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Tell me everything about ABG , its analysis and its interpretations. All put light upon the procedure of allens test done before blood gas analysis. Tell me few example cases to know it more. And your job is to provide me the complete theoretical, analytical and clinical picture of it. Do not compromise the accuracy and clinical value of your response. Think like a clinician and a teacher who teaches young doctors. Try to make it fmge exam centered also.
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Arterial Blood Gas (ABG) - The Complete Clinical & Exam Guide
Sources: Tintinalli's Emergency Medicine, Roberts & Hedges' Clinical Procedures in Emergency Medicine, Rosen's Emergency Medicine, Murray & Nadel's Respiratory Medicine, Pfenninger & Fowler's Procedures for Primary Care, Symptom to Diagnosis (4th Ed.), Morgan & Mikhail's Clinical Anesthesiology
SECTION 1: WHAT IS AN ABG AND WHY DO WE DO IT?
An Arterial Blood Gas is the gold standard test that simultaneously measures:
- pH (acid-base status)
- PaO2 (oxygenation)
- PaCO2 (ventilation)
- HCO3- (calculated, reflects metabolic component)
- SaO2 (oxygen saturation)
- Lactate (often included on modern analyzers)
- Hemoglobin, electrolytes (on point-of-care analyzers)
The arterial sample is drawn after the blood has passed through the lungs and before it reaches peripheral tissues - making it the definitive picture of oxygenation, ventilation, and acid-base status together.
Why artery and not vein?
Venous blood has already undergone peripheral gas exchange. Venous pH correlates within ±0.05 units of arterial pH, but venous PO2 cannot be used for oxygenation assessment. A normal venous PCO2 is reassuring, but an elevated venous PCO2 needs arterial confirmation. - Tintinalli's Emergency Medicine, p.121
SECTION 2: THE MODIFIED ALLEN'S TEST
Anatomical Basis
The radial artery is the preferred puncture site for ABG. Before puncturing it, you must confirm that the hand has adequate collateral circulation through the ulnar artery via the superficial palmar arch - because if the radial artery thromboses after puncture, the hand should not become ischemic.
The superficial palmar arch connects both arteries. The thumb, index finger, and thenar eminence are most vulnerable if radial artery is compromised.
Why Modified Allen's Test?
The original Allen test (1929) had many false positives. The modified Allen's test minimizes these and is the current standard.
Step-by-Step Procedure (from Pfenninger & Fowler)
Preparation:
- Hand should be at least room temperature (>70°F / ~21°C). Warm in water if needed.
- Patient sits or lies with arm at or below heart level.
Step 1 - Exsanguination:
- Ask the patient to raise the arm above heart level and open and close the fist several times to drain blood from the hand.
- Ask them to clench the fist tightly.
Step 2 - Compression:
- The clinician compresses BOTH the radial and ulnar arteries simultaneously with the thumbs/fingers.
- Maintain compression for about 1 minute.
Step 3 - Observation of pallor:
- Lower the fist below heart level.
- Ask the patient to unclench (open) the hand slowly. The hand should appear cadaveric (pale/white).
- Important: Do NOT hyperextend the wrist or fingers - this causes false positivity.
Step 4 - Release ulnar artery only:
- Release pressure from the ulnar artery (keep radial artery compressed).
- Watch the hand for return of color.
Step 5 - Interpretation:
| Time to color return | Interpretation |
|---|---|
| < 6 seconds | Normal (Negative test) - proceed with radial puncture |
| 6-15 seconds | Equivocal - caution; consider Doppler assessment |
| > 15 seconds | Abnormal (Positive test) - DO NOT puncture radial artery at this site |
FMGE High-Yield: An abnormal (positive) Allen test means continued pallor beyond 5-15 seconds after release of radial compression. This suggests inadequate collateral circulation from the ulnar artery. - Roberts & Hedges', Rosen's Emergency Medicine
Clinical Pearls on Allen's Test
- A positive test is NOT an absolute contraindication - it alerts you to potential complications and need for close monitoring.
- Alternatives if Allen test is positive: Brachial artery or femoral artery puncture.
- More sensitive alternatives: Hand-held Doppler ultrasonography, pulse oximetry with waveform monitoring, formal arterial Doppler.
- Many anesthesiologists now consider the Allen's test of questionable utility for routine pre-cannulation assessment, as large series have shown safe radial artery cannulation even without testing. - Morgan & Mikhail's Clinical Anesthesiology, Barash's Clinical Anesthesia
SECTION 3: NORMAL ABG VALUES (MEMORIZE THESE)
| Parameter | Normal Value | Clinical Significance |
|---|---|---|
| pH | 7.35 - 7.45 | Acid-base status |
| PaO2 | 80 - 100 mmHg | Oxygenation |
| PaCO2 | 35 - 45 mmHg | Ventilation ("respiratory parameter") |
| HCO3- | 22 - 26 mEq/L | Metabolic component (calculated) |
| SaO2 | 95 - 100% | Oxygen saturation |
| Base Excess (BE) | -2 to +2 mEq/L | Net metabolic component |
Trick to remember: pH 7.40, PaCO2 40, HCO3- 24, PaO2 80-100. Everything revolves around "40."
SECTION 4: THE HENDERSON-HASSELBALCH EQUATION
$$\text{pH} = \text{pK} + \log_{10} \left(\frac{[\text{HCO}_3^-]}{0.03 \times \text{PaCO}_2}\right)$$
Where pK = 6.1, [HCO3-] in mmol/L, PaCO2 in mmHg.
What this tells you:
- pH is determined by the ratio of HCO3- to PaCO2
- When the ratio is normal (HCO3- = 24, PaCO2 = 40), pH = 7.40
- Lungs control PaCO2 (respiratory component)
- Kidneys control HCO3- (metabolic component)
SECTION 5: SYSTEMATIC ABG INTERPRETATION - THE 6-STEP APPROACH
Use this approach on EVERY ABG. Never skip steps.
Step 1: Look at the pH
| pH | Interpretation |
|---|---|
| < 7.35 | Acidemia |
| 7.35 - 7.45 | Normal (but may still have mixed disorder!) |
| > 7.45 | Alkalemia |
Key concept: pH < 7.35 = acidemia; pH > 7.45 = alkalemia. These are properties of the blood. "Acidosis" and "alkalosis" are the processes causing those states. - Rosen's Emergency Medicine
Step 2: Identify the Primary Disorder
Ask: "Which parameter (PaCO2 or HCO3-) is moving in the same direction as the pH change?"
| Primary Disorder | pH | PaCO2 | HCO3- |
|---|---|---|---|
| Metabolic Acidosis | ↓ | N or ↓ | ↓ (primary) |
| Metabolic Alkalosis | ↑ | N or ↑ | ↑ (primary) |
| Respiratory Acidosis | ↓ | ↑ (primary) | N or ↑ |
| Respiratory Alkalosis | ↑ | ↓ (primary) | N or ↓ |
Rule: In respiratory disorders, PaCO2 and pH move in opposite directions. In metabolic disorders, PaCO2 and pH move in the same direction.
Step 3: Check for Compensation (Is it adequate?)
The body never overcompensates. If compensation appears more than expected, a second primary process is present.
Compensation Formulas - HIGH YIELD FMGE TABLE
| Primary Disorder | Expected Compensation |
|---|---|
| Metabolic Acidosis | PaCO2 = (1.5 × HCO3-) + 8 ± 2 (Winter's Formula) |
| Metabolic Alkalosis | PaCO2 increases by 0.6 mmHg per 1 mEq/L rise in HCO3- |
| Respiratory Acidosis (Acute) | HCO3- rises by 1 mEq/L per 10 mmHg rise in PaCO2 |
| Respiratory Acidosis (Chronic) | HCO3- rises by 3-4 mEq/L per 10 mmHg rise in PaCO2 |
| Respiratory Alkalosis (Acute) | HCO3- falls by 2 mEq/L per 10 mmHg fall in PaCO2 |
| Respiratory Alkalosis (Chronic) | HCO3- falls by 5 mEq/L per 10 mmHg fall in PaCO2 |
FMGE Trick: Remember metabolic compensation takes 3-5 days (renal adjustment). Respiratory compensation is immediate (minutes to hours).
