Arterial line and blood gas (ABG)

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Arterial Cannulation

Indications

  • Beat-to-beat arterial blood pressure and mean arterial pressure (MAP) monitoring during major surgery, haemodynamic instability, extracorporeal circuits (e.g. ECMO, IABP) and thrombolysis or hypertensive emergencies.
  • Frequent arterial blood gas (ABG) analysis or lactate trending.
  • Continuous sampling for laboratory investigation when venous access is unreliable.
  • Advanced haemodynamic calculations (pulse-contour cardiac output, stroke-volume or pulse-pressure variation).
  • Neuro-anaesthesia, trauma or stroke cases in which tight cerebral perfusion pressure control is required.
  • Major burns, obstetric crises (e.g. massive haemorrhage) and paediatric cardiac surgery where invasive pressures guide resuscitation.

Contraindications

Absolute

  • Absent distal pulse or proven inadequate collateral circulation (Doppler, plethysmography).
  • Local infection, burn or traumatic disruption at the proposed site.
  • Prior radial artery harvest/prosthetic graft in the limb.
  • Critical limb ischaemia or unreconstructable peripheral vascular disease.

Relative

  • Coagulopathy (platelets < 50 × 10⁹ L⁻¹ or INR > 2) or therapeutic anticoagulation.
  • Raynaud phenomenon, Buerger disease, severe vasospasm.
  • ipsilateral arteriovenous fistula/lymphoedema/axillary node dissection.
  • High-dose vasopressor infusion (risk of digital ischaemia).
  • Sugical field proximity or planned limb positioning incompatible with line security.

Site Selection

Site Advantages Disadvantages Comment
Radial Superficial, low infection rate, palmar collateral flow Small calibre in shock/children Preferred; ultrasound first-pass success >90 %
Ulnar Preservation of radial grafts Deeper, smaller, proximity to ulnar nerve Reserve for failed radial
Brachial Large calibre, easy ultrasound view End artery, median nerve injury risk Acceptable for ≤48 h with ≤20 G catheter
Axillary Central pressure, mobile limb Plexus proximity, technical Useful when femoral contraindicated
Femoral Rapid access in shock/CPR, reliable waveform Higher bleed/infection if asepsis poor Ideal in major vasoconstriction or CPB gradients
Dorsalis pedis / Posterior tibial Accessible prone/upper-limb burns Amplified systolic BP, distal ischaemia Continuous foot perfusion checks

Technique

  • Ultrasound guidance (short-axis out-of-plane or long-axis in-plane) is recommended; meta-analysis shows higher first-pass success, fewer attempts and haematomata than palpation.
  • Direct over-the-needle, Seldinger or modified Seldinger techniques are acceptable; choose smallest catheter that provides reliable waveform (20–22 G adults, 22–24 G paediatrics).
  • Zero transducer at the phlebostatic axis (4th intercostal, mid-axillary); re-zero after patient repositioning >15 °.
  • Fast-flush test daily to confirm adequate natural frequency (>10 Hz) and optimal damping (1–2 oscillations).

Maintenance & Infection Prevention

  • Pressurised (300 mmHg) 0.9 % saline at 2–3 mL h⁻¹; routine heparinised flush offers no patency benefit and risks thrombocytopenia—avoid unless repeated clotting occurs.
  • Chