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Background
Orthostatic hypotension is a sudden decrease in blood pressure when a person moves from sitting to standing, often due to factors such as dehydration, blood volume changes, pharmaceutical side effects, and medical disorders like diabetes, Parkinson’s disease, and nervous system diseases. The body’s normal response to standing involves narrowing blood vessels and increasing heart rate to maintain blood flow to the brain, but in individuals with orthostatic hypotension, this mechanism fails, causing symptoms like dizziness, light-headedness, and fainting. Postprandial hypotension, on the other hand, refers to a drop in blood pressure after a meal. When we eat, blood is redirected to the digestive system to aid digestion and absorption of nutrients. In healthy individuals, the body compensates for this redistribution of blood by increasing heart rate and constricting blood vessels to maintain normal blood pressure. However, in some people, particularly older adults, this compensatory response is impaired, leading to a significant decrease in blood pressure after eating. In severe cases, postprandial hypotension can cause dizziness, light-headedness, fatigue, and syncope (fainting). The exact cause of postprandial hypotension is not fully understood. Still, it is believed to involve various factors, including an exaggerated response by the autonomic nervous system, impaired baroreceptor reflexes, and inadequate vasoconstriction.
Epidemiology
Orthostatic Hypotension (OH):
Postprandial Hypotension (PH):
Anatomy
Pathophysiology
Orthostatic hypotension occurs when the autonomic nervous system fails to maintain blood pressure due to postural changes, leading to vasoconstriction and elevated heart rate. Factors such as medication, autonomic neuropathy, volume depletion, and fundamental autonomic control problems can contribute to this phenomenon. Postprandial hypotension is not fully understood, but some theories suggest that blood flow to the splanchnic vasculature increases after a meal, causing a decrease in central circulation and a drop in blood pressure. However, in individuals with postprandial hypotension, these mechanisms are impaired, possibly due to baroreceptor dysfunction or abnormal vasoactive substance release or response.
Etiology
Orthostatic hypotension is caused by volume depletion, medication, autonomic dysfunction and rare disorders like Shy-Drager syndrome and familial dysautonomia. It is more common in older adults due to diminished baroreceptor reflexes and impaired vasoconstrictor responses. Autonomic dysfunction like diabetic neuropathy and Parkinson’s disease can increase the risk of postprandial hypotension. Digestive system factors like the release of vasoactive substances during digestion can also contribute to postprandial hypotension. Abnormalities in releasing or responding to these substances can disrupt blood pressure regulation. Meal composition particularly high-carbohydrate meals has been associated with a higher incidence of postprandial hypotension. Tese factors contribute to the development and progression of orthostatic and postprandial hypotension.
Genetics
Prognostic Factors
Orthostatic hypotension can be influenced by various factors, including medical conditions like diabetes, Parkinson’s, autonomic neuropathy or cardiovascular disease, severity of symptoms like dizziness, lightheadedness and syncope, blood pressure response, age and overall health. Postprandial hypotension is influenced by the severity of blood pressure drop after a meal, meal-related factors and response to treatment can all impact the prognosis. Effective management and treatment can improve the prognosis, while severe symptoms like dizziness, lightheadedness and syncope increase the risk of falls, injuries, and complications. Older age and poor overall health can also affect the ability to tolerate and manage the condition effectively.
Clinical History
Age group:
Orthostatic hypotension is a condition more common in the older adults which can lead to falls and injuries due to syncope or near-fainting episodes. Postprandial hypotension is more common in older adult and affecting individuals of any age.
Physical Examination
Orthostatic Hypotension:
It is measured in supine and standing position to check the orthostatic changes.
It is measured in standing and supine positions. An elevated levels of heart rate by 10 beats per min or more may indicate the compensatory autonomic response.
It includes Dizziness, near fainting while standing or light-headedness.
It assesses the symptoms of autonomic neuropathy like abnormal sweating or loss of deep tendon reflexes.
Postprandial Hypotension:
It measure the blood pressure before and after the meal.
Assess for the postprandial symptoms like light-headedness, dizziness or fatigue.
Evaluate the causes and signs of autonomic dysfunction or comorbidities.
Assess for any postural change during the examination.
Age group
Associated comorbidity
Orthostatic hypotension is linked to comorbidities like diabetes, Parkinson’s disease, autonomic neuropathy, cardiovascular disease and certain medications. Symptoms can get worse during the continuous standing or sudden changes in body position. Postprandial hypotension may be triggered by larger carbohydrate-rich meals and can be exacerbated by standing upright after eating. These conditions can be exacerbated by sudden changes in body position.
Associated activity
Acuity of presentation
Orthostatic hypotension can be gradual or sudden, with some experiencing chronic symptoms over time or acute symptoms following medication changes or illness. Postprandial hypotension typically occurs 30-60 minutes after a meal, with symptoms being intermittent or consistent depending on the individual and the condition’s severity.
