What causes diastolic blood pressure to increase

In general, mean BP change in a population, rather than the response rate (i.e., percentage of the population that reaches a prespecified goal BP or has a change of a specified magnitude) has been used as the metric to evaluate antihypertensive efficacy. Although the response rate, relative to comparator, will generally track mean BP changes, it depends on the starting BP and the non–drug-related component of response (i.e., digit preference), and thus may be misleading. On the other hand, there may be cases in which it would be useful to examine the distribution of responses rather than simply mean response, such as when responder and nonresponder subsets exist, as would be the case for low- and high-renin patients in responding to ACE-Is, ARBs, or β-adrenergic receptor blockers. Racial/ethnic differences in antihypertensive response to agents that block the renin-angiotensin system are well described. The FDA has not defined a minimum magnitude of BP-lowering required for antihypertensive approval. In theory, an antihypertensive that reduced BP on average by as little as 2 mm Hg could be considered approvable if the drug had no significant safety issues, although most antihypertensive drugs currently approved have mean BP reductions substantially greater than this, and it is hard to imagine that such a drug would be considered very useful. If used, such a drug might also create a delay for patients to receive other more potent antihypertensives. Approval of such a drug would make most sense if the drug provided a novel mechanism, so that it could be added to maximal medical therapy in a patient not at goal BP. A more interesting possibility, however, is that a drug might have a small effect in the general population, but a sizeable effect in some patients, possibly, but not necessarily, a genetically or proteomically definable subset of the population. Even if that subset were only a small fraction of the population, such a drug, if properly targeted, might be useful for the responsive subset.

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Hypertrophic Cardiomyopathy

SHEMY CARASSO MD, HARRY RAKOWSKI MD, in Diastology, 2008

Geometry

Dynamic diastolic pressure-volume (P-V) curves measured during filling (PVRfill) in patients with HCM are often considerably shallower than would be anticipated if one assumed high chamber stiffness,25–27 and they markedly deviate from the passive end diastolic pressure-volume relationship (EDPVR) recorded during balloon catheter obstruction of inferior vena cava inflow. This is in contrast to the concordance of dynamic and passive curves in normal subjects, hypertensive hypertrophy, and dilated cardiomyopathy.27 The unusual behavior in HCM cannot be attributed directly to increased viscosity, enhanced pericardial constraint, or preload dependence of isovolumic relaxation. Regional heterogeneity of relaxation may play a role, but probably the major mechanism involves the end systolic distal chamber being virtually emptied, so that unfolding of the chamber in early diastole can accommodate substantial volumes by pure shape change without increasing the endocardial surface area and thus without stretching the myocardium.25,26 This may account for the fact that there was very little change in LV pressure during early filling in HCM hearts, yielding shallow PVRfill. This in turn may be directly related to the unique fiber and chamber architecture seen with HCM and possibly to enhanced ventricular interaction. These observations complicate the interpretation of diastolic P-V data in HCM, as well as conclusions regarding the influence of therapies based on analysis of single cardiac cycles.27

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Cardiovascular Assessment

Dany E. Weisz BSc, MD, MSc, Patrick Joseph McNamara MD, MRCPCH, MSc, in Assisted Ventilation of the Neonate (Sixth Edition), 2017

Diastolic Hypotension

Low DBP generally reflects reduced SVR or intravascular volume depletion, and treatment should target the underlying etiology (see Table 14-7). Intravascular volume expansion with a 10 to 20 mL/kg bolus of 0.9% sodium chloride is a first-line therapy in the setting of dehydration, capillary leak, or warm septic shock. Additional volume may be administered based on clinical evaluation and the biochemical and echocardiographic response to the initial bolus. Diastolic hypotension due to reduced SVR but refractory to fluid resuscitation may be treated with intravenous vasopressor infusions such as dopamine (5 to 15 mcg/kg/min), which has been consistently demonstrated to be superior to dobutamine at increasing blood pressure. Epinephrine may be considered in the setting of diastolic hypotension and concomitant LV dysfunction. Norepinephrine is a potent β1- and α-adrenergic agonist, which increases systolic and DBP and SVR, with limited evidence in term neonates that it may be effective in septic shock refractory to fluid resuscitation, dopamine, and dobutamine.48

Glucocorticoids have been demonstrated to increase blood pressure in neonates with refractory hypotension by upregulating catecholamine production and adrenergic receptor expression and should be considered in cases of refractory hypotension. Hydrocortisone has been well studied in neonates and is typically administered at a dose of 0.5 to 1 mg every 6 hours.