Winter's Formula for Metabolic Acidosis:
Expected PaCO2 = (1.5 × HCO3-) + 8 ± 2
If measured PaCO2 > expected → concomitant Respiratory Acidosis (e.g., impending respiratory failure)
If measured PaCO2 < expected → concomitant Respiratory Alkalosis (e.g., salicylate poisoning)
Quick trick: In metabolic acidosis, the last two digits of expected pH ≈ expected PaCO2. (e.g., pH expected 7.23 → PCO2 ≈ 23) - Roberts & Hedges'
Step 4: Calculate the Anion Gap (Always do this in metabolic acidosis)
$$\text{Anion Gap (AG)} = [\text{Na}^+] - ([\text{HCO}_3^-] + [\text{Cl}^-])$$
Normal AG = 8-12 mEq/L (some institutions use 12-16 depending on albumin correction)
| AG > 12 (Wide AG) | AG normal (Hyperchloremic) |
|---|---|
| MUDPILES causes | HARDUP causes |
MUDPILES mnemonic (High Anion Gap Metabolic Acidosis):
- M - Methanol
- U - Uremia
- D - Diabetic Ketoacidosis (DKA)
- P - Paraldehyde / Paracetamol (Acetaminophen) / Polyethylene glycol
- I - Iron / Isoniazid
- L - Lactic acidosis
- E - Ethylene glycol
- S - Salicylates
HARDUP mnemonic (Normal Anion Gap Metabolic Acidosis):
- H - Hyperalimentation / Hospital-acquired saline administration
- A - Acid infusion / Addison's disease / Acetazolamide (Carbonic anhydrase inhibitors)
- R - Renal Tubular Acidosis (RTA)
- D - Diarrhea (most common cause!)
- U - Ureterosigmoidostomy
- P - Pancreatic fistula / drainage
Albumin correction of AG: Corrected AG = Measured AG + 2.5 × (4 - measured albumin in g/dL). Critical in hypoalbuminemic patients (cirrhosis, nephrotic syndrome) - a hidden high AG acidosis may be masked.
Step 5: Calculate the Delta-Delta Gap (In Wide AG Metabolic Acidosis)
This detects a hidden mixed disorder in a patient with wide AG acidosis.
$$\frac{\Delta \text{AG}}{\Delta \text{HCO}_3^-} = \frac{(\text{Measured AG} - 12)}{(24 - \text{Measured HCO}_3^-)}$$
| Delta/Delta ratio | Interpretation |
|---|---|
| < 1 | AG acidosis + concurrent normal AG acidosis |
| 1 - 2 | Pure AG metabolic acidosis |
| > 2 | AG acidosis + concurrent metabolic alkalosis |
Typical values: ~1.6:1 in lactic acidosis; ~1:1 in ketoacidosis. - Symptom to Diagnosis, 4th Ed.
Step 6: Assess Oxygenation
PaO2 and the A-a gradient:
$$\text{PAO}_2 = \text{FiO}2 \times (P\text{atm} - \text{PH}_2\text{O}) - \frac{\text{PaCO}_2}{0.8}$$
At room air (FiO2 = 0.21, sea level):
PAO2 ≈ 150 - (PaCO2/0.8)
Normal A-a gradient = age/4 + 4 (or approximately 5-15 mmHg in young adults)
| A-a gradient | Implication |
|---|---|
| Normal (< 15 mmHg) | Hypoxia from hypoventilation (CNS depression, neuromuscular disease) |
| Elevated (> 15 mmHg) | Hypoxia from V/Q mismatch, shunt, or diffusion defect |
SECTION 6: THE ACID-BASE MAP (VISUAL INTERPRETATION TOOL)
The Acid-Base Map plots pH against PaCO2. The center "N" zone is normal. Points falling in the colored zones outside the compensation bands indicate mixed disorders:
- Zone 1 (red): Mixed respiratory + metabolic acidosis
- Zone 2 (pink): Mixed respiratory + metabolic alkalosis
- Zone 3 (yellow): Metabolic alkalosis + respiratory acidosis
- Zone 4 (gold): Metabolic acidosis + respiratory alkalosis
Any ABG value falling outside a compensation band on this map = mixed disorder present.
SECTION 7: OSMOLAR GAP (When to calculate in ABG workup)
When you have a high AG metabolic acidosis and suspect toxic alcohol ingestion:
$$\text{Osmolar Gap} = \text{Measured Osmolality} - \left[(2 \times \text{Na}) + \frac{\text{Glucose}}{18} + \frac{\text{BUN}}{2.8}\right]$$
Normal osmolar gap < 10 mOsm/kg
- Wide osmolar gap (>10) in context of high AG acidosis = methanol or ethylene glycol poisoning
- To estimate methanol concentration: Osmolar gap × 3 = methanol in mg/dL
- To estimate ethylene glycol concentration: Osmolar gap × 6 = ethylene glycol in mg/dL
FMGE Alert: A normal osmolar gap does NOT rule out toxic alcohol - because as the alcohol is metabolized to its toxic acids, the osmolar gap normalizes while the AG gap rises.
