Quick Review: Acid Base Disorders
T Fujii, B Phillips
Citation
T Fujii, B Phillips. Quick Review: Acid Base Disorders. The Internet Journal of Internal Medicine. 2002 Volume 3 Number 2.
Abstract
Normal blood pH is 7.40 (7.36 - 7.44), which corresponds to a [H+] of 40 nEq/L (44-36).
Systemic arterial pH is maintained by complex buffering mechanisms as well as renal and respiratory compensatory responses. This brief article reviews the basics of acid-base disorders.
General Concepts
The kidneys regulate HCO3¯ by the following mechanisms:
Reabsorption of filtered HCO3¯
Formation of titrable acid
Excretion of NH4+ in the urine
Acidemia: serum pH < 7.36
Alkalemia: serum pH > 7.44
Acidosis: pathophysiologic processes, which favor development of acidemia
Alkalosis: pathophysiologic processes, which favor development of alkalosis
Buffer: A substance, which can absorb or donate H+ ions in order to mitigate changes pH.
H2CO3¯ H+ + HCO3¯ H2O + CO2
* Remember: [H+] ion concentration and pH are inversely related.
Henderson-Hasselbalch equation:
pH = pK + log
Kassirer-Bleich equation:
H+ = 24 x PCO2/HCO3 ¯
Reflects how the acidity of blood is determined by the relative availability of acid and alkali, i.e. HCO3¯, PaCO2. Stresses how H+ ion concentration is determined by the ratio of PCO2/HCO3, rather than the absolute value of either value alone.
Metabolic Acidosis
Anion Gap: Na+ - (Cl¯- + HCO3¯) (represents unmeasured anions in plasma, normally 10-12 mmol/L)
Figure 1
Compensation:
Winter's formula: PaCO2 = 1.5 x HCO3¯ + 8 (+/-2)
(PaCO2 = last 2 digits of pH - chronic metabolic acidosis)
Treatment:
Should be directed at the underlying cause Bicarbonate therapy can be considered with severe acidosis with physiologic compromise:
Bicarbonate deficit (mEq) = LBW x 0.5 x (Desired HCO3¯– actual HCO3¯)
Osmolal Gap:
Measured OSM – Calculated OSM
Calculated Osmolality:
2 x Na + Glc/18 + BUN/2.8 + ETOH/4.6
Elevated OG (> 10 mOsm/L):
Methanol
Ethylene glycol
Paraldehyde
ETOH ketoacidosis
Isopropyl alcohol
Mannitol
Metabolic Alkalosis
Figure 2
Compensation:
PaCO2 = 0.9 x HCO3¯ + 9
Treatment:
Acetazolamide (Diamox): 250 -375 mg po qd-bid
HCl infusion: 0.1-0.2 N @ < 0.2 mEq/hour via central line (=100-200 mEq H+/L)
HCL (mmol) = (LBW x 0.5) x Actual HCO3- desired HCO3)
Hemodialysis: severe alkalosis with cardiac/renal dysfunction
Respiratory Acidosis
CNS:
Sedatives, morphine, anesthetics
Trauma, Stroke
Infection
NM Disorders:
Myopathies (MD, K+ depletion)
Neuropathies (GB, polio)
Acute-Chronic Lung disease
COPD
PNA, pulmonary edema
ARDS
Acute obstruction (aspiration, tumor, spasm)
Obesity
Pneumothorax
Pleural effusion
Kyphoscoliosis
Scleroderma
Crush injury
Mechanical ventilation
Cardiopulmonary arrest
Compensation:
Acute: HCO3¯ increases by 1 mmol/L for each 10 mm Hg increase in PaCO2
Chronic: HCO3¯ increases by 4 mmol/L for each 10 mm Hg increase in PaCO2
Respiratory Alkalosis
-
Anxiety, Pain
-
CNS Disorders (CVA, tumor, infection)
-
Lung Disease:
-
-
Restrictive disorders
-
Pulmonary embolus
-
PNA
-
-
Sepsis, fever
-
Hyperthryoidism
-
Hypoxia
-
Hepatic insufficiency
-
Pregnancy
-
Salicylates, Catecholamines
-
Mechanical ventilation
Compensation:
Acute: HCO3¯ decreases by 2 mmol/L for each 10 mm Hg decrease in PaCO2
Chronic: HCO3¯ decreases by 5-7 mmol/L for each 10 mm Hg decrease in PaCO2
Delta Gap:
Identifies triple acid base disorders
Figure 3
Summary of Acid Base Compensatory Responses
Figure 4