Identifying the etiology of diastolic hypotension in very preterm infants on the first day of life is challenging. A combined clinical–echocardiographic evaluation is important to define and manage the relative contributions of intravascular volume depletion, reduced SVR, and PDA, which all merit different therapeutic approaches. Diastolic hypotension due to a large PDA may be supportively managed with strategies to judiciously increase PVR (see next section) or with intravenous dobutamine. Adrenocortical insufficiency is common in extremely preterm infants and intravenous hydrocortisone is effective in the treatment of refractory hypotension without an increase in short-term adverse effects.49

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THE PULMONARY CIRCULATION

Andrew Davies MA PhD DSc, Carl Moores BA BSc MB ChB FRCA, in The Respiratory System (Second Edition), 2010

Gravity

The diastolic blood pressure in the systemic circulation is about 80 mmHg, which is enough pressure to raise a column of water by a height of over a metre. In other words, there is more than enough pressure to carry blood from the heart up to the head. However, in the pulmonary circulation the diastolic blood pressure is about 12 mmHg, enough pressure to raise a column of water about 15 cm. In other words, there is only just enough pressure to pump blood from the right ventricle up to the lung apices. On the other hand, at the lung bases the blood pressure in the pulmonary circulation is equal to the pressure generated by the right ventricle plus the hydrostatic pressure of a column of blood extending up to the heart. Because the pressure generated by the right ventricle is not very high, this extra hydrostatic pressure makes a very significant difference. Thus there is a very considerable difference in arterial blood pressure between the bases and the apices of the lungs owing to gravity. In other words, gravity tends to direct blood towards the lung bases.

Case 7.1

The pulmonary circulation: bringing blood and gas together: 2

What causes a pulmonary embolus and how can it be diagnosed?

A pulmonary embolus occurs when something, usually a thrombus (blood clot), occludes part of the pulmonary artery tree. Generally the thrombus forms in the veins of the pelvis or lower limb, and part of that thrombus or the whole thrombus may dislodge and pass through the vena cava, through the right atrium and ventricle and into the pulmonary artery. The thrombus finally lodges in a branch of the pulmonary artery, occluding it. The segment of lung tissue supplied by the obstructed artery has a reduced blood supply (although it often receives some blood – remember the bronchial circulation) and may finally infarct.

In a small number of cases (probably less than 10% of the total number of pulmonary emboli) the thrombus does not form in the veins of the pelvis or leg but forms in the heart. This may be as a result of atrial fibrillation, in which the atria of the heart do not beat properly, or thrombus may form on a part of the myocardium which has infarcted. Very occasionally the embolus is not formed from thrombus but from other substances, such as fat or amniotic fluid.

Conditions that lead to the formation of thrombus in the pelvic and lower limb veins include prolonged immobility, lower limb or pelvic fractures, abdominal surgery, pregnancy, the presence of cancer and clotting abnormalities. Mrs Dodds had two of these risk factors, including immobility (she was bedridden) and a lower limb fracture. If the thrombus forms in the lower limb it may become swollen and painful, which is why the doctor examined Mrs Dodds' legs. If thrombus occurs in the lower limbs it usually occurs in the deep veins in the muscle, rather than the veins near the skin. Hence the condition is usually called deep venous thrombosis (DVT). Several cases have been reported of patients suffering DVTs and pulmonary emboli following the prolonged immobility that occurs during a long-distance flight, sometimes in rather cramped conditions. The true incidence of this so-called ‘economy class syndrome’ is yet to be established, however.

Small emboli in the lungs cause no symptoms and no haemodynamic problems and go unnoticed. Larger emboli, particularly if they result in pulmonary infarction, can cause clinical symptoms, including pleuritic chest pain and sometimes haemoptysis. Very large emboli are a medical emergency (see Box 4).

Usually there is very little to find on clinical examination of a patient who has suffered a pulmonary embolus – occasionally there may be a few crackles on auscultation. Occasionally, though, a pleural rub may be heard over an area of infarcted lung. A plain chest X-ray is not generally very helpful in diagnosing a pulmonary embolus: if there is quite a large embolus it is said that the affected lung fields can appear ‘oligaemic’: in other words, they appear darker on the chest X-ray as those areas of lung contain less blood. This is not always easy to see, however. Larger pulmonary emboli increase the amount of work that the right ventricle has to do, as it has to pump blood into a partially obstructed pulmonary circulation. This can result in changes in the ECG. Classically these changes consist of S waves in lead I and Q waves and inverted T waves in lead III (hence the mnemonic: ‘S1 Q3 T3’), but these changes are rarely seen in practice.

Diagnosis of a pulmonary embolus can be made using a radioisotope scan of the blood flow in the lungs, but nowadays is often made with a CT pulmonary angiogram. In this test, X-ray contrast is injected into a vein and its flow through the lungs is monitored with a fast CT scanner. Clot in the pulmonary vessels can then be identified.

A CT pulmonary angiogram of a patient with a large pulmonary embolus is shown in Figure 7.5A. The CT shows a cross-section of the patient's chest at the point where the aorta arches over the dividing pulmonary artery. CT scans are usually shown as if the cross-section is being viewed from below, in other words, the left-hand side of the scan corresponds to the right-hand side of the body. X-ray contrast, which shows up white on the scan, has been injected into a cannula lying in the superior vena cava – the white dot in the otherwise dark vena cava is the contrast within the cannula. Blood which contains contrast is clearly visible in the ascending and descending aorta. There is blood in the right and left pulmonary arteries; however, dark areas are visible within these arteries which correspond to thrombus. This pulmonary embolus is a large one, and thrombus is visible in both pulmonary arteries.

The regional flow of blood within the lungs can be demonstrated by dissolving a radioactive gas (usually Xenon-133 (133Xe)) in saline and then injecting this into the right side of the heart via an intravenous catheter. During the injection the subject holds his breath, and some of the radioactive xenon leaves the blood and enters the alveoli. By measuring the level of radioactivity from outside the body it is possible to estimate the blood flow to different regions of the lungs (Fig. 7.6).

Although the difference in regional blood flow between the apices and bases of the lungs is thought to be due largely to the effect of gravity, it is nevertheless the case that the gradient remains in subjects who are in the supine position. Furthermore, the anatomy of the branching pulmonary vessels results in greater variation between different parts of the same level in the lung than between mean flow in adjacent levels.

Gravity is one factor influencing regional differences in blood flow within the lungs. However, other factors include the air pressure in the alveoli around the pulmonary capillaries, and hypoxic pulmonary vasoconstriction.

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Normal and Abnormal Cardiopulmonary Responses to Exercise

Scot Irwin, in Cardiopulmonary Physical Therapy (Fourth Edition), 2004

Diastolic blood pressure abnormalities

The second, less commonly cited, abnormal blood pressure response is a persistent rise in diastolic pressure with increase in exercise workload. This finding has been correlated with increasing severity of coronary artery disease.23 Numerous articles in the literature describe normal diastolic blood pressure responses.4,24 Many of these articles and texts contradict one another, but generally, the normal response to exercise is for diastolic blood pressure to fall slightly (by 10 to 20 mm Hg) or rise slightly in younger persons, or to remain the same in older persons.

A common sequel to a progressive rise in diastolic pressure with exercise is for the diastolic pressure to remain abnormally elevated several minutes after exercise. No literature describes the significance of this finding, but in the author's clinical experience, it is an abnormal finding.

For the purposes of this discussion, an abnormal diastolic blood pressure response occurs when the diastolic pressure rises 20 mm Hg or more above 90 mm Hg with increasing levels of exercise. Both a patient's actual abnormal response and the generally accepted normal response are depicted in Fig. 3-15. Patients who exhibit this response may have coronary artery disease, even in the absence of ST-segment changes.25 Patient E (see Fig. 3-15) exhibited the following findings upon cardiac catheterization: All atrial and ventricular pressures were mildly to moderately elevated; the left ventricular end-diastolic pressure was 22 mm Hg at rest (0 to 12 mm Hg is normal); the ejection fraction and contractile pattern were normal; the right coronary artery was irregular throughout its course but without severe stenosis; the left main and circumflex arteries were normal; the left anterior descending artery (LAD) was normal to its midpoint, where a 95% to 100% lesion appeared to the end of the LAD, but a large diagonal branch took off at this same point; this branch and the remnants of the LAD continued to be irregular throughout the rest of their courses but without significant stenosis.

Mechanisms.

The causes of progressive diastolic blood pressure increases during exercise are open to speculation. Once again, any combination of humoral, neurological, and hemodynamic factors could be the cause. It is of interest to note though that patients exhibiting a progressive diastolic response to exercise have increased coronary artery blood flow by increasing the driving pressure (diastolic blood pressure). Patients with severe coronary disease generally have some additional peripheral vascular disease, which can dramatically affect systolic and diastolic pressures.

