in these guidelines besides the National...

Decompressive Craniectomy

Decompressive craniectomy is indicated in patients with persistent elevated ICP refractory to medical treatments. In patients with unilateral swelling following hematoma evacuation or tumor resection, hemicraniectomy or removal of a large cranial flap with dural patching has been successful in reducing ICP. In patients with cerebral edema of both hemispheres, bilateral craniectomy may be necessary. Rarely, removal of damaged tissue or lobectomy may be performed as a last-ditch effort to decrease the intracranial contents in the most severe cases of intracranial hypertension. This procedure appears to be effective both for traumatic brain injury as well as for swelling secondary to stroke or subarachnoid hemorrhage. A multicenter trial to assess its efficacy as an early treatment for traumatic brain injury will determine its future role as a definitive treatment for intracranial hypertension 10 .

Excessive Sympathetic Nervous System Output Is Detrimental to Health

Stimulation of the SNS is a hallmark of the acute stress response (Goldstein, 1987). SNS activation has many physiological consequences that work in concert to promote the fight-or-flight response (Jansen et al., 1995 Goldstein, 1996) and facilitate features of innate immunity (Campisi and Fleshner, 2003 Johnson et al., 2005). SNS activation is a powerful feature of the acute stress response that is adaptive when the response is acute and constrained. If, however, SNS activation is frequent or excessive, it can produce negative health consequences (Seals and Dinenno, 2004). For example, chronically elevated SNS responses are believed to mechanistically contribute to the etiology of metabolic syndrome, a key antecedent to clinical atherosclerotic diseases that includes visceral adiposity, glucose intolerance, insulin resistance, dyslipidemia, and hypertension (Baron, 1990 Julius et al., 1992 Lind and Lithell, 1993). In addition, it has been reported in both the human and animal...

Pharmacogenetic Targets In Cardiovascular Disease

Atherosclerosis is, at least in part, attributed to an underlying immune-mediated process with onset early in life, ultimately leading to severe clinical manifestations, such as myo-cardial infarction, unstable angina, and cerebral stroke. The increased incidence of cardiovascular events in the western societies is attributed to the underlying immune process, which is amplified by additional cardiovascular risk factors, such as hypercholesterolemia, hypertension, smoking, diabetes, and obesity, which by themselves have their own genetic background. This section provides a summary of some of the key issues for a full discussion, see the chapter on cardiovascular disease.

Hemorrhagic and Ischemic Stroke

In patients with hemorrhagic stroke, control of blood pressure is important to prevent further hemorrhage. However, it is important to rule out the occurrence of hypertension secondary to increase in ICP (Cushing's response), in which event the mean arterial pressure should be reduced gradually, and not below 130 mmHg in known hypertensive patients, and lower (100 mmHg) in previously normotensive patients. On the other hand, mild-to-moderate hypertension (160-180 systolic and 90-100 diastolic blood pressure) should be left untreated in patients with ischemic stroke. Vasopressors to support blood pressure may be necessary.

Absorption Metabolism Excretion

Prazosin is readily absorbed after oral administration, peak serum levels occur approximately 2 hours after a single oral dose, and the antihypertensive effect of pra-zosin persists for up to 10 hours. Its half-life in plasma ranges from 2.5 to 4 hours, and elimination from plasma appears to follow first-order kinetics. The drug is extensively (perhaps as high as 97 ) bound to plasma proteins this observation partially explains the lack of correlation between plasma drug levels and persistence of antihypertensive effect.

Cadaver And Living Kidney Donation

Numerous strides have been made to increase the total number of cadaver kidneys available by public education programs encouraging organ donation. There is also a new classification of expanded criteria organ donors, and more liberal consideration of controlled and uncontrolled non-heart-beating donors. In addition, many programs are expanding their living kidney donor experience by including distantly related donors such as spouses, cousins, aunts, uncles, close friends, and even emotionally unrelated donors. This has resulted in an increase in the proportion of all kidney transplants performed in the U.S. by living donors to almost 45 . In many transplant programs, living kidney donation accounts for nearly 75 of all the kidney transplants. There are few medical ethical issues related to accepting kidneys from living donors. The donor mortality risk is

