Orthostatic syncope

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Orthostatic syncope refers to syncope resulting from a postural decrease in blood pressure, termed orthostatic hypotension. [1]

Contents

Orthostatic hypotension occurs when there is a persistent reduction in blood pressure of at least 20mmHg systolic or 10mmHg diastolic within 3 minutes of standing or being upright to 60 degrees on the head-up tilt table. [2] [1] In people with initial orthostatic hypotension, the decrease in blood pressure occurs within 15 seconds, while in those with delayed orthostatic hypotension it occurs after over 3 minutes of assuming an upright position. [3] [2] [1]

Signs and symptoms

Orthostatic syncope may occur suddenly with no warning or may be preceded by symptoms. [1] Associated symptoms are usually because of cerebral hypoperfusion occurring in the upright position and include dizziness, feeling faint or nauseated, diaphoresis, a sense of warmth or blurred vision. [1] Other general symptoms regardless of the position include a feeling of generalized weakness, headache, fatigue, cognitive slowing and shortness of breath. [2] [3] [4]

Symptoms may be sudden or gradual, getting progressively worse until the patient loses consciousness. [1] Patients may have a single episode with an identifiable precipitating factor or recurrent episodes without an overt, identifiable, precipitating factor. [1]

Blood pressure and heart rate should be measured in supine and standing positions. As described above, orthostatic hypotension diagnosis is when there is a drop of greater than or equal to 20 mmHg or greater or equal to 10 mmHg in systolic and diastolic blood pressures, respectively within 3 minutes of standing. [1] In the case of hypovolemia, there is also a compensatory rise in heart rate of greater than 15 beats/minute. [1]

Complications

Complications of orthostatic syncope include: [1]

  1. Trauma or injury from falls during an episode of orthostatic syncope.
  2. Stroke from changes in blood pressure due to decrease blood flow to the brain.
  3. Cardiovascular complications including heart failure, chest pain, and arrhythmias.

Etiology

There are multiple causes of orthostatic hypotension which could lead to syncope including neurally mediated (neurogenic) and non-neurally mediated causes. [3]

Neurally mediated causes include conditions that cause either primary or secondary failure of the autonomic system: [3]

Non-neurally mediated causes include: [3]

Pathophysiology

The autonomic nervous system regulates various body processes and comprises the sympathetic (adrenergic) and parasympathetic (cholinergic) nervous system. These systems work in balance to respond to changes throughout the body. When the body assumes an upright position, there is an immediate gravitational pooling of about 500 to 1000ml of blood to the lower extremities, splanchnic and pulmonary circulations. [4] The decrease in venous return to the heart reduces cardiac output and eventually causes a drop in blood pressure. Baroreceptors in the carotid and aortic arteries sense this decrease in blood pressure and activate the sympathetic nervous system which leads to increased heart rate, systemic vasoconstriction, and increased cardiac muscle contractility all of which eventually increase blood pressure. [3] [4] In a healthy individual, this sympathetic activation causes a physiological increase in heart rate by 10 to 20 bpm, diastolic blood pressure by 5mmHg, but minimal to no change in systolic blood pressure. [3] In patients with autonomic dysfunction, there is an inadequate engagement of the autonomic nervous system in response to a decrease in blood pressure leading to persistent hypotension. [1]

Diagnosis

Orthostatic vitals including blood pressure and heart rate in response to upright posture for at least 3 minutes is essential for the diagnosis of orthostatic syncope. A resting 12-lead electrocardiogram is useful to rule out arrhythmias. Targeted blood testing is reasonable including complete hematology, glycemic and metabolic profiles to rule out associated conditions such as anemia, metabolic or renal derangements. In selected patients with suspected neurodegenerative disease and syncope, referral for autonomic evaluation is reasonable to improve diagnostic and prognostic accuracy. [5]

Differential Diagnosis

Differential diagnosis includes other causes of loss of consciousness: [1]

Management

The history and physical examination are essential components in the evaluation of a patient with orthostatic syncope. The history may reveal a cause for hypovolemia such as vomiting, diarrhea, and decreased oral intake. Melena, hematemesis, hematuria, menorrhagia or hematochezia point to blood loss. Elderly deconditioned patients, especially after prolonged hospitalization, may have reduced muscle tone. [1]

Review of the patients' medication list may show polypharmacy, culprit medications (including diuretics, vasodilators, other antihypertensives) and steroids (a clue to steroid-induced adrenal insufficiency). [1]

Review of the past medical history will reveal associated predisposing medical conditions (diabetes, Parkinsonism, dementia). [1] Patient compliance with both pharmacological and nonpharmacological therapy is recommended for successful treatment. [1]

