Deconditioning, orthostatic intolerance, exercise and chronic illness: Part 1
- Deconditioning is when the body becomes acclimated to less physical stress and becomes less able to function properly under normal conditions.
- Bed rest can cause deconditioning.
- The cardiovascular system changes within 24 hours of bed rest.
- In less than a week, 10% of blood volume is lost.
- When deconditioned, your body does not make appropriate changes when changing position.
- This is called orthostatic intolerance (OI).
- Chronic illness can cause deconditioning.
Deconditioning, orthostatic intolerance, exercise and chronic illness: Part 2
- Orthostatic intolerance(OI) is symptoms that interfere with or prevent standing up.
- OI affects heart rate, blood pressure and distribution of blood to the brain.
- In OI, the body incorrectly initiates a fight or flight response.
- Orthostatic hypotension is a reduction of systolic blood pressure of more than 20 mm Hg or diastolic blood pressure of more than 10 mm Hg within three minutes of standing.
- POTS patients have daily OI symptoms with excessive tachycardia when standing (increase of 30 bpm when standing or over 120 bpm in adults).
- Postural syncope (fainting) can be caused by orthostatic intolerance or vasovagal syncope (VVS).
- Fainting is caused by lack of blood flow to the brain.
- Mast cell disease is known to cause orthostatic intolerance.
Deconditioning, orthostatic intolerance, exercise and chronic illness: Part 3
- POTS (postural orthostatic tachycardia syndrome) is one type of orthostatic intolerance (OI).
- POTS is characterized by an increase of heart rate of 30 bpm or more when standing in the absence of orthostatic hypotension.
- Neuropathic POTS is caused by the veins in the legs not constricting enough to maintain blood pressure when standing.
- Hyperadrenergic POTS is caused by the nervous system telling the heart to beat faster and harder.
- HyperPOTS patients have fluctuating or elevated blood pressure, tachycardia, hypertension and excessive sweating.
- One study found that 38% of mast cell patients had hyperPOTS.
- One study found that 28.9% of POTS patients had less blood volume than normal.
- POTS patients have persistent tachycardia, push less blood out of the heart per beat than normal, have a smaller than normal part of the heart, and do not use oxygen effectively during exercise.
- POTS is often associated with conditions that provoke exercise intolerance, like fibromyalgia, chronic fatigue syndrome and deconditioning.
Deconditioning, orthostatic intolerance, exercise and chronic illness: Part 4
- Syncope (fainting) is loss of consciousness due to temporary loss of blood supply to the brain.
- About 40% of people will faint in their lifetime.
- Vasovagal syncope(VVS) is a form of orthostatic intolerance (OI).
- VVS is often preceded by lightheadedness, sweating, weakness, nausea and visual disturbances.
- VVS patients can go long periods without OI symptoms.
- Ingestion of 16 oz of water in five minutes effectively treats OI episodes of all types.
- OI symptoms can be triggered by large meals, sudden change in position, extended time laying down, heat and alcohol.
- Physical maneuvers and compression garments can decrease OI symptoms in some patients.
- Increasing salt and water intake is recommended for adults with orthostatic hypotension or POTS.
Deconditioning, orthostatic intolerance, exercise and chronic illness: Part 5
- Deconditioning and physical inactivity increase risk for cardiovascular disease.
- A person can lose 10-20% of muscle strength in one week of bed rest.
- Muscle loss is greatest in lower back and legs.
- After three days of bed rest, connective tissue and muscles begin to contract.
- Osteoporosis is more likely in deconditioned patients.
- After twelve weeks of bed rest, almost 50% of bone density can be lost.
- Frequent bed rest increases risk of blood clots.
- Bed rest can reduce strength of muscles supporting the respiratory system, leading to cough and pneumonia.
- 15-30% of bedrest patients develop kidney stones.
- Frequent bed rest can cause neurologic, cognitive and psychiatric disturbances.
- Thyroid, adrenal and pituitary hormones become dysregulated with bed rest.
Exercise and mast cell activity
- Exercise induces mast cell degranulation and release of newly made mediators.
- Histamine, tryptase and leukotrienes increase following exercise in patients who have exercise induced bronchoconstriction.
- Treating with montelukast and loratadine suppressed release of histamine and leukotrienes.
- Leptin is elevated in obese patients.
- Leptin makes airways more reactive and more inflamed.
- Leptin increases the allergic response including leukotriene production.
- Asthmatics who are obese are less likely to respond to inhaled corticosteroids but respond to anti-leukotriene medications.
- Leukotriene E4 was elevated in both obese and lean asthmatics after exercise.
- 9a,11b-PGF2 (metabolite of PGD2) was elevated in obese and lean asthmatics after exercise.
Histamine depletion in exercise
- Regular exercise can be protective against asthma.
- Histamine is released in lungs due to exercise.
- Histamine becomes depleted during exercise.
- Plasma epinephrine does not rise in asthmatics following exercise.
- Inhalation of cromolyn before exercise can prevent or mitigate induced asthma in many patients.
- Treating with H1 and H2 antihistamines decreased endurance during exercise.
- Histamine is important in inducing exercise tolerance.
Chronic urticaria and angioedema: Part 3
- There are several pathways that can cause urticaria and angioedema:
- IgE activation of mast cells
- C3a and C5a activation of mast cells
- Production of bradykinin
- IgG activation of mast cells
- Non-immunologic methods such as radiocontrast dyes, pressure on the skin, heat, etc.
Chronic urticaria and angioedema: Part 4
- There are several conditions that present similarly to chronic urticaria and angioedema.
- Development of urticaria during pregnancy is not unusual.
- Cutaneous mast cell patients often have urticaria like lesions.
- MCAS can also cause angioedema and urticaria.
- Angioedema in the absence of urticaria is rare.
- Hereditary angioedema (HAE) is caused by deficiency or dysfunction of C1 esterase inhibitor in most patients.
- HAE patients do not have coincident urticaria.
- Acquired angioedema is caused by antibodies to the C1 esterase inhibitor, which can be from cancer.
- Angioedema can affect any part of the body.
Chronic urticaria and angioedema: Part 5
- Treatment scheme:
- Second generation H1 antihistamine
- Increase dose of second generation H1 antihistamine
- Add another second generation H1 antihistamine
- Add an H2 antihistamine
- Add a leukotriene receptor antagonist.
- Add a first generation H1 at bedtime.
- Add a strong antihistamine like hydroxyzine.
- Consider Xolair or immunosuppressants.
Premedication and surgical concerns in mast cell patients
- Exact incidence of immediate anaphylaxis from surgery or anesthesia is unknown in mast cell patients
- Mast cell patients should premedicate for surgery.
- Anxiety, temperature changes, irritation of skin, physical trauma and pain can all cause mast cell activation.