Orthostatic hypotension (OH) occurs when the body has an inadequate response to postural changes and, as a result, is unable to maintain a steady blood pressure when moving from a lying to standing position. It is defined as a decrease in systolic or diastolic blood pressure that occurs within three minutes of moving from a sitting or supine position to a standing position. The parameter for OH is a decrease of 20 mmHg systolic or a decrease of 10 mmHg diastolic. 

Orthostatic hypotension physiology

Upon standing, gravity causes a significant amount of circulating blood to shift into the lower part of the body. In an adult, this is between 300 and 800 ml. So, if the average adult has about five liters of circulating blood volume, this represents up to 16% of total volume. 

In normal physiology, baroreceptors in the aortic arch and carotid sinus alert the central nervous system that blood pressure has decreased. This causes the CNS to trigger an increase in heart rate and systemic vasoconstriction as compensatory mechanisms to prevent blood from pooling in the lower extremities and to maintain adequate venous return. With adequate venous return and an increase in heart rate, cardiac output is maintained and the organs (especially the brain) are perfused.

When these mechanisms are not working properly, the individual can have symptoms, though some cases of OH are asymptomatic. Symptoms include dizziness, lightheadedness, palpitations, nausea, blurred vision, and headache. Some individuals may even experience syncope, neck and shoulder pain (from those muscles not getting adequately perfused), and even chest pain and dyspnea. 

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Acute vs. chronic orthostatic hypotension

Orthostatic hypotension can be classified as acute or chronic. Acute orthostatic hypotension is often associated with certain medications or an acute condition that, once treated, no longer causes the patient to have orthostatic symptoms. Examples include dehydration, orthostatic hypotension associated with a medication, or sepsis. 

Chronic orthostatic hypotension develops over a longer period of time and is often asymptomatic while it is developing. Many times chronic OH is simply a result of age-related changes such as decreased baroreflex sensitivity, decreased parasympathetic activity, decreased vasoconstriction, and increased vascular stiffness. Chronic OH can also be due to impaired blood pressure regulatory mechanisms and chronic conditions that involve autonomic dysfunction. 

As you will see as we dive into the interventions, treating chronic orthostatic hypotension can be complex.

Neurogenic vs. non-neurogenic orthostatic hypotension

Neurogenic orthostatic hypotension is related to conditions that affect autonomic function such as diabetic neuropathy and Parkinson’s disease. It typically involves inadequate release of norepinephrine (which is a vasoconstrictor) in response to the drop in blood pressure along with an inadequate increase in heart rate. 

Non-neurogenic orthostatic hypotension is associated with conditions of reduced cardiac output and/or impaired vascular tone not related to autonomic dysfunction. Examples include:

  • Vasodilation secondary to fever or sepsis
  • Reduced cardiac output related to cardiac dysfunction such as aortic stenosis or heart failure
  • Decreased circulating volume related to adrenal insufficiency or dehydration

Conditions that exacerbate orthostatic hypotension

Note that symptoms of orthostatic hypotension will be pronounced in circumstances where vasodilation is present and/or cardiac output is already reduced. This includes:

  • Hot weather – Blood vessels dilate in hot weather as a way to bring the blood toward the surface of the skin, allowing it to dispel heat and keep the body cooler.
  • Adrenal fluid volume deficit – This may be related to decreased fluid intake, diuresis and even fluid losses through diarrhea, vomiting or large wounds such as burns.
  • Alcohol intake – Not only does alcohol have a diuretic effect, it also causes vasodilation.
  • Prolonged standing – Standing for long periods of time can cause blood to pool in the lower extremities. Over time this can increase pressure in the veins, causing weak valves and venous distention. This leads to the development of varicose veins and predisposes the individual to increased venous pooling.
  • Prolonged bed rest – Though bed rest is common in the clinical setting (especially with critically ill individuals), studies show that it contributes significantly to cardiovascular deconditioning and impaired hormonal response to changes in blood pressure. Be very aware of this when getting your patient out of bed if they have been on bed rest of any duration. 