Differential Diagnoses
Orthostatic hypotension can be caused by various factors such as vasovagal syncope, cardiac arrhythmias, medication side effects, hypovolemia and postprandial hypotension. Vasovagal syncope can occur due to emotional stress, pain or prolonged standing while cardiac arrhythmias can cause low blood pressure. Hypovolemia can result from blood loss, dehydration or inadequate fluid intake. Postprandial hypotension can be caused by gastrointestinal disorders, adverse food reactions, cardiac issues like angina and metabolic disorders like hypoglycemia or glucose metabolism disorders. Monitoring blood glucose and metabolic evaluations can help identify these conditions.
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Treatment paradigm
Orthostatic and postprandial hypotension are treated with a mix of lifestyle changes and pharmaceutical therapies. The primary objective is to increase and regulate blood pressure in order to relieve symptoms and enhance general well-being. Lifestyle adjustments include increasing hydration and salt consumption, wearing compression stockings and avoiding abrupt changes in body posture. In postprandial hypotension, eating smaller, more frequent meals and avoiding large carbohydrate-rich meals may help alleviate symptoms. Pharmacological therapies like fludrocortisone, midodrine, and droxidopa are used to increase blood volume or vasoconstriction in orthostatic hypotension, and alpha-adrenergic agonists or acetylcholinesterase inhibitors in postprandial hypotension.
by Stage
by Modality
Chemotherapy
Radiation Therapy
Surgical Interventions
Hormone Therapy
Immunotherapy
Hyperthermia
Photodynamic Therapy
Stem Cell Transplant
Targeted Therapy
Palliative Care
use-of-the-non-pharmacological-therapy-for-modifying-the-environment
Discontinue exacerbating drugs:
Identifying and discontinuing medications that induce orthostatic hypotension (OH) are the initial measures to be taken. In cases where it is impossible to discontinue the medication in question or for patients with mild symptoms, reducing the dosage may be adequate. Several medications have been associated with OH, including beta-adrenergic blockers, alpha-adrenergic agonists, and tricyclic antidepressants.
Enhance salt and water intake:
Individuals diagnosed with orthostatic hypotension (OH) must augment their dietary salt and water intake to bolster intravascular volume. The rapid water consumption triggers an osmopressor reflex within an hour of ingestion by decreasing osmolarity in the portal vein.
In addition to consuming water during meals and before exercise, it is advisable to keep a water pitcher near the bedside and down it before getting out of bed in the morning. Ingesting 500 mL of water upon awakening and aiming for a daily intake of 1.5 to 3 liters is a reasonable goal.
Including high-sodium foods in the diet or utilizing salt tablets can also prove beneficial for managing OH.
Modification of daily activities and lifestyle changes:
Patients are advised to transition gradually and in stages from a supine position to a seated one and then to a standing one. This maneuver holds particular significance in the morning, as orthostatic tolerance is typically at its lowest.
During defecation, patients should also avoid performing Valsalva-like maneuvers involving frequent, forceful coughing or straining with a closed glottis. Constipation may require treatment with stool softeners and dietary modifications, while cough suppressants may sometimes be necessary.
Patients should restrict walking in excessively hot or humid weather and avoid situations that may lead to overheating. Additionally, minimizing exposure to hot showers and saunas is recommended, as warm temperatures can cause skin vasodilation, leading to decreased venous return and exacerbation of orthostatic hypotension (OH).
Use compression stockings and abdominal binders:
Utilizing custom-fitted elastic compression stockings allows for applying pressure that varies across the lower extremities and lower abdomen. This helps to reduce peripheral blood pooling, aiding in the management of orthostatic hypotension (OH).
Abdominal binders have improved the decline in orthostatic blood pressure for specific individuals with orthostatic hypotension (OH). They may be better tolerated than compression stockings applied to the legs and abdomen.
Use of fludrocortisone as initial treatment for managing orthostatic and postprandial hypotension
In cases where orthostatic hypotension (OH) experiences modest or temporary improvement in symptoms through nonpharmacologic methods aimed at increasing intravascular volume, such as consuming more salt and water, fludrocortisone can relieve symptoms. This particularly applies to patients who continue to experience persistent volume depletion despite these measures. Fludrocortisone may help address the underlying volume depletion and alleviate symptoms of OH.
Fludrocortisone a synthetic mineralocorticoid increases blood pressure by enhancing renal reabsorption of sodium and water. However, after weeks of treatment, blood volume may return to pre-treatment levels potentially due to elevated peripheral vascular resistance. This sustained effect can lead to long-term adverse effects. Fludrocortisone can also enhance the pressor effect of sympathomimetic agents further affecting blood pressure regulation.