Pharmacological Actions

The actions of p-blockers on blood pressure are complex. After acute administration, blood pressure is only slightly altered. This is because of the compensatory reflex increase in peripheral vascular resistance that results from a p-blocker-induced decrease in cardiac output. Vasoconstriction is mediated by a-receptors, and a-receptors are not antagonized by p-receptor blocking agents. Chronic administration of p-blockers, however, results in a reduction of blood pressure, and this is the reason for their use in primary hypertension (see Chapter 20).The mechanism of this effect is not well understood, but it may include such actions as a reduction in renin release, antagonism of p-receptors in the central nervous system, or antagonism of presynaptic facilita-tory p-receptors on sympathetic nerves. The release of renin from the juxtaglomerular cells of the kidney is believed to be regulated in part by preceptors most p-blockers decrease renin release. While the drug-induced decrease...

Management of Vasospasm

Angiographic vasospasm occurs in up to 70 of patients after aneurysmal SAH, although only about 30-40 of patients become clinically symptomatic. Although nimodipine prophylaxis improves the neurological outcome of patients, it neither decreases the incidence nor alters the magnitude of vasospasm. Vasospasm typically occurs on day 3 after SAH, peaks on day 7, and generally subsides by the end of 14 days. Vasospasm is the main cause of delayed ischemic deficit, resulting in brain infarction or death. Early vasospasm results in elevated flow velocities, which can be detected by TCD, but the diagnosis must be confirmed with angiogra-phy in symptomatic patients. SPECT can detect regional differences in perfusion and facilitate management. Currently, the only medical treatment for symptomatic vasospasm is augmentation of cerebral perfusion by elevation of blood pressure, and cardiac output. Although its value has not been established with randomized clinical trials, triple-H therapy...

Fluid and Electrolytes

To maintain adequate cerebral perfusion, it is important to maintain normovolemia. The practice of keeping neurological patients dehydrated to minimize cerebral edema is outdated, and in head-injured patients is associated with poor outcome 15 . Fluid balance tallying total input and output should be monitored daily, and insensible loss of 500-800 ml per day should be allowed. Patients with head injury often suffer multiple injuries that may result in significant blood loss, contributing to hypovolemia and hypotension. On the other hand, patients who suffer SAH can develop acute decrease in circulating blood volume unrelated to blood loss. Patients with hemorrhagic or ischemic stroke may also be hypovolemic, and the volume status cannot be assessed by the presence or absence of systemic hypertension. A thorough history and clinical examination is crucial to the establishment of the correct diagnosis. To ensure normovolemia, isotonic fluids or normal saline should be given, although...

Physician as Catalyst

Given this environment, how the physician sees himself or herself in the doctor-patient relationship is important. Primary care physicians shift between various doctor-patient roles throughout the day. For instance, a patient who presents to the office having just experienced the death of a spouse needs a physician who will empathetically listen more than talk. In this situation, the physician is a counselor. For the patient presenting with an anaphylactic reaction, the physician must quickly take action. It is not time to be a counselor but instead to take control and make rapid decisions. In either case, the physician's role is based on the presenting needs of the patient. Treating patients with tobacco dependency, alcoholism, or drug addiction requires a triage approach that is different from treating hypertension or diabetes. My responsibility is to identify how willing a patient is to fight an addiction and then be a catalyst in providing the right intervention at the right...

Noninvasive investigations

The resting ECG may be normal or show evidence of previous myocardial infarction in one or more territories. There may be evidence of hypertension, such as left ventricular hypertrophy. ECG changes may be subtle and non-specific, such as ST segment flattening in the lateral leads or T-wave inversion inferiorly.

Epidemiology Of Chd In Subsaharan African Populations

Numerous publications have emphasized the rarity of CHD in sub-Saharan African populations. In 1960, CHD was considered extremely rare in Uganda.1 A general review in 1977 noted that Africans were regarded as virtually free of hypertension and CHD. 2 In the same year at Enugu, Nigeria, not 1 patient among 348 with cardiac disorders over a 4-year period had CHD.3 As to international appreciation, a leading article titled British and African Hearts published in 1983 in the U.K. emphasized the tremendous contrast between the experiences of CHD in the two types of populations.4 In 1993, a rural hospital in Tanzania reported a low prevalence of CHD risk factors and the absence of the disease.5 The latter phenomenon was also noted in rural Nigeria.6 In a rural hospital at Gelukspan in the Northwest Province of South Africa, none of the 2593 adult admissions in 1994 arose from CHD.7 Around the same time, the same observation related to 2010 admissions was noted at the rural Manguzi Hospital...

