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The Henderson-Hasselbach (H-H) equation, from a medical
perspective, is about reflexes. When bicarbonate
concentration [HCO3‾] drops as a result of
metabolic acidosis, e.g., lactic acidosis during anaerobic exercise,
breathing is considered to be a reflexive compensatory response that
contributes to restoration of acid-base balance. When PCO2 is too low,
extracellular pH rises with resulting respiratory alkalosis, a condition
identified as hypocapnia. When PCO2
is too high, extracellular pH falls with resulting respiratory acidosis, a
condition identified as hypercapnia. The medical perspective offers up organic
explanations that may give rise to these conditions. Integrating behavioral psychology with the
H-H equation, however, sets the stage for examining these conditions from a
learning perspective where the denominator of the equation may be directly
regulated by powerful reinforcement of operant breathing behaviors that
compromise acid-base balance. Thus,
the equation might be rewritten as follows:
acid-base regulation (pH) = physiology [HCO3‾] ÷ behavior
(breathing for PCO2 changes). The implications are impressive. Learned overbreathing behavior results in behavioral
hypocapnia, where breathing rate and depth are mismatched. Its consequence is an increased level of
pH, or respiratory alkalosis, which may have profound immediate and long-term
effects that may trigger, exacerbate, and/or cause a wide variety of
emotional (anxiety, anger), cognitive (attention, learning), behavioral
(public speaking, test taking), and physical (pain, asthma) changes that may
seriously impact health and performance (Fried, 1987; Laffey & Kavanagh,
2002). Practically speaking,
behavioral hypocapnia is defined as ETCO2 readings below 35 mmHg
brought about by learned breathing patterns:
30-35 mmHg is mild to moderate, 25-30 mmHg is serious, and 20-25 mmHg
is severe hypocapnia. Behavioral
hypocapnia reduces respiratory fitness and disturbs acid-base chemistry as
follows: ● Hypocapnia increases red blood cell alkalinity and
reduces red cell CO2 levels, thereby increasing hemoglobin’s
affinity for oxygen (Bohr Effect). The consequence is “unfriendly” hemoglobin:
oxygen saturation rises (HbO2) but oxygen distribution to tissues
is compromised. Note that the
uninformed practitioner may mistakenly interpret higher saturation readings
taken with an oximeter as a sign of improved respiration. The same red blood cell physiology also
restricts the amount of nitric oxide (a potent vasodilator) released by
hemoglobin, resulting in significant vasoconstriction, even ischemia. These two factors together may very significantly
reduce reduction of oxygen and glucose to cells that require them. ● Hypocapnia increases plasma alkalinity, thereby
triggering significant electrolyte changes.
Calcium ions migrate into muscles in exchange for hydrogen ions,
resulting in their immediate constriction, e.g., arteries, gut, and
bronchioles. Vasoconstriction can
lower cerebral and coronary blood flow/volume by up to 50 percent in a matter
of seconds. Bronchiole constriction
increases airway resistance and may trigger asthma symptoms or precipitate an
attack. Gut constriction may result in
nausea and cramping, as in the case of altitude sickness. Calcium-magnesium imbalance in skeletal
muscles may increase the likelihood of spasm and fatigue. Sodium and potassium ions in interstitial
fluids migrate into cells in exchange for hydrogen ions resulting in sodium
and potassium deficiencies. ● Chronic hypocapnia orchestrates yet different
physiological changes. The kidney
requires CO2 for the reabsorption of both bicarbonate and sodium
ions, as well as for generating new bicarbonates lost in the urine as a
result of buffering acids generated by protein breakdown (e.g., phosphoric
acid). The resulting bicarbonate and
sodium deficiencies may include some of the same effects as those identified
with chronic stress, e.g., fatigue.
Other effects include: elevated platelet level, aggregation, and
“adhering” propensity; antioxidant depletion as a result of excitotoxin
production (e.g., glutamate); and systemic inflammation. ● Hypocapnia may set the stage for intracellular lactic
acidosis (e.g., in neurons) by significant reductions in oxygen supply and
increased cellular metabolism resulting from the influx of sodium and
potassium. Here are some of the symptoms and deficits triggered, exacerbated,
caused, or perpetuated by hypocapnia: RESPIRATION: shortness of breath, breathlessness, bronchial
constriction and spasm, airway resistance, reduced lung compliance, asthma
symptoms; CHEST: tightness, pressure,
and pain; PERIPHERAL CHANGES: trembling,
twitching, shivering, sweatiness, coldness, tingling, and numbness; HEART: palpitations, increased rate, angina
symptoms, arrhythmias, nonspecific pain, ECG abnormalities; EMOTION: anxiety, anger, panic,
apprehension, worry, crying, low mood, frustration, performance anxiety,
phobia, generalized anxiety; STRESS:
tenseness, acute fatigue, chronic fatigue, effort syndrome weakness,
headache, burnout; SENSES: blurred vision,
dry mouth, sound seems distant, reduced pain threshold; CONSCIOUSNESS: dizziness, loss of balance,
fainting, black-out, confusion, disorientation, disconnectedness,
hallucinations, traumatic memories, self-esteem, personality shifts; COGNITION: attention deficit, inability to
think, poor memory, learning deficits;
MUSCLES: tetany, hyperreflexia, spasm, weakness, fatigue, pain; ABDOMEN: nausea, cramping, and
bloatedness; MOVEMENT: coordination,
reaction time, balance; VASCULAR:
hypertension, migraine, digital artery spasm, ischemia; BLOOD: red blood cell rigidity, thrombosis; SLEEP: apnea; PERFORMANCE: endurance, altitude sickness. Fried, R. The hyperventilation syndrome: Research
and clinical treatment. Baltimore:
John Hopkins University Press, 1987. Laffey, J.G., & Kavanagh, B.P. Hypocapnia.
New England Journal of Medicine
(2002); 347(1): 43-53. Levitzky, M. G. Pulmonary Physiology. New York: McGraw Hill, 2007 (7th edition). Copyrighted by Behavioral Physiology
Institute, Santa Fe, New Mexico USA |