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Hypovolemia and orthostatic hypertension

Hypovolemia and orthostatic hypertension


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What is the physiological mechanism behind the occurrence of orthostatic hypertension in the presence of hypovolemia?


The pathophysiology of orthostatic hypertension has not been elucidated. It is believed it involves activation of the sympathetic nervous system [1], vascular adrenergic hypersensitivity and diabetic neuropathy [2]. High levels of plasma atrial natriuretic peptide and antidiuretic hormone were observed in children [3].

Hypovolemia causes:

  • baroreflex-mediated increase in muscle sympathetic nerve activity [4]
  • release of epinephrine and norepinephrine [5]
  • activation of renin-angiotensin axis [5], thus increasing ADH levels

All these reactions result in vasoconstriction and blood pressure raising. But not up to absolute hypertension.

Orthostatic hypertension is diagnosed by a rise in systolic blood pressure of 20 mmHg or more when standing [6].

This is possible. A raise of 20 mmHg from hypotension could result due to vasoconstriction.


References:

  1. Fessel J, Robertson D. Orthostatic hypertension: when pressor reflexes overcompensate. Nat Clin Pract Nephrol. 2006 Aug;2(8):424-31. doi: 10.1038/ncpneph0228. PubMed PMID: 16932477.

  2. Chhabra L, Spodick DH. Orthostatic hypertension: recognizing an underappreciated clinical condition. Indian Heart J. 2013 Jul 5;65(4):454-6. doi: 10.1016/j.ihj.2013.06.023. PubMed PMID: 23993009.

  3. Zhao J, Yang J, Du S, Tang C, Du J, Jin H. Changes of atrial natriuretic peptide and antidiuretic hormone in children with postural tachycardia syndrome and orthostatic hypertension: a case control study. Chin. Med. J. 2014 May;127(10):1853-7. PubMed PMID: 24824244.

  4. Ryan KL, Rickards CA, Hinojosa-Laborde C, Cooke WH, Convertino VA. Sympathetic responses to central hypovolemia: new insights from microneurographic recordings. Front Physiol. 2012 Apr 26;3:110. doi: 10.3389/fphys.2012.00110. PubMed PMID: 22557974.

  5. Wikipedia contributors, "Shock (circulatory)," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Shock_(circulatory)&oldid=612494727 (accessed June 26, 2014).

  6. Wikipedia contributors, "Orthostatic hypertension," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Orthostatic_hypertension&oldid=603984647 (accessed June 26, 2014).


I presumed you meant orthostatic hypotension.

Blood pressure falls on standing and is caused primarily by increased gravity causing blood pooling in the legs. This reduces venous return and subsequently cardiac output and therefore arterial blood pressure. Usually however standing doesn't usually cause a massive fall in blood pressure as standing immediately triggers vasoconstriction (baroreceptor reflex), pressing the blood up into the body again. However when there's a secondary factor reducing blood pressure such as hypovolaemia, the fall in pressure is higher than the body may sometimes be able to compensate for. This causes symptomatic orthostatic hypotension.


Abstract

PURPOSE: To investigate whether body sodium content and blood volume contribute to the pathogenesis of orthostatic hypotension in patients with diabetes mellitus.

SUBJECTS AND METHODS: Exchangeable sodium, plasma and blood volumes, and catecholamine, renin, and aldosterone levels were assessed in 10 patients with Type II diabetes mellitus who had orthostatic hypotension and control groups of 40 diabetic patients without orthostatic hypotension and 40 normal subjects of similar age and sex. In subgroups, clinical tests of autonomic function and cardiovascular reactivity to norepinephrine and angiotensin II infusions were performed.

RESULTS: In diabetic patients with orthostatic hypotension, mean (± SD) supine blood pressure was 165/98 ± 27/12 mm Hg (P <0.05 compared with other groups) and mean upright blood pressure was 90/60 ± 38/18 mm Hg. Compared with controls, diabetic patients with orthostatic hypotension had a 10% lower blood volume. They also had less exchangeable sodium than patients with diabetes who did not have orthostatic hypotension (P <0.01). Compared with both groups of controls, diabetic patients with orthostatic hypotension had decreased 24-hour urinary norepinephrine excretion and a reduced diastolic blood pressure response to handgrip (P <0.05). Moreover, they displayed reduced products of exchangeable sodium or blood volume and sympathetic function indexes. Cardiovascular pressor reactivity to norepinephrine was enhanced (P <0.01) and beat-to-beat variation decreased (P <0.01) in both groups of diabetic patients. Microvascular complications were more prevalent in the diabetic patients with orthostatic hypotension (90% vs 35%).

CONCLUSIONS: Patients who have Type II diabetes mellitus and orthostatic hypotension are hypovolemic and have sympathoadrenal insufficiency both factors contribute to the pathogenesis of orthostatic hypotension.


Blood pressure assessment in the hypovolemic shock patient

Historically, EMS professionals relied on the vital signs, specifically blood pressure, in conjunction with other physical findings to determine if a patient was in hypovolemic shock. Shock is a state of inadequate tissue perfusion. However, it has become clearer that blood pressure and heart rate may not be a good early indicator of a hypovolemic shock state and may actually mislead the EMS practitioner when considering a differential diagnosis.

Alteration in vital signs primarily results from both a reduction in blood volume and a cascade of neural and hormonal responses in an attempt to increase the blood pressure and conserve body fluid. We have always looked for profound changes in the blood pressure to assist in making a differential diagnosis of shock.

For example, a drop in the systolic blood pressure to 90 mmHg is an indication that the shock state deteriorated from a compensatory stage to a decompensatory, or progressive stage. This dramatic drop, which is a clear but late finding, represents approximately a 30% blood loss in a healthy individual. The literature suggests that a patient could be in a true shock state and not initially present with a dramatic decrease in blood pressure or increase in heart rate [1,2]. Therefore, it is imperative to understand what the blood pressure is indicating and that the signs of poor perfusion can be assessed to identify early indicators of shock.

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Blood pressure changes from fluid loss

Blood pressure is determined by the cardiac output (CO) and peripheral vascular resistance (PVR). The equation BP = CO × PVR represents the interaction of the two variables. Cardiac output is the amount of blood ejected from the left ventricle in one minute. Peripheral vascular resistance is the resistance in the peripheral arteries and arterioles determined by the vessel size. A decrease in the vessel lumen will increase the resistance whereas, a decrease in the vessel size will decrease the peripheral vascular resistance. An increase in the cardiac output or peripheral vascular resistance will lead to an increase in the blood pressure whereas, a decrease will cause a decrease in blood pressure.

Cardiac output is an interaction of heart rate (HR) and stroke volume (SV), which is reflected in the equation CO = HR × SV. The stroke volume is defined as the amount of blood ejected from the left ventricle with each contraction and is determined by the preload, myocardial contractility and afterload. In general, an increase in heart rate or stroke volume will lead to an increase in cardiac output. Inversely, a reduction in heart rate or stroke volume will lead to a decrease in cardiac output.

The loss of blood associated with hypovolemic shock causes a reduction in the venous volume, which in turn diminishes the preload, stroke volume and cardiac output. A drop in cardiac output, which is reflected by a falling systolic blood pressure, results in a decrease in pressure in the carotid bodies and aortic arch, and triggers the baroreceptors (inhibitory stretch-sensitive receptors that constantly measure arterial pressure). When the baroreceptors sense a decrease in the arterial pressure, the sympathetic nervous system is prompted to initiate a cascade of neural and hormonal responses in an attempt to restore the pressure back to a normal state.

The direct neural stimulation and hormonal influence will increase the heart rate, increase myocardial contractility and increase peripheral vascular resistance through systemic vasoconstriction. The diastolic blood pressure is an indirect measure of peripheral vascular resistance thus, as the vessels constrict and vascular resistance increases, the diastolic blood pressure is maintained or increases.

EMS provider assessment of blood pressure

Even though the patient is losing blood and the venous volume and pressure is decreasing, the blood pressure will look relatively stable as the heart rate, myocardial contractility and peripheral vascular resistance increase as a means to compensate. This could produce a blood pressure that is deceiving and may lead the EMS practitioner into a false sense of patient stability.

For example, a blood pressure of 102/88 mm Hg surely falls within a normal limit however, it could also be a clear sign of hypovolemia when assessed closer. It is important to not only look at the overall blood pressure, but also the pulse pressure, which can provide valuable information about the hemodynamic state. The pulse pressure is the difference between the systolic blood pressure and the diastolic blood pressure.

For example, using the pressure discussed previously, the pulse pressure is calculated at 14 mm Hg (102 – 88 = 14 mm Hg). If the difference is less than 25 percent of the systolic blood pressure, the pulse pressure is considered to be narrow. A wide pulse pressure is considered to be greater than 50 percent of the systolic blood pressure.

A narrow pulse pressure in a hypovolemic shock patient indicates a decreasing cardiac output and an increasing peripheral vascular resistance. The decreasing venous volume from blood loss and the sympathetic nervous system attempt to increase or maintain the falling blood pressure through systemic vasoconstriction. This increase in heart rate and myocardial contractility is reflected in the decreasing systolic BP, the increasing diastolic BP and the narrowing pulse pressure. Thus, a blood pressure of 102/88 mmHg no longer appears to be “normal” and requires further assessment of heart rate, respiratory rate and other signs of perfusion, such as the skin color, temperature, condition and the patient’s mental status.

Be careful when assigning a blood pressure assessment as “normal.” The pulse pressure may provide more valuable and important information than the actual blood pressure itself. Blood pressure should be considered in the whole assessment of the patient and not purely as an independent finding.

1. Edelman D.A., White M.T., Tyburski J.G., et al: Post-traumatic hypotension: should systolic blood pressure of 90–109 mm Hg be included?. Shock 27. (2): 134-138.2007.

2. Victorino G.P., Battistella F.D., Wisner D.H.: Does tachycardia correlate with hypotension after trauma?. J Am Coll Surg 196. (5): 679-684.2003.

This article was originally posted Apr. 7, 2009. It has been updated.


Comparison between men and women of volume regulating hormones and aquaporin-2 excretion following graded central hypovolemia

Central hypovolemia induced by orthostatic loading causes reno-vascular changes that can lead to orthostatic intolerance. In this study, we investigated volume regulating hormonal responses and reno-vascular changes in male and female subjects as they underwent central hypovolemia, induced by graded lower body negative pressure (LBNP). Aquaporin-2 (AQP2) excretion was measured as a biomarker for the renal system response to vasopressin. 37 young healthy subjects (n = 19 males n = 18 females) were subjected to graded LBNP until - 40 mmHg LBNP. Under resting conditions, males had significantly higher copeptin (a stable peptide derived from vasopressin) levels compared with females. Adrenocorticotropin (ACTH), adrenomedullin (ADM), vasopressin (AVP) and brain natriuretic peptide (BNP) were not affected by our experimental protocol. Nevertheless, an analysis of ADM and BNP with the data normalized as percentages of the baseline value data showed an increase from baseline to 10 min after recovery in the males in ADM and in the females in BNP. Analysis of BNP and ADM raises the possibility of a preferential adaptive vascular response to central hypovolemia in males as shown by the normalized increase in ADM, whereas females showed a preferential renal response as shown by the normalized increase in BNP. Furthermore, our results suggest that there might be a difference between men and women in the copeptin response to alterations in orthostatic loading, simulated either using LBNP or during posture changes.

Keywords: Adrenomedullin Aquaporins Copeptin Lower body negative pressure Orthostatic loading Vasopressin.


Treatment

NONPHARMACOLOGIC THERAPY

Compared with the general population, athletes and other physically active patients are often more motivated to comply with nonpharmacologic interventions, because these measures have virtually no side effects. Although lifestyle modifications cannot eliminate the need for antihypertensive drug therapy in all patients, dietary and behavioral changes may reduce the amount of medication needed and, thus, the possibility of side effects. Dietary and lifestyle changes may include decreasing sodium intake, increasing potassium intake, losing weight, decreasing alcohol consumption, avoiding stimulant use, applying relaxation techniques, and performing aerobic exercise.

Dietary Changes

A reduction in sodium intake can lead to a decrease in blood pressure.5 In particular, patients should be advised to reduce their intake of processed foods such as luncheon meat and fast foods. Processed foods provide 75 percent of the sodium recommended for the typical American diet.9 These foods are particularly common in the diets of adolescent athletes. Blacks, older persons, and those with diabetes mellitus seem to be especially sensitive to the effects of dietary sodium.9

Potatoes and bananas, as well as many other fruits, contain significant amounts of potassium. These foods should be included in the diet of athletes and other physically active patients. High dietary potassium intake may provide some protection against high blood pressure or may improve blood pressure control.10 A high-potassium diet is especially important in endurance athletes, who may tend to be hypokalemic.5

Calcium or magnesium supplementation for the sole purpose of improving blood pressure control is not routinely recommended in physically active patients.5

Weight Loss

Losing just 4.5 kg (10 lb) can reduce blood pressure in overweight patients who have hypertension.11 Loss of this much weight also seems to enhance the blood pressure–lowering effects of many medications.12 The weight reduction plan should include foods that are high in fiber and low in saturated fats.13

Lifestyle Changes

Excessive alcohol use can decrease the effectiveness of antihypertensive drug therapy. Adults should limit alcohol intake to the equivalent of two beers per day. Women and lighter weight persons should consume no more than the equivalent of one beer per day.5

Some athletes routinely use biofeedback, muscle relaxation techniques, meditation, yoga, and stress management techniques. These stress reduction tools may have value as adjunctive therapy in patients with hypertension.

Regular aerobic exercise adequate to achieve moderate fitness can lower blood pressure, enhance weight loss, and reduce mortality.14 The effects of exercise on hypertension are even more dramatic in patients with hypertension secondary to renal dysfunction.

Recommendations on exercise and sports participation for patients with hypertension are provided in Table 3 .15

Exercise and Sports Participation in Athletes and Other Physically Active Persons with Hypertension

The recommended mode, frequency, duration, and intensity of exercise are generally the same as those for persons without hypertension.

Blood pressure should be controlled before resumption of participation in vigorous sports, because both dynamic and isometric exercise can cause remarkable increases in blood pressure.

Recommendations on exercise restrictions

High-normal blood pressure

Controlled mild to moderate hypertension (<140/90 mm Hg)

No restrictions on dynamic exercise possible limit on isometric training or sports in some patients

Uncontrolled hypertension (>140/90 mm Hg)

Limited to low-intensity dynamic exercise avoid isometric sports.

Controlled hypertension with end-organ damage

Limited to low-intensity dynamic exercise avoid isometric sports.

Severe hypertension with no end-organ involvement

Limited to low-intensity dynamic exercise, with participation only if blood pressure is under adequate control.

Secondary hypertension of renal origin

Limited to low-intensity dynamic exercise avoid 𠇌ollision” sports that could lead to kidney damage.

Information from 26th Bethesda Conference: recommendations for determining eligibility for competition in athletes with cardiovascular abnormalities. January 6𠄷, 1994. J Am Coll Cardiol 199424:845� .

Exercise and Sports Participation in Athletes and Other Physically Active Persons with Hypertension

The recommended mode, frequency, duration, and intensity of exercise are generally the same as those for persons without hypertension.

Blood pressure should be controlled before resumption of participation in vigorous sports, because both dynamic and isometric exercise can cause remarkable increases in blood pressure.

Recommendations on exercise restrictions

High-normal blood pressure

Controlled mild to moderate hypertension (<140/90 mm Hg)

No restrictions on dynamic exercise possible limit on isometric training or sports in some patients

Uncontrolled hypertension (>140/90 mm Hg)

Limited to low-intensity dynamic exercise avoid isometric sports.

Controlled hypertension with end-organ damage

Limited to low-intensity dynamic exercise avoid isometric sports.

Severe hypertension with no end-organ involvement

Limited to low-intensity dynamic exercise, with participation only if blood pressure is under adequate control.

Secondary hypertension of renal origin

Limited to low-intensity dynamic exercise avoid 𠇌ollision” sports that could lead to kidney damage.

Information from 26th Bethesda Conference: recommendations for determining eligibility for competition in athletes with cardiovascular abnormalities. January 6𠄷, 1994. J Am Coll Cardiol 199424:845� .

PHARMACOLOGIC THERAPY

Athletes and other physically active patients need to monitor medication effects, because some antihypertensive drugs may have an adverse influence on exercise tolerance. Other drugs, including NSAIDs, may decrease the action of antihypertensive medications, including diuretics, beta blockers, and angiotensin-converting enzyme (ACE) inhibitors.16 Physicians and patients also need to be aware that the U.S. Olympic Committee (USOC) and the National Collegiate Athletic Association (NCAA) have banned the use of some antihypertensive medications.16 – 18 The effects of anti-hypertensive drug classes are summarized in Table 4 .5 , 6 , 16 – 21

Summary of Pharmacologic Treatment for Hypertension in Athletes and Other Physically Active Patients

No effect or decrease in endurance

Hypovolemia, orthostatic hypotension, and urinary loss of potassium and magnesium, which can lead to muscle cramps, arrhythmias, and rhabdomyolysis in patients exercising intensely or competing in warm weather

Elderly patients, black patients, patients with CHF

Endurance athletes, collegiate athletes

Use banned by USOC and NCAA

Dry, nonproductive cough (angiotensin I blockers)

Patients with diabetes mellitus, renal insufficiency, CHF, asthma, or hyperlipidemia

Female patients who are not using contraception

First-dose hypotensive effect with alpha1 blockers, especially in elderly patients

Patients with hyperlipidemia or BPH

May want to avoid in men older than 55 years

Centrally acting agents may cause drowsiness, dry mouth, and impotence rebound hypertension can occur with abrupt discontinuation of clonidine (Catapres).

Increase in perceived exertion levels, impairment of cardiac output and maximum oxygen uptake, earlier fatigue and lactate threshold, possible exacerbation of exercise-induced bronchospasm or asthma

Patients with coronary artery disease

Patients with asthma, endurance athletes, collegiate athletes

Use banned in precision sports (i.e., shooting, archery, diving, ice skating)

Decrease, increase, or no effect

Nondihydropyridines (e.g., verapamil [Calan], diltiazem [Cardizem]) can cause heart rate suppression and minor impairment of maximum heart rate, decreased left ventricular contractility, and constipation.

Patients with asthma, black patients

Dihyrdopyridines (e.g., amlodipine [Norvasc], nifedipine [Procardia]) can cause reflex tachycardia, fluid retention, and vascular headaches.

CHF = congestive heart failure USOC = U.S. Olympic Committee NCAA = National Collegiate Athletic Association ACE = angiotensin-converting enzyme BPH = benign prostatic hyperplasia .

*— Loop diuretics are inappropriate for the treatment of hypertension in competitive athletes and other physically active patients .

†— Because of insufficient data documenting cardiac and renal protective effects, angiotensin-II receptor blockers are generally recommended only in patients who cannot tolerate ACE inhibitors. Angiotensin-II receptor blockers do not cause dry, nonproductive cough .

Information from references 5 , 6, and 16 through 21 .

Summary of Pharmacologic Treatment for Hypertension in Athletes and Other Physically Active Patients

No effect or decrease in endurance

Hypovolemia, orthostatic hypotension, and urinary loss of potassium and magnesium, which can lead to muscle cramps, arrhythmias, and rhabdomyolysis in patients exercising intensely or competing in warm weather

Elderly patients, black patients, patients with CHF

Endurance athletes, collegiate athletes

Use banned by USOC and NCAA

Dry, nonproductive cough (angiotensin I blockers)

Patients with diabetes mellitus, renal insufficiency, CHF, asthma, or hyperlipidemia

Female patients who are not using contraception

First-dose hypotensive effect with alpha1 blockers, especially in elderly patients

Patients with hyperlipidemia or BPH

May want to avoid in men older than 55 years

Centrally acting agents may cause drowsiness, dry mouth, and impotence rebound hypertension can occur with abrupt discontinuation of clonidine (Catapres).

Increase in perceived exertion levels, impairment of cardiac output and maximum oxygen uptake, earlier fatigue and lactate threshold, possible exacerbation of exercise-induced bronchospasm or asthma

Patients with coronary artery disease

Patients with asthma, endurance athletes, collegiate athletes

Use banned in precision sports (i.e., shooting, archery, diving, ice skating)

Decrease, increase, or no effect

Nondihydropyridines (e.g., verapamil [Calan], diltiazem [Cardizem]) can cause heart rate suppression and minor impairment of maximum heart rate, decreased left ventricular contractility, and constipation.

Patients with asthma, black patients

Dihyrdopyridines (e.g., amlodipine [Norvasc], nifedipine [Procardia]) can cause reflex tachycardia, fluid retention, and vascular headaches.

CHF = congestive heart failure USOC = U.S. Olympic Committee NCAA = National Collegiate Athletic Association ACE = angiotensin-converting enzyme BPH = benign prostatic hyperplasia .

*— Loop diuretics are inappropriate for the treatment of hypertension in competitive athletes and other physically active patients .

†— Because of insufficient data documenting cardiac and renal protective effects, angiotensin-II receptor blockers are generally recommended only in patients who cannot tolerate ACE inhibitors. Angiotensin-II receptor blockers do not cause dry, nonproductive cough .

Information from references 5 , 6, and 16 through 21 .

Diuretics

Both thiazide and loop diuretics decrease plasma volume, cardiac output, and vascular resistance.20 The thiazide diuretics have less pronounced effects.

Thiazide diuretics are often recommended as initial therapy in patients with hypertension. In several randomized, controlled trials (conducted primarily in the elderly),22 – 28 these agents have been associated with decreases in both mortality and morbidity.

Thiazide diuretics are useful as second-line therapy in salt-sensitive athletes and physically active patients with hypertension.5 These agents should be given in a low dosage and, in some patients, combined with a potassium-sparing agent. Thiazide diuretics are inexpensive and a good choice in patients who exercise only casually, in physically active elderly patients, and in black patients. Possible side effects include hypovolemia, orthostatic hypotension, and urinary loss of potassium and magnesium. These side effects can lead to muscle cramps, arrhythmias, and rhabdomyolysis in patients who are exercising intensely or competing in warm weather.

The side effects associated with thiazide diuretics are magnified with the more potent loop diuretics. Consequently, loop diuretics are inappropriate for use in the treatment of hypertension in athletes and other physically active patients. These agents have also been shown to cause short-term increases in plasma cholesterol, glucose, and uric acid levels.21

Sports regulatory bodies have banned the use of all diuretics. These agents cannot be used by elite athletes who are required to undergo drug testing.16 – 18

ACE Inhibitors

These agents block the conversion of angiotensin I to angiotensin II, which is a potent vasoconstrictor and a source of sodium retention.19 ACE inhibitors are associated with a slight decrease in heart rate, an increase in stroke volume, and a decrease in total peripheral resistance.20

ACE inhibitors have been shown to have beneficial effects in patients with heart failure, systolic dysfunction or nephropathy. They reverse ventricular hypertrophy and microalbuminuria, with preservation of renal function. In exercise, ACE inhibitors have no major effects on energy metabolism and cause no impairment of maximum oxygen uptake. In general, these drugs have no deleterious effects on training or competition.20

The major side effect of ACE inhibitors is a dry, nonproductive cough. Because there have been anecdotal reports of postural hypotension after intense exercise in patients taking ACE inhibitors, an adequate cool-down period is recommended.

ACE inhibitors are excellent for treating mild to moderate hypertension. They are often the first-line agents for the treatment of high blood pressure in physically active patients, especially those with diabetes.5 Their effectiveness may be improved by adding a thiazide in a low dosage, with the drugs taken separately or in combination.

The potassium-sparing effect of ACE inhibitors may be increased when these agents are taken concomitantly with NSAIDs.19 Use of ACE inhibitors is contraindicated in pregnancy. Therefore, patients of childbearing age should use some form of contraception if they are taking an ACE inhibitor.

Angiotensin-II receptor blockers produce similar effects as ACE inhibitors. However, because of their action at the receptor level, they do not cause a dry cough. Currently, insufficient data are available to document whether angiotensin-II receptor blockers have cardiac and renal protective effects. Therefore, these agents are generally recommended only for patients who cannot tolerate ACE inhibitors.5

Alpha Blockers

The alpha1-receptor antagonists competitively block postsynaptic alpha1 arteriolar smooth muscle receptors. They decrease systemic vascular resistance, with no reflex increase in heart rate or cardiac output. A first-dose hypotensive effect can occur, especially in the elderly.

Alpha blockers cause no major changes in energy metabolism during exercise, and maximum oxygen uptake is preserved. Therefore, these agents have no major effects on training or sports performance.20 Alpha blockers have been used in athletes with diabetes mellitus who have hypertension and hypercholesterolemia, because they do not exacerbate these conditions.7

The doxazosin arm of the ongoing Antihypertensives and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT)29 was discontinued because of an increased incidence of congestive heart failure, compared with use of a diuretic. The ALLHAT findings should be taken into consideration, especially in athletes older than 55 years.

Centrally acting alpha agonists have no major effects on training or sports performance.19 Because of their side effects, however, these agents are rarely used. These effects may include mild to moderate drowsiness, dry mouth, and impotence. Rebound hypertension can occur with the abrupt discontinuation of orally administered clonidine (Catapres).7

Beta Blockers

Noncardioselective beta blockers significantly decrease contractility of the heart and decrease heart rate. Systemic vascular resistance is increased, especially in the muscle and skin. Because these drugs inhibit lipolysis and glycogenolysis, hypoglycemia may occur after intense exercise. In addition, athletes who take beta blockers perceive greater exertion during exercise, which may affect adherence to the prescribed medication regimen.20 An increased total cholesterol level and a decreased HDL cholesterol level may also be noted.7

Although cardioselective beta blockers have fewer side effects than noncardioselective agents, they also impair cardiac output and maximum oxygen uptake, particularly in athletes. Cardioselective beta blockers should not be used in athletes and other physically active patients unless there is an underlying condition (e.g., coronary artery disease) that requires their use.20

When combined alpha-beta blockers are used, the beta effects are greater than the alpha effects. There is a decrease in the systemic vascular resistance, but less impairment of muscle blood flow and maximum oxygen uptake. If beta blockade is necessary, a combined alpha-beta blocker may be the best choice.21

The USOC has banned the use of beta blockers in athletes participating in precision events such as archery, shooting, diving, and ice skating.16 – 18

Calcium Channel Blockers

These drugs inhibit calcium slow-channel conduction, thereby reducing the calcium concentration in vascular smooth muscle cells, which results in decreased systemic vascular resistance with generalized vasodilation.19 Calcium channel blockers are effective in reversing ventricular hypertrophy.

Dihydropyridines such as amlodipine (Norvasc) and nifedipine (Procardia) can cause reflex tachycardia, fluid retention (pedal edema), and vascular headaches. Nondihydropyridines such as verapamil (Calan) and diltiazem (Cardizem) can cause heart rate suppression, minor impairment of maximal heart rate, decreased left ventricular contractility, and constipation.5

Calcium channel blockers have no major effects on energy metabolism during exercise, and maximum oxygen uptake is generally preserved.20 There is a potential for competitive “steal” of muscle blood flow (because of vasodilatation) and earlier onset of the lactate threshold.30 However, calcium channel blockers, especially the dihydropyridines, are generally well tolerated and effective in physically active patients. They are often used as first-line agents in black athletes.5


Is Absolute Hypovolemia a Risk Factor for Vasovagal Response to Head-Up Tilt?

To test the hypothesis that hypovolemia is associated with an increased incidence of vasovagal syncope during head-up tilt (HUT) 45 patients with history of syncope or presyncope were studied. Blood volume (radio-iodinated serum albumin) was determined, then subjects underwent a graded HUT (from 15°–60° HUT) with cuff blood pressure and ECG monitoring. All patients were kept on their own medications during evaluation. Thirty patients (12 male, 18 female, mean age 50 ± 19 [SD] years) had hypovolemia, defined as blood volume < 90% of lab normal for corresponding sex, while 15 patients (7 male, 8 female, mean age 52 ± 21 years) were normovolemic with blood volume ranging from 91%-110% of sex-matched normal subjects. The normovolemic patients served as controls. During HUT, a vasovagal response was elicited in 5 of the 30 hypovolemics and in 4 of the 15 normovoiemic (16.7% and 26.7%, respectively, P = NS). In those who developed vasovagal response, the changes of heart rate and blood pressure during HUT were not significantly different between hypovolemics and normovolemics, neither at the endpoint (vasovagal response) nor immediately before the development of the vasovagal response. In patienis with nonvasovagal events, four types of hemodynamic responses to tilt were observed normal blood pressure response associated with normal heart rate increase, normal blood pressure response in association with accentuated increase in heart rate, orthostatic hypotension with normal acceleration of heart rate, and orthostatic hypotension with accelerated increase in heart rate. The percent distribution of these responses were 44%, 20%. 0%, and 36% in the 25 nonvasovagal hypovoiemics versus 73%, 0%, 18%, and 9% in the 11 nonvasovagal normovolemics. The results demonstrate that supine total blood volume does not predict the occurrence of vasovagal response to HUT. However, accentuated orthostatic tachycardia was more prevalent in hypovolemics as compared to normovolemics with nonvasovagal response to tilt.


RESULTS

Technical limitations prevented collection of complete data from all study segments in all subjects. Specifically, during hypovolemia, complete CVP data were collected from six subjects at −5, −10, and −20 mmHg LBNP and from four subjects only at −15 mmHg. Otherwise, complete hemodynamic and MSNA data were obtained from seven subjects at −10 and −20 mmHg LBNP during hypovolemia and from six subjects at −15 mmHg LBNP (normovolemia) and −40 mmHg LBNP (hypovolemia).

Baseline and LBNP responses.

There was no effect of time or repeated LBNP periods on cardiovascular hemodynamic or sympathetic variables measured in the intervening rest segments (Table 1). Moreover, the average of the intervening rest periods was not different than the pre-LBNP baseline data for all variables (Table 1). Spironolactone administration increased hematocrit from 43.6 ± 0.6% to 47.8 ± 0.5% (P < 0.05), resulting in a 15.5 ± 1.7% (P < 0.05) reduction in resting PV (range = 8–20% reduction). This hypovolemia was associated with a 1.4-mmHg reduction in baseline CVP (P < 0.05), an 11.7% reduction in SV (P < 0.05), and corresponding reductions in cardiac output and FBF (P< 0.05) (Table 1). Baseline MAP, HR, and IVC diameter were not altered by spironolactone administration. Subsequently, baseline FVR and TPR were augmented in association with a ∼23% increase in MSNA (all P < 0.05) (Table 1).

Table 1. Baseline (0 mmHg LBNP) cardiovascular and sympathetic variables before (normovolemia) and after (hypovolemia) diuretic administration

Values are means ± SE. Pre-LBNP, baseline period before first administered level of lower body negative pressure HR, heart rate SV, stroke volume MAP, mean arterial pressure TPR, total peripheral resistance FBF, forearm blood flow FVR, forearm vascular resistance IVC, inferior vena cava diameter CVP, central venous pressure a.u., arbitrary units.

* P < 0.05, hypovolemia vs. normovolemia.

Effects of LBNP.

Compared with baseline, CVP was reduced during LBNP, becoming statistically significant at −40 mmHg LBNP (Fig.1). The diuretic-induced reductions in CVP observed at rest were sustained during LBNP (main effect of spironolactone, P < 0.05) (Figs. 1 and2). There was no difference in the IVC response to LBNP between conditions (Fig. 1). During normovolemia, HR increased by 5 and 13 beats/min at −20 and −40 mmHg, respectively (P < 0.05 Fig. 3). Hypovolemia did not change the HR response, with increases of 9 ± 3 and 16 ± 5 beats/min at −20 and −40 mmHg LBNP, respectively (Fig. 3).

Fig. 1.Inferior vena cava (IVC) diameter and estimated central venous pressure (CVP) responses during graded lower body negative pressure (LBNP) before and after diuretic administration. Values are means ± SE. *P < 0.05 vs. 0 mmHg.


Fig. 2.Changes in arterial blood pressure (ABP), estimated CVP, and muscle sympathetic nerve activity (MSNA) for a representative participant from baseline (0 mmHg) to −40 mmHg LBNP during both diuretic (hypovolemia) and placebo (normovolemia) conditions.


Fig. 3.Heart rate (HR), stroke volume (SV), and cardiac output (Q) responses during graded LBNP before and after diuretic administration. Values are means ± SE. *P < 0.05 vs. 0 mmHg.

SV decreased, with LBNP becoming statistically significant by −20 mmHg LBNP (P < 0.05 Fig. 3). The reduction in baseline SV in hypovolemia was sustained throughout LBNP (main effect of condition,P < 0.05 Fig. 3). Specifically, during normovolemia, SV was reduced from a baseline value of 103 ± 11 to 80 ± 11 and 69 ± 9 ml/beat at −20 and −40 mmHg of LBNP, respectively. Hypovolemic levels decreased from 91 ± 11 to 67 ± 7 and 54 ± 5 ml/beat at −20 and −40 mmHg, respectively.

Cardiac output was reduced with −40 mmHg of LBNP (P < 0.05 Fig. 3), decreasing from 6,550 ± 755 to 5,208 ± 643 ml/min during normovolemia and from 5,905 ± 707 to 4,416 ± 449 ml/min during hypovolemia (main effect of spironolactone,P < 0.05).

Original tracings of arterial blood pressure, CVP, and MSNA recordings at baseline and −40 mmHg LBNP for a single individual are shown in Fig. 2. These data highlight the reduction in CVP and increase in arterial blood pressure with hypovolemia in association with augmented MSNA, particularly at −40 mmHg LBNP. Compared with baseline values, MAP did not change in either condition on going from −5 to −20 mmHg of LBNP (Fig. 4). During normovolemia, MAP decreased by 5 ± 2 mmHg from baseline to −40 mmHg (P < 0.05) (Figs. 2 and 4). In contrast, MAP increased by 6 ± 3 mmHg from baseline to −40 mmHg LBNP during hypovolemia (P < 0.05) (Figs. 2 and 4).

Fig. 4.Percent change (from 0 mmHg) in total MSNA, mean arterial pressure (MAP), and total peripheral resistance (TPR) responses during graded LBNP before and after diuretic administration. a.u., Arbitrary units. Values are means ± SE. *P < 0.05 vs. 0 mmHg.

Graded levels of LBNP produced consistent and progressive increases in the %MSNA (Fig. 4). Compared with normovolemia, the %MSNA was augmented in hypovolemia (main effect of spironolactone,P < 0.05). Specifically, the %MSNA at −5 to −40 mmHg increased by 127 ± 12% during normovolemia and by 137 ± 15% in hypovolemia.

The diuretic-induced augmentation of TPR was also maintained throughout LBNP (main effect of spironolactone, P < 0.05). Compared with rest (0 mmHg), TPR was elevated at −20 and −40 mmHg in both trials (Fig. 4) (P < 0.05). TPR at −40 mmHg during hypovolemia [23 ± 3 arbitrary units (a.u.)] was greater than that during normovolemia (18 ± 3 a.u.) (P < 0.05).

The spironolactone-induced increase in baseline FVR and reduction in FBF were both maintained during all levels of LBNP (main effect of spironolactone, P < 0.05 Fig.5). FBF was reduced from baseline by ∼9 ± 3 ml/min (P < 0.05) at −40 mmHg LBNP during normovolemia and by ∼11 ± 5 ml/min (P < 0.05) during hypovolemia (Fig. 5). The reduction in FBF was due to increases in (P < 0.05) FVR at −40 mmHg during both normovolemia (19 ± 6%, P < 0.05) and hypovolemia (29 ± 10%, P < 0.05) (Fig. 5).

Fig. 5.Forearm blood flow (FBF) and forearm vascular resistance (FVR) responses during graded LBNP before and after diuretic administration. Values are means ± SE. *P < 0.05 vs. 0 mmHg.

Cardiopulmonary baroreflex response.

The absence of CVP data at −15 mmHg did not affect determination of the reflex response. When the slope of the regression lines between −5 and −10 mmHg and −15 and −20 mmHg were compared using the mean data points, no differences were observed (Table2), thus indicating that the baroreflex response to low levels of LBNP was linear across the range of data.

Table 2. Cardiopulmonary baroreflex slope changes between −5 and −10 mmHg and −15 and −20 mmHg both before (normovolemia) and after (hypovolemia) diuretic administration for TPR, FVR, and %MSNA

Values are means ± SE. ΔTPR, baseline change in TPR ΔFVR, change in FVR from baseline %ΔMSNA, percent change in total MSNA from baseline ΔCVP, change in CVP from baseline (0 mmHg).

Average stimulus-response characteristics of the cardiopulmonary baroreflex control of TPR, FVR, and MSNA in normovolemia and hypovolemia are shown in Fig. 6. Values between −5 and −20 mmHg were used to optimize analysis of the cardiopulmonary baroreflex and to facilitate direct comparisons with earlier reports (16, 36). Differences in the slope (ΔTPR/ΔCVP, ΔFVR/ΔCVP, and %ΔMSNA/ΔCVP) between normovolemia and hypovolemia were compared after determining the mean slopes generated by all subjects. There were no significant differences found between the mean slopes of the two conditions for any relationship. Mean slopes for normovolemia and hypovolemia, respectively, were as follows: ΔTPR/ΔCVP, −1.72 ± 0.12 vs. −1.54 ± 0.08 a.u. ΔFVR/ΔCVP, −0.17 ± 0.004 vs. −0.12 ± 0.001 a.u. and %ΔMSNA/ΔCVP, −36 ± 12 vs. −39 ± 16 a.u. It is noteworthy that this approach to developing the mean regression did not affect the outcome. Specifically, there was no difference in the slope of the relationships when the data were plotted as a regression line through the mean data points. Slope values using this latter method for normovolemia and hypovolemia were as follows: ΔTPR/ΔCVP, −1.75 ± 0.13 vs. −1.55 ± 0.07 a.u. ΔFVR/ΔCVP, −0.19 ± 0.005 vs. −0.14 ± 0.002 a.u. and %ΔMSNA/ΔCVP, −40 ± 13 vs. −44 ± 16 a.u., respectively.

Fig. 6.Baroreflex stimulus-response relationships during graded LBNP from −5 to −20 mmHg betweem ΔTPR, ΔFVR, and %ΔMSNA and estimated ΔCVP before and after diuretic administration. Values are means ± SE for normovolemia and hypovolemia respectively. *Significant (P < 0.05) upward shift of they-intercept during hypovolemia.

The y-intercept for the %ΔMSNA/ΔCVP increased from −10.2 ± 2.2 a.u. in normovolemia to 34.3 ± 11.3 a.u. after diuretic administration (P < 0.05). Compared with normovolemia (−1.0 ± 0.4 a.u.), they-intercept for the ΔTPR/ΔCVP relationship during hypovolemia was 4.0 ± 0.6 a.u. (P < 0.05). For the ΔFVR/ΔCVP relationship, the y-intercept increased from 0.24 ± 0.07 a.u. during normovolemia to 0.37 ± 0.08 a.u. during hypovolemia (P < 0.05).

Integrated baroreflex response.

The changes in TPR, FVR, and MSNA at the level of −40 mmHg LBNP relative to changes in CVP were examined from five individuals to assess average stimulus-response characteristics of integrated baroreflex cardiovascular control (Fig.7). Compared with normovolemia (1.2 ± 0.2 a.u.), the ΔTPR/ΔCVP relationship increased during hypovolemia (2.6 ± 0.6 a.u.) (P < 0.05). Similar increases were observed for ΔFVR/ΔCVP (from 0.11 ± 0.07 to 0.63 ± 0.17 a.u.) (P < 0.05) and %ΔMSNA/ΔCVP (from 49 ± 12 to 96 ± 25 a.u.) during normovolemia and hypovolemia, respectively (P < 0.05). Thus, for a given decrease in CVP, there were greater increases in TPR, FVR, and MSNA during hypovolemia at −40 mmHg LBNP.

Fig. 7.Integrated baroreflex stimulus-response relationships at −40 mmHg between %ΔMSNA, ΔTPR, and ΔFVR and estimated ΔCVP before (normovolemia) and after (hypovolemia) diuretic administration. Values are mean ± SE. *Significant difference (P< 0.05) between conditions.


Review of the Evidence

Background on Orthostatics

  • The development of orthostatic criteria appear to be derived from measuring blood pressure and HR before and after young, healthy patients donate blood
  • Baseline OH in Adolescents
    • Orthostatic HR changes common ( Skinner 2010 )
    • Transient OH common ( Stewart 2002 )
    • Blood pressure changes usually fall within normal adult ranges
    • Positional SBP changes occur in 11 – 50% of patients > 65 years of age ( Ooi 1997 , Aronow 1988 )
    • Varies based on time of day and irrelevant of accompanying symptoms

    Orthostatic Hypotension Take Home Point: At baseline, orthostatic vital signs are common and increases in frequency with age.

    Orthostatics in Blood Loss

    Witting MD et al. Defining the positive tilt test: a study of healthy adults with moderate acute blood loss. Ann Emerg Med 1994 23(6): 1320-3. PMID: 8198307

    What they did: Measured postural BP and HR changes after blood donation (450 ml) by healthy volunteers

    McGee S et al. The rational clinical examination. Is this patient hypovolemic. JAMA 1999 281(11): 1022-9. PMID: 10086438

    Orthostatics in Non-Blood Volume Loss (i.e. vomiting, diarrhea)

    Johnson DR et al. Dehydration and orthostatic vital signs in women with hyperemesis gravidarum. Acad Emerg Med 1995 2(8): 692-7. PMID: 7584747

    Orthostatic Hypotension Take Home Point: Orthostatic measurements had poor sensitivity for diagnosing moderate blood loss or significant dehydration. Performance characteristics were improved in large blood loss but, these patients are unlikely to be missed

    Orthostatic Symptoms

    Question: If the utility of the vital sign changes with position aren’t useful, what about simply using symptoms (I.e. the patient feels lightheaded when they stand.)?

    Moderate volume loss: symptoms have limited predictive value

    • Excellent performance characteristics of inability to stand for vital signs to be measured
      • Sensitivity: 97%
      • Specificity: 98%
      • (+) LR = 48.5
      • (-) LR = 0.03

      Orthostatic Vital Signs + Serious Outcomes

      Question: Are the presence of abnormal orthostatic vital signs associated with 30-day serious outcomes in older adults presenting with syncope?

      Abnormal orthostatic vital signs or symptoms are not associated with an increased risk of adverse outcomes at 30-days. ( White 2019 )

      Odds Ratio for Serious Outcomes: 1.05 (95% CI 0.62 – 1.10)

      Summary: Based on the limited available evidence, it’s unlikely orthostatic vital sign measurement can be used to determine which patients have volume loss and which do not. The baseline prevalence of orthostatic vital signs is common and patients will not always develop orthostatic vital signs in response to volume loss. Therefore, there will both be patients who are orthostatic by numbers without volume loss and there will be patients with volume loss who are not orthostatic by numbers. Symptoms, with the exception of inability to stand to have orthostatics performed, are not useful either. Finally, there doesn’t appear to be an association between the presence of orthostatics after syncope and adverse outcomes.

      Bottom Line: Based on the low overall sensitivity of orthostatic vital sign measurements, they should not be used to influence clinical decision making.

      References:

      1. Skinner JE et al. Orthostatic heart rate and blood pressure in adolescents: reference ranges. J Child Neuro 2010 25(10): 1210-5. PMID: 20197269
      2. Stewart JM. Transient orthostatic hypotension is common in adolescents. J Pediatr 2002 140: 418-24. PMID: 12006955
      3. Ooi WL et al. Patterns of orthostatic blood pressure change and the clinical correlates in a frail, elderly population. JAMA 1997 277: 1299-1304. PMID: 9109468
      4. Aronow WS et al. Prevalence of postural hypotension in elderly patients in a long-term health care facility. Am J Cardiology 1988 62(4): 336-7. PMID: 3135742
      5. Witting MD et al. Defining the positive tilt test: a study of healthy adults with moderate acute blood loss. Ann Emerg Med 1994 23(6): 1320-3. PMID: 8198307
      6. McGee S et al. The rational clinical examination. Is this patient hypovolemic. JAMA 1999 281(11): 1022-9. PMID: 10086438
      7. Johnson DR et al. Dehydration and orthostatic vital signs in women with hyper emesis gravidarum. Acad Emerg Med 1995 2(8): 692-7. PMID: 7584747
      8. White JL et al. Orthostatic vital signs do not predict 30 day serious outcomes in older emergency department patients with syncope: A multi center observational study. Am J Emerg Med 2019. PMID: 30928476

      Post Peer Reviewed By: Salim R. Rezaie (Twitter: @srrezaie)

      Anand Swaminathan

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      3 Comments
      Natalie OH

      Just a question on your last statement “should not be used to influence clinical decision making”. Obviously sensitivity is poor, but specificity looks quite high.
      Postural BP is usually part of my syncope screen. And having a persistent drop >20mmHg would exclude an elderly patient from going home. I notice Ooi states that it’s quite common in the elderly, however in those who have just had a fall, I would be reluctant to send them home with persistent drop.
      Would be interested to know if someone has compared this to frequency of falls…

      Anand Swaminathan

      Natalie, Fantastic questions and you bring up some great points.
      I’m not very concerned with specificity in this case. Orthostatics are most commonly used as a screening test to pick up those who have occult blood or volume loss. Sensitivity here is key and, as you noted, the sensitivity is quite low.
      For blood loss, I agree that specificity isn’t bad and so maybe there’s a role there. The limitations are that all of this data is in the setting of healthy volunteers who were phlebotomized as opposed to patients who actually had trauma and blood loss or GI bleeds and blood loss. We have no idea how orthostatics would perform in those settings.
      As for non-blood volume loss, the limited evidence we have speaks to orthostatics having poor performance characteristics.
      As for long term outcomes, we have little on it except for this study:
      Raiha I et al. Prevalence, predisposing factors and prognostic importance of postural hypotension. Arch Intern Med 1995 155: 930-935.
      Raiha performed a prospective random sample cohort study with 10-year follow up. The data showed neither systolic nor mean blood pressure changes with standing predicted mortality at 10 years follow up, however a diastolic drop of 10 mmHg with standing was associated with increased vascular mortality (odds ratio 2.7, 95% CI, 1.3 to 5.6). When further analyzed this association disappeared in multivariate analysis after adjusting for background factors such as underlying cardiovascular disease. The thought being those patients with a more labile diastolic pressure likely had underlying risk factors that predisposed them to increased vascular mortality such as stroke and MI.


      Get Up, Stand Up: Orthostatics

      Orthostatic vital signs. Nurses think they’re a pain in the neck. Some doctors think they’re of marginal usefulness. Many providers simply think they’re a dying breed.

      Like many old-school physical exam techniques, though, they’re dying only because high-tech imaging and laboratory techniques have largely replaced their role. And I don’t know about you, but my ambulance doesn’t come equipped for an ultrasound or serum electrolytes. Diagnostically, EMS lives in the Olden Days — the days of the hands-on physical, the stethoscope, the palpation and percussion, the careful and detailed history. For us, orthostatics have been and still are a valuable tool in patient assessment.

      How are they performed? Orthostatic vital signs are essentially multiple sets of vitals taken from the patient in different positions. (They’re also sometimes known as the tilt test or tilt table, which is indeed another way to perform them — if you have a big, pivoting table available. Postural vitals is yet another name.) They usually include blood pressure and pulse, and are taken in two to three positions — supine (flat on the back) and standing are the most common, but a sitting position is sometimes also included, or used instead of standing. This is useful when a patient is unable to safely stand, although it’s not quite as diagnostically sensitive.

