Acidosis: Process lowering blood pH below 7.35. Respiratory refers to failure of respiratory system in pH balance.
Normal Respiration:
Inhalation: Diaphragm and chest muscles contract, chest expands, air enters.
Exhalation: Muscles relax, lungs recoil due to elastin, air exits.
Lungs facilitate oxygen intake and carbon dioxide removal.
Carbon dioxide binds with blood water to form carbonic acid (H2CO3).
Carbonic acid dissociates into hydrogen ions (H^+) and bicarbonate ions (HCO_3^-, a buffer).
Partial pressure of carbon dioxide (pCO2) must be in a narrow range to prevent pH fluctuations.
Lungs maintain a ventilation rate that matches carbon dioxide production by tissues.
Chemoreceptors in carotid arteries and aortic arch detect rising pCO2 and falling pH.
Respiratory centers in the brainstem increase respiratory rate and depth.
Minute ventilation is increased, which is the volume of air moving in and out of the lungs per minute.
Increased ventilation removes more carbon dioxide, reduces pCO2, and raises pH.
Normal ventilation mechanism disrupted.
Minute ventilation inadequate for pH balance.
Potential Causes:
Brainstem Issues: Stroke or overdose (opioids, barbiturates) slowing respiratory centers.
Neuromuscular Disorders: Myasthenia gravis impairs nerve stimulation of muscles.
Muscle Impairment: Trauma or obesity hindering diaphragm and chest wall muscles.
Airway Obstruction: Foreign object blocking bronchus.
Impaired Gas Exchange: COPD, pneumonia (fluid in alveoli), pulmonary edema (fluid between alveoli/capillaries).
Result: Inefficient carbon dioxide removal.
Carbon dioxide accumulates, raising pCO2 above 45 mmHg.
Blood pH decreases below 7.35.
If respiratory centers function, increased rate and depth of ventilation occur.
Excess carbon dioxide diffuses into cells (especially red blood cells).
Carbon dioxide reacts with water to form carbonic acid, then hydrogen ions and bicarbonate ions.
Bicarbonate escapes to the circulation to counteract high pCO2.
Hydrogen ions are buffered by intracellular proteins (amine groups like in hemoglobin).
Issue: Limited intracellular protein concentration relative to carbon dioxide levels.
Only small amounts of carbon dioxide enter cells to avoid disrupting intracellular pH.
Limited bicarbonate generation (approximately 1 mEq/L increase per 10 mmHg increase in pCO2).
Example: An acute rise of pCO2 from 40 to 60 mmHg (increase of 20 mmHg) only raises plasma bicarbonate from 24 to 26 mEq/L which has minimal impact of pH.
Acute phase: pH remains low.
Kidney Compensation (after 3-5 days):
Kidneys sense low pH and increase bicarbonate reabsorption in proximal convoluted tubules.
Kidneys increase bicarbonate concentration by roughly 4 mEq/L for each 10 mmHg increase in pCO2.
Example: If pCO2 increases from 20 to 40 mmHg (increase of 20 mmHg), plasma bicarbonate increases by 8 mEq/L (from 24 to 32 mEq/L).
This leads to a substantial pH increase.
Lungs fail to eliminate carbon dioxide.
Carbon dioxide builds up, lowering blood pH below 7.35.
Divided into acute (no renal compensation) and chronic phases (renal compensation present).
Renal compensation raises bicarbonate concentration.
Alkalosis: Process causing alkali accumulation or acid loss.
Respiratory: Failure of the respiratory system in pH balance.
Inhalation: Diaphragm and chest muscles contract, chest expands, air enters.
Exhalation: Muscles relax, lungs recoil due to elastin, air exits.
Lungs facilitate oxygen intake and carbon dioxide removal.
Carbon dioxide binds with blood water to form carbonic acid (H2CO3).
Carbonic acid dissociates into hydrogen ions (H^+) and bicarbonate ions (HCO_3^-, a buffer).
Partial pressure of carbon dioxide (pCO2) must be in a narrow range to prevent pH fluctuations.
Lungs maintain a ventilation rate that matches carbon dioxide production by tissues.
Chemoreceptors in carotid arteries and aortic arch detect falling pCO2 and rising pH.
Respiratory centers in the brainstem decrease respiratory rate and depth.
Minute ventilation is decreased, which is the volume of air moving in and out of the lungs per minute.
Decreased ventilation means less carbon dioxide moves out, which increases pCO2 and lowers pH.
Normal ventilation mechanism disturbed.
Minute ventilation exceeds what's needed to balance the pH.
Respiratory centers fire more than usual for ventilation to increase.
Causes:
Normal Response: Hypoxia (low oxygen) due to pneumonia, pulmonary embolism, or high altitude.
Abnormal Response: Anxiety, panic attacks, sepsis, salicylate overdoses.
Rare: Brainstem disorders irritating respiratory centers.
Iatrogenic: Over-ventilation (incorrect ventilator settings).
Result: Lungs eliminate too much carbon dioxide.
Carbon dioxide depleted, pCO2 falls below 35 mmHg.
Blood pH increases above 7.45.
Acidic molecules (carboxyl groups from proteins like hemoglobin) in cells (especially red blood cells) release hydrogen ions.
Hydrogen ions diffuse into blood and combine with bicarbonate to form carbonic acid, which breaks down into carbon dioxide and water.
Plasma bicarbonate concentration decreases slightly.
Limited intracellular protein concentration means limited hydrogen ions available to neutralize bicarbonate.
Bicarbonate decrease is small (about 2 mEq/L for each 10 mmHg decrease in pCO2).
Example: An acute drop of pCO2 from 40 to 20 mmHg (decrease of 20 mmHg) only decreases plasma bicarbonate from 24 to 20 mEq/L which has minimal impact of pH.
Acute phase: pH remains high.
Kidney Compensation (after 3-5 days):
Kidneys sense high pH and decrease bicarbonate reabsorption in proximal convoluted tubules.
Bicarbonate is excreted more in the urine.
Kidneys decrease bicarbonate concentration by roughly 4-5 mEq/L for each 10 mmHg decrease in pCO2.
Example: If pCO2 decreases from 40 to 20 mmHg (decrease of 20 mmHg), plasma bicarbonate decreases by 8 mEq/L (from 24 to 16 mEq/L).
This leads to a substantial pH decrease.
Lungs blow off more carbon dioxide than needed.
Blood pH increases above 7.45.
Divided into acute (no renal compensation) and chronic phases (renal compensation present).
Renal compensation decreases bicarbonate concentration.