Again, a progressive rise in diastolic blood pressure to above 90 mm Hg with exercise is an abnormal clinical measure. This finding should be recognized and incorporated into exercise test interpretations and individualized exercise-training programs. If the diastolic pressure rises by more than 20 mm Hg above 90 during increasing levels of exercise, the exercise should be terminated, and the patient's physician should be notified.

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Naturopathic Physical Medicine Approaches to General Health Enhancement and Specific Conditions

Leon Chaitow ND DO, ... Roger Newman Turner ND DO BAc, in Naturopathic Physical Medicine, 2008

Massage and hypertension

Massage lowers diastolic blood pressure: Noting that high blood pressure is associated with elevated anxiety, stress and stress hormones, hostility, depression and catecholamines, massage therapy and progressive muscle relaxation were evaluated as treatments for reducing blood pressure and these associated symptoms. Adults who had been diagnosed as hypertensive received ten 30-minute massage sessions over 5 weeks, or were given progressive muscle relaxation instructions (control group). Sitting diastolic blood pressure decreased after the first and last massage therapy sessions, and reclining diastolic blood pressure decreased from the first to the last day of the study. Although both groups reported less anxiety, only the massage therapy group reported less depression and hostility and showed decreased urinary and salivary stress hormone levels (cortisol). The results suggest that massage therapy may be effective in reducing diastolic blood pressure and symptoms associated with hypertension (Hernandez-Reif et al 2000a).

Hypertension reduced by massage: A preliminary study (Olney 2005) tested the effects of a regularly applied back massage on the blood pressure (BP) of patients with clinically diagnosed hypertension. In this experimental, pretest/post-test study, a 10-minute back massage was given to the experimental group (n = 8), three times a week for 10 sessions. The control group (n = 6) relaxed in the same environment for 10 minutes, three times a week for 10 sessions. Analysis of variance-determined systolic BP changed significantly between groups over time as did the diastolic BP. This preliminary study suggested that regular massage may lower BP in hypertensive persons.

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Obesity

Samuel Klein, Johannes A. Romijn, in Williams Textbook of Endocrinology (Thirteenth Edition), 2016

Hypertension

Systolic and diastolic blood pressures decrease with weight loss, independent of sodium restriction.269 In the Trials of Hypertension Prevention Phase II (TOHP II), approximately 1200 overweight and obese patients were randomly assigned to a dietary weight loss intervention or usual care.270 The study showed a dose-response relationship between weight loss and change in blood pressure at 36 months. During the first 6 months, patients who successfully lost weight experienced a marked reduction in blood pressure. However, among patients who regained most or all of their lost weight, blood pressure steadily increased to near-baseline values.

The marked weight loss induced by gastric surgery improves or completely resolves hypertension in about two thirds of extremely obese hypertensive patients.271 However, data from the SOS (Swedish Obese Subjects) study indicated that the beneficial effect of weight loss on blood pressure might not persist.272 Much of the improvement in blood pressure observed at 1 and 2 years after gastric surgery disappeared by 3 years, and both systolic and diastolic pressures increased over the next 5 years. These findings imply that the current energy balance and the direction of weight change are important in blood pressure control.

A decreased incidence of hypertension with weight loss has been reported by several large, prospective, epidemiologic and intervention studies. For example, TOHP II found that persons who maintained a weight loss of at least 4.5 kg at 36 months had a 65% decrease in the risk of hypertension compared with control group participants who gained 1.8 kg.270 The Nurses' Health Study observed a direct correlation between the risk of developing hypertension and changes in body weight among normotensive women who were observed for 12 to 15 years. With weight loss of 5.0 to 9.9 kg, the risk of developing hypertension decreased by 15%; with a loss of 10 kg or more, it decreased by 26%.36

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Neurologic Complications of Hypertension

Anthony S. Kim, S.Claiborne Johnston, in Aminoff's Neurology and General Medicine (Fifth Edition), 2014

Epidemiology

Both systolic and diastolic blood pressures are distributed approximately normally in the population. For convenience, physicians have defined pathologic states such as hypertension based on specific blood pressure thresholds, typically a systolic blood pressure of 140 mmHg or greater or a diastolic blood pressure of 90 mmHg or greater, or both. Thus defined, hypertension is common, affecting approximately 78 million adults in the United States.1 The number of hypertensive adults worldwide is expected to reach 1.54 billion by 2025.2 In the Framingham study, individuals who were normotensive at age 55 had an approximately 90 percent lifetime risk of developing hypertension.3