Use of Sympathomimetic agents as initial treatment for managing orthostatic and postprandial hypotension
Midodrine
Midodrine is an orally taken alpha-1 adrenergic agonist that increases peripheral vascular resistance and improves blood pressure by constricting blood vessels and reducing orthostatic hypotension symptoms and has a short duration of action.
Droxidopa
Droxidopa, a synthetic precursor of norepinephrine, enhances blood pressure regulation by increasing peripheral vasoconstriction. Enzymes convert droxidopa to norepinephrine thereby improving blood pressure control
Use of NET inhibitors as initial treatment for managing orthostatic and postprandial hypotension
In cases where orthostatic hypotension (OH) patients do not improve despite nonpharmacologic measures and their serum norepinephrine level exceeds 220 pg/mL, atomoxetine is the primary pharmacotherapy. Atomoxetine is a norepinephrine transporter (NET) inhibitor that enhances good blood pressure and reduces symptoms in patients with nOH, as it is the primary medication used to address OH symptoms.
Use of Second-line combination treatment for managing orthostatic and postprandial hypotension
For people who cannot handle the side effects of fludrocortisone a sympathomimetic medication can be given in addition to or instead of it. Combining fludrocortisone with an alpha agonist might result in lower doses. Using droxidopa in conjunction with norepinephrine reuptake inhibitors or midodrine increases pressor effect but use caution since supine blood pressure may rise.
Use of Pyridostigmine as an Adjunctive/alternative treatment option for managing orthostatic and postprandial hypotension
Pyridostigmine, a cholinesterase inhibitor, augments cholinergic neurotransmission in both sympathetic and parasympathetic ganglia. Pyridostigmine, on average, led to a modest increase in systolic blood pressure of only four mmHg. The combination of midodrine with pyridostigmine exhibited slightly superior efficacy compared to pyridostigmine alone. Likewise, the concurrent administration of pyridostigmine and atomoxetine produces a synergistic effect, resulting in heightened blood pressure and improved tolerance to orthostatic challenges.
Use of Erythropoietin as an Adjunctive/alternative treatment option for managing orthostatic and postprandial hypotension
Using recombinant human erythropoietin raises standing blood pressure and enhances orthostatic tolerance in patients experiencing anemia commonly associated with autonomic failure. Initiating a trial of erythropoietin should be considered the primary treatment approach for all individuals affected by orthostatic hypotension (OH) and anemia, particularly those exhibiting low serum erythropoietin concentrations.
use-of-intervention-with-a-procedure-in-treating-orthostatic-and-postprandial-hypotension
Orthostatic Hypotension:
Postprandial Hypotension:
use-of-phases-in-managing-orthostatic-and-postprandial-hypotension
Assessment and Lifestyle Modifications:
The initial phase of orthostatic or postprandial hypotension involves a comprehensive evaluation to identify the underlying causes and factors. This includes reviewing medical history, physical examinations and diagnostic tests. Lifestyle modifications like increasing fluid and salt intake, maintaining hydration and modifying meal composition may be initiated.
Pharmacological Interventions:
If lifestyle changes do not provide sufficient symptom relief or the condition is severe and pharmacological interventions may be introduced. These may include medications targeting blood volume expansion, vasoconstriction or autonomic function. The choice of medication depends on the individual’s condition, comorbidities and response to treatment.
Specialist Consultation and Interventions:
If symptoms persist or become refractory to lifestyle modifications and pharmacological interventions, a specialist consultation may be necessary. The specialist can evaluate the individual’s condition and recommend additional interventions, such as baroreceptor stimulation, gastric pacing, or endoscopic procedures. These interventions are done for severe symptoms or case of unresponsive to other treatments.
Ongoing Management and Follow-up:
The final management phase involves long-term monitoring and follow-up to assess the treatment plan’s effectiveness, adjust medications, and address new concerns. Regular visits with healthcare professionals are crucial for optimal symptom control, treatment response, and managing changes in the individual’s condition or medication needs.
Medication
Future Trends
Orthostatic hypotension is a sudden decrease in blood pressure when a person moves from sitting to standing, often due to factors such as dehydration, blood volume changes, pharmaceutical side effects, and medical disorders like diabetes, Parkinson’s disease, and nervous system diseases. The body’s normal response to standing involves narrowing blood vessels and increasing heart rate to maintain blood flow to the brain, but in individuals with orthostatic hypotension, this mechanism fails, causing symptoms like dizziness, light-headedness, and fainting. Postprandial hypotension, on the other hand, refers to a drop in blood pressure after a meal. When we eat, blood is redirected to the digestive system to aid digestion and absorption of nutrients. In healthy individuals, the body compensates for this redistribution of blood by increasing heart rate and constricting blood vessels to maintain normal blood pressure. However, in some people, particularly older adults, this compensatory response is impaired, leading to a significant decrease in blood pressure after eating. In severe cases, postprandial hypotension can cause dizziness, light-headedness, fatigue, and syncope (fainting). The exact cause of postprandial hypotension is not fully understood. Still, it is believed to involve various factors, including an exaggerated response by the autonomic nervous system, impaired baroreceptor reflexes, and inadequate vasoconstriction.
