Acid-Base Disorders 3 (other acid-base abnormalities) Flashcards
Compensation in metabolic alkalosis
- As a guideline, PCO2 in patients with significant metabolic alkalosis should rise by 0.7 mm Hg for each mEq increase in HCO3
- The PCO2 also rarely rises above 55 mm Hg in compensation for metabolic alkalosis
Examples of chloride-sensitive metabolic alkalosis
Vomiting
Diarrhea
Diuretic use
Chloride-wasting diseases (cystic fibrosis, chloride-wasting enteropathy)
Examples of chloride-unresponsive metabolic alkalosis
Renal artery stenosis
Renin secreting tumors
Adrenal hyperplasia
Hyperaldosteronism
Cushing’s syndrome
Exogenous mineralocorticoids (licorice, fludrocortisone)
(usually normovolemia or hypervolemia)
Treatment of metabolic alkalosis
In the emergency setting, metabolic alkalosis rarely requires active management
- treat the underlying cause
- hydrate, and replace volume with sodium chloride and potassium
- aggressive therapy, such as IV hydrochloric acid, requires ICU admission and monitoring
In respiratory acidosis, regardless of the underlying cause, the final common path is
Inadequate ventilation
This most frequently results from
- head trauma
- chest trauma
- lung disease
- excess sedation
chronic hypoventilation in extremely obese patients
Pickwickian syndrome
How to determine if respiratory acidosis is acute or chronic?
Ratio of change in pH and change in PCO2
(delta pH / Δ PCO2)
>0.8: concomitant metabolic acidosis
=0.8:acute
0.33-0.8: acute on chronic
=0.33: chronic
<0.33: concomitant metabolic alkalosis
Precaution in patients with severe emphysema / COPD
- If the arterial PCO2 chronically exceeds 60-70 mmHg, respiratory acidosis may depress the respiratory center
- Under such circumstances, the stimulus for ventilation is provided primarily by hypoxemia acting on chemoreceptors in the carotid and aortic bodies.
- Giving oxygen could REMOVE the main stimulus TO BREATHE, causing the PCO2 to rise abruptly to extremely dangerous levels
- Consequently, when administering oxygen to patients with COPD, carefully monitor for apnea or hypoventilation
- However, do not withold oxygen in the case of severe hypoxemia
Treatment of respiratory acidosis
- Improvement of alveolar ventilation
- In general, if the minute ventilation is doubled, the PCO2 will be reduced by 50%
- Treat COPD
- Provide NIV support or tracheal intubation as needed
Remarks on chronic respiratory acidosis
- The arterial PCO2 should not be reduced by more than 5.0 mm Hg/hour
- Rapid correction of a severe chronic respiratory acidosis can cause sudden development of a severe metabolic alkalosis, with resulting dysrhythmias
- A rapid rise in pH can cause an abrupt increase in ionized calcium levels and hypokalemia
respiratory alkalosis and tetany
- Acute reduction in PCO2 produces a reduction in H+, resulting in an increase in negative charge on anionic buffers
- The now negatively charged proteins instead bind calcium
- If the effect is sufficiently large, the reduction in ionized calcium produces tetany (e.g., carpopedal spasm) and paresthesias
respiratory alkalosis and cerebral blood flow
- Hypocapnia also produces substantial reductions in cerebral blood flow and
- results in reduced tissue oxygen delivery due to a leftward shift in the oxygen-hemoglobin dissociation curve (i.e., increased hemoglobin-oxygen binding)
Remarks on chronic respiratory alkalosis
- Chronic respiratory alkalosis is unique among acid-base disorders in that its compensation may be complete.
- Compensatory events include bicarbonaturia and a reduction in acid excretion, requiring 6 to 72 hours to develop full and at least 1 week to normalize pH
Treatment of respiratory alkalosis
- Treat the underlying cause
- For patients with anxiety and hyperventilation, do NOT use “paper-bag” rebreathing because it may lead to hypoxia
Chronic respiratory alkalosis can be expected in
High altitudes
- particulary among mountaineers climbing over 12,000 feet, where the partial pressure of oxygen is significantly diminised
- acetazolamide is frequently prescribed to counter the physiologic respiratory effect of such ascents