Despite the frequent division of blood pressure into diagnostic categories such as hypertension and normotension, there is no obvious threshold at which higher blood pressure begins affecting the risk of complications, and even patients with diastolic blood pressures of 80 to 90 mmHg are at increased risk of stroke compared with those with blood pressures of 70 to 80 mmHg (Fig. 7-1).4 Reflecting a growing awareness of the continuous risk associated with blood pressure, blood pressures in the range of 120–140/80–90 mmHg, once considered to be “normal,” are now labeled as “prehypertensive.”5

What causes diastolic blood pressure to increase

Figure 7-1. Relative risks of stroke. Estimates of the usual diastolic blood pressure (DBP) in each baseline DBP category are taken from mean DBP values 4 years after baseline in the Framingham study. Solid squares represent disease risks in each category relative to risk in the whole study population; sizes of squares are proportional to the number of events in each DBP category; and 95 percent confidence intervals for estimates of relative risk are denoted by vertical lines.

(From MacMahon S, Peto R, Cutler J, et al: Blood pressure, stroke, and coronary heart disease. Lancet 335:764, 1990, with permission.)

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Hypertension

Ihab Hajjar M.D., M.S., F.A.C.P., A.G.S.F, in Practice of Geriatrics (Fourth Edition), 2007

General approach

Historically, diastolic blood pressure has been the critical blood pressure by which management was decided. It is now established that systolic blood pressure is the more critical blood pressure to lower in elderly patients. Many clinical trials have shown that lowering systolic blood pressure prevents morbidity and mortality in these patients. Pooled estimates from these trials in older adults (N = 15,693; age 60 years or older; median follow-up, 3.8 years) have shown that lowering systolic blood pressure by 10 mm Hg is associated with a decrease of 13% in total mortality, 30% in stroke risk, 28% in cardiovascular mortality, and 23% in coronary events risk.13 In addition, a subgroup meta-analysis of hypertension trials in the very old (80 years or older) found that treatment is associated with a 34% decrease in stroke risk and a 22% decrease in cardiovascular events. However, there was no benefit in cardiovascular and overall mortality.14 These findings suggest that although lowering systolic blood pressure in the very old may not produce an overall mortality benefit, it produces morbidity benefit. A similar finding was found in the pilot study of Hypertension in the Very Elderly Trial (HYVET), in which the use of a diuretic to lower blood pressure was associated with a decrease in strokes but not in cardiovascular or overall mortality.15 All this evidence suggests that lowering systolic blood pressure in the geriatric patient is beneficial in lowering morbidity, but may not effect mortality, especially in the very old. It also suggests that when a target blood pressure cannot be achieved—for example, because of an adverse drug effect, even a mild reduction in systolic blood pressure (7 to 10 mm Hg) is still beneficial and may be attempted.

Certain patient populations, such as patients in extended-care or assisted living facilities or frail older adults, may pose a special management challenge. Target blood pressure levels for treatment have not been defined. In these patients, the global assessment should include assessing the risks of antihypertensive therapy, such as the number of already prescribed medications, which has been linked to falls, orthostatic and postprandial hypotension, limited life expectancy, and quality of life issues. Although not specific to extended-care facility residents, all frail patients need to be monitored closely. Lifestyle modifications, their effects on blood pressure, and overall outcomes in this patient population have been not well studied. Because the risk of adult failure to thrive in this frail patient population is high, caloric restriction is better avoided.

What would cause diastolic blood pressure to be high?

Lifestyle: Smoking, heavy use of alcohol increase the risk of diastolic hypertension. Diets low in potassium and high in salt can increase diastolic blood pressure. A sedentary lifestyle can make you overweight, leading to high blood pressure. Stress, both mental and physical, can temporarily raise blood pressure.

What factors affect diastolic blood pressure?

The factors discussed are heart rate, arterial pressure, coronary perfusion pressure, the pericardium, and the mechanical interplay between ventricles. The influence of heart rate, arterial pressure, and coronary perfusion pressure can be considered as minor provided they remain within their normal physiological range.

How can I lower my diastolic blood pressure immediately?

Follow the 20 tips below to help lower your overall blood pressure, including diastolic blood pressure..
Focus on heart-healthy foods. ... .
Limit saturated and trans fats. ... .
Reduce sodium in your diet. ... .
Eat more potassium. ... .
Lay off the caffeine. ... .
Cut back on alcohol. ... .
Ditch sugar. ... .
Switch to dark chocolate..