      Why would we do such a dance? The main badness that orthostatics reveal is hypovolemia. With a full tank of blood, what ordinarily happens when I stand up? Gravity draws some of my blood into the lower portion of my body (mostly these big ol’ legs). This reduces perfusion to the important organs upstairs, especially my brain, so my body instantly compensates by increasing my heartrate a bit and tightening up my vasculature. No problem. However, what if my circulating volume is low — whether due to bleeding, dehydration, or even a “relative” hypovolemia (in distributive shocks such as sepsis or anaphylaxis)? In that case, when my smaller volume of blood is pulled away by gravity, my body will have a harder time compensating. If it’s not fully able to, then my blood pressure will drop systemically.

      “But,” you cry, “surely this is all just extra steps. Can’t I recognize hypovolemia from basic vital signs — no matter what position you’re in?”

      Well, yes and no. If it’s severe enough, then it will be readily apparent even if I’m standing on my head. But we routinely take baseline vitals on patients who are at least somewhat horizontal, and this is the ideal position to allow the body to compensate for low volume. By “challenging” the system with the use of gravity, we reveal the compensated hypovolemias… rather than only seeing the severely decompensated shock patients, who we can easily diagnose from thirty paces anyway. Like a cardiac stress test, we see more by pushing the body until it starts to fail that’s how you discover the cracks beneath the surface.

      Do we run on patients with hypovolemia? Oh, yes. External bleeding is a gimme, but how about GI bleeds? Decreased oral fluid intake? Increased urination due to diuretics? How about the day after a frat party kegger? Any of this sound familiar? It would be foolish to take the time to do this when it won’t affect patient care — such as in the obviously shocked patient — but there are times when what it reveals can be important, such as in patients who initially appear well and are considering refusing transport.

      Here’s the process I’d recommend for taking orthostatics:

      1. Start with your initial, baseline set of vitals. Whatever position your patient is found in, that’s fine. Deal with your initial assessment in the usual fashion.
      2. Once you’re starting to go down a diagnostic pathway that prominently includes hypovolemic conditions in the differential, start thinking about orthostatics. If your initial vitals were taken while seated, try lying the patient flat and taking another pulse and BP. If possible, wait a minute or so between posture change and obtaining vitals this will allow their system to “settle out” and avoid capturing aberrant numbers while they reestablish equilibrium.
      3. Ask yourself: can the patient safely stand? Even in altered or poorly-ambulatory individuals, the answer might be “yes” with your assistance, up to and including a burly firefighter supporting them from behind with a bearhug. (Caution here is advised even in basically well patients, because significant orthostatic hypotension may result in a sudden loss of consciousness upon standing. You don’t want your “positive” finding to come from a downed patient with a fresh hip fracture.) If safe to do so, stand the patient and take another pulse and BP. Again, waiting at least a minute is ideal, but if that’s not possible, don’t fret too much.
      4. For totally non-ambulatory patients, substitute sitting upright for standing. Ideally, this should be in a chair (or off the side of the stretcher) where their legs can hang, rather than a Fowler’s position with legs straight ahead.
      5. For utterly immobile patients who can’t even sit upright, or if attempting orthostatics in the truck while already transporting, you’ll need to do your best to position them with the stretcher back itself. Fully supine will be your low position, full upright Fowler’s will be your high position, and a semi-Fowler’s middle ground can be included if desired.

      On interpretation: healthy, euvolemic patients can exhibit small orthostatic changes, so hypovolemia is only appreciable from a significant drop in BP or increase in heart rate. From supine to standing, a drop in the systolic blood pressure of over 20 is usually considered abnormal, as is an increase in pulse of over 30. (Changes from supine to sitting, or sitting to standing, will obviously be smaller, and therefore harder to distinguish from ordinary physiological fluctuations.) A drop in diastolic pressure of over 10 is also considered aberrant. You can remember this as the 󈫺–20–30” rule.

      Try to remember what’s going on here. As the patient shifts upright, their available volume is decreasing, for which their body attempts to compensate — in part by increasing their heart rate. It’s a truism that younger, healthier, less medicated patients are more able to compensate than older and less well individuals. So for the same volume status, you would be more likely to see an increase in pulse from the younger patient, perhaps with no change in pressure whereas the older patient might have less pulse differential but a greater drop in pressure. (On the whole, the pulse change tends to be a more sensitive indicator than pressure, since almost everyone is able to compensate somewhat for orthostatic effects. As always, if you look for the compensation rather than the decompensation — the patch, rather than the hole it’s covering — you’ll see more red flags and find them sooner.)

      Are substantial orthostatic changes definitive proof of hypovolemia? No, nothing’s certain in this world. Another possible cause is autonomic dysregulation, which essentially means that the normal compensating mechanisms (namely baroreceptors that detect the drop in pressure and stimulate vasoconstriction, chronotropy, and inotropy) fail to function properly. You do have enough juice, but your body isn’t doing its job of keeping it evenly circulating. Vasovagal syncope is one common example of this I’ve got it myself, in fact, and hence have a habit of passing out while squatting. This sort of thing is not related to volume status, although if you combine the two the effect can be synergistic. A good history can help distinguish them: ask the patient if they have a prior history of dizziness upon standing.

      Finally, pulse and pressure are not the only changes you can assess. One of the best indicators of orthostatic hypotension is simply a subjective feeling of light-headedness reported by the patient. Although sudden light-headedness upon standing can have other causes (the other big possibility is benign paroxysmal positional vertigo — although strictly speaking, BPPV tends to cause “dizziness,” which is not the same as “lightheadedness”), hypovolemia is certainly one of the most likely. So stand ’em up when it’s safe and reasonable, ask how they feel, grab the vitals if you can, and maybe even take the opportunity to see how well they walk (a nice, broad neurological test — the total inability to ambulate in a normally ambulatory patient is a very ominous sign).

      Orthostatics are usually recorded on documentation by drawing little stick figures of the appropriate postures. For those who find this goofy, or are documenting on computers without “stick figure” keys, a full written description will do.


      Management

      • Stop external bleeding.
      • Stabilize fractured long bones, noting discoloration from tissue blood accumulation.
      • Aggressive fluid replacement, if hypotensive, initially with repeated 500 cc bolus of (isotonic) normal saline (NS) or Ringer's Lactate (RL) until a systolic BP of 90 mmHg is achieved.

      (Caveat: excessive NS or RL can cause metabolic acidosis or metabolic alkalosis, respectively.)

      • Warm and position the patient.
      • Rapidly transport to a trauma center, where blood products can be used.

      The sooner blood products can be used for replacement instead of NS or RL, the better chance of avoiding end-organ failure.

      Medications such as dopamine, dobutamine, epinephrine, and norepinephrine may be needed to maintain blood pressure and tissue perfusion and improve cardiac output.



Comments:

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