Treatment of orthostatic syncope depends on the underlying cause and includes both nonpharmacological and pharmacological measures. [3] [4]

Nonpharmacological treatment measures aim at either increasing venous return to the heart while decreasing venous pooling in the lower extremities or increasing blood volume to maintain blood pressure in the supine position and include [3] [4] :

  1. Avoiding physical deconditioning in the elderly which helps maintain muscle tone in lower extremities
  2. External compression devices such as waist-high compression stockings, abdominal binders
  3. Physical maneuvers such as lunges, calf-raise, squatting, leg crossing
  4. Review of home medications and discontinue diuretics and vasodilators if possible
  5. Increase water and fluid intake to about 2-3 liters per day, avoid dehydration, bolus water ingestion of 500mls of water in 2 to 3 minutes especially in the morning
  6. Dietary measures including liberal salt diet 6-10g/day, eating small frequent low carbohydrate meals a day in case of postprandial orthostatic hypotension, avoid alcohol intake
  7. In patients with autonomic dysfunction and supine hypertension, raising the head of the bed to 10 degrees at night reduces nocturnal diuresis
  8. Life style modification by avoiding activities that increase core temperature and cause peripheral vasodilatation such as avoiding saunas, spas, hot tubs, prolonged hot showers, and excessive high-intensity exercise

The goal of pharmacological treatment is to increase blood volume or peripheral vascular resistance and includes [3] [4] :

  1. Midodrine 2.5 to 15 mg orally once to thrice daily
  2. Fludrocortisone 0.1 to 0.2 mg daily in the morning titrated up to 1 mg daily if needed
  3. Pyridostigmine 30 to 60 mg orally trice daily
  4. Yohimbine 5.4 to 10.8 mg orally trice daily
  5. Octreotide 12.5 to 50 ug subcutaneously twice daily
  6. Cafergot such as caffeine 100 mg and ergotamine 100 mg

Prognosis

Prognosis for orthostatic syncope depends on the underlying cause of orthostatic hypotension. The prognosis is good in non-neurally mediated orthostatic syncope once the cause of postural hypotension is identified and treated - fluid resuscitation in dehydration or volume depletion, transfusion for blood loss, discontinuation of offending antihypertensive medications. In neurally mediated syncope, prognosis depends on the course of the underlying medical condition. However, in the Framingham heart study, patients with syncope of unknown cause or neurologic syncope had an increased risk of death from any cause in multivariable-adjusted hazard ratios of 1.32 and 1.54 respectively. [6]

Orthostatic hypotension is one of the most frequently identified causes of syncope in the general population. Effective treatment depends on determining the underlying etiology and instituting appropriate interventions to reduce the risk of harm to the patient. If the history suggests neurogenic orthostatic hypotension as a cause of syncope, a definitive diagnosis may require a complete autonomic workup and coordination of care between the primary care provider, cardiologist, and neurologist. [1]

Epidemiology

Orthostatic hypotension is more frequent in elderly patients because of multiple factors such as supine hypertension, age-related changes in baroreflexes and vasoconstrictor responses and a decrease in muscle tone, cardiac and vascular compliance. Neurogenic orthostatic hypotension showed a prevalence of 18% in patients older than 65 years and resulted in syncope in 9.4% of patients in the NIH funded Framingham cohort. [3] [6]

Related Research Articles

<span class="mw-page-title-main">Blood pressure</span> Pressure exerted by circulating blood upon the walls of arteries

Blood pressure (BP) is the pressure of circulating blood against the walls of blood vessels. Most of this pressure results from the heart pumping blood through the circulatory system. When used without qualification, the term "blood pressure" refers to the pressure in a brachial artery, where it is most commonly measured. Blood pressure is usually expressed in terms of the systolic pressure over diastolic pressure in the cardiac cycle. It is measured in millimeters of mercury (mmHg) above the surrounding atmospheric pressure, or in kilopascals (kPa). The difference between the systolic and diastolic pressures is known as pulse pressure, while the average pressure during a cardiac cycle is known as mean arterial pressure.

Orthostatic hypotension, also known as postural hypotension, is a medical condition wherein a person's blood pressure drops when standing up or sitting down. Primary orthostatic hypotension is also often referred to as neurogenic orthostatic hypotension. The drop in blood pressure may be sudden, within 3 minutes or gradual. It is defined as a fall in systolic blood pressure of at least 20 mmHg or diastolic blood pressure of at least 10 mmHg after 3 minutes of standing. It occurs predominantly by delayed constriction of the lower body blood vessels, which is normally required to maintain adequate blood pressure when changing the position to standing. As a result, blood pools in the blood vessels of the legs for a longer period, and less is returned to the heart, thereby leading to a reduced cardiac output and inadequate blood flow to the brain.

