- The term used to define the acidity or alkalinity of solutions or blood, pH, is the negative logarithm of the hydrogen ion concentration ([H+]).
- Normal pH = -log [H+] = 7.40 (7.35-7.45)
- Acid = proton donor (H+)
- Base = proton acceptor
- Solution acidity reflects [H+]
- Pa02: Partial pressure of oxygen in arterial blood (mmHg). Normal is 40
- PaCo2: Partial pressure of carbon dioxide in arterial blood (mmHg). Normal 75-100 mm Hg
- A buffer is solution containing a weak acid and its conjugate base or a weak base and its conjugate acid
- It minimizes changes in pH by accepting or giving up H+
- Examples: Bicarbonate, hemoglobin, proteins, phosphates, amnonia
Physiologic Responses to pH Changes
- Immediate chemical buffering
- Respiratory compensation (if possible)
- Renal compensation (slower)
- Mediated by chemoreceptors in brain stem
- VO2 1-4 L/min for every 1mm Hg PaCO2
- Response to metabolic acidosis is hyperventilation, response to metabolic alkalosis is hypoventilation (but less predictable)
- PaCO2 usually does not rise above 55 mmHg in response to metabolic alkalosis because hypoxemia produced by hypoventilation drives ventilation and limits compensation
- PaCO2 decreases 1-1.5 mmHg for every 1 mEq/L decrease in HCO3-
- PaCO2 increases 0.25-1 mmHg for every 1 mEq/L increase in HCO3- up to 55mmHg
- Enormous ability of kidneys to eliminate H+ and reabsorb or form new HCO3-
- Increased absorption of HCO3-
- Increased excretion of acids
- Increased NH3 production
- Increased secretion of HCO3-
- Generally occurs only with concomitant Na+ deficit or with mineralocorticoid excess
- Metabolic acidosis, usually characterized by an acidemic pH (<7.35) and hypobicarbonatemia
- Lactic Acidosis
- Diabetic Ketoacidosis
- Alcoholic Ketoacidosis
- Uremic Acidosis
- Gastrointestinal HCO3- Loss
- Renal Tubular Acidosis
- Treatment is aimed at the underlying disorder, such as insulin and fluid therapy for diabetes and appropriate volume resuscitation to restore tissue perfusion.
- Characterized by an alkalemic pH (>7.45)
- Factors that generate metabolic alkalosis include nasogastric suction and diuretic administration
- Abnormalities that generate HCO3- within the body are called “initiation factors” of metabolic alkalosis, whereas abnormalities that promote renal conservation of HCO3- are called “maintenance factors.”
- Mild alkalosis is generally well tolerated.
- Severe or symptomatic alkalosis (pH > 7.60) requires urgent treatment.
- Depending on the degree of hypovolemia, adequate amounts of 0.9% NaCl and KCl should be administered.
- Discontinuation of diuretics and administration of H2-blockers in patients whose alkalosis is due to nasogastric suction can be useful.
- Increase in PaCO2 > 45 mmHg
- Respiratory acidosis, usually characterized by a low pH (<7.35) and always characterized by hypercarbia, occurs when minute ventilation is insufficient to eliminate CO2 production without an increased capillary–alveolar CO2 gradient.
- Occurs when an acute or chronic rise in arterial CO2
- Respiratory acidosis results from decreased alveolar ventilation and subsequent hypercapnia
- Inadequate Elimination of CO2
- Increased Production of CO2
Symptoms and Signs
- With acute onset, there is somnolence and confusion, and myoclonus with asterixis may be seen. Coma from CO2 narcosis ensues.
- Severe hypercapnia increases cerebral blood flow and cerebrospinal fluid pressure.
- Signs of increased intracranial pressure (papilledema, pseudotumor cerebri) may be seen.
- Since drug overdose is an important reversible cause of acute respiratory acidosis, administration of naloxone (opiate antagonist), 0.04-2 mg intravenously is given to all such patients if no obvious cause for respiratory depression is present
- In all forms of respiratory acidosis, treatment is directed at the underlying disorder to improve ventilation.
Definition & etiology:
- Decrease in PaCO2 < 35 mmHg