A. Causes [1]
- Shock
- Volume depletion - hemorrhage, severe dehydration
- Sepsis Syndrome
- Cardiogenic Shock
- Neurogenic Shock - usually due to spinal cord injury
- Orthostatic Changes
- Increasing incidence with age
- Symptoms and objective signs are most common in morning hours [2]
- Autonomic Instability [7]
- Age related; quite common in the elderly
- Neuropathy due to systemic disease (eg. Diabetes)
- Autonomic Insufficiency
- Parkinsonism (hypotension is exacerbated by many anti-Parkinsonian Drugs)
- Pure Autonomic Insufficiency
- Shy-Drager Syndrome (Multiple Systems Atrophy)
- Endocrine Failure
- Adrenal Insufficiency
- Hyperthyroidism
- Pituitary Failure / Pituitary Apoplexy [3]
- Drugs (usually have autonomic action)
- L-dopa
- Anti-depressants (anti-alpha adrenergic activity)
- Monoamine oxidase inhibitors
- Anti-hypertensives (such as ß-blockers and alpha-blockers)
- Cholinergics
- Phenothiazines (anti-alpha adrenergic activity)
- alpha-adrenergic blockers for benign prostatic hyperplasia (BPH)
- Normal blood pressure (BP) range for particular persons
B. Orthostatic Hypotension [1,7]
- Orthostatic hypotension is a classic manifestation of sympathetic vasoconstrictor failure
- Definition
- On standing up from sitting or lying down:
- Systolic BP decrease of at least 20mm Hg OR
- Diastolic BP decrease of at least 10mm Hg
- Heart rate typically and normally increases >10bpm on standing
- In most cases of orthostatic hypotension, heart rate does not increase (<10bpm) on standing
- Physiology
- On rising to standing position, 500-1000 mL of blood pools in lower extremities
- BP and particularly cerebral and cardiac perfusion must be maintained
- Baroreceptors mainly in carotid and aortic vessels detect drop in pressure
- This normally stimulates sympathetic nervous system
- Both neurological and hormonal systems are rapidly activated
- Heart rate usually increases and vasoconstriction occurs
- Failure of any of these systems can lead to orthostatic changes
- Major Systems for Maintaining BP on Standing
- Muscle contraction in legs and abdomen compress veins, reduces blood pooling
- In euvolemia, extra blood is held normally in venous system, acting as a reservoir
- Sympathetic nervous system adjusts arterial, venous, and cardiac tone
- Increased cardiac inotropy and chronotropy (contractility and rate) normally occur
- Renin-Angiotensin-Aldosterone system activated
- Vasopressin (antidiuretic hormone) levels increase
- Classification of Orthostatic Hypotension
- Neurogenic
- Non-Neurogenic: Cardiogenic and others
- Iatrogenic: usually due to medications, overall most common cause
- Differential Diagnosis
- Symptomatic or asymptomatic orthostatic hypotension
- Lightheadedness / Dizziness
- Pres-syncope or Syncope from other causes
- True Vertigo
- Neurogenic Causes
- Spinal cord problems: syrngomyelia, transverse myelitis, tumors, tabes dorsalis
- Peripheral Nervous System: HIV/AIDs, diabetes, alcoholism, amyloidosis, renal failure, paraneoplastic syndrome, Guillain-Barre syndrome, vitamin B12 or folate deficiency
- Autonomic Failure: Parkinson's disease, dysautonomias, multiple system atrophy, pure autonomic failure
- Central Nervous System: stroke, multiple sclerosis, brain tumors, brain-stem lesions
- Carotid sinus hypersensitivity
- Neurocardiogenic syncope
- Non-Neurogenic Causes
- Cardiac Pump Failure: congestive heart failure, cardiomyopathies, many other causes
- Reduced intravascular volume: dehydration, burns, diarrhea, hemorrhage, vomiting
- Salt-lsing nephropathies
- Cirrhosis with ascites
- Endocrinopathies: adrenal insufficiency, thyroid dysfunction
- Venous pooling: alcoholism, fever, heat stroke, sepsis, postprandial splanchnic dilation
- Vigorous exercise with dilation of skeletal vessel beds
- Drugs
- alpha and beta blockers
- Other antihypertensives
- Dopamine Agonists: bromocriptine, levodopa
- Diuretics
- Monoamine oxidase inhibitors
- Narcotics, sedatives, minor tranquilizers
- Nitrates
- Phenothiazines
- Phosphodiesterase 5 Inhibitors: sildenafil, vardenafil, others
- Sympatholytics
- Tricyclic antidepressants
- Vincristine > vinblastine
C. Treatment [1]
- Correction of Underlying Problem
- Volume repletion - fluids, blood products
- Cardiac support
- Correct septic causes
- Stop or change medications
- Some patients with hypotension will require specific BP raising therapy
- Intravenous Sympathomimetics
- Dopamine
- Phenylephrine
- Norepinephrine
- Oral Sympathomimetics
- Midodrine
- Pseudoephedrine
- Clonidine (0.4mg po qd) - may be effective in some patients [4]
- Dihydroergotamine - generally not recommended for chronic use [4]
- Midodrine (ProAmatine®) [2,5]
- Improves vascular resistance by agonist action on alpha1-adrenergic receptors
- Shown to be effective in increasing BP ~22mm at 10mg po tid
- Side effects minimal, mainly supine hypertension
- Scalp pruritis may also occur due to drug, but no cardiotoxic effects seen
- Initiate therapy at 2.5-5mg po tid; last dose taken before 6:00 PM
- Fludrocortisone (Flurinef®)
- Used to increase vascular volume (fluid loading)
- Mineralocorticoid replacement; aldosterone analog
- Baseline and follow-up potassium, sodium, magnesium
- Begin 0.1mg qd-bid po, up to ~ 0.4mg qd-bid
- Orthostatic Hypotension with Anemia [6]
- Treatment with erythropoietin (Epogen®, Procrit®)
- SBP increased ~20 mmHg and DBP increased ~15 mmHg
- HCT increased from 34% to 45%
- Dizziness resolves in many of the patients
- Long term effects not known, but some patients develop mild supine hypertension
Resources
Mean Arterial Pressure (MAP)
References
- Bradley JG and Davis KA. 2003. Am Fam Phys. 68(12):2393
- Low PA, et al. 1997. JAMA. 277:1046
- Kaiser UB and Hedley-Whyte ET. 2001. NEJM. 344(20):1536 (Case Record)
- Victor RG and Talman WT. 2002. Am J Med. 112(5):361
- Midodrine. 1997. Med Let. 39(1003):59
- Ward C and Kenny RA. 1996. Am J Med. 100(4):418
- Freeman R. 2008. NEJM. 358(6):615