“An interesting fact about pH is that it is measured in log scale—meaning pH of 6 is 10 times more acidic than pH of 7 and 100 times more acidic than pH of 8.”
5.1 General Principles
How to interpret arterial blood gas (ABG) to diagnose acid-base disorder?
Step 1 : Look at serum pH (normal pH = 7.35-7.45). If abnormal, is it acidic (low pH) or alkalotic (high pH)?
Step 2: Find out which component (PaCO2 or HCO3 –) correlates with the abnormal pH, as this will point toward the primary disorder:
CO2 is an acidic gas. It increases the acid content of blood by reacting with H2O to form carbonic acid. Normal value of PaCO2 (H+) is 40 mmHg, and it is always controlled by respiratory system.
HCO3 – is a base and an important buffer of hydrogen ions in the blood. Normal value of HCO3 – is 24 mEq/L +/- 3, and HCO3 – content is always controlled by metabolic components, largely through the kidneys.
Example: If pH is acidotic and PaCO2 is elevated, then the primary disorder is respiratory acidosis. If pH is acidotic and HCO3 is low, then the primary disorder is metabolic acidosis.
Step 3: Know that compensation is almost always never complete (e.g., respiratory compen-sation of metabolic acidosis can never bring back the pH to normal). Hence the rule is that “primary disorder always reflects the pH status.” And, if pH is normal and HCO3 – or PaCO2 is abnormal, then it should be a mixed disorder of primary acid/primary base, because “compensation is never complete.”
1 The only exception to this rule is high-altitude respiratory alkalosis, where compensation can be complete resulting in normal pH.
Compensation
Respiratory compensation is immediate, so most of the nonrespiratory causes of acid-base disorders will have respiratory compensation.
Metabolic compensation, which is mostly by the kidneys, is not immediate and can take 2 to 3 days to kick in. Thus, in primary respiratory acid-base disorder, metabolic compensation may not be present, especially if the respiratory pathology is acute.
In acidosis, kidneys increase reabsorption of HCO3 – and increase H+ excretion.
In alkalosis, kidneys increase excretion of HCO3 – and increase reabsorption of H+.
5.2 Respiratory Alkalosis
5.2.1 Acute Respiratory Alkalosis
Etiology
Any cause of hypoxia (e.g., acute pulmonary embolus, asthma exacerbation, pneumonia) can lead to compensatory increase in ventilatory drive, which increases minute ventilation resulting in patients blowing off their CO2. If hypoxemia is not corrected in time, respiratory muscle fatigue can ensue resulting in acute respiratory acidosis.
Central nervous system pathology (e.g., intracranial or subarachnoid hemorrhage): protective mechanism of hyperventilation kicks in, which has the final effect of decreasing intracranial pressure.
2 Compensatory hyperventilation → decreased arterial PaCO2 → arterial vasoconstriction → decreased cerebral blood flow → compensatory decrease in intracranial pressure
Respiratory stimulation due to aspirin, caffeine abuse, high fever, etc.
Iatrogenic: if minute ventilation in intubated patients is set too high.
A Complication of Acute Respiratory Alkalosis: Acute Hypocalcemia
Mechanism: alkalosis → less H+ ions concentration → less H+ (positive ion) binding to albumin → more sites are available for Ca++ (another positive ion) to bind with albumin → low free ionized calcium → acute hypocalcemia.
Clinical features: neuromuscular excitation leading to paresthesias, hyperactive deep tendon reflexes, perioral numbness, carpopedal spasms (early tetany) and sometimes, even seizures.
A 30-year-old female patient with prior medical hx of anxiety disorder presents with sudden onset of severe shortness of breath. Exam reveals increased respiratory rate. ABG done reveals normal PaO2 on room air, pH of 7.51, PaCO2 of 30 and HCO3 – of 23.
Patient develops hand and leg paraesthesias. While taking blood pressure, her wrist hand muscles go into a transient spasm.
13. What is the underlying cause?
5.2.2 Chronic Respiratory Alkalosis
Etiology
Pregnancy: progesterone is a respiratory stimulant
Cirrhosis: due to decreased metabolism of progesterone and other endogenous respiratory stimulants
Complication: if chronic, it can lead to renal parathyroid hormone (PTH) resistance and pseudo-hypoparathyroidism (hyperphosphatemia and hypocalcemia despite high-normal or high PTH).
5.3 Primary Metabolic Acidosis
Approach to identify the cause of metabolic acidosis
aAnion gap is the sum of all the positively charged ions minus sum of all negatively charged ions in serum electrolyte panel:
