• a. Modified Allen test: It is used to assess the integrity of the ulnar artery before radial artery puncture or cannulation at that site, to verify ulnar artery collateral circulation, and to ensure blood flow to the hand if occlusion of radial artery occurs due to thrombus or embolization.
• b. Radial artery is the common site chosen; other sites include femoral artery, brachial artery, and rarely dorsalis pedis artery.
• c. Preheparinized ABG syringes if available or a normal syringe flushed with 0.05 mL of 1:1,000 heparin solution and emptied, gloves, and alcohol swabs.
• d. Procedure is performed after taking aseptic precautions, needle directed at an angle of 30–45° from the surface, and after 2 mL is collected, needle is removed, firm occlusive local pressure applied for over 5 minutes, check for hemostasis and apply adhesive plaster. If ABG syringe is used, needle protective sleeve applied, untwisted and removed with needle and placed in sharp container. Excess air removed by holding upright, gently tapped to bring air bubble if any to the top so that air can be expelled and after capping placed in ice bag and sent for analysis immediately after noting the details of the patient’s name, FiO2, temperature, date, and time.
• e. Reasons for precautions:
  • Aseptic precautions to prevent sepsis.
  • Needle is directed at an angle 30–45° in the direction of the artery to avoid trauma and allow smooth muscle fibers to occlude the site of puncture after the procedure.
  • Firm occlusion to avoid bleeding and hematoma.
  • Air bubbles expelled as they will increase PaO2 and cause error in interpretation.
  • Sent in ice because change in pH is 0.001, PCO2 is 0.1 mm Hg and PaO2 is 0.01% in ice; without ice, change in pH is 0.01, PCO2 is 1 mm Hg and PaO2 is 0.1%.
  • Patient’s details for avoiding errors and correct interpretation based on parameters like FiO2.

• a. Oxygen—hemoglobin dissociation curve: Correlates the oxygen saturation of hemoglobin across a range of partial pressures of oxygen.
• b. The p50 is the pressure at which hemoglobin is 50% saturated (27 mm Hg on the X-axis).
• c. Left shift (dashed blue line) increases oxygen affinity (hemoglobin holds more tightly to oxygen and delivers less to tissues at a given arterial oxygen pressure): e.g., fetal hemoglobin (HbF), carboxyhemoglobin, methemoglobinemia (MetHb), low 2,3-diphosphoglycerate (2,3-DPG), higher pH (alkalosis), decrease in body temperature (hypothermia).
• d. Right shift (dashed red line) decreases oxygen affinity (hemoglobin delivers more oxygen to tissues at a given arterial oxygen pressure): e.g., increase in body temperature (fever/hyperthermia), higher 2,3-DPG, lower pH (acidosis), increased PaCO2.
• e. Determinants of PaO2: Age (as age increases PaO2 decreases: PaO2 ≈ 104.2 − 0.27 × age in years), FiO2 (roughly 5 × FiO2 percentage), barometric pressure, alveolar ventilation, and ventilation-perfusion matching.

The AaDO2 is calculated as follows:

${\text{AaDO}}_2={\text{PAO}}_2-{\text{PaO}}_2$

${\text{PAO}}_2=[{\text{FiO}}_2\times (760-47)-1.25\times {\text{PaCO}}_2]$
${\text{PAO}}_2=[0.5\times 713-1.25\times 65]=356.5-81.25=275.25\text{ mm Hg}$

${\text{AaDO}}_2=275.25-160=115.25\text{ mm Hg}$

Inference: Marked increase in alveolar-arterial oxygen gradient.

• a. Anion gap: $\text{Na}-(\text{Cl}+{\text{HCO}}_3)=136-(100+12)=24\text{ mEq/L}$.
• b. High anion gap metabolic acidosis (HAGMA) with normal oxygenation.
• c. Compensation using Winter’s formula:
  $\text{Expected }{\text{PCO}}_2=({\text{HCO}}_3\times 1.5)+8\pm 2=(12\times 1.5)+8\pm 2=26\pm 2=24\text{–}28\text{ mm Hg}$
  Actual ${\text{PCO}}_2$ is $32\text{ mm Hg}$ ($>28$), so there is concurrent respiratory acidosis.
• d.
  • $\text{Delta anion gap}=24-12=12$
  • $\text{Delta }{\text{HCO}}_3=24-12=12$
  • $\text{Delta-delta ratio}=\frac{12}{12}=1.0$ (Pure HAGMA with concurrent respiratory acidosis).
• e. Conditions with decreased anion gap: Hypoalbuminemia, paraproteinemia (multiple myeloma), bromide intoxication, lithium toxicity, and hypermagnesemia.