Orthostatic Hypotension (OH):
Postprandial Hypotension (PH):
Orthostatic hypotension occurs when the autonomic nervous system fails to maintain blood pressure due to postural changes, leading to vasoconstriction and elevated heart rate. Factors such as medication, autonomic neuropathy, volume depletion, and fundamental autonomic control problems can contribute to this phenomenon. Postprandial hypotension is not fully understood, but some theories suggest that blood flow to the splanchnic vasculature increases after a meal, causing a decrease in central circulation and a drop in blood pressure. However, in individuals with postprandial hypotension, these mechanisms are impaired, possibly due to baroreceptor dysfunction or abnormal vasoactive substance release or response.
Orthostatic hypotension is caused by volume depletion, medication, autonomic dysfunction and rare disorders like Shy-Drager syndrome and familial dysautonomia. It is more common in older adults due to diminished baroreceptor reflexes and impaired vasoconstrictor responses. Autonomic dysfunction like diabetic neuropathy and Parkinson’s disease can increase the risk of postprandial hypotension. Digestive system factors like the release of vasoactive substances during digestion can also contribute to postprandial hypotension. Abnormalities in releasing or responding to these substances can disrupt blood pressure regulation. Meal composition particularly high-carbohydrate meals has been associated with a higher incidence of postprandial hypotension. Tese factors contribute to the development and progression of orthostatic and postprandial hypotension.
Orthostatic hypotension can be influenced by various factors, including medical conditions like diabetes, Parkinson’s, autonomic neuropathy or cardiovascular disease, severity of symptoms like dizziness, lightheadedness and syncope, blood pressure response, age and overall health. Postprandial hypotension is influenced by the severity of blood pressure drop after a meal, meal-related factors and response to treatment can all impact the prognosis. Effective management and treatment can improve the prognosis, while severe symptoms like dizziness, lightheadedness and syncope increase the risk of falls, injuries, and complications. Older age and poor overall health can also affect the ability to tolerate and manage the condition effectively.
Age group:
Orthostatic hypotension is a condition more common in the older adults which can lead to falls and injuries due to syncope or near-fainting episodes. Postprandial hypotension is more common in older adult and affecting individuals of any age.
Orthostatic Hypotension:
It is measured in supine and standing position to check the orthostatic changes.
It is measured in standing and supine positions. An elevated levels of heart rate by 10 beats per min or more may indicate the compensatory autonomic response.
It includes Dizziness, near fainting while standing or light-headedness.
It assesses the symptoms of autonomic neuropathy like abnormal sweating or loss of deep tendon reflexes.
Postprandial Hypotension:
It measure the blood pressure before and after the meal.
Assess for the postprandial symptoms like light-headedness, dizziness or fatigue.
Evaluate the causes and signs of autonomic dysfunction or comorbidities.
Assess for any postural change during the examination.
Orthostatic hypotension is linked to comorbidities like diabetes, Parkinson’s disease, autonomic neuropathy, cardiovascular disease and certain medications. Symptoms can get worse during the continuous standing or sudden changes in body position. Postprandial hypotension may be triggered by larger carbohydrate-rich meals and can be exacerbated by standing upright after eating. These conditions can be exacerbated by sudden changes in body position.
Orthostatic hypotension can be gradual or sudden, with some experiencing chronic symptoms over time or acute symptoms following medication changes or illness. Postprandial hypotension typically occurs 30-60 minutes after a meal, with symptoms being intermittent or consistent depending on the individual and the condition’s severity.
Orthostatic hypotension can be caused by various factors such as vasovagal syncope, cardiac arrhythmias, medication side effects, hypovolemia and postprandial hypotension. Vasovagal syncope can occur due to emotional stress, pain or prolonged standing while cardiac arrhythmias can cause low blood pressure. Hypovolemia can result from blood loss, dehydration or inadequate fluid intake. Postprandial hypotension can be caused by gastrointestinal disorders, adverse food reactions, cardiac issues like angina and metabolic disorders like hypoglycemia or glucose metabolism disorders. Monitoring blood glucose and metabolic evaluations can help identify these conditions.
Treatment paradigm
Orthostatic and postprandial hypotension are treated with a mix of lifestyle changes and pharmaceutical therapies. The primary objective is to increase and regulate blood pressure in order to relieve symptoms and enhance general well-being. Lifestyle adjustments include increasing hydration and salt consumption, wearing compression stockings and avoiding abrupt changes in body posture. In postprandial hypotension, eating smaller, more frequent meals and avoiding large carbohydrate-rich meals may help alleviate symptoms. Pharmacological therapies like fludrocortisone, midodrine, and droxidopa are used to increase blood volume or vasoconstriction in orthostatic hypotension, and alpha-adrenergic agonists or acetylcholinesterase inhibitors in postprandial hypotension.