<span class="mw-page-title-main">Dysautonomia</span> Any disease or malfunction of the autonomic nervous system

Dysautonomia, autonomic failure, or autonomic dysfunction is a condition in which the autonomic nervous system (ANS) does not work properly. This may affect the functioning of the heart, bladder, intestines, sweat glands, pupils, and blood vessels. Dysautonomia has many causes, not all of which may be classified as neuropathic. A number of conditions can feature dysautonomia, such as Parkinson's disease, multiple system atrophy, dementia with Lewy bodies, Ehlers–Danlos syndromes, autoimmune autonomic ganglionopathy and autonomic neuropathy, HIV/AIDS, mitochondrial cytopathy, pure autonomic failure, autism, and postural orthostatic tachycardia syndrome.

<span class="mw-page-title-main">Hypotension</span> Abnormally low blood pressure

Hypotension is low blood pressure. Blood pressure is the force of blood pushing against the walls of the arteries as the heart pumps out blood. Blood pressure is indicated by two numbers, the systolic blood pressure and the diastolic blood pressure, which are the maximum and minimum blood pressures, respectively. A systolic blood pressure of less than 90 millimeters of mercury (mmHg) or diastolic of less than 60 mmHg is generally considered to be hypotension. Different numbers apply to children. However, in practice, blood pressure is considered too low only if noticeable symptoms are present.

<span class="mw-page-title-main">Reflex syncope</span> Brief loss of consciousness due to a neurologically induced drop in blood pressure

Reflex syncope is a brief loss of consciousness due to a neurologically induced drop in blood pressure and/or a decrease in heart rate. Before an affected person passes out, there may be sweating, a decreased ability to see, or ringing in the ears. Occasionally, the person may twitch while unconscious. Complications of reflex syncope include injury due to a fall.

<span class="mw-page-title-main">Hypovolemic shock</span> Medical condition

Hypovolemic shock is a form of shock caused by severe hypovolemia. It could be the result of severe dehydration through a variety of mechanisms or blood loss. Hypovolemic shock is a medical emergency; if left untreated, the insufficient blood flow can cause damage to organs, leading to multiple organ failure.

Orthostatic intolerance (OI) is the development of symptoms when standing upright that are relieved when reclining. There are many types of orthostatic intolerance. OI can be a subcategory of dysautonomia, a disorder of the autonomic nervous system occurring when an individual stands up. Some animal species with orthostatic hypotension have evolved to cope with orthostatic disturbances.

<span class="mw-page-title-main">Postural orthostatic tachycardia syndrome</span> Abnormally high heart rate when standing

Postural orthostatic tachycardia syndrome (POTS) is a condition characterized by an abnormally large increase in heart rate upon sitting up or standing. POTS is a disorder of the autonomic nervous system that can lead the individual to experience a variety of symptoms. Symptoms may include lightheadedness, brain fog, blurred vision, weakness, fatigue, headaches, heart palpitations, exercise intolerance, nausea, diminished concentration, tremulousness (shaking), syncope (fainting), coldness or pain in the extremities, chest pain and shortness of breath. Other conditions associated with POTS include migraine headaches, Ehlers–Danlos syndrome, asthma, autoimmune disease,vasovagal syncope and mast cell activation syndrome. POTS symptoms may be treated with lifestyle changes such as increasing fluid and salt intake, wearing compression stockings, gentler and slow postural changes, avoiding prolonged bedrest, medication and physical therapy.

<span class="mw-page-title-main">Neurogenic shock</span> Insufficient blood flow due to autonomic nervous system damage

Neurogenic shock is a distributive type of shock resulting in hypotension, often with bradycardia, caused by disruption of autonomic nervous system pathways. It can occur after damage to the central nervous system, such as spinal cord injury and traumatic brain injury. Low blood pressure occurs due to decreased systemic vascular resistance resulting from loss of sympathetic tone, which in turn causes blood pooling within the extremities rather than being available to circulate throughout the body. The slowed heart rate results from a vagal response unopposed by a sympathetic nervous system (SNS) response. Such cardiovascular instability is exacerbated by hypoxia, or treatment with endotracheal or endobronchial suction used to prevent pulmonary aspiration.

<span class="mw-page-title-main">Beck's triad (cardiology)</span> Medical condition

Beck's triad is a collection of three medical signs associated with acute cardiac tamponade, a medical emergency when excessive fluid accumulates in the pericardial sac around the heart and impairs its ability to pump blood. The signs are low arterial blood pressure, distended neck veins, and distant, muffled heart sounds.

<span class="mw-page-title-main">Tilt table test</span> Medical procedure often used to diagnose dysautonomia or syncope

A tilt table test (TTT), occasionally called upright tilt testing (UTT), is a medical procedure often used to diagnose dysautonomia or syncope. Patients with symptoms of dizziness or lightheadedness, with or without a loss of consciousness (fainting), suspected to be associated with a drop in blood pressure or positional tachycardia are good candidates for this test.

<span class="mw-page-title-main">Hypertensive emergency</span> Profoundly elevated blood pressure resulting in symptomatic end-organ injury

A hypertensive emergency is very high blood pressure with potentially life-threatening symptoms and signs of acute damage to one or more organ systems. It is different from a hypertensive urgency by this additional evidence for impending irreversible hypertension-mediated organ damage (HMOD). Blood pressure is often above 200/120 mmHg, however there are no universally accepted cutoff values.

<span class="mw-page-title-main">Droxidopa</span> Synthetic amino acid/norepinephrine prodrug

Droxidopa is a synthetic amino acid precursor which acts as a prodrug to the neurotransmitter norepinephrine (noradrenaline). Unlike norepinephrine, droxidopa is capable of crossing the protective blood–brain barrier (BBB).

The Bezold–Jarisch reflex involves a variety of cardiovascular and neurological processes which cause hypopnea, hypotension and bradycardia in response to noxious stimuli detected in the cardiac ventricles. The reflex is named after Albert von Bezold and Adolf Jarisch Junior. The significance of the discovery is that it was the first recognition of a chemical (non-mechanical) reflex.

<span class="mw-page-title-main">Syncope (medicine)</span> Transient loss of consciousness and postural tone

Syncope, commonly known as fainting, or passing out, is a loss of consciousness and muscle strength characterized by a fast onset, short duration, and spontaneous recovery. It is caused by a decrease in blood flow to the brain, typically from low blood pressure. There are sometimes symptoms before the loss of consciousness such as lightheadedness, sweating, pale skin, blurred vision, nausea, vomiting, or feeling warm. Syncope may also be associated with a short episode of muscle twitching. Psychiatric causes can also be determined when a patient experiences fear, anxiety, or panic; particularly before a stressful event, usually medical in nature. When consciousness and muscle strength are not completely lost, it is called presyncope. It is recommended that presyncope be treated the same as syncope.

<span class="mw-page-title-main">Orthostatic headache</span> Medical condition

Orthostatic headache is a medical condition in which a person develops a headache while vertical and the headache is relieved when horizontal. Previously it was often misdiagnosed as different primary headache disorders such as migraine or tension headaches. Increasing awareness of the symptom and its causes has prevented delayed or missed diagnosis.

<span class="mw-page-title-main">Dopamine beta hydroxylase deficiency</span> Medical condition

Dopamine beta (β)-hydroxylase deficiency is a condition involving inadequate dopamine beta-hydroxylase. It is characterized by increased amounts of serum dopamine and the absence of norepinephrine (NE) and epinephrine. Dopamine is released, as a false neurotransmitter, in place of norepinephrine. Other names for norepinephrine include noradrenaline (NA) and noradrenalin. This condition is also sometimes referred to as "norepinephrine deficiency". Researchers of disorders such as schizophrenia are interested in studying this disorder, as patients with these specific diseases can have an increase in the amount of dopamine in their system and yet do not show other symptoms of DβH deficiency.

Orthostatic hypertension is a medical condition consisting of a sudden and abrupt increase in blood pressure (BP) when a person stands up. Orthostatic hypertension is diagnosed by a rise in systolic BP of 20 mmHg or more when standing. Orthostatic diastolic hypertension is a condition in which the diastolic BP raises to 98 mmHg or over in response to standing, but this definition currently lacks clear medical consensus, so is subject to change. Orthostatic hypertension involving the systolic BP is known as systolic orthostatic hypertension.

Supine hypertension is a paradoxical elevation in blood pressure upon assuming a supine position from a standing or sitting position. It is assumed to be a manifestation of disorders of the autonomic nervous system or due to side effects of medications such as midodrine and droxidopa.

Adrenergic neurone blockers, commonly known as adrenergic antagonists, are a group of drugs that inhibit the sympathetic nervous system by blocking the activity of adrenergic neurones. They prevent the action or release of catecholamines such as norepinephrine and epinephrine. They are located throughout the body, causing various physiological reactions including bronchodilation, accelerated heartbeat, and vasoconstriction. They work by inhibiting the synthesis, release, or reuptake of the neurotransmitters or by antagonising the receptors on postsynaptic neurones. Their medical uses, mechanisms of action, adverse effects, and contraindications depend on the specific types of adrenergic blockers used, including alpha 1, alpha 2, beta 1, and beta 2.

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