Drug-induced orthostatic hypotension

One of the most common causes for acute orthostatic hypotension you’ll see in the clinical setting is drug-induced orthostatic hypotension. This generally occurs due to one or more mechanisms: 

  • The medication interferes with the body’s compensatory response to standing. For example, a beta blocker would prevent the heart rate from increasing.
  • The medication causes fluid volume losses, such as a diuretic.
  • The medication increases venous pooling, such as nitrates, which cause vasodilation.

Other common medications that contribute to orthostatic hypotension are insulin, alpha blockers used for prostatic hyperplasia, and antidepressants.

  • Insulin – Insulin has a blood pressure lowering effect in some patients. When combined with autonomic neuropathy, this can certainly lead to orthostatic hypotension.
  • Alpha blockers – Terazosin, which is an antihypertensive often used to treat benign prostatic hyperplasia, causes systemic vasodilation.
  • Antidepressants – Orthostatic hypotension is very common with TCAs but can also occur with serotonin modulators such as trazodone, among others.

Other causes of orthostatic hypotension

In addition to drug-induced OH, there are many other circumstances that can lead to an individual experiencing a drop in blood pressure upon standing. This includes both neurogenic and non-neurogenic OH as well as some that would be considered acute.

Cardiovascular issues – Patients with cardiovascular dysfunction are at higher risk for OH. This includes congestive heart failure, myocardial infarction, venous insufficiency, and anemia.

Adrenal insufficiency – Patients with adrenal insufficiency are volume depleted due to reduced mineralocorticoid function. Recall that aldosterone (the main mineralocorticoid) plays a key role in blood pressure regulation by influencing sodium and water balance.

Parkinson’s disease – Studies show about 20 percent of patients with Parkinson’s disease have symptomatic orthostatic hypotension caused by inadequate norepinephrine release. This is a prime example of neurogenic orthostatic hypotension.

Multiple sclerosis – Up to 42 percent of people with MS have cardiovascular autonomic dysfunction, which puts them at high risk for falls secondary to orthostatic hypotension. Again, this is classified as a type of neurogenic orthostatic hypotension.

Conditions associated with decreased blood volume – Any condition that causes decreased circulating volume can cause orthostatic hypotension. Common culprits include sepsis, dehydration, severe vomiting or diarrhea, and large surface area burns.

Postprandial orthostatic hypotension – Orthostatic hypotension after eating a meal occurs due to blood flowing to the intestines for the purpose of digestion. In healthy individuals, the other blood vessels constrict to compensate. When this compensatory mechanism fails (which is not uncommon in older individuals and those with neurogenic OH), the individual experiences the drop in blood pressure.

What are the complications of orthostatic hypotension?

The main complication of OH is that it puts the patient at much higher risk for falling, especially if they have an underlying condition that affects mobility or are of advanced age. Other potential complications of orthostatic hypotension are:

  • Concussion and subdural hematoma – Head injuries are common with falls, especially in the elderly. If your patient is elderly or taking an anticoagulant, be aware that subdural hematomas can occur if they hit their head. In fact, falls are the most common reason for subdural hematoma in the elderly.
  • Bone fractures – Fractures associated with falls can occur anywhere in the body, though common sites include the hip, knee, ankle, wrist, arm, and shoulder. According to the CDC, more than 95% of hip fractures are caused by falls.
  • Stroke and TIA – The decrease in cerebral perfusion pressure can increase the risk of stroke and transient ischemic attacks, especially in patients who have lower blood pressure at baseline.
  • Heart disease – Though the exact causative role is not fully understood, studies show that fluctuating blood pressure plays a role in the pathogenesis of cardiovascular disease and is recognized as a risk factor for heart failure.