Cardiology, General
Discontinue exacerbating drugs:
Identifying and discontinuing medications that induce orthostatic hypotension (OH) are the initial measures to be taken. In cases where it is impossible to discontinue the medication in question or for patients with mild symptoms, reducing the dosage may be adequate. Several medications have been associated with OH, including beta-adrenergic blockers, alpha-adrenergic agonists, and tricyclic antidepressants.
Enhance salt and water intake:
Individuals diagnosed with orthostatic hypotension (OH) must augment their dietary salt and water intake to bolster intravascular volume. The rapid water consumption triggers an osmopressor reflex within an hour of ingestion by decreasing osmolarity in the portal vein.
In addition to consuming water during meals and before exercise, it is advisable to keep a water pitcher near the bedside and down it before getting out of bed in the morning. Ingesting 500 mL of water upon awakening and aiming for a daily intake of 1.5 to 3 liters is a reasonable goal.
Including high-sodium foods in the diet or utilizing salt tablets can also prove beneficial for managing OH.
Modification of daily activities and lifestyle changes:
Patients are advised to transition gradually and in stages from a supine position to a seated one and then to a standing one. This maneuver holds particular significance in the morning, as orthostatic tolerance is typically at its lowest.
During defecation, patients should also avoid performing Valsalva-like maneuvers involving frequent, forceful coughing or straining with a closed glottis. Constipation may require treatment with stool softeners and dietary modifications, while cough suppressants may sometimes be necessary.
Patients should restrict walking in excessively hot or humid weather and avoid situations that may lead to overheating. Additionally, minimizing exposure to hot showers and saunas is recommended, as warm temperatures can cause skin vasodilation, leading to decreased venous return and exacerbation of orthostatic hypotension (OH).
Use compression stockings and abdominal binders:
Utilizing custom-fitted elastic compression stockings allows for applying pressure that varies across the lower extremities and lower abdomen. This helps to reduce peripheral blood pooling, aiding in the management of orthostatic hypotension (OH).
Abdominal binders have improved the decline in orthostatic blood pressure for specific individuals with orthostatic hypotension (OH). They may be better tolerated than compression stockings applied to the legs and abdomen.
Cardiology, General
Neurology
In cases where orthostatic hypotension (OH) experiences modest or temporary improvement in symptoms through nonpharmacologic methods aimed at increasing intravascular volume, such as consuming more salt and water, fludrocortisone can relieve symptoms. This particularly applies to patients who continue to experience persistent volume depletion despite these measures. Fludrocortisone may help address the underlying volume depletion and alleviate symptoms of OH.
Fludrocortisone a synthetic mineralocorticoid increases blood pressure by enhancing renal reabsorption of sodium and water. However, after weeks of treatment, blood volume may return to pre-treatment levels potentially due to elevated peripheral vascular resistance. This sustained effect can lead to long-term adverse effects. Fludrocortisone can also enhance the pressor effect of sympathomimetic agents further affecting blood pressure regulation.
Cardiology, General
Neurology
Midodrine
Midodrine is an orally taken alpha-1 adrenergic agonist that increases peripheral vascular resistance and improves blood pressure by constricting blood vessels and reducing orthostatic hypotension symptoms and has a short duration of action.
Droxidopa
Droxidopa, a synthetic precursor of norepinephrine, enhances blood pressure regulation by increasing peripheral vasoconstriction. Enzymes convert droxidopa to norepinephrine thereby improving blood pressure control
Cardiology, General
In cases where orthostatic hypotension (OH) patients do not improve despite nonpharmacologic measures and their serum norepinephrine level exceeds 220 pg/mL, atomoxetine is the primary pharmacotherapy. Atomoxetine is a norepinephrine transporter (NET) inhibitor that enhances good blood pressure and reduces symptoms in patients with nOH, as it is the primary medication used to address OH symptoms.
Neurology
For people who cannot handle the side effects of fludrocortisone a sympathomimetic medication can be given in addition to or instead of it. Combining fludrocortisone with an alpha agonist might result in lower doses. Using droxidopa in conjunction with norepinephrine reuptake inhibitors or midodrine increases pressor effect but use caution since supine blood pressure may rise.
Cardiology, General
Neurology
Pyridostigmine, a cholinesterase inhibitor, augments cholinergic neurotransmission in both sympathetic and parasympathetic ganglia. Pyridostigmine, on average, led to a modest increase in systolic blood pressure of only four mmHg. The combination of midodrine with pyridostigmine exhibited slightly superior efficacy compared to pyridostigmine alone. Likewise, the concurrent administration of pyridostigmine and atomoxetine produces a synergistic effect, resulting in heightened blood pressure and improved tolerance to orthostatic challenges.