Immediate Questions

Are there treatable causes of cardiopulmonary arrest Consider the 5 H's and 4 T's Hypoxemia Hypovolemia Hypothermia Hyperkalemia or hypokalemia and metabolic disorders intracranial Hypertension cardiac Tamponade Tension pneumothorax Toxins, poisons, and drugs and Thromboembolism.

Allele Frequencies and Their Equilibrium Properties

Genetic changes at a specific site are generally termed polymorphic if they occur commonly in the population (i.e., two alternative forms with frequencies of 1 or more). Polymorphisms are classified into several major classes including single nucleotide polymorphisms (SNPs), short tandem repeats (STRs), and variable number of tandem repeats (VNTRs). STRs and VNTRs have proven extremely useful for the localization of disease genes through linkage analysis (Gyapay et al., 1994). Linkage, however, does not have fine enough resolution to lead to the identification of the disease-causing gene and allele. The latter require fine mapping, and it is in this area that the single nucleotide changes are most useful (Johnson et al., 2001). Furthermore, susceptibility alleles (whether changing disease susceptibility or response to treatment) are likely to fall into the class of single nucleotide differences. In Mendelian diseases, such single nucleotide changes result in truncated proteins,...

Physical Exam Key Points

Fast rate can indicate a toxic or metabolic abnormality. Slow rate is often an ominous sign that is suggestive of impending respiratory arrest, a toxin, or intracranial hypertension. Assess oxygenation by pulse oximetry. c. BP. Is BP high (intracranial hypertension, toxin, or hypertensive emergency) or low (decompensated shock) 2. CNS. Low Glasgow Coma Scale score may indicate head injury. Examine head and fontanelle bulging fontanelle can occur with intracranial hypertension or meningitis, whereas sunken fontanelle indicates hypovolemia and dehydration. Look for boggy swelling, palpable fracture, or other signs of trauma. Note presence of a ventricular shunt. 3. Eyes. Examine for signs of trauma (raccoon's eyes) or hypovolemia and dehydration (sunken). Assess pupil size and reaction. Pupillary size can give clues to the presence of a toxin. Depressed or absent reaction may indicate structural CNS lesion, herniation or impending herniation, or cardiopulmonary...

Anatomical considerations

With advancing age, elastin fragmentation, fibrosis, and medial necrosis lead to degeneration of the aortic lamellas. These changes are most pronounced in the ascending aorta and become less prominent as the aorta descends into the abdomen. These changes occur as part of the normal aging process but are more prominent in hypertensive patients. Pre-existing dilation of the aorta (as occurs in Marfan's syndrome) may also be relevant. Laplace's law relates wall stress to pressure and diameter as the aorta dilates, so wall stress increases. Medial degeneration may result from structural abnormalities (e.g. Marfan's and Ehlers-Danlos syndromes) in which dissection may occur without pre-existing hypertension or, possibly, from ischemic necrosis due to occlusion of the vasa vasorum.

Cause and Incidence of Pancreatic Ischemia

Some authors have described the various causes of pancreatic ischemia or infarct, such as periarteritis nodosa, malignant essential hypertension, embolism, and splenic or superior mesenteric arterial thrombosis 2 . Recently our investigations revealed pancreatic ischemia caused by disseminated intravascular coagulation (DIC) and cholesterol emboli 5, 6 . McKay et al. suggested that cardiac failure with hypotension or shock can cause pancreatic ischemia 3 . The incidence of pancreatic ischemia is unclear. McKay described that pancreatic infarcts were found in only 0.19 of 21,481 consecutive necropsies at the Mayo Clinic 3 . Our study revealed that fresh ischemic lesions were found in 20 (7 35) of cases of DIC and in 12 (2 17) of cases of cholesterol emboli 5, 6 .