Diagnosing orthostatic hypotension

Orthostatic hypotension is often diagnosed by taking heart rate and blood pressure measurements in the lying and standing positions. To assess a patient for orthostatic hypotension, follow these steps: 

  1. Have the patient assume a supine position for at least five minutes.
  2. Measure their heart rate and blood pressure in the supine position.
  3. Have the patient stand. Be ready for OH just in case so the patient doesn’t fall. If the patient experiences lightheadedness or you sense they are about to fall, assist them back to a seated position.
  4. After one minute, measure heart rate and blood pressure.
  5. Wait another two minutes and then measure heart rate and blood pressure again.
  6. Compare the standing measurements against the supine measurement. If there is an increase of 20 mmHg or more in the systolic blood pressure, or an increase of 10 mmHg or more in the diastolic blood pressure, this is indicative of orthostatic hypotension.

Diagnosis may also be conducted via a tilt-table test. In this diagnostic procedure, the patient is exposed to orthostatic stress by tilting the table into the upright position. For some examinations, the response may be intentionally exaggerated with the use of medication. During the procedure, the patient’s heart rate, oxygen saturation level, and ECG tracing are continuously monitored. Blood pressure is also closely monitored and, while continuous non-invasive monitoring is preferred, it may not be available. In these cases, cuff pressure measurements may be utilized at regular intervals.

In addition to measuring vital signs, the patient will be observed for syncope, sweating and other outward signs of orthostatic hypotension. Additionally, they will be instructed to tell the examiner if they feel any symptoms such as lightheadedness, blurred vision, nausea or palpitations. 

If the patient has no symptoms after about 45 minutes in the upright position, a drug may be utilized to provoke the response. Commonly used medications include nitroglycerin and isoproterenol.

The upright tilt is abandoned if the patient’s blood pressure drops below a certain threshold (usually 70 mmHg, but this can vary) or if the patient has a syncopal episode. Additionally, some patients will require a fluid bolus to reverse hypotension, even after resuming the supine position.

Though a tilt table test is generally considered to be a safe procedure, the patient could have hypotension and/or weakness that persists for several hours.

Orthostatic hypotension treatments and risk reduction

The management of chronic orthostatic hypotension can be complex. One approach is to utilize an A-to-F mnemonic which provides several options for patients to try.

  • A: Abdominal binder – Wearing an abdominal binder when out of bed can help patients with autonomic dysfunction retain adequate blood pressure. The binder works by reducing splanchnic venous pooling and making more blood volume available for circulation.
  • B: Bed up position – Sleeping with the head of bed slightly elevated by about 4 inches has been shown to help with orthostatic hypotension. It is thought that over time, this slightly upward tilting position retrains the body’s sensors and gradually increases vascular tone to lessen incidences of orthostatic hypotension. Additionally, the slight upward tilt helps reduce nocturnal hypertension and diuresis, so the body holds onto fluids which is beneficial when the patient stands.
  • B: Bolus – Drinking 16 ounces of water prior to prolonged standing can help an individual experience less orthostatic stress and can increase blood pressure by up to 20 mmHg for up to two hours.
  • C: Countermaneuvers – Contracting the muscles of the lower body can help improve venous return and cardiac output. It has also been shown that clenching the hands into fists prior to and upon standing can also help increase blood pressure and decrease orthostatic hypotension.
  • D: Drugs – Pharmacologic treatment of orthostatic hypotension may be necessary. We’ll talk more about the specific drugs further down.
  • E: Exercise – Individuals with orthostatic hypotension (and especially elderly individuals who have suffered a fall) may feel tentative about increasing their activity. Encourage the patient to exercise as it’s an important component in venous return and preservation of vascular tone. Beneficial exercises that don’t increase fall risk include recumbent cycling, swimming and lifting light weights. 
  • E: Education – Ensure the patient understands factors that put them at risk for orthostatic hypotension and to change positions slowly (especially upon waking). It’s also important to teach them techniques for improving their blood pressure such as those mentioned above. And, of course, make sure the patient knows the symptoms of orthostatic hypotension so they can recognize it quickly and (hopefully) avoid a fall.
  • F: Fluids and salt – Many patients with orthostatic hypotension benefit from increased fluids and salt in order to have optimal fluid balance. They may get enough salt from adding extra salt to their foods, or they may need to take a salt tablet.