Cardiology, General
Neurology
Using recombinant human erythropoietin raises standing blood pressure and enhances orthostatic tolerance in patients experiencing anemia commonly associated with autonomic failure. Initiating a trial of erythropoietin should be considered the primary treatment approach for all individuals affected by orthostatic hypotension (OH) and anemia, particularly those exhibiting low serum erythropoietin concentrations.
Cardiology, General
Neurology
Orthostatic Hypotension:
Postprandial Hypotension:
Cardiology, General
Neurology
Assessment and Lifestyle Modifications:
The initial phase of orthostatic or postprandial hypotension involves a comprehensive evaluation to identify the underlying causes and factors. This includes reviewing medical history, physical examinations and diagnostic tests. Lifestyle modifications like increasing fluid and salt intake, maintaining hydration and modifying meal composition may be initiated.
Pharmacological Interventions:
If lifestyle changes do not provide sufficient symptom relief or the condition is severe and pharmacological interventions may be introduced. These may include medications targeting blood volume expansion, vasoconstriction or autonomic function. The choice of medication depends on the individual’s condition, comorbidities and response to treatment.
Specialist Consultation and Interventions:
If symptoms persist or become refractory to lifestyle modifications and pharmacological interventions, a specialist consultation may be necessary. The specialist can evaluate the individual’s condition and recommend additional interventions, such as baroreceptor stimulation, gastric pacing, or endoscopic procedures. These interventions are done for severe symptoms or case of unresponsive to other treatments.
Ongoing Management and Follow-up:
The final management phase involves long-term monitoring and follow-up to assess the treatment plan’s effectiveness, adjust medications, and address new concerns. Regular visits with healthcare professionals are crucial for optimal symptom control, treatment response, and managing changes in the individual’s condition or medication needs.
Orthostatic hypotension is a sudden decrease in blood pressure when a person moves from sitting to standing, often due to factors such as dehydration, blood volume changes, pharmaceutical side effects, and medical disorders like diabetes, Parkinson’s disease, and nervous system diseases. The body’s normal response to standing involves narrowing blood vessels and increasing heart rate to maintain blood flow to the brain, but in individuals with orthostatic hypotension, this mechanism fails, causing symptoms like dizziness, light-headedness, and fainting. Postprandial hypotension, on the other hand, refers to a drop in blood pressure after a meal. When we eat, blood is redirected to the digestive system to aid digestion and absorption of nutrients. In healthy individuals, the body compensates for this redistribution of blood by increasing heart rate and constricting blood vessels to maintain normal blood pressure. However, in some people, particularly older adults, this compensatory response is impaired, leading to a significant decrease in blood pressure after eating. In severe cases, postprandial hypotension can cause dizziness, light-headedness, fatigue, and syncope (fainting). The exact cause of postprandial hypotension is not fully understood. Still, it is believed to involve various factors, including an exaggerated response by the autonomic nervous system, impaired baroreceptor reflexes, and inadequate vasoconstriction.
Orthostatic Hypotension (OH):
Postprandial Hypotension (PH):
Orthostatic hypotension occurs when the autonomic nervous system fails to maintain blood pressure due to postural changes, leading to vasoconstriction and elevated heart rate. Factors such as medication, autonomic neuropathy, volume depletion, and fundamental autonomic control problems can contribute to this phenomenon. Postprandial hypotension is not fully understood, but some theories suggest that blood flow to the splanchnic vasculature increases after a meal, causing a decrease in central circulation and a drop in blood pressure. However, in individuals with postprandial hypotension, these mechanisms are impaired, possibly due to baroreceptor dysfunction or abnormal vasoactive substance release or response.
Orthostatic hypotension is caused by volume depletion, medication, autonomic dysfunction and rare disorders like Shy-Drager syndrome and familial dysautonomia. It is more common in older adults due to diminished baroreceptor reflexes and impaired vasoconstrictor responses. Autonomic dysfunction like diabetic neuropathy and Parkinson’s disease can increase the risk of postprandial hypotension. Digestive system factors like the release of vasoactive substances during digestion can also contribute to postprandial hypotension. Abnormalities in releasing or responding to these substances can disrupt blood pressure regulation. Meal composition particularly high-carbohydrate meals has been associated with a higher incidence of postprandial hypotension. Tese factors contribute to the development and progression of orthostatic and postprandial hypotension.