• a. Disorder: Metabolic alkalosis as the HCO3 is high (34 mEq/L) with alkalemia (pH 7.48).
• b. Compensation: Expected PaCO2 rises 0.5–1 mm Hg for each 1 mEq/L rise in HCO3:
  $\mathrm{\Delta }{\text{HCO}}_3=34-24=10\text{ mEq/L}⟹\text{Expected rise in }{\text{PaCO}}_2=5\text{–}10\text{ mm Hg}⟹\text{Expected }{\text{PaCO}}_2=45\text{–}50\text{ mm Hg}$
  Actual PaCO2 is 47 mm Hg, indicating appropriate respiratory compensation.
• c. Is there another disorder: No.
• d. Cause for low Na and K: Loss of HCl through gastric vomiting, contraction alkalosis, secondary hyperaldosteronism leading to renal potassium loss, and hypovolemic hyponatremia.
• e. Oxygenation and oxygen content: Normal oxygenation (PaO2 96 mm Hg).
  $\text{Oxygen content }({\text{CaO}}_2)=(\text{Hb}\times 1.34\times {\text{SaO}}_2)+({\text{PaO}}_2\times 0.003)$
  ${\text{CaO}}_2=(8\times 1.34\times 1.0)+(96\times 0.003)=10.72+0.288=11.0\text{ mL/dL}$

• a. Metabolic acidosis (acidemia with low HCO3 18 mEq/L).
• b. Estimated compensation using Winter’s formula:
  $\text{Expected }{\text{PCO}}_2=(18\times 1.5)+8\pm 2=27+8\pm 2=35\pm 2=33\text{–}37\text{ mm Hg}$
• c. Simple metabolic acidosis with appropriate respiratory compensation (actual PaCO2 is 33 mm Hg).
• d. Normal anion gap metabolic acidosis (NAGMA / hyperchloremic metabolic acidosis) as AG is 12.

• a. Primary disturbance: Metabolic alkalosis (elevated pH 7.51 and HCO3 36 mEq/L).
• b. Compensation: Expected PaCO2 rises 0.5–1 mm Hg for each 1 mEq/L rise in HCO3:
  $\mathrm{\Delta }{\text{HCO}}_3=36-24=12⟹\text{Expected }{\text{PaCO}}_2=40+(6\text{ to }12)=46\text{–}52\text{ mm Hg}$
  Actual PaCO2 is 49 mm Hg; compensation is appropriate.
• c. Oxygenation status: Normal oxygenation (PaO2 93 mm Hg, SaO2 95%).
• d. Simple metabolic alkalosis.
• e. Clinical implication: Classic for hypochloremic hypokalemic metabolic alkalosis seen in infantile hypertrophic pyloric stenosis (IHPS). Look for visible peristalsis, palpable olive mass, perform abdominal ultrasound, and obtain surgical consultation.

• a. Initial impression: Severe high anion gap metabolic acidosis, hyperglycemia with normal oxygenation.
• b. Diabetic ketoacidosis (DKA).
• c. Compensation: Using Winter’s formula:
  $\text{Expected }{\text{PCO}}_2=(1.5\times 11)+8\pm 2=16.5+8\pm 2=24.5\pm 2=22.5\text{–}26.5\text{ mm Hg}$
  Actual PCO2 is 16 mm Hg ($<22.5$), indicating additional/superimposed respiratory alkalosis (or partial overcompensation).
• d. Anion gap: $136-(99+11)=26\text{ mEq/L}$ (High anion gap).
• e. Conditions with HAGMA: Diabetic ketoacidosis, uremia/renal failure, toxic ingestions (methanol, ethylene glycol, salicylates), and lactic acidosis (sepsis, tissue hypoperfusion).

• a. Anion gap: $\text{Na }138-(\text{Cl }100+{\text{HCO}}_{3}2.7)=35.3\text{ mEq/L}$.
• b. Severe uncompensated high anion gap metabolic acidosis with hyperoxia (PaO2 396.4 mm Hg).
• c. Expected PCO2: $(1.5\times 2.7)+8\pm 2=4.05+8\pm 2=10\text{–}14\text{ mm Hg}$.
  Actual PCO2 is 25.8 mm Hg ($>14$), indicating concurrent respiratory acidosis.
• d.
  • $\text{Delta anion gap}=35.3-12=23.3$
  • $\text{Delta }{\text{HCO}}_3=24-2.7=21.3$
  • $\text{Delta gap}=\text{Delta AG}-\text{Delta }{\text{HCO}}_3=23.3-21.3=2.0$
  • $\text{Delta-delta ratio}=\frac{23.3}{21.3}=1.09$
• e. Final interpretation: Mixed High Anion Gap Metabolic Acidosis (HAGMA) + Respiratory Acidosis (delta gap between −6 and +6 and ratio between 0.8 and 2.0 confirms pure HAGMA component with superimposed respiratory failure).

