Arterial blood Gas Analysis with sampling method cases and discussions

A small description with examples of ABG analysis helpful for medical students

1. Arterial Blood Gas Analysis & Acid Base Disorders Presenter Dr Famna Moderator Dr Rajvir

2. What is an acid and base? According to Bronsted-Lowry theory Acid : H +  donor Base : H +  acceptor Conjugate acid-base pairs No concept of neutrality

3. Acidosis  - an abnormal process or condition which would lower arterial pH if there were no secondary changes in response to the primary aetiological factor. Alkalosis  - an abnormal process or condition which would raise arterial pH if there were no secondary changes in response to the primary aetiological factor. Simple (Acid-Base) Disorders   are those in which there is a single primary aetiological acid-base disorder. Mixed (acid-Base) Disorders  are those in which two or more primary aetiological disorders are present simultaneously. Acidaemia  -  Arterial pH <7.36([ H +]>44 nM ) Alkalaemia   -  Arterial pH >7.44([ H +]<36 nM ) Terminology

4. Metabolic refers to disorders that result from a primary alteration in [H + ] or [HCO 3 - ]. Respiratory refers to disorders that result from a primary alteration in PCO 2 due to altered CO 2 elimination.

5. Types of acid in the body Types of Acids in the Body Respiratory Acid (Carbonic Acid / CO₂) • Carbon dioxide (CO₂) is a “volatile acid” because it can be excreted via the lungs. • While CO₂ itself isn’t an acid, it forms carbonic acid (H₂CO₃) in water. • The body produces around 12,000–24,000 mmol /day of CO₂ through metabolism. Metabolic (Fixed) Acids • These are non-volatile • Examples include lactic acid, sulphuric acid, phosphoric acid, and ketone bodies. • Net fixed acid production is around 70–100 mmol /day , primarily excreted by the kidneys. Excretion Pathways • Lungs : Remove CO₂, preventing respiratory acidosis. • Kidneys : Excrete fixed acids and regulate bicarbonate (HCO₃⁻) levels

6. Body’s response to acid base imbalance 1. Buffering (immediate response) • Chemical buffers (e.g., bicarbonate, proteins, and phosphates) neutralize excess H⁺ ions 2. Respiratory Compensation (Minutes to Hours) • Changes in breathing rate alter CO₂ levels to correct pH imbalances. • Hyperventilation removes CO₂ (useful in metabolic acidosis), while hypoventilation retains CO₂ (useful in metabolic alkalosis). 3. Renal Compensation (Hours to Days) • Kidneys regulate HCO₃⁻ and excrete fixed acids to maintain long-term acid-base balance. This interplay of buffer systems, respiration, and renal function ensures the body’s acid-base homeostasis

7. When & Why

8. Overview of Arterial Blood Gas (ABG) Sampling Before sampling • Confirm the need for the ABG and identify any contraindications Inadequate collateral circulation at the puncture site Should not be performed through a lesion or a surgical shunt , Evidence of peripheral vascular disease distant to the puncture site A coagulopathy or medium- to high-dose anticoagulation therapy ) Always record details of O 2  therapy and respiratory support (e.g. ventilator settings). • Unless results are required urgently, allow at least 20 minutes after any change in O 2  therapy before sampling (to achieve a steady state). • Explain to the patient why you are doing the test, what it involves and the possible complications (bleeding, bruising, arterial thrombosis, infection and pain); then obtain consent to proceed. • Prepare the necessary equipment ( heparinised syringe with cap, 20–22G needle, sharps disposal container, gauze) and don universal precautions. • Identify a suitable site for sampling by palpating the radial, brachial or femoral artery Routine sampling should, initially, be attempted from the radial artery of the non-dominant arm. Allen’s test

9. Technical errors - Syringe flushed with 0.5ml 1:1000 heparin Do not leave excess heparin - inc. dilutional effects, decreased HCO3 & pCO2 Risk of alteration of results with: Increased size of syringe Decreased vol of sample Syringes must gave >50% of blood Use only 3ml or less syringe 25% lower values if 1ml sample taken in 10ml syringe(0.25ml) heparin in needle) Air bubble inc pO2 & pCO2 dec

10. Approaches to Acid-Base Compensation 1. Boston Method (Empirical, Bicarbonate-Based) • Approach: Uses bicarbonate-based bedside rules derived from in vivo titration experiments. • Key Feature: Predicts expected bicarbonate (HCO₃⁻) or PaCO₂ compensation for acid-base disorders Acute Respiratory Acidosis: ↑PaCO₂ by 10 → ↑HCO₃⁻ by 1 • Chronic Respiratory Acidosis: ↑PaCO₂ by 10 → ↑HCO₃⁻ by 4 • Acute Respiratory Alkalosis: ↓PaCO₂ by 10 → ↓HCO₃⁻ by 2 • Chronic Respiratory Alkalosis: ↓PaCO₂ by 10 → ↓HCO₃⁻ by 5 • Metabolic Acidosis: Expected PaCO₂ = (1.5 × HCO₃⁻) + 8 (Winters formula ) • Metabolic Alkalosis: Expected PaCO₂ = (0.7 × HCO₃⁻) + 20 • Pros: Practical, widely used in ICU exams and bedside assessments. • Cons: Requires actual bicarbonate calculation and can be inaccurate with significant respiratory derangements

11. CopenHagen a pproach: 2. Copenhagen Method (Theoretical, Base Excess-Based) • Uses Standard Base Excess (SBE) to separate metabolic and respiratory effects on acid-base balance. • Key Feature: Focuses on metabolic acid-base status independent of respiratory changes. • Rules: • Acute Respiratory Disorders: No change in SBE (expected SBE = 0) • Chronic Respiratory Disorders: Expected SBE = 0.4 × (PaCO₂ - 40) • Metabolic Acidosis: Expected PaCO₂ = 40 + (1.0 × SBE) • Metabolic Alkalosis: Expected PaCO₂ = 40 + (0.6 × SBE) • Pros: Used by most ABG machines, removes respiratory influence on metabolic assessment. • Cons: Standard bicarbonate (HCO₃⁻ st ) is misleading if used with Boston rules

12. Base Excess An empirical expression that approximates the amount of acid or base required to titrate one liter of blood back to a normal pH of 7.40 It allows the estimation of the number of equivalents of sodium- bicarbonate or ammonium chloride required to correct the patient’s pH to normal. SBE = (HCO3)– 24.8 + 16.8 (pH – 7.4) -2 to +2 mEq/L (or mmol /L) Positive BE (above +2 mEq/L):  Suggests a metabolic alkalosis, meaning there's an excess of base in the blood.  Negative BE (below -2 mEq/L):  Indicates a metabolic acidosis, meaning there's a deficit of base in the blood. 

13. Steward approach 3. Stewart Method (Physicochemical, Complex but Comprehensive) • Approach: Describes acid-base status based on strong ion difference (SID), PCO₂, and weak acid concentrations. • Key Feature: More mechanistic and complete but mathematically complex. • Pros: Offers deeper physiological understanding. • Cons: Hard to apply bedside, requires significant computation, not widely used clinically

14. Comprehensive history and physical examination. Evaluate simultaneously performed ABG & serum electrolytes. Ventilatory and oxygenation status (gas exchange) Identification of the dominant disorder. Calculation of compensation. Calculate the anion gap and the Δ. Anion Gap Δ AG Δ Bicarbon ate Clinical correlation Step wise evaluation of acid-base disorder Boston approach

15. Step 3 : Assessment of gas exchange PaO2 Vs SpO2 PaO2 dependent upon age, FiO2, Patm PaO2 = 109-0.4(age), as age increases PaO2 decreases As FiO2 increases the expected PaO2increases Alveolar arterial O2 gradient

16. PaO2/FiO2 ratio PaCO2 Is directly proportional to CO2 production and inversely proportional to alveolar ventilators Normal – 35-45 mmHg

17. Identification of the dominant disorder Primary disorder pH Initial change Compensatory change Metabolic acidosis ↓ ↓ HCO 3 ↓ PCO 2 Metabolic alkalosis ↑ ↑ HCO 3 ↑ PCO 2 Respiratory acidosis ↓ ↑ PCO 2 ↑ HCO 3 Respiratory alkalosis ↑ ↓ PCO 2 ↓ HCO 3

18. Dictums in ABG Analysis Primary change & Compensatory change always occur in the same direction. pH and Primary parameter change in the same direction suggests a metabolic problem. pH and Primary parameter change in the opposite direction suggests a respiratory problem. Renal and pulmonary compensatory mechanisms return pH toward but rarely to normal. A normal pH in the presence of changes in PCO 2 or HCO 3 suggets a mixed acid- base disorder.

19. Clues to Mixed Acid-Base Disorders Normal pH (with the exception of chronic respiratory alkalosis) PCO 2 and HCO 3 deviating in opposite directions pH change in the opposite direction of a known primary (dominant) acid- base disorder

20. Metabolic Acidosis Definition: Metabolic acidosis is a primary condition that leads to an excess of fixed acids in the blood , causing a drop in plasma bicarbonate (HCO₃⁻) levels. This occurs because HCO₃⁻ is used to neutralize excess H⁺ ions. • A primary metabolic acidosis directly results from increased acid production or decreased acid excretion. • A secondary bicarbonate drop due to another condition (e.g., compensatory response to respiratory alkalosis) should not be mistaken for metabolic acidosis. • Mixed acid-base disorders can occur, such as in salicylate overdose , where both metabolic acidosis and respiratory alkalosis coexist due to respiratory center stimulation.

21. Step 5 : Calculate the “gaps” Anion gap = Δ AG = Δ HCO 3 = Na + − [Cl − + HCO 3 ] Anion gap − 12 24 − HCO 3 The anion gap represents the difference in charge between measured cations and measured anions. The missing negative charge is made up of weak acids (A- ), such as albumin and phosphate, and strong unmeasured anions (UMAs), such as lactate.

22. Corrected anion gap : Anion gap corrected (for albumin) = calculated anion gap + 2.5 × (normal albumin [in g/dL] − observed albumin [in g/dL]) The delta gap is a concept used in acid-base balance analysis to assess the presence of mixed acid-base disorders. • AG (Anion Gap) represents unmeasured anions in the blood. • 12 is the normal anion gap (mEq/L). • 24 is the normal bicarbonate (HCO₃) level (mEq/L). • The numerator represents the increase in AG (AG excess). • The denominator represents the decrease in bicarbonate (HCO₃ deficit). >26 – additional met. Alkalosis < 22 – additional NAGMA This ratio, sometimes called the gap-gap , helps determine if there is an additional metabolic disorder, such as a concurrent metabolic alkalosis or a normal anion gap metabolic acidosis.

23. Metabolic Alkalosis Metabolic alkalosis is characterized by an increase in bicarbonate (HCO₃⁻) concentration in the blood, typically >30 mEq/L. It is caused by factors such as extracellular volume changes, aldosterone activity, kidney function, and electrolyte imbalances (chloride and potassium). Causes & Mechanisms • Loss of Gastric Acid: Vomiting or nasogastric suction leads to H⁺ loss, which increases HCO₃⁻. • Hypovolemia: Decreased plasma volume reduces glomerular filtration and activates the renin-angiotensin-aldosterone system, promoting HCO₃⁻ retention. • Aldosterone: Increases Na⁺ retention and K⁺ loss, contributing to metabolic alkalosis. • Chloride Depletion: Reduces bicarbonate excretion, sustaining alkalosis. • Hypokalemia: Causes H⁺ to move into cells, raising plasma HCO₃⁻. • Diuretics: Increase sodium and chloride loss, promoting bicarbonate reabsorption

24. Clinical Consequences • Neurologic Effects: Symptoms like confusion, seizures, and muscle spasms may occur but are rare. • Hypoventilation: The body compensates by reducing breathing rate, increasing CO₂ (PaCO₂) retention. • Oxyhemoglobin Dissociation Curve Shift: to left. Reduced oxygen release to tissues due to alkalosis-induced hemoglobin affinity changes. Evaluation Metabolic alkalosis is assessed by analyzing extracellular volume status and urinary chloride concentration, which help determine the underlying cause s.

25. Types of Metabolic Alkalosis • Low ECV, Low Urine Cl⁻ (Chloride-Sensitive) • High ECV, High Urine Cl⁻ (Chloride-Resistant) • Other Causes : Hypokalemia and hypomagnesemia can contribute Management • Chloride-Responsive : Treated with isotonic saline and potassium chloride ( KCl ). • Edematous States : Diuretics are counterproductive ; acetazolamide may be used. • Severe Cases : Hydrochloric acid infusion ( HCl ) can be used cautiously.

26. Respiratory acidosis A respiratory acidosis is a primary acid-base disorder in which arterial pCO 2  rises to a level higher than expected. Mechanisms of Increased Arterial pCO₂ (Hypercapnia) 1. Excess CO₂ in inspired gas (e.g., rebreathing, anesthesia). 2. Decreased alveolar ventilation (most common cause). 3. Increased CO₂ production (e.g., malignant hyperthermia). An adult at rest produces ~200 mL of CO₂ per minute , which is efficiently excreted by the lungs. If CO₂ production increases but ventilation remains constant, respiratory acidosis occurs. However, the body rapidly increases ventilation in response to high pCO₂, preventing acidosis—except in fixed ventilation settings (e.g., mechanical ventilation in critically ill patients).

27. Alveolar Hypoventilation & Hypoxaemia • Hypoventilation can impair oxygen uptake, leading to hypoxaemia . • Increasing inspired O₂ can correct hypoxaemia if the issue is purely hypoventilation. • If pulmonary disease (e.g., shunt, V/Q mismatch ) is present, hypoxaemia persists despite high O₂ .

28. • Acute: Only intracellular buffering; HCO₃⁻ increases slightly . • Chronic: Kidneys retain bicarbonate , HCO₃⁻ rises significantly , and pH moves closer to normal

29. Respiratory Alkalosis Respiratory alkalosis is a primary acid-base disorder where arterial pCO₂ falls below expected levels . • If no compensation or other acid-base disorder is present, this raises arterial pH . • Hypocapnia ≠ Respiratory Alkalosis : • If hypocapnia occurs as compensation for metabolic acidosis , it is not considered respiratory alkalosis. ‘ Always Due to Increased Alveolar Ventilation ’ • Alveolar ventilation , not total (minute) ventilation, determines pCO₂ levels. • Difference between minute ventilation & alveolar ventilation : • Minute ventilation = Respiratory rate × Tidal volume • Alveolar ventilation = Respiratory rate × (Tidal volume - Dead space volume) • Example: Increased dead space (e.g., pulmonary embolism) may increase minute ventilation without lowering pCO₂. Interpretation of Hypocapnia (Low pCO₂) 1. Primary hypocapnia = Respiratory alkalosis (due to direct hyperventilation). 2. Secondary hypocapnia = Compensatory response to metabolic acidosis (not respiratory alkalosis).

30. Clinical Importance : • Misinterpreting compensatory hypocapnia as respiratory alkalosis can miss a serious respiratory disorder . • Example: A patient with both metabolic acidosis + respiratory acidosis might be misdiagnosed as only metabolic acidosis , leading to inappropriate treatment.

