ABG CONFERENCE - COPD and obesity – Respiratory acidosis due to

hypoventilation and impaired chest wall mobility

A 62 year old obese man (BMI 46 kg/m2), known case of
chronic obstructive pulmonary disease related to smoking, on
inhalation drugs (salmeterol, fluticasone, and tiotropium), and
hypertensive on perindopril 4 mg OD and spironolactone 50
mg OD, presented to the emergency room with dyspnea.
Three weeks PTA, he was given furosemide 40 mg OD because
of peripheral edema. No other abnormalities noted.
At the Emergency Room, patient had two runs of ventricular
tachycardia.
Physical Examination:
General Survery: Awake, in respiratory distress
BP 180/110 CR 89 RR 28 SPO2 90%
HEENT: No neck vein distention
C/L: No rales, occasional wheezes
Extremities: Grade 1 pedal edema
ABG 7.61/55/77/54
- Hypokalemia – Metabolic alkalosis is generated
primarily by an intracellular shift of protons. However,
potassium depletion is also associated with enhanced
renal ammonia production
- Hypoalbuminemia - Metabolic alkalosis because of the
diminution of the negative charge that albumin normally
contributes to the anion gap and the shift in the buffering
curve for plasma
- Chloruretic agents - all directly produce the loss of
chloride, sodium, and fluid in the urine. These losses, in
turn, promote metabolic alkalosis by several possible
mechanisms. (1) Diuretic-induced increases in sodium
delivery to the distal nephron accelerate potassium and
proton secretion. (2) ECF volume contraction stimulates
renin and aldosterone secretion, which blunts sodium
loss but accelerates the secretion of potassium and
protons. (3) Potassium depletion will independently
augment bicarbonate reabsorption in the proximal
tubule and (4) stimulate ammonia production, which, in
turn, will increase urinary net acid excretion.

CXR: Pulmonary emphysema without an infiltrate Verify the accuracy of the ABG result

TEE: Normal atrial dimensions, normal systolic function, Modified Henderson equation:
normal heart valves and normal vena cava inferior diameter [H+] = 24 x PCO2/HCO3-
= 24 x 55/54
= 24
Serum Electrolytes
This pH is then compared to the measured pH. If the values are
Na (mmol/L) 134 134-145 similar the sample is valid and if the values are far apart, there
K (mmol/L) 2.0 3.5-5.0 may be a measurement error.
HCO3 in the ABG is derived or calculated and is not directly
Cl (mmol/L) 67 97-107 measured

Mg (mmol/L) 0.87 0.7-1.05 What is the primary or dominant disorder?

Urea (mmol/L) 19 2.5-6.4 Metabolic alkalosis
Crea (mOSm/kg) 160 64-104
Check the compensatory response
Osm (mOSm/kg) 299 275-300
Change in pCO2 = 0.75 x Change in HC03
Albumin (g/L) 30 35-50 = 0.75 x 24 – 54
= 0.75 x -30
= 16.5
Urine
Actual pCO2 = 55 -> Compensated
Na (mmol/L) 7
Secondary acid base disorder
K (mmol/L) 38
None
Cl (mmol/L) <10
What other tests would you do?
Crea (mOSm/kg) 10.4

Osm (mOSm/kg) 351 - ECG

pH 5.5 How would you manage this case?

Protein (g/L) 0.84 - Discontinue or avoid use of diuretic

- IVF: NaCl to correct for hypochloremia and volume
Transtubular gradient 0.16 depletion
- Start KCl drip 40 meqs in 250 PNSS x 8 hours
What is the acid base problem and electrolytes - Repeat electrolytes post correction
abnormality?

- Tachypnea RR 28 – Respiratory alkalosis due to excess

CO2 excretion