Orthostatic hypotension can be influenced by various factors, including medical conditions like diabetes, Parkinson’s, autonomic neuropathy or cardiovascular disease, severity of symptoms like dizziness, lightheadedness and syncope, blood pressure response, age and overall health. Postprandial hypotension is influenced by the severity of blood pressure drop after a meal, meal-related factors and response to treatment can all impact the prognosis. Effective management and treatment can improve the prognosis, while severe symptoms like dizziness, lightheadedness and syncope increase the risk of falls, injuries, and complications. Older age and poor overall health can also affect the ability to tolerate and manage the condition effectively.
Age group:
Orthostatic hypotension is a condition more common in the older adults which can lead to falls and injuries due to syncope or near-fainting episodes. Postprandial hypotension is more common in older adult and affecting individuals of any age.
Orthostatic Hypotension:
It is measured in supine and standing position to check the orthostatic changes.
It is measured in standing and supine positions. An elevated levels of heart rate by 10 beats per min or more may indicate the compensatory autonomic response.
It includes Dizziness, near fainting while standing or light-headedness.
It assesses the symptoms of autonomic neuropathy like abnormal sweating or loss of deep tendon reflexes.
Postprandial Hypotension:
It measure the blood pressure before and after the meal.
Assess for the postprandial symptoms like light-headedness, dizziness or fatigue.
Evaluate the causes and signs of autonomic dysfunction or comorbidities.
Assess for any postural change during the examination.
Orthostatic hypotension is linked to comorbidities like diabetes, Parkinson’s disease, autonomic neuropathy, cardiovascular disease and certain medications. Symptoms can get worse during the continuous standing or sudden changes in body position. Postprandial hypotension may be triggered by larger carbohydrate-rich meals and can be exacerbated by standing upright after eating. These conditions can be exacerbated by sudden changes in body position.
Orthostatic hypotension can be gradual or sudden, with some experiencing chronic symptoms over time or acute symptoms following medication changes or illness. Postprandial hypotension typically occurs 30-60 minutes after a meal, with symptoms being intermittent or consistent depending on the individual and the condition’s severity.
Orthostatic hypotension can be caused by various factors such as vasovagal syncope, cardiac arrhythmias, medication side effects, hypovolemia and postprandial hypotension. Vasovagal syncope can occur due to emotional stress, pain or prolonged standing while cardiac arrhythmias can cause low blood pressure. Hypovolemia can result from blood loss, dehydration or inadequate fluid intake. Postprandial hypotension can be caused by gastrointestinal disorders, adverse food reactions, cardiac issues like angina and metabolic disorders like hypoglycemia or glucose metabolism disorders. Monitoring blood glucose and metabolic evaluations can help identify these conditions.
Treatment paradigm
Orthostatic and postprandial hypotension are treated with a mix of lifestyle changes and pharmaceutical therapies. The primary objective is to increase and regulate blood pressure in order to relieve symptoms and enhance general well-being. Lifestyle adjustments include increasing hydration and salt consumption, wearing compression stockings and avoiding abrupt changes in body posture. In postprandial hypotension, eating smaller, more frequent meals and avoiding large carbohydrate-rich meals may help alleviate symptoms. Pharmacological therapies like fludrocortisone, midodrine, and droxidopa are used to increase blood volume or vasoconstriction in orthostatic hypotension, and alpha-adrenergic agonists or acetylcholinesterase inhibitors in postprandial hypotension.
Cardiology, General
Discontinue exacerbating drugs:
Identifying and discontinuing medications that induce orthostatic hypotension (OH) are the initial measures to be taken. In cases where it is impossible to discontinue the medication in question or for patients with mild symptoms, reducing the dosage may be adequate. Several medications have been associated with OH, including beta-adrenergic blockers, alpha-adrenergic agonists, and tricyclic antidepressants.
Enhance salt and water intake:
Individuals diagnosed with orthostatic hypotension (OH) must augment their dietary salt and water intake to bolster intravascular volume. The rapid water consumption triggers an osmopressor reflex within an hour of ingestion by decreasing osmolarity in the portal vein.
In addition to consuming water during meals and before exercise, it is advisable to keep a water pitcher near the bedside and down it before getting out of bed in the morning. Ingesting 500 mL of water upon awakening and aiming for a daily intake of 1.5 to 3 liters is a reasonable goal.
Including high-sodium foods in the diet or utilizing salt tablets can also prove beneficial for managing OH.
Modification of daily activities and lifestyle changes:
Patients are advised to transition gradually and in stages from a supine position to a seated one and then to a standing one. This maneuver holds particular significance in the morning, as orthostatic tolerance is typically at its lowest.
During defecation, patients should also avoid performing Valsalva-like maneuvers involving frequent, forceful coughing or straining with a closed glottis. Constipation may require treatment with stool softeners and dietary modifications, while cough suppressants may sometimes be necessary.
Patients should restrict walking in excessively hot or humid weather and avoid situations that may lead to overheating. Additionally, minimizing exposure to hot showers and saunas is recommended, as warm temperatures can cause skin vasodilation, leading to decreased venous return and exacerbation of orthostatic hypotension (OH).