31. The compensatory response is a fall in bicarbonate level. As can be seen by inspection of the Henderson-Hasselbalch equation (below), a decreased [HCO3-] will counteract the effect of a decreased pCO2 on the pH. Mathematically, it returns the value of the  [HCO3] / 0.03 pCO2  ratio towards normal. pH = pKa + log {([HCO3]/ 0.03 pCO2 }

32. Case Scenarios in Acid- Base Disorders

33. Case 1: A 15-year-old juvenile diabetic • Presentation: Abdominal pain, vomiting, fever, and tiredness for one day. Stopped taking insulin three days ago. • Examination: Tachycardia, blood pressure 100/60 mmHg, signs of dehydration, normal abdominal examination. On NP @ 2L ABG - • pH: 7.31 • PaCO₂: 26 mmHg • HCO₃: 12 mEq/L • PaO₂: 150 mmHg FiO2 : 36% • Sodium (Na): 140 mEq/L • Potassium (K): 5.0 mEq/L • Chloride (Cl): 100 mEq/

34. Step 1: Check pH → Acidemia • pH = 7.31 (low) → Indicates acidosis . Step 2: Determine the primary disturbance (Respiratory vs. Metabolic) • PaCO₂ = 26 mmHg (low) • HCO₃ = 12 mEq/L (low) • Since both HCO₃ and pH are low , this suggests primary metabolic acidosis . Step 3: Check respiratory compensation (Winter’s formula) • Expected PaCO₂ = (1.5 × HCO₃) + 8 ± 2 • = (1.5 × 12) + 8 ± 2 • = 18 + 8 ± 2 • = 26 ± 2 (expected range: 24-28 mmHg) • Measured PaCO₂ = 26 mmHg (within range → appropriate respiratory compensation). Step 4: Calculate the Anion Gap (AG) A G = Na - (Cl + HCO₃) • = 140 - (100 + 12) • = 140 - 112 • = 28 (Elevated Anion Gap Metabolic Acidosis - HAGMA) Step 5: Calculate Delta Ratio (to check for mixed disorders) Δ AG / Δ HCO₃ = (AG - 12) / (24 - HCO₃) • = (28 - 12) / (24 - 12) • = 16 / 12 • = 1.33 Interpretation: • Δ ratio between 1-2 suggests pure High Anion Gap Metabolic Acidosis (HAGMA), likely due to Diabetic Ketoacidosis (DKA). • No additional metabolic alkalosis or normal anion gap acidosis is present. Final Diagnosis: • High Anion Gap Metabolic Acidosis (HAGMA) → Diabetic Ketoacidosis (DKA) • Appropriate respiratory compensation

35. Management: 1. IV fluids (0.9% normal saline) to correct dehydration. 2. IV insulin infusion to correct hyperglycemia and ketoacidosis . 3. Monitor potassium —expect an initial high-normal level that may drop with insulin therapy. 4. Frequent blood gas and glucose monitoring to assess resolution. 5. Transition to subcutaneous insulin once the anion gap normalizes and patient is stable

36. Case 2 : 75 yr old female presents with fever and profuse diarrhea for 2 days, vitals T: 100.4; HR: 130, BP: 78/30 PH: 7.29 / PaCO2: 30 / HCO3: 14 / pO2 – 90/ FiO2 - 21% Na: 128 / K: 3.2 / Cl: 94 / HCO3: 14 STEP 1: PH STEP 2: pCO2 STEP 3: evaluate compensation (PaCO2 = 1.5 × HCO3 + 8) + or - 2 STEP 4: calculate AG (AG = Na - (Cl + HCO3)) STEP 5: calculate DELTA RATIO (delta AG / delta HCO3)

37. 75 yr old female presents with fever and profuse diarrhea for 2 days, vitals T: 100.4; HR: 130, BP: 78/30 PH: 7.29 / PaCO2: 30 / HCO3: 14 / pO2 – 90/ FiO2 - 21% Na: 128 / K: 3.2 / Cl: 94 / HCO3: 14 STEP 1: PH dec STEP 2: pCO2 dec STEP 3: evaluate compensation (PaCO2 = 1.5 × HCO3 + 8) 29 ( 27 to 31) STEP 4: calculate AG (AG = Na - (Cl + HCO3)) 20 STEP 5: calculate DELTA RATIO (delta AG / delta HCO3) 0.8 (<1)

38. High anion gap metabolic acidosis with normal anion gap metabolic acidosis

39. Case 3: A 58-year-old male with a history of type 2 diabetes mellitus and hypertension presents to the emergency department with: • Fever (38.9°C), chills, and altered mental status • Tachypnea (Respiratory rate: 28 breaths/min), tachycardia (HR: 120 bpm) • Low blood pressure (BP: 85/50 mmHg) despite IV fluids • Oliguria (low urine output), cool extremities • SpO₂: 91% on 40% FiO₂ via face mask pH 7.22 pCO₂ 30 mmHg HCO₃⁻ (Bicarbonate) 16 mmol /L Base Excess -8 mmol /L Lactate 5.5 mmol /L PaO₂ 70 mmHg FiO₂ 40% (Room air: 21%) Na = 140 mmol /L • Cl = 104 mmol /L • HCO₃ = 16 mmol /

40. Step 1: Check pH • pH = 7.22 (Low) → Indicates acidemia . Step 2: Identify the primary disturbance (Respiratory vs. Metabolic) • PaCO₂ = 30 mmHg (low) • HCO₃ = 16 mmol /L (low) • Since both bicarbonate (HCO₃) and pH are low , so primary metabolic acidosis . Step 3: Evaluate Respiratory Compensation (Winter’s formula) • Expected PaCO₂ = (1.5 × HCO₃) + 8 ± 2 • = (1.5 × 16) + 8 ± 2 • = 24 + 8 ± 2 • = 30 ± 2 (Expected range: 28–32 mmHg) • Measured PaCO₂ = 30 mmHg → Within expected range (appropriate respiratory compensation) . Step 4: Calculate the Anion Gap (AG) = 140 - 120 = 20 (Elevated Anion Gap Metabolic Acidosis - HAGMA) Step 5: Calculate the Delta Ratio Δ AG / Δ HCO₃ = (AG - 12) / (24 - HCO₃) = (20 - 12) / (24 - 16) = 8 / 8 = 1.0 ( Interpretation: • (HAGMA). • No additional metabolic alkalosis or normal anion gap acidosis   Lactic Acidosis (Lactate = 5.5 mmol /L, indicating sepsis ( urosepsis or shock) • Appropriate respiratory compensation (no secondary respiratory disorder). PaO₂ is lower than expected for the given FiO₂ , raising concerns about early acute respiratory distress syndrome (ARDS) . Possible Causes of HAGMA in This Case: 1. Sepsis-induced lactic acidosis (most likely) • Fever, tachycardia, hypotension, and high lactate suggest septic shock. 2. Diabetic ketoacidosis (DKA) • Less likely as glucose levels are not provided. 3. Renal failure • Could contribute, but not enough information provided

41. Septic shock with metabolic (lactic) acidosis and hypoxia, possibly progressing to ARDS Management: 1. Oxygen therapy: FiO₂ may need to be increased or consider high-flow nasal cannula (HFNC) or non-invasive ventilation (NIV) if respiratory distress worsens. 2. Aggressive IV fluid resuscitation (crystalloids) to improve perfusion. 3. Empirical IV antibiotics (broad-spectrum, covering Gram-negative and Gram-positive bacteria). 4. Vasopressors (norepinephrine) for persistent hypotension after fluids. 5. Close monitoring of ABG, lactate, and kidney function to assess response. 6. Consider intubation and mechanical ventilation if respiratory failure progresses (PaO₂/FiO₂ ratio worsening).