• a. Severe mixed respiratory acidosis (PaCO2 75 mm Hg) and metabolic acidosis (HCO3 12.7 mEq/L, AG 24) with severe hypoxemia (PaO2 38.6 mm Hg).
• b.
  • $\text{Delta anion gap}=24-12=12$
  • $\text{Delta bicarbonate}=24-12.7=11.3$
• c. $\text{Delta gap}=12-11.3=0.7$ and $\text{delta-delta ratio}=\frac{12}{11.3}=1.06$, confirming pure HAGMA with severe respiratory acidosis and severe hypoxemia (PaO2 < 40 mm Hg).

• a. Normal oxygenation (PaO2 92 mm Hg, normal > 80 mm Hg).
• b. Classification of hypoxemia:
  • Mild hypoxemia: PaO2 60–79 mm Hg (tachypnea)
  • Moderate hypoxemia: PaO2 40–59 mm Hg (tachycardia, cool extremities)
  • Severe hypoxemia: PaO2 < 40 mm Hg (cyanosis, arrhythmias, brain injury, and arrest)
• c. Initial impression: Metabolic alkalosis.
• d. Final interpretation: For 1 mEq/L rise in HCO3, PCO2 increases by 0.5–1 mm Hg. For $\mathrm{\Delta }{\text{HCO}}_3=33-24=9\text{ mEq/L}$, expected PCO2 rise is 4.5–9 mm Hg (expected PCO2: 44.5–49 mm Hg). Actual PCO2 is 49 mm Hg, confirming adequately compensated metabolic alkalosis.

• a. Severe metabolic acidosis.
• b. $\text{Anion gap}=141-(105+8)=28\text{ mEq/L}$ (High anion gap).
• c. $\text{Expected }{\text{PCO}}_2=(1.5\times 8)+8\pm 2=12+8\pm 2=18\text{–}22\text{ mm Hg}$. Actual PCO2 is 34 mm Hg ($>22$), so there is superimposed respiratory acidosis.
• d. $\text{Delta AG}=28-12=16$; $\text{Delta }{\text{HCO}}_3=24-8=16$; $\text{Delta-delta ratio}=\frac{16}{16}=1.0$; $\text{Delta gap}=16-16=0$. Final impression: Pure HAGMA with concurrent respiratory acidosis.
• e. Possible clinical conditions: Inborn errors of metabolism (IEM) with respiratory depression, chronic kidney disease (CKD) with pneumonia, septic shock with respiratory failure, or postcardiac arrest state.

• a. Acute respiratory acidosis with moderate hypoxia on FiO2 0.6 and adequate metabolic compensation (in acute respiratory acidosis, for every 10 mm Hg rise in PaCO2, HCO3 rises by 1 mEq/L: $\mathrm{\Delta }{\text{PaCO}}_2=20⟹\text{expected }{\text{HCO}}_3=24+2=26\text{ mEq/L}$).
• b. Normal PaO2 in room air with normal lungs: 80–100 mm Hg.
• c. Normal PaCO2: 35–45 mm Hg (average 40 mm Hg).
• d. Normal serum bicarbonate: 22–26 mmol/L (average 24 mmol/L or mEq/L).

• a. Mixed disorder: Respiratory alkalosis with metabolic alkalosis.
• b. Compensation: For a 10 mm Hg acute fall in PCO2, HCO3 should fall by 2 mEq/L (expected HCO3: 22 mEq/L). Actual HCO3 is 28 mEq/L, confirming concurrent metabolic alkalosis with mild hypoxemia (PaO2 70 mm Hg).

• a. Normal pH (7.39) with markedly abnormal HCO3 (6 mEq/L) and PCO2 (12 mm Hg), indicating a mixed acid-base disorder (metabolic acidosis + respiratory alkalosis) with normal oxygenation.
• b. $\text{Anion gap}=134-(106+6)=22\text{ mEq/L}$ (High anion gap).
• c. Expected compensation: For ${\text{HCO}}_3=6\text{ mEq/L}$, expected ${\text{PCO}}_2=(1.5\times 6)+8\pm 2=17\pm 2=15\text{–}19\text{ mm Hg}$. Actual PCO2 is 12 mm Hg ($<15$), indicating added primary respiratory alkalosis.
• d.
  • $\text{Delta AG}=22-12=10$
  • $\text{Delta }{\text{HCO}}_3=24-6=18$
  • $\text{Delta-delta ratio}=\frac{10}{18}=0.55$ ($<0.8$)
  • $\text{Delta gap}=10-18=-8$ ($<-6$)
  • Inference: Mixed High Anion Gap Metabolic Acidosis (HAGMA) + Normal Anion Gap Metabolic Acidosis (NAGMA) + Respiratory Alkalosis.
• e. Clinical situation: Inborn error of metabolism (IEM) complicated by diarrhea and dehydration, chronic kidney disease (CKD) with gastroenteritis/diarrhea, or salicylate toxicity with vomiting.