General interventions for all patients also include:

A key nursing implication of orthostatic hypotension is that it puts your patient at high risk for falls, especially in the morning when blood pressure tends to be at its lowest.

  • Identify the underlying cause for the orthostatic hypotension and address it when able. For example, if the OH is related to anemia, the patient may need a hematopoietic agent such as epoetin alfa or even a blood transfusion.
  • Teach the patient to change position slowly, use assistive devices (such as a walker) or call for help prior to getting out of bed. Your main goal is to prevent falls!
  • Compression stockings can improve venous return, especially in individuals who stand for long periods of time. However, a 2015 study showed that an abdominal binder is more beneficial, so that may be tried first.
  • Patients should avoid drinking alcohol, which acts as a vasodilator and diuretic.
  • For patients who experience postprandial orthostatic hypotension, limiting high carbohydrate meals can help reduce symptoms. Additionally, small frequent meals are preferred while hot foods/beverages may also need to be avoided. In severe cases, the medication octreotide may be used to reduce the amount of blood flowing to the intestine.

A key nursing implication of orthostatic hypotension is that it puts your patient at high risk for falls, especially in the morning when blood pressure tends to be at its lowest.

Pharmacology for orthostatic hypotension

Midodrine – Midodrine is a vasopressor that activates alpha-1 adrenergic receptors on both the arterial and venous side. The result is increased vascular tone and increased blood pressure. It is typically taken three times per day, with the first dose occurring soon after getting up in the morning and the last dose taken at least four hours before bed so as to not cause nocturnal hypertension. One bothersome side effect of midodrine is urinary frequency.

Fludrocortisone – Fludrocortisone is a mineralocorticoid often used in cases of adrenal insufficiency. For orthostatic hypotension, it is used to help the body retain sodium and adequate circulating plasma volume. Because it also causes potassium excretion, patients may need to be advised to consume high-potassium foods or even take a potassium supplement. Note that fludrocortisone can cause significant supine hypertension.

Pyridostigmine – Pyridostigmine is a cholinesterase inhibitor that prevents the breakdown of acetylcholine. In orthostatic hypotension it is used to improve neurotransmission in the baroreflex pathway. It is typically used in patients with only mild to moderate orthostatic hypotension as its effects as a vasopressor are not significant. It may also be used in conjunction with midodrine. Side effects of pyridostigmine are cholinergic in nature and include bradycardia, diarrhea, abdominal cramps, nausea and vomiting, excessive sweating, and excessive salivation.

Droxidopa – Droxidopa is an adrenergic agent that causes peripheral vasoconstriction to increase blood pressure. Serious cardiovascular adverse effects include heart failure, myocardial ischemia, and arrhythmias.

Hematopoietic agents – If the cause of orthostatic hypotension is reduced circulating volume related to anemia, then increasing RBCs may help. A common medication used for this purpose is epoetin alfa (brand names Epogen and Procrit).

Desmopressin – Synthetic vasopressin may be used to decrease nocturia which can help mitigate morning orthostatic hypotension.

In summary, orthostatic hypotension can be related to a wide variety of clinical conditions and underlying disorders. The biggest risk to your patients is falling, so instruct them to change positions from a supine to upright position slowly and to call for assistance before getting out of bed.

You can review orthostatic hypotension again while you’re on the go in episode 297 of the Straight A Nursing podcast. Tune in wherever you get your podcast fix, or straight from the website here.

The information, including but not limited to, audio, video, text, and graphics contained on this website are for educational purposes only. No content on this website is intended to guide nursing practice and does not supersede any individual healthcare provider’s scope of practice or any nursing school curriculum. Additionally, no content on this website is intended to be a substitute for professional medical advice, diagnosis or treatment.


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