42. Case 4 : A 45-year-old female presents with: • 3-day history of severe vomiting due to gastroenteritis • Weakness, dizziness, and muscle cramps • BP: 95/60 mmHg, HR: 105 bpm, RR: 14 bpm • Physical exam: Dry mucous membranes, reduced skin turgor, no peripheral edem a pH 7.50 45 pCO₂ 45 mmHg HCO₃⁻ (Bicarbonate) 35 mmol /L Base Excess +10 mmol /L Chloride (Cl⁻) 88 mmol /L Potassium (K⁺) 2.9 mmol /L PaO₂ 90 mmHg FiO₂ 21%

43. Step 1: Assess pH • pH = 7.50 - alkalosis . Step 2: Check PaCO₂ (Respiratory Component) • PaCO₂ = 45 mmHg Normal Step 3: Check HCO₃⁻ (Metabolic Component) • is elevated , which suggests metabolic alkalosis . Step 4: Assess Compensation • In metabolic alkalosis, the expected compensatory response is hypoventilation (increased PaCO₂) . • Here, PaCO₂ is at the upper normal limit (45 mmHg) , suggesting partial compensation . Step 5: Evaluate Underlying Cause • Clinical History : 3-day history of severe vomiting → leads to loss of gastric acid ( HCl ), which increases HCO₃⁻ , causing metabolic alkalosis . • Hypokalemia (K⁺ = 2.9 mmol /L) : Vomiting leads to potassium loss , contributing to muscle cramps and weakness. • Signs of Dehydration : Weakness, dizziness, reduced skin turgor → likely hypovolemia due to fluid loss. • Hypochloremia (Cl⁻ = 88 mmol /L) : Vomiting leads to chloride loss, which helps maintain alkalosis.

44. Step 6: Final Diagnosis • Primary disorder : Metabolic alkalosis • Likely cause : Severe vomiting leading to loss of gastric acid, dehydration, and hypokalemia • Compensation : Partial respiratory compensation (mild hypoventilation Management: 1. IV normal saline (0.9% NaCl) and potassium replacement 2. Identify and treat the cause of vomiting 3. Monitor electrolytes (K⁺, Cl⁻) and acid-base statu s

45. Case 5: A 68-year-old male with a history of chronic obstructive pulmonary disease (COPD) presents with: • Progressive shortness of breath and cough with purulent sputum for 3 days • Use of accessory muscles, audible wheezing • SpO₂: 86% on room air, RR: 26 bpm, BP: 140/85 mmHg • Breath sounds: Decreased with bilateral expiratory wheeze pH 7.28 pCO₂ 60 mmHg HCO₃⁻ (Bicarbonate) 30 mmol /L Base Excess +5 mmol /L PaO₂ 55 mmHg FiO₂ 21%

46. Interpretation: • Primary respiratory acidosis (high pCO₂, low pH) • Partially compensated by metabolic alkalosis (elevated HCO₃⁻) • Hypoxemia due to chronic respiratory diseas e Diagnosis: Acute on chronic respiratory acidosis due to COPD exacerbation. Management: 1. Controlled oxygen therapy (target SpO₂: 88–92%) 2. Nebulized bronchodilators (albuterol + ipratropium ) 3. Systemic corticosteroids (prednisone or IV methylprednisolone) 4. Consider non-invasive ventilation (BiPAP) if respiratory distress worsen

47. Case 6 : 32-year-old female presents with: • Sudden onset of shortness of breath, dizziness, and tingling in her hands • Recent emotional stress and history of anxiety disorder • RR: 30 bpm, HR: 110 bpm, BP: 130/80 mmHg • No wheezing or stridor, normal oxygen saturatio n pH 7.52 pCO₂ 28 mmHg HCO₃⁻ (Bicarbonate) 22 mmol /L Base Excess +1 mmol /L PaO₂ 98 mmHg FiO₂ 21%

48. Interpretation: • Primary respiratory alkalosis (low pCO₂, high pH) • Normal bicarbonate (acute process with no metabolic compensation yet) • Normal oxygenatio n Diagnosis: Acute respiratory alkalosis due to hyperventilation from a panic attack Management: 1. Reassurance and breathing exercises (slow breathing into a paper bag or cupped hands) 2. Rule out other causes (pulmonary embolism, hypoxia) if risk factors present 3. Consider short-term benzodiazepines if severe anxiet

