Hypertension Causes And Treatment Pdf

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Hypertension , also called high blood pressure , condition that arises when the blood pressure is abnormally high. Although the heart and blood vessels can tolerate increased blood pressure for months and even years, eventually the heart may enlarge a condition called hypertrophy and be weakened to the point of failure. Injury to blood vessels in the kidneys, brain, and eyes also may occur.

Everything You Need to Know About High Blood Pressure (Hypertension)

Resistant hypertension is defined as uncontrolled blood pressure despite the use of three antihypertensive drugs, including a diuretic, in optimal doses. Treatment resistance can be attributed to poor adherence to antihypertensive drugs, excessive salt intake, physician inertia, inappropriate or inadequate medication, and secondary hypertension.

Drug-induced hypertension, obstructive sleep apnoea, primary aldosteronism, and chronic kidney disease represent the most common secondary causes of resistant hypertension.

Several drugs can induce or exacerbate pre-existing hypertension, with non-steroidal anti-inflammatory drugs being the most common due to their wide use.

Obstructive sleep apnoea and primary aldosteronism are frequently encountered in patients with resistant hypertension and require expert management. Hypertension is commonly found in patients with chronic kidney disease and is frequently resistant to treatment, while the management of renovascular hypertension remains controversial. A step-by-step approach of patients with resistant hypertension is proposed at the end of this review paper.

Hypertension represents a major public health problem affecting more than one billion individuals worldwide [ 1 ]. The advent of antihypertensive therapy has substantially reduced the occurrence of cardiovascular events.

However, antihypertensive therapy failed to achieve blood pressure control in all patients, with hypertension control rates remaining in general disappointingly low. Blood pressure goals are not attained in some patients despite the simultaneous use of several antihypertensive medications. Resistant hypertension is currently defined as uncontrolled blood pressure despite the use of optimal doses of three antihypertensive medications, of which one is a diuretic [ 2 ].

Several factors have been identified as contributors to resistant hypertension. Poor patient adherence, physician inertia, inadequate doses or inappropriate combinations of antihypertensive drugs, excess alcohol intake, and volume overload are some of the most common causes of resistance [ 2 — 10 ].

Secondary forms of hypertension represent another very important contributor to drugresistance. The list of secondary forms of hypertension is long and covers a large variety of conditions Table 1. Most of these conditions may result in resistance to pharmacologic therapy of hypertension. The management of patients with resistant hypertension requires a gratifying combination of clinical acumen and common sense. An extensive workup of all patients with uncontrolled hypertension is scientifically unsound, is very costly and requires immense human and technical resources.

Therefore, practicing physicians need to implement evidence-based medicine. The effective management of patients with resistant hypertension requires an appropriate combination of physiology and pharmacology, taking into account the unique characteristics of each case in order to tailor the therapeutic approach to the individual patient.

This paper will address the most common secondary causes of resistant hypertension drug-induced, obstructive sleep apnea, primary aldosteronism, and chronic kidney disease , which are frequently encountered in hypertensive patients and are, therefore, the most interesting from the clinical point of view.

In addition, this paper will attempt to provide a rational for the workup and treatment of patients with resistant hypertension. The exact prevalence of resistant hypertension in the general population remains unknown. It has to be noted, however, that atypical drug combinations have been used in most of these studies as required by study protocols. Therefore, the evaluation of the prevalence of resistant hypertension requires a large, prospective, population-based study, specially designed for this aim.

Similarly, the prognosis of resistant hypertension is currently unknown [ 2 — 10 ]. Available evidence addressing the prognosis of resistant hypertension is scarce, since virtually no longitudinal study has addressed this topic.

Data from small clinical studies point towards an increased cardiovascular risk in patients with resistant hypertension. In addition, patients with resistant hypertension frequently have comorbidities that are known to increase cardiovascular morbidity and mortality, such as chronic kidney disease, diabetes, and obesity.

Moreover, patients with resistant hypertension have higher rates of target organ damage than the general hypertensive population and are thus at increased cardiovascular risk. Resistance to antihypertensive treatment is affected by several lifestyle factors. Excessive dietary salt intake is common in patients with resistant hypertension and contributes to treatment resistance by blunting the blood pressure reduction of most antihypertensive drugs, including diuretics and inhibitors of the renin-angiotensin axis [ 2 — 10 ].

Obesity can also contribute to treatment resistance [ 2 — 10 ]. It has been shown that blood-pressure control is more difficult to be achieved in obese than lean hypertensive patients.

Several lines of evidence indicate a graded positive correlation between body mass index and blood pressure levels, while weight loss results in blood pressure reduction.

Insulin resistance, sympathetic nervous system overactivity, sodium retention, and activation of the renin-angiotensin system have been implicated in the pathogenesis of obesity-induced hypertension.

Alcohol consumption is another important factor [ 2 — 10 ]. In addition, blood pressure control might be achieved more difficult in heavy drinkers due to poor adherence in antihypertensive therapy. The role of physical inactivity in patients with resistant hypertension has not been adequately studied.

A variety of prescription or over the counter medicines as well as other exogenous substances may induce hypertension or contribute to treatment resistance. Drug-induced hypertension is among the most common causes of secondary hypertension and is frequently encountered in everyday clinical practice. However, despite the frequent occurrence of drug-induced hypertension, primary care physicians frequently miss the opportunity to detect and appropriately manage this iatrogenic form of secondary hypertension.

Therefore, a detailed and meticulous medical history is of utmost importance in patients with resistant hypertension, since the identification and subsequent withdrawal of the offending drug may alleviate treatment resistance.

Another very important aspect relates to the great variability of the effects of administered drugs on blood pressure. The administration of offending drugs can result in excessive blood pressure elevation in some individuals, while most individuals will experience little or no increases of blood pressure.

This variability represents a rule without exception. Therefore, it would be very important to identify predictors of blood pressure elevation, in order to individualize drug treatment. Up to now, however, no such reliable predictors have been identified. A descriptive list of all exogenous agents capable of inducing or exaggerating hypertension is presented in Table 2. However, this paper will focus on the drugs that are widely used, represent the most common causes of drug-induced hypertension, and are thus of major clinical importance: nonsteroidal anti-inflammatory drugs NSAIDs and oral contraceptives.

In addition, a brief comment regarding specific antineoplastic agents anti-VEGF that have emerged as inducers of hypertension is presented at the end of this chapter, since many clinicians are not aware of this condition. Osteoarthritis is highly prevalent in the general population, and its prevalence would be even greater due to population aging and the obesity epidemic [ 11 , 12 ]. Osteoarthritis and hypertension often coexist, since both conditions are age related.

Although lifestyle modification, exercise, and weight loss are considered as first-line therapeutic measures for patients with osteoarthritis, the vast majority of such patients require the systematic or intermittent use of either acetaminophen or NSAIDs for pain relief.

Two large prospective cohort studies in normotensive women reported higher risks of subsequent hypertension among NSAIDs users than in women without regular NSAIDs administration [ 14 , 15 ]. In the first study, the risk of developing hypertension was increased about two times in women using acetaminophen or NSAIDs [ 14 ]. Acetaminophen consumption for 1—4 days per month and NSAIDs consumption for 5—14 days per month was necessary for the risk to be apparent.

It has to be noted that although acetaminophen is considered to have a better safety profile than NSAIDs [ 16 , 17 ], its use was associated with a moderate increase in the risk for incident hypertension in both males and females [ 18 , 19 ]. In the first meta-analysis, mean arterial pressure was increased by 3. On the contrary, data reporting no or little effect of NSAIDs on blood pressure exist in the literature as well.

In two cross-sectional studies, no association between use of NSAIDs and hypertension was found [ 23 , 24 ]. Similar findings were observed in two small randomized studies regarding the effects of acetaminophen on blood pressure [ 25 , 26 ], as well as in studies evaluating the effects of aspirin on blood pressure in hypertensive patients [ 27 , 28 ].

In addition, in a large prospective cohort of 8, male normotensive physicians, analgesic use was not associated with increased risk of developing hypertension hazard ratio: 1. The corresponding hazard ratios were 1. This apparent heterogeneity of available data on the effects of traditional NSAIDs on blood pressure becomes even more complicated when recent data with selective COX-2 inhibitors are taken in account. In a meta-analysis of randomized trials, use of COX-2 inhibitors was associated with a significant increase in blood pressure compared to placebo 3.

However, it was shown that a great part of blood pressure elevation could be attributed to rofecoxib. Indeed, rofecoxib use is associated with greater blood pressure elevations than celecoxib in both hypertensive and normotensive individuals [ 31 ]. The above-mentioned study highlights another important aspect: the potential differences on blood pressure effects between the various NSAIDs.

In a meta-analysis of randomized trials, conducted mainly in hypertensive patients, naproxen and indomethacin were associated with the largest blood pressure elevations, while piroxicam, sulindac, ibuprofen, and aspirin exhibited little if any effect on blood pressure [ 21 ].

On the contrary, a randomized study in patients with controlled hypertension showed that the blood pressure was significantly higher with ibuprofen than with lumiracoxib [ 32 ]. Moreover, in 34, participants at the MEDAL Multinational Etoricoxib and Diclofenac Arthritis Long term program, patients assigned to etoricoxib discontinued the study due to hypertension more frequently than patients randomized to diclofenac [ 33 ].

Finally, the potential differences of the effects of NSAIDs on blood pressure according to the various antihypertensive agents coadministered are of great clinical importance. In a study of elderly hypertensives with osteoarthritis, indomethacin had no effect on blood pressure in patients taking calcium antagonists whereas significant blood pressure elevations were detected in patients taking ACE-inhibitors [ 34 ].

On the contrary, celecoxib exerted similar to placebo effects in patients taking ACE-inhibitors [ 35 ]. Another study among hypertensive patients with osteoarthritis, comparing the effects of rofecoxib and celecoxib, revealed no differences on blood pressure between the two drugs in patients taking diuretics or calcium antagonists, whereas larger blood pressure elevations were observed with rofecoxib than with celecoxib in patients taking ACE-inhibitors or beta blockers [ 36 ]. The above presented information clearly indicates that available data on the effects of NSAIDs on blood pressure are sometimes contradictory and in total far from conclusive.

Convincing data coming from carefully designed randomized studies are necessary to: a detect potential differences between the various NSAIDs on blood pressure, b clarify the effects of coadministering each NSAID with each one of the various antihypertensive drug categories, and c identify predictors of blood pressure response to NSAIDs use. Withdrawal of NSAIDs is indicated in patients with resistant hypertension, exacerbation of prior hypertension, or incident hypertension.

Pain relief is more likely in patients with osteoarthritis and pain of muscular skeletal origin. However, this is not always possible in everyday clinical practice, since patients with chronic inflammatory arthritic diseases rheumatoid arthritis respond better to anti-inflammatory agents. In such cases, hydrocodone, tramadol, or nerve blocking might be of help, constituting effective alternatives to NSAIDs. In cases, however, where NSAIDs are still necessary, the lower effective dose should be administered, since existing data point towards dose-related effects of NSAIDs on blood pressure.

NSAIDs affect blood pressure levels via different mechanisms: activation of the renin-angiotensin-aldosterone system, sodium and water retention, induction of vasoconstriction through endothelin-1 and arachidonic acid metabolites, and mainly inhibition of renal vasodilatory prostaglandins E 2 and I 2 [ 37 — 43 ].

These detrimental effects of NSAIDs may lead to deterioration of renal function and acute kidney injury, especially in patients of older age, preexisting hypertension, chronic kidney disease, or diabetes. In such patients, calcium antagonists seem to be more suitable than drugs inhibiting the renin-angiotensin system, since the concomitant administration of NSAIDs and calcium antagonists is not accompanied by blood pressure elevation [ 36 , 39 ].

The development of NSAIDs that apart from cyclo-oxygenase inhibition possess nitric oxide promoting properties might significantly ameliorate current situation and alleviate the effects of NSAIDs on blood pressure. Naproxcinod is the first CINOD in clinical trials with very promising preliminary results [ 44 — 47 ]. Oral contraceptives represent another class of drugs that are widely used and are capable of inducing hypertension [ 48 , 49 ].

However, withdrawal of oral contraceptives abolished this increased risk, underlining the need for close monitoring in women taking oral contraceptives. A study in hypertensive women revealed that those taking oral contraceptives had more severe hypertension and lower blood-pressure control rates than women using other contraceptive methods [ 51 ].

The type of oral contraceptives seems also to be of clinical importance. Combined oral contraceptives progestin and estradiol , which were widely used in the past, were associated with blood pressure elevations more frequently than progestin-only oral contraceptives. On the contrary, drospirenone a fourth generation progestin reduces blood pressure when combined with estradiol [ 52 ].

Therefore, current guidelines recommend the use of progestin-only oral contraceptives in women with established cardiovascular disease, or major cardiovascular risk factors such as hypertension [ 53 , 54 ].

It can, therefore, be summarized that oral contraceptives may contribute to resistance in hypertensive women, but the type of oral contraceptive is important. Close monitoring of women and withdrawal of oral contraceptives may alleviate the effects on blood pressure.

Another class of agents that emerged as inducers of hypertension are the antineoplastic drugs that target the VEGF pathway.

Severe Asymptomatic Hypertension: Evaluation and Treatment

Hypertension HTN or HT , also known as high blood pressure HBP , is a long-term medical condition in which the blood pressure in the arteries is persistently elevated. High blood pressure is classified as primary essential hypertension or secondary hypertension. Blood pressure is classified by two measurements, the systolic and diastolic pressures, which are the maximum and minimum pressures, respectively. Lifestyle changes and medications can lower blood pressure and decrease the risk of health complications. Hypertension is rarely accompanied by symptoms, and its identification is usually through screening , or when seeking healthcare for an unrelated problem. Some people with high blood pressure report headaches particularly at the back of the head and in the morning , as well as lightheadedness , vertigo , tinnitus buzzing or hissing in the ears , altered vision or fainting episodes.

Resistant hypertension is defined as uncontrolled blood pressure despite the use of three antihypertensive drugs, including a diuretic, in optimal doses. Treatment resistance can be attributed to poor adherence to antihypertensive drugs, excessive salt intake, physician inertia, inappropriate or inadequate medication, and secondary hypertension. Drug-induced hypertension, obstructive sleep apnoea, primary aldosteronism, and chronic kidney disease represent the most common secondary causes of resistant hypertension. Several drugs can induce or exacerbate pre-existing hypertension, with non-steroidal anti-inflammatory drugs being the most common due to their wide use. Obstructive sleep apnoea and primary aldosteronism are frequently encountered in patients with resistant hypertension and require expert management.

diseases and stroke are becoming major causes of illness and death. They account for Advances in the diagnosis and treatment of hypertension have played a major role in recent dramatic policy/lotusdream.org). Cutler JA.

Common Secondary Causes of Resistant Hypertension and Rational for Treatment

Hypertension affects one-third of Americans and is a significant modifiable risk factor for cardiovascular disease, stroke, renal disease, and death. Severe asymptomatic hypertension is defined as severely elevated blood pressure mm Hg or more systolic, or mm Hg or more diastolic without symptoms of acute target organ injury. The short-term risks of acute target organ injury and major adverse cardiovascular events are low in this population, whereas hypertensive emergencies manifest as acute target organ injury requiring immediate hospitalization. Individuals with severe asymptomatic hypertension often have preexisting poorly controlled hypertension and usually can be managed in the outpatient setting.

High blood pressure, or hypertension, occurs when your blood pressure increases to unhealthy levels. Your blood pressure measurement takes into account how much blood is passing through your blood vessels and the amount of resistance the blood meets while the heart is pumping. Narrow arteries increase resistance. The narrower your arteries are, the higher your blood pressure will be. Over the long term, increased pressure can cause health issues, including heart disease.

High Blood Pressure

Blood pressure is the force of your blood pushing against the walls of your arteries. Each time your heart beats, it pumps blood into the arteries. Your blood pressure is highest when your heart beats, pumping the blood.


High blood pressure hypertension is a common condition in which the long-term force of the blood against your artery walls is high enough that it may eventually cause health problems, such as heart disease. Blood pressure is determined both by the amount of blood your heart pumps and the amount of resistance to blood flow in your arteries. The more blood your heart pumps and the narrower your arteries, the higher your blood pressure. A blood pressure reading is given in millimeters of mercury mm Hg. It has two numbers. You can have high blood pressure for years without any symptoms.

We include products we think are useful for our readers. If you buy through links on this page, we may earn a small commission. Hypertension is another name for high blood pressure. It can lead to severe health complications and increase the risk of heart disease, stroke, and sometimes death. This pressure depends on the resistance of the blood vessels and how hard the heart has to work.

 Может быть, Стратмор решил посмотреть на звезды. - Джабба, мне не до шуток. - Ну хорошо, - сказал он, приподнимаясь на локтях.  - Может быть, у них закоротило генератор. Как только освобожусь, загляну в шифровалку и… - А что с аварийным питанием. Если закоротило генератор, почему оно не включилось. - Не знаю.

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В желающих принять его на работу не было недостатка, а увидав, что он может творить на компьютере, они уже не хотели его отпускать. Профессионализм Хейла достиг высокого уровня, и у него появились знакомые среди интернет-пользователей по всему миру. Он был представителем новой породы киберпсихов и общался с такими же ненормальными в других странах, посещая непристойные сайты и просиживая в европейских чатах. Его дважды увольняли за использование счета фирмы для рассылки порнографических снимков своим дружкам. - Что ты здесь делаешь? - спросил Хейл, остановившись в дверях и с недоумением глядя на Сьюзан.

Там открывался вид на стоянку автомобилей агентства, а из окна комнаты для заседаний был виден внушительный ряд корпусов АНБ - в том числе и купол шифровалки, это вместилище высочайших технологий, возведенное отдельно от основного здания и окруженное тремя акрами красивого парка. Шифровалку намеренно разместили за естественной ширмой из высоченных кленов, и ее не было видно из большинства окон комплекса АНБ, а вот отсюда открывался потрясающий вид - как будто специально для директора, чтобы он мог свободно обозревать свои владения. Однажды Мидж предложила Фонтейну перебраться в эту комнату, но тот отрезал: Не хочу прятаться в тылу. Лиланд Фонтейн был не из тех, кто прячется за чужими спинами, о чем бы ни шла речь. Мидж открыла жалюзи и посмотрела на горы, потом грустно вздохнула и перевела взгляд на шифровалку. Вид купола всегда приносил ей успокоение: он оказался маяком, посверкивающим в любой час суток. Но сегодня все было по-другому.

Юлий Цезарь всегда с нами. Мидж развела руками. - О чем. - Квадрат Цезаря, - просияла Сьюзан.  - Читается сверху .

У него никогда не возникало сомнений по поводу того, кто убьет Танкадо.

Но одно не давало Фонтейну покоя - то, что Стратмор решил прибегнуть к услугам Халохота. Тот, конечно, был мастером своего дела, но наемник остается наемником. Можно ли ему доверять. А не заберет ли он ключ .

Мидж повернулась на вращающемся стуле. - Такой список выдает только принтер Фонтейна. Ты это отлично знаешь. - Но такие сведения секретны. - У нас чрезвычайная ситуация, и мне нужен этот список.

Где-то там, на летном поле, в одном из трех частных ангаров севильского аэропорта стоит Лирджет-60, готовый доставить его домой. Пилот сказал вполне определенно: У меня приказ оставаться здесь до вашего возвращения. Трудно даже поверить, подумал Беккер, что после всех выпавших на его долю злоключений он вернулся туда, откуда начал поиски. Чего же он ждет. Он засмеялся.

 Дипломатическая любезность? - изумился старик. - Да, сэр. Уверен, что человеку вашего положения хорошо известно, что канадское правительство делает все для защиты соотечественников от неприятностей, которые случаются с ними в этих… э-э… скажем так, не самых передовых странах. Тонкие губы Клушара изогнулись в понимающей улыбке.

 Это не имеет никакого отношения к Попрыгунчику, - резко парировала. Вот это чистая правда, - подумал Джабба. - Послушай, Мидж, к Стратмору я не отношусь ни плохо ни хорошо. Ну, понимаешь, он криптограф.

Мотоцикл и такси с грохотом въехали в пустой ангар. Беккер лихорадочно осмотрел его в поисках укрытия, но задняя стена ангара, громадный щит из гофрированного металла, не имела ни дверей, ни окон. Такси было уже совсем рядом, и, бросив взгляд влево, Беккер увидел, что Халохот снова поднимает револьвер.

Он потерял равновесие, шатаясь, выскочил на слепящее солнце и прямо перед собой увидел лестницу. Перепрыгнув через веревку, он побежал по ступенькам, слишком поздно сообразив, куда ведет эта лестница.

Люди на подиуме с недоумением переглянулись. Дэвид подмигнул крошечной Сьюзан на своем мониторе. - Шестьдесят четыре буквы. Юлий Цезарь всегда с нами. Мидж развела руками.

Она смутилась. - Боже, вы, кажется, сумели прочесть. Он посмотрел еще внимательнее.

 - Имея партнера в Америке, Танкадо мог разделить два ключа географически. Возможно, это хорошо продуманный ход. Сьюзан попыталась осознать то, что ей сообщил коммандер.

Его взял немец. Дэвид почувствовал, как пол уходит у него из-под ног. - Немец. Какой немец. - Тот, что был в парке.

Полагаю, Росио и ее гость ушли на вечернюю прогулку. Если вы оставите для нее записку, она получит ее прямо с утра.  - Он направился к полке с ячейками для ключей и почты. - Быть может, я мог бы позвонить в номер и… - Простите, - сказал консьерж, и вся его любезность мгновенно улетучилась.

В разделе Служба сопровождения в справочнике было только три строчки; впрочем, ничего иного все равно не оставалось. Беккер знал лишь, что немец был с рыжеволосой спутницей, а в Испании это само по себе большая редкость. Клушар вспомнил, что ее звали Капля Росы. Беккер скорчил гримасу: что это за имя.

Вспомнив всю услышанную от шефа ложь, она похолодела и посмотрела на него, в глазах ее мелькнуло подозрение. - Это вы убили Танкадо. Стратмор вздрогнул и замотал головой: - Конечно.


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