Use compression stockings and abdominal binders:
Utilizing custom-fitted elastic compression stockings allows for applying pressure that varies across the lower extremities and lower abdomen. This helps to reduce peripheral blood pooling, aiding in the management of orthostatic hypotension (OH).
Abdominal binders have improved the decline in orthostatic blood pressure for specific individuals with orthostatic hypotension (OH). They may be better tolerated than compression stockings applied to the legs and abdomen.
Cardiology, General
Neurology
In cases where orthostatic hypotension (OH) experiences modest or temporary improvement in symptoms through nonpharmacologic methods aimed at increasing intravascular volume, such as consuming more salt and water, fludrocortisone can relieve symptoms. This particularly applies to patients who continue to experience persistent volume depletion despite these measures. Fludrocortisone may help address the underlying volume depletion and alleviate symptoms of OH.
Fludrocortisone a synthetic mineralocorticoid increases blood pressure by enhancing renal reabsorption of sodium and water. However, after weeks of treatment, blood volume may return to pre-treatment levels potentially due to elevated peripheral vascular resistance. This sustained effect can lead to long-term adverse effects. Fludrocortisone can also enhance the pressor effect of sympathomimetic agents further affecting blood pressure regulation.
Cardiology, General
Neurology
Midodrine
Midodrine is an orally taken alpha-1 adrenergic agonist that increases peripheral vascular resistance and improves blood pressure by constricting blood vessels and reducing orthostatic hypotension symptoms and has a short duration of action.
Droxidopa
Droxidopa, a synthetic precursor of norepinephrine, enhances blood pressure regulation by increasing peripheral vasoconstriction. Enzymes convert droxidopa to norepinephrine thereby improving blood pressure control
Cardiology, General
In cases where orthostatic hypotension (OH) patients do not improve despite nonpharmacologic measures and their serum norepinephrine level exceeds 220 pg/mL, atomoxetine is the primary pharmacotherapy. Atomoxetine is a norepinephrine transporter (NET) inhibitor that enhances good blood pressure and reduces symptoms in patients with nOH, as it is the primary medication used to address OH symptoms.
Neurology
For people who cannot handle the side effects of fludrocortisone a sympathomimetic medication can be given in addition to or instead of it. Combining fludrocortisone with an alpha agonist might result in lower doses. Using droxidopa in conjunction with norepinephrine reuptake inhibitors or midodrine increases pressor effect but use caution since supine blood pressure may rise.
Cardiology, General
Neurology
Pyridostigmine, a cholinesterase inhibitor, augments cholinergic neurotransmission in both sympathetic and parasympathetic ganglia. Pyridostigmine, on average, led to a modest increase in systolic blood pressure of only four mmHg. The combination of midodrine with pyridostigmine exhibited slightly superior efficacy compared to pyridostigmine alone. Likewise, the concurrent administration of pyridostigmine and atomoxetine produces a synergistic effect, resulting in heightened blood pressure and improved tolerance to orthostatic challenges.
Cardiology, General
Neurology
Using recombinant human erythropoietin raises standing blood pressure and enhances orthostatic tolerance in patients experiencing anemia commonly associated with autonomic failure. Initiating a trial of erythropoietin should be considered the primary treatment approach for all individuals affected by orthostatic hypotension (OH) and anemia, particularly those exhibiting low serum erythropoietin concentrations.
Cardiology, General
Neurology
Orthostatic Hypotension:
Postprandial Hypotension:
Cardiology, General
Neurology
Assessment and Lifestyle Modifications:
The initial phase of orthostatic or postprandial hypotension involves a comprehensive evaluation to identify the underlying causes and factors. This includes reviewing medical history, physical examinations and diagnostic tests. Lifestyle modifications like increasing fluid and salt intake, maintaining hydration and modifying meal composition may be initiated.
Pharmacological Interventions:
If lifestyle changes do not provide sufficient symptom relief or the condition is severe and pharmacological interventions may be introduced. These may include medications targeting blood volume expansion, vasoconstriction or autonomic function. The choice of medication depends on the individual’s condition, comorbidities and response to treatment.
Specialist Consultation and Interventions:
If symptoms persist or become refractory to lifestyle modifications and pharmacological interventions, a specialist consultation may be necessary. The specialist can evaluate the individual’s condition and recommend additional interventions, such as baroreceptor stimulation, gastric pacing, or endoscopic procedures. These interventions are done for severe symptoms or case of unresponsive to other treatments.
Ongoing Management and Follow-up:
The final management phase involves long-term monitoring and follow-up to assess the treatment plan’s effectiveness, adjust medications, and address new concerns. Regular visits with healthcare professionals are crucial for optimal symptom control, treatment response, and managing changes in the individual’s condition or medication needs.
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