49. Case 7 : 55-year-old male with a history of chronic obstructive pulmonary disease (COPD) and chronic kidney disease (CKD) presents to the emergency department with progressive shortness of breath, confusion, and generalized weakness . Clinical Findings: • BP : 90/60 mmHg, HR : 110 bpm, RR : 30 bpm • Physical exam : Tachypnea, decreased breath sounds, pedal edema • History : Reports vomiting for the past 2 days Arterial Blood Gas (ABG) and Electrolytes: • pH = 7.21 ( Acidemia ) • PaCO₂ = 55 mmHg (↑) ( Respiratory Acidosis ) • HCO₃⁻ = 15 mmol /L (↓) ( Metabolic Acidosis ) • Base Excess = -10 • Na⁺ = 140 mmol /L, Cl⁻ = 112 mmol /L • K⁺ = 5.5 mmol /L • Lactate = 4 mmol /L ( Elevated

50. Step 1: Assess pH - is acidosis . Step 2: Identify the Primary Disorder (Respiratory or Metabolic?) • PaCO₂ = 55 mmHg (Normal: 35–45 mmHg) → Respiratory Acidosis • HCO₃⁻ = 15 mmol /L (Normal: 22–26 mmol /L) → Metabolic Acidosis Since both PaCO₂ and HCO₃⁻ are abnormal in a way that worsens acidosis , this suggests a mixed acid-base disorder (Metabolic & Respiratory Acidosis). Step 3: Determine Compensation • Expected HCO₃⁻ in Chronic Respiratory Acidosis (Using Winter’s Formula for expected HCO₃⁻ in chronic respiratory acidosis): HCO3 = 24 + 0.4 ( delta PaCO2 ) = 24 + 3.75 = 27.75 • Actual HCO₃⁻ = 15 (much lower than expected) → Indicates an additional Metabolic Acidosis , not just compensatory changes. Step 4: Evaluate the Anion Gap (AG) for Metabolic Acidosis AG = Na⁺ - (Cl⁻ + HCO₃⁻) AG = 140 - (112 + 15) = 140 - 127 = 13 \text{ (High Anion Gap Metabolic Acidosis)} • Causes of High Anion Gap Metabolic Acidosis: • Lactic Acidosis (Lactate = 4) • Renal Failure (CKD leading to retention of acids like phosphate, sulfate, urate

51. Step 5: Identify the Cause of the Respiratory Acidosis • The patient has COPD , which leads to chronic CO₂ retention → Chronic Respiratory Acidosis . • However, acute worsening (RR 30 bpm, confusion, hypoxia) suggests acute on chronic respiratory failure due to possible COPD exacerbation . Final Diagnosis: Mixed Acid-Base Disorder 1. Chronic Respiratory Acidosis from COPD (PaCO₂ = 55 mmHg). 2. High Anion Gap Metabolic Acidosis from lactic acidosis & renal failure (HCO₃⁻ = 15 mmol /L, AG = 13). 3. Possible Contributing Factors: • Vomiting could lead to metabolic alkalosis , but in this case, the acidosis is dominant Step 6: Management Approach 1. Treat COPD Exacerbation : • Oxygen therapy (target SpO₂ 88-92% to avoid worsening CO₂ retention). • Bronchodilators (e.g., albuterol, ipratropium ) . • Consider Non-Invasive Ventilation (BiPAP) or mechanical ventilation if CO₂ rises further. 2. Address Metabolic Acidosis : • IV fluids to improve perfusion and lactate clearance. • Treat underlying cause (e.g., sepsis, renal failure, dehydration). • Dialysis if CKD leads to severe acidosis. 3. Monitor Potassium (K⁺ = 5.5) : • If worsening, consider calcium gluconate , insulin, or dialysis to prevent hyperkalemia complications

52. Thank you