SECTION 8: CAUSES, CLINICAL FEATURES & TREATMENT
Metabolic Acidosis
Causes: See MUDPILES / HARDUP above
Clinical features:
- Kussmaul breathing (deep, sighing hyperventilation - the respiratory compensation)
- Cardiovascular: decreased contractility, vasodilation, arrhythmias
- CNS: confusion, lethargy, coma
- Hyperkalemia (H+ enters cells, K+ exits)
Treatment:
- Treat the underlying cause
- Sodium bicarbonate: consider when pH < 7.10, or pH < 7.20 with acute kidney injury
- In DKA: insulin + fluids; in lactic acidosis: treat sepsis/hypoperfusion
Metabolic Alkalosis
Causes:
- Vomiting (loss of HCl), NG suction
- Diuretic use (loop/thiazides - K+ and H+ loss)
- Hyperaldosteronism, Cushing's syndrome
- Alkali ingestion
- Post-hypercapnia alkalosis
Clinical features:
- Hypoventilation
- Hypokalemia, hypocalcemia (tetany)
- Arrhythmias
Saline-responsive vs. saline-resistant:
- Saline-responsive (urine Cl- < 15 mEq/L): vomiting, NG suction, diuretics - treat with IV NaCl
- Saline-resistant (urine Cl- > 25 mEq/L): hyperaldosteronism, severe hypokalemia - treat underlying cause
Respiratory Acidosis
Causes (decreased CO2 clearance):
- CNS depression (opioids, sedatives, stroke)
- Neuromuscular disease (GBS, MG, muscular dystrophy)
- Chest wall (kyphoscoliosis, obesity hypoventilation)
- Lung disease (severe asthma, COPD exacerbation, ARDS)
Acute vs. Chronic:
| Acute | Chronic | |
|---|---|---|
| HCO3- change per 10 mmHg CO2 rise | +1 | +3-4 |
| Cause | Sudden CNS/NM failure | COPD, OHS |
| Treatment | Mechanical ventilation if needed | Treat underlying, BiPAP |
Respiratory Alkalosis
Causes (increased CO2 clearance = hyperventilation):
- Anxiety / panic attacks (most common in outpatients)
- Pain
- Sepsis (early - direct stimulation of respiratory center)
- Pulmonary embolism
- Salicylate poisoning (direct stimulation of brainstem)
- Pregnancy (progesterone stimulates breathing)
- High altitude
- Hepatic encephalopathy
Clinical features: Perioral/finger tingling, carpopedal spasm, dizziness, tetany
SECTION 9: WORKED CLINICAL CASES
Case 1: Diabetic Ketoacidosis (FMGE Classic)
Patient: 22-year-old with Type 1 DM, not taking insulin for 3 days. Vomiting, abdominal pain, Kussmaul breathing.
ABG: pH 7.08, PaCO2 18 mmHg, HCO3- 5 mEq/L, Na 134, Cl 98, Glucose 480
Step 1 - pH: 7.08 → Acidemia
Step 2 - Primary: HCO3- ↓↓ → Metabolic Acidosis
Step 3 - Compensation (Winter's):
Expected PaCO2 = (1.5 × 5) + 8 = 7.5 + 8 = 15.5 ± 2 (range 13.5-17.5)
Measured PaCO2 = 18 → slightly higher than expected → likely adequate/borderline; no additional respiratory acidosis
Step 4 - AG:
AG = 134 - (5 + 98) = 31 → High AG metabolic acidosis
Step 5 - Delta-Delta:
(31 - 12) / (24 - 5) = 19/19 = 1.0 → Pure AG acidosis (consistent with ketoacidosis)
Diagnosis: Severe DKA with pure high-AG metabolic acidosis with appropriate respiratory compensation (Kussmaul breathing)
Pearls: DKA is the classic delta-delta = 1. Treat with IV fluids, insulin infusion. Do not give bicarb unless pH < 6.9.
Case 2: COPD Exacerbation (Chronic Respiratory Acidosis)
Patient: 68-year-old chronic smoker, on home O2. Increased dyspnea, purulent sputum. SpO2 82% on room air.
ABG: pH 7.32, PaCO2 68 mmHg, HCO3- 34 mEq/L
Step 1: pH 7.32 → Acidemia
Step 2: PaCO2 68 (↑↑) → Primary Respiratory Acidosis
Step 3 - Chronic or Acute?
PaCO2 has risen 28 mmHg above normal (68-40=28)
- Acute compensation: HCO3- should rise by 28/10 × 1 = 2.8 mEq/L → HCO3- = 26.8
- Chronic compensation: HCO3- should rise by 28/10 × 3.5 = ~10 mEq/L → HCO3- = 34
Measured HCO3- = 34 → Chronic respiratory acidosis with full renal compensation (COPD baseline)
Diagnosis: Chronic respiratory acidosis with complete metabolic compensation - this is the patient's baseline COPD. This is NOT an acute decompensation in itself - but the clinical picture demands treating the trigger (infection).
Pearl: Do NOT give high-flow O2 to a COPD patient with chronic CO2 retention. Controlled O2 to target SpO2 88-92% prevents loss of hypoxic drive. Give BiPAP if not improving.
Case 3: Sepsis with Lactic Acidosis (from Roberts & Hedges' Textbook)
Patient: 74-year-old, fever 39°C, hypotension 96/70, E. coli bacteremia (septic shock).
ABG/Labs: pH 7.49, PaCO2 25, HCO3- 22, Na 138, K 3.2, Cl 105
Step 1: pH 7.49 → Alkalemia
Step 2: PaCO2 25 (↓) → Primary Respiratory Alkalosis
Step 3 - Compensation:
PaCO2 fell 15 mmHg. Expected HCO3- fall:
- Acute: 2 mEq/L per 10 mmHg → 3 mEq/L fall → HCO3- should be ≈ 21 Measured HCO3- = 22 → appropriate acute respiratory alkalosis compensation
Diagnosis: Acute respiratory alkalosis due to sepsis (direct stimulation of respiratory center by endotoxins/cytokines)
Pearl: Early sepsis classically presents with respiratory alkalosis BEFORE lactic acidosis takes over. As sepsis worsens, it transitions to high-AG metabolic acidosis (lactic acidosis). This makes "MUDPILES" important in septic patients.
Case 4: Profuse Diarrhea (Normal AG Metabolic Acidosis - from Roberts & Hedges')
Patient: 58-year-old woman, 1 week of profuse diarrhea.
Labs: Na 133, K 2.8, Cl 118, pH 7.26, PaCO2 13, HCO3- 5
Step 1: pH 7.26 → Acidemia
Step 2: HCO3- 5 (↓↓) → Primary Metabolic Acidosis
Step 3 - Winter's Formula:
Expected PaCO2 = (1.5 × 5) + 8 = 15.5 ± 2 (range 13.5-17.5)
Measured PaCO2 = 13 → within expected range → pure metabolic acidosis
Step 4 - AG:
AG = 133 - (5 + 118) = 10 → Normal AG!
Diagnosis: Normal-AG (hyperchloremic) metabolic acidosis from diarrhea. Diarrhea loses HCO3- directly; chloride rises to maintain electroneutrality.
Pearl: Diarrhea = Normal AG acidosis (loss of bicarb-rich fluid). Vomiting = Metabolic alkalosis (loss of HCl). This distinction is CLASSIC for FMGE.
Case 5: Salicylate Poisoning (Mixed Disorder)
Patient: 19-year-old found with empty aspirin bottles. Confused, tinnitus, hyperventilating.
ABG: pH 7.46, PaCO2 20, HCO3- 14
Analysis:
- pH 7.46 → alkalemia
- PaCO2 20 ↓ → respiratory alkalosis (direct CNS stimulation by salicylates)
- HCO3- 14 ↓ → ALSO metabolic acidosis (salicylate = organic acid, high AG)
Calculate AG: (assume Na 140, Cl 106) → AG = 140 - (14+106) = 20 (high)
Diagnosis: Mixed respiratory alkalosis + high-AG metabolic acidosis - the classic pattern of salicylate toxicity
Pearl: If PaCO2 is lower than Winter's formula would predict, think respiratory alkalosis on top of metabolic acidosis → Salicylates.
SECTION 10: SPECIAL TOPICS (FMGE FAVORITES)
Oxygenation - Hypoxemia Classification
| PaO2 (mmHg) | Severity |
|---|---|
| 60-80 | Mild hypoxemia |
| 40-60 | Moderate hypoxemia |
| < 40 | Severe hypoxemia |
| < 20 | Life-threatening |
5 Causes of Hypoxemia (classic teaching):
- Hypoventilation - Normal A-a gradient, PaCO2 elevated
- V/Q mismatch - Most common cause in clinical practice (PE, COPD, asthma)
- Shunt - Does NOT respond to supplemental O2 (ASD, AVM, consolidation)
- Diffusion impairment - Responds to O2 (pulmonary fibrosis)
- Low FiO2 - High altitude; normal A-a gradient
Base Excess (BE)
- Represents the excess or deficit of base needed to restore pH to 7.40 at PaCO2 40 mmHg
- BE > +2: metabolic alkalosis
- BE < -2: metabolic acidosis (also called "base deficit")
- Base deficit > 6 in trauma suggests significant hemorrhagic shock (FMGE alert)
Oxygen Content and Delivery
- CaO2 = (Hb × 1.34 × SaO2) + (0.003 × PaO2)
- Hemoglobin is far more important than dissolved PaO2 for oxygen delivery
SECTION 11: FMGE RAPID-FIRE HIGH-YIELD FACTS
| Topic | Key Fact |
|---|---|
| Allen's test - normal return time | < 6 seconds |
| Allen's test - positive (abnormal) | > 5-15 seconds pallor persists |
| Preferred ABG site | Radial artery |
| Second choice site | Brachial or femoral artery |
| pH of death | < 6.8 or > 7.8 |
| Kussmaul breathing | Respiratory compensation for metabolic acidosis |
| CO2 retention in COPD | Do NOT give high-flow O2; target SpO2 88-92% |
| Winter's formula | Expected PaCO2 = 1.5 × HCO3- + 8 ± 2 |
| Diarrhea | Normal AG metabolic acidosis |
| Vomiting | Metabolic alkalosis |
| DKA | High AG metabolic acidosis |
| Salicylate poisoning | Mixed: Resp alkalosis + Met acidosis (most classic mixed disorder) |
| Sepsis early | Respiratory alkalosis |
| Sepsis late | High AG metabolic acidosis (lactic) |
| MUDPILES | High AG acidosis causes |
| HARDUP | Normal AG acidosis causes |
| Acute resp acidosis | HCO3- ↑ 1 per 10 mmHg CO2 |
| Chronic resp acidosis | HCO3- ↑ 3-4 per 10 mmHg CO2 |
| Delta-delta < 1 | AG acidosis + normal AG acidosis |
| Delta-delta > 2 | AG acidosis + metabolic alkalosis |
| Osmolar gap > 10 | Toxic alcohol (methanol / ethylene glycol) |
| Pregnancy | Chronic respiratory alkalosis (progesterone) |
| A-a gradient elevated | V/Q mismatch, shunt, diffusion defect |
| A-a gradient normal + hypoxia | Pure hypoventilation |
SECTION 12: A CLINICIAN'S ABG INTERPRETATION CHECKLIST
When you get an ABG, do this in order:
1. Look at pH → acidemia or alkalemia?
2. Look at PaCO2 → primary respiratory?
3. Look at HCO3- → primary metabolic?
4. Does the secondary change match the primary? (compensation vs. mixed?)
5. Calculate AG → high or normal?
6. If high AG → Winter's formula → is compensation adequate?
7. Calculate delta-delta → any hidden mixed disorder?
8. In high AG + suspected toxin → calculate osmolar gap
9. Look at PaO2 and A-a gradient → oxygenation status
10. Correlate with the clinical picture ALWAYS
The numbers tell you the story, but the patient tells you the title. Always interpret the ABG in the context of the clinical history. A pH of 7.32 means something very different in a COPD patient on BiPAP versus a young previously healthy patient with no explanation for acidosis.
Sources: Roberts and Hedges' Clinical Procedures in Emergency Medicine | Tintinalli's Emergency Medicine | Rosen's Emergency Medicine | Murray & Nadel's Textbook of Respiratory Medicine | Pfenninger and Fowler's Procedures for Primary Care | Morgan and Mikhail's Clinical Anesthesiology | Symptom to Diagnosis 4th Edition | Barash's Clinical Anesthesia
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