APatient is pulseless

If patient is in shock, provide fluid boluses of 20 mL kg of isotonic (NS or Ringer lactate) solution at least twice. Reassess patient after each fluid bolus. Consider infusion of inotrope if there is no or minimal improvement after second fluid bolus. Consider the 5 H's and 4 T's (see II, G, earlier). Involve consultants promptly for the following conditions congenital or acquired heart disease, arrhythmias (cardiologist) injuries (trauma surgeon) head injury, and intracranial hypertension (neurosurgeon). Other actions

Hypoxia Inducible Factor

In summary, HIF-1-dependent gene expression warrants classification as an endogenous cytoprotective mechanism by allowing for adaptation to cellular hypoxia, whether it be secondary to low oxygen tension per se or due to decreased blood flow (ischemia). While some of the aforementioned cytoprotective mechanisms (e.g., the heat shock response) allow for more immediate forms of cytoprotection, the cytoprotective responses and adaptations associated with HIF-1 activation are comparatively slower to develop. In addition, some of the responses induced by HIF-1 activation can be maladaptive pathologic depending on duration of activation (e.g., the development of pulmonary hypertension in the setting of chronic hypoxia). Thus a greater understanding of HIF-1 regulation and activity will be necessary in order to manipulate HIF-1 activity as a therapeutic option. These options will include, depending on the therapeutic goals and clinical scenario, either augmenting HIF-1 activity (e.g., in...

The Isoactin Network Drives Retinal Microvascular Morphogenesis

There are multiple lines of genetic, cellular, and biochemical data demonstrating functional diversity of the actin isoforms. Functional distinction is evidenced by altered expression profiles, biophysical properties, cellular localization, and overexpression studies. For example, in retinal pericytes or vascular smooth muscle cells that are actively dividing, nonmuscle isoactins are prevalent however, when the cells are contractile, a-VSM actin (among other smooth muscle-specific proteins) prevails 9 . Expression of aVSM actin is strongly regulated during wound contraction, as seen in myofibroblasts, during mesangial cell damage in hypertension, and in de-differentiated, intimal vascular smooth muscle cells present in atherosclerotic lesions. This regulated pattern of vascular cell isoactin

Pulmonary Vasodilation

The cyclo-oxygenase metabolite prostacyclin is a potent, short-lived vasodilator and antithrombotic agent. Intravenous administration of the commercially available form of prostacyclin, epoprostenol, relieves the symptoms of primary pulmonary hypertension by dilating the pulmonary vasculature 99 . A stable prostacyclin analogue, iloprost, appears to be similarly effective when administered as an aerosol and obviates the logistical problems associated with maintained intravenous administration 100 .

Disease Prevalence In The Elderly

The prevalence of many diseases is age-related and several may co-exist in the same patient. These include hypertension (Hawthorne et al., 1974) osteoarthrosis (Lawrence, 1977) and prostatic hypertrophy (Berry et al., 1984). Age-specific mortality rates are shown for cardiovascular and cerebrovascular diseases, together with data for cancers, in Table 7.1 (British Heart Foundation, 2000) and morbidity data in Table 7.2 (British Heart Foundation, 2001).

Hypertensive Cardiovascular Disease

Ganglionic blockers were once widely used in the management of essential hypertension, and they constituted an important advance in the treatment of that disease. Unfortunately, the development of tolerance to these drugs and their numerous undesirable side effects resulting from their nonselective ganglion-blocking properties led to a decline in their use. They have now been completely replaced by more effective and less toxic drugs. They do, however, retain some usefulness in the emergency treatment of hypertensive crisis.

Atrioventricular conduction block

Conduction abnormalities may have abnormalities in autonomic tone, particularly heightened vagal stimulation. Atrioventricular conduction block may be due to myocardial ischemia, chronic hypertension, digoxin toxicity, b-blockers, calcium-channel blockers, myocarditis, acute rheumatic fever, myocardial calcification, aortic stenosis, mitral stenosis, and congenital atrioventricular block.

Firstdegree atrioventricular block

First-degree atrioventricular block occurs when the PR interval is prolonged (0.20 s or longer, or 0.18 s or longer if the heart rate exceeds 90 beats min). If the QRS interval is normal, the delay in conduction is in the atrioventricular node. With a prolonged QRS, the conduction delay may be in the His-Purkinje system. It is usually asymptomatic, and may be due to drugs (e.g. digoxin, b-blockers, calcium-channel blockers), intrinsic conduction system disease, and hypertension. It can be ominous if it is due to endocarditis with abscess formation involving the conduction system.

Diet And Heart Failure

While gender, obesity, heredity, and insulin resistance may explain some of the variance in LVH, hypertension (HBP) is generally regarded as the primary culprit.55 Thus, the risks associated with LVH and HBP are intimately linked. Recent data also suggest that low dietary intake of polyunsaturated fatty acids and high intake of saturated fatty acids along with HBP and obesity at age 50 predicted the prevalence of LVH 20 years later.56 Although the source of saturated fatty acids is usually animal fat, the source of unsaturated

Chapter References

Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure (1993). Fifth Report. Archives of Internal Medicine, 153, 154-83. Panacek, E.A. (1994). Hypertensive emergencies and urgencies. In Emergency cardiac care (ed. W.B. Gibbler and T.P. Aufderhide), pp. 528-48. Mosby Year Book, St Louis, MO. Powers, W.J. (1993). Acute hypertension after stroke the scientific basis for treatment decisions. Neurology, 43, 461-7.

Aetiology and pathophysiology Aetiology

Risk factors for vascular dementia can be divided into vascular factors (e.g. arterial hypertension, atrial fibrillation, myocardial infarction, coronary heart disease, diabetes, generalized atherosclerosis, lipid abnormalities, smoking), demographic factors (e.g age, education), genetic factors (e.g. family history, individual genetic features), and stroke-related factors (e.g. type of cerebrovascular disease, site and size of stroke). (1, ,19) Hypoxic ischaemic events (cardiac arrhythmias, congestive heart failure, myocardial infarction, seizures, pneumonia) may be an important risk factor for incident dementia in patients with stroke.

Intracranial hemorrhage

Per cent, or to an mean arterial pressure of 110 to 120 mmHg, over a period of 6 to 12 h. Initial therapeutic agents include calcium-channel blockers (e.g. nimodipine or nifedipine), starting with low doses, or sodium nitroprusside in patients unable to take oral medication. If blood pressure reduction appears to worsen the patient's overall status, the antihypertensive agents should be discontinued immediately and blood pressure allowed to return to moderately elevated levels. Experiences with hypertensive intraparenchymal cerebral hemorrhage are limited and there no controlled trials. Currently, the recommendations are the same as those for subarachnoid hemorrhage, with similar goals for target blood pressure and time frame (C hoy0 aDd O.p rL 1990).

Acute cardiac impairment

When acute cardiac impairment occurs with severe hypertension, immediate blood pressure reduction will decrease cardiac work and myocardial oxygen demand. If neurological complications are not an active concern, the pressure should be quickly reduced to near-normal levels (diastolic blood pressure 85-90 mmHg). With ongoing myocardial ischemia the agent of choice is intravenous nitroglycerin (glyceryl trinitrate). However, this agent is not a very effective antihypertensive, and so sodium nitroprusside may be needed. A loop diuretic may also be considered in appropriate patients.

Hypertensive urgencies

Hypertensive urgencies are much more common than emergencies. Therapy should be initiated within the initial few hours, at least within 24 h, and oral medications are usually adequate (PanacekJ994). The most popular agent for urgencies is currently nifedipine. Clonidine hydrochloride is a common alternative. There is also increasing experience with oral angiotensin-converting enzyme inhibitors and with intravenous or oral labetalol. The hypertension should be reduced but need not be normalized. These patients require close follow-up but not usually hospital admission.

Possibilities for prevention

For primary prevention the target is the brain at risk of cerebrovascular disease and cognitive impairment. The methods relate to the treatment of putative risk factors of vascular dementia, and the promotion of potential protective factors. Risk factors include those related to cerebrovascular disorders and stroke, to vascular dementia, to post-stroke dementia, to white-matter lesions, and to cognitive impairment or dementia, and also those related to Alzheimer's disease. (8) The vascular risk factors include arterial hypertension, atrial fibrillation, myocardial infarction, coronary heart disease, diabetes, generalized atherosclerosis, lipid abnormalities, and smoking. The demographic factors include age and education. One putative protective factor is oestrogen. (83 Knowledge of effects of primary prevention on these risk factors in populations free of cognitive impairment is still scant. (884) In a European study, treatment of mild systolic hypertension decreased the incidence of...

Pharmacological Interventions Aimed at Decreasing CVD Risk

Theoretically, if insulin sensitivity is enhanced in insulin-resistant persons, the associated improvement in CVD risk factors should lead to a decrease in CVD. Although there is substantive evidence that weight loss and treatment with TZD compounds will improve insulin sensitivity in insulin-resistant individuals, associated with an improved CVD risk profile, there are no clinical trials that provide experimental evidence that either approach will decrease CVD events. In the absence of such information, it is necessary to consider the potential clinical utility of addressing specific CVD risk factors, associated with the IRS, in an effort to decrease CVD. In the next section, therapeutic approaches to two such factors - dyslipidemia and hypertension - will be considered.

Acute respiratory failure and sepsis

In acute respiratory failure, several mechanisms promote the development of pulmonary hypertension. The inflammatory character of the disease leads to neutrophil permeability of the pulmonary capillary bed leads to a subsequent fluid shift to the interstitium, eventually resulting in pulmonary permeability edema. The increase in interstitial pressure compromises capillary blood flow, thus promoting ventilation-perfusion mismatch with hypoxia and respiratory acidosis. Because a high shunt fraction and a patchy distribution of atelectasis is characteristic in acute respiratory failure, hypoxic pulmonary vasoconstriction is an important factor in redistribution of blood flow to ventilated parts of the lung in order to reduce shunt perfusion and prevent hypoxic vasoconstriction in non-injured parts of the lung. The high airway pressures produced by mechanical ventilation cause distortion and high shear forces in the capillary bed of the overinflated part of the diseased lung this hampers...

Mechanisms of vascular remodeling

Persistent pulmonary hypertension, whether acute in onset or chronic and slowly progressive, induces structural changes to the pulmonary arterial tree. Remodeling of pulmonary arteries is a response to high flow and high pressures and or any underlying inflammatory or toxic process. Shear stress to vascular endothelial cells and the subsequent restructuring of their surface properties and shape are considered important factors for remodeling. Pulmonary arteriosclerosis is the most common initial alteration, presenting as a thickening and hypertrophy of smooth muscle of the vascular medial layer. An increase in connective tissue can also be observed. The consequence is a narrowing of the arterial lumen, already the major site of pulmonary vascular resistance under physiological conditions. Furthermore, a reduced compliance of the vascular wall to changing blood flows enhances the development of pulmonary hypertension. The anatomical localization of the injury is The late presentation...

Prognosis and outcome

Remodeling of the vessel structure is potentially reversible when caused by mechanical forces. A reduction in blood flow and perfusion pressure also normalizes shear stresses to intact endothelial cells which are essential for reversal of vascular remodeling. The potential recovery of the pulmonary circulation has been demonstrated in many clinical entities, for example after correction of mitral valve disease, pulmonary artery banding in congenital pulmonary hypertension, or closure of cardiac septal defects. Depending on the duration of pulmonary hypertension, it may take years for the vessels to restructure and pulmonary artery pressures to normalize. Involvement of the right and left ventricles in the disease process must also be considered as this will influence or limit restoration of a normal pulmonary circulation. In contrast with chronic pulmonary hypertension resulting from increased blood flow or high pressures, remodeling of pulmonary vasculature is almost irreversible in...

Etiology And Risk Factors

The main risk factor for most forms of dementia is advanced age, with prevalence roughly doubling every five years over the age of 65 years. Onset before this age is very unusual and, in the case of AD, often suggests a genetic cause. Single gene mutations at one of three loci (beta amyloid precursor protein, presenilinl and presenilin2) account for most of these cases. For late-onset AD both environmental (lifestyle) and genetic factors are important. A common genetic polymorphism, the apolipoprotein E (apoE) gene e4 allele greatly increases risk of going on to suffer from dementia up to 25 of the population have one or two copies (4, 5). However, it is not uncommon for one identical twin to suffer from dementia and the other not. This implies a strong influence of the environment (6). Evidence from cross-sectional and case-control studies suggests associations between AD and limited education (7) and head injury (8, 9), which, however, are only partly supported by longitudinal...

Intravenously administered vasodilators

Global vasodilatation of the pulmonary vasculature increases blood flow to areas of intrapulmonary shunt which further reduces the already compromised PaO2, particularly in patients with acute respiratory distress syndrome. Moreover, concurrent dilatation of the systemic vasculature may result in a dose-dependent arterial hypotension which may possibly lead to ventricular ischemia and consequent heart failure. Nevertheless, vasodilator agents play a major role in the therapeutic strategy of primary pulmonary hypertension. Continuous epoprostenol infusion not only improves the well being of patients considered for heart-lung transplantation, but also doubles median survival time ( Higenbottam,,, 1.9.93).

Alterations Of The Bloodocular Barrier In Diseased State

The blood-ocular barrier shares similar embryological origin, microanat-omy, and many physiological functions with the blood-brain barrier. There are many natural (e.g., diabetes, hypertension) or iatrogenic (chemotherapy, retinal photocoagulation) conditions that cause blood-ocular barrier breakdown. Disruption of the tight junctions between the endothe-lium of the retinal blood vessels (inner blood-retinal barrier) and the tight junctions between adjacent RPE cells (outer blood-retinal barrier) results in breakdown of the BOB and subsequent changes in drug ocular penetration.

What caused this stroke

The list of potential causes is long and obviously differs for ischaemic35 and haemorrhagic stroke.36 In individual patients, even after extensive investigation it may be difficult to establish the cause many will have competing causes (for example, atrial fibrillation (AF) and carotid disease). Thus in practice, the precise cause of stroke is often uncertain. Accepting this, we estimate that about 50 of ischaemic strokes are due to atherothromboembolism, 25 due to intracranial small vessel disease, and 20 due to cardiac embolism, with only 5 due to rarer causes. Most haemorrhagic strokes are thought to be due to small vessel disease (often associated with hypertension), although amyloid angiopathy commonly underlies lobar haemorrhages vascular abnormalities such as aneurysms and arteriovenous malformations may also underlie haemorrhage and the risk of haemorrhage with anticoagulants increases with the international normalised ratio (INR).

General Comments

The only significant human exposure to bismuth involves pharmaceutical uses. A number of trivalent and, rarely, pentavalent salts of bismuth have been used orally or intramuscularly over the past two centuries for the treatment of a number of conditions syphilis, malaria, hypertension, warts, stomatitis, upper respiratory tract infections, amebiasis, dyspepsia and diarrhea. Bismuth compounds have also been used as radiocontrast agents in diagnostic testing and as topical astringents having slight antiseptic action (1). With the introduction of more effective therapeutic agents, primarily antibiotics and antimicrobials, the internal use of certain trivalent bismuth salts (subnitrates, subcarbonates, subgallates, tartrates, subcitrates, and subsalicylates) is now limited primarily to oral preparations for the prevention and treatment of gastric and intestinal disorders, such as ulcers and diarrhea. Available as over-the-counter products, the (presumed) insoluble bismuth salts were long...

Transplant Related Complications

Hepatic Veno-occlusive Disease (VOD) VOD is a clinical syndrome characterized by painful hepatomegaly, jaundice, ascites, fluid retention, and weight gain.116,117 The onset is usually before day + 35 after stem cell reinfusion, and other causes of these symptoms and signs are absent. VOD develops in 2 to 40 of patients after SCT and ranges in severity from mild, reversible disease to a severe syndrome associated with multiorgan failure and death, with established severe VOD shown to have a mortality rate approaching 100 by day + 100 post-SCT. VOD is believed to be caused by primary conditioning regimen-induced injury to sinusoidal endothelial cells and hepatocytes with subsequent damage to the central veins in zone 3 of the hepatic acinus.118 Early changes include deposition of fibrinogen, factor VIII, and fibrin within venular walls and sinusoids. As the process of venular microthrombosis, fibrin deposition, ischemia, and fibrogenesis advances, widespread zonal disruption leads to...

Cardiovascular Reflexes

The injection of a vasoconstrictor, which causes an increase in mean arterial blood pressure, results in activation of the baroreceptors and increased neural input to the cardiovascular centers in the medulla oblongata. The reflex compensation for the drug-induced hypertension includes an increase in parasympathetic nerve activity and a decrease in sympathetic nerve activity. This combined alteration in neural firing reduces cardiac rate and force and the tone of vascular smooth muscle. As a consequence of the altered neural control of both the heart and the blood vessels, the rise in blood pressure induced by the drug is opposed and blunted.

Withdrawal without complications

When alcohol is completely withdrawn or substantially reduced a characteristic withdrawal syndrome can develop. It includes autonomic hyperactivity like hand tremor, insomnia, sweating, tachycardia, hypertension, and anxiety. The symptoms generally occur between 6 and 12 h after the last alcohol consumption. Depending on their severity they may last for up to 4 or 5 days. The neurobiological basis for withdrawal is a gradual upregulation of W-methyl-D-aspartate receptors under the influence of chronic alcohol use. As soon as the alcohol, which acts as a central nervous system depressant, is withdrawn, we observe an overwhelming excitatory action on the brain mediated by the glutamatergic system.

Mechanism of Action

Arterial blood pressure (afterload) is also reduced by propranolol. Although the mechanisms responsible for this antihypertensive effect are not completely understood, they are thought to involve (1) a reduction in cardiac output, (2) a decrease in plasma renin activity, (3) an action in the central nervous system, and (4) a resetting of the baroreceptors . Thus, propranolol may exert a part of its beneficial effects in secondary angina by decreasing three of the major determinants of myo-cardial oxygen demand, that is, heart rate, contractility, and systolic wall tension.

Calcium Entry or Calcium Channel Blockers

These compounds block L-type voltage-dependent calcium channels in vascular smooth muscle and the heart, block platelet aggregation, and are particularly effective in the prophylaxis of coronary vasospasm or variant angina. In addition, these compounds are used in the chronic treatment of secondary angina. Two members of this group, vera-pamil (Calan) and diltiazem (Cardiazem), also have been approved for use in the therapy of certain supraventricular tachyarrhythmias (see Chapter 16). Other potential clinical uses of these compounds include systemic and pulmonary hypertension and Raynaud's syndrome

The Reninangiotensin System

The renin-angiotensin system is important for the regulation of vascular smooth muscle tone, fluid and electrolyte balance, and the growth of cardiac and vascular smooth muscle. A normally functioning renin-angiotensin system contributes to the routine control of arterial blood pressure. A variety of basic and clinical investigations have resulted in a broader understanding of the role of the renin-angiotensin system in the cardiovascular pathophysiology of hypertension, congestive heart failure, and more recently, atherosclerosis. Whether or not abnormal activity of the renin-angiotensin system contributes to the primary etiology of these diseases, pharmacological inhibition of the renin-angiotensin system has proved to be a valuable therapeutic strategy in the treatment of hypertension and congestive heart failure.

Obesity see chapter

Obesity is a risk factor for the development of Type 2 diabetes. Weight gain (particularly centrally distributed) is associated with metabolic processes that increase the risk of cardiovascular disease. These metabolic disturbances include an atherogenic lipid profile, hyperinsulinaemia, hypertension and thrombogenesis. Diabetes UK estimate 75-90 of people with diabetes have Type 2 diabetes, of these 80 are overweight or obese. The risks of hypertension, For overweight Type 2 diabetic patients, the most important dietary objective is to achieve and maintain a desirable weight and BMI. However, the weight loss required to achieve this is often not realistic, even in the long term and weight loss of 5 can result in some clinical improvement. Whereas 10 weight loss can produce major benefits improving glycaemic control by reducing insulin resistance improving lipid profile and reducing hypertension

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Your heart pumps blood throughout your body using a network of tubing called arteries and capillaries which return the blood back to your heart via your veins. Blood pressure is the force of the blood pushing against the walls of your arteries as your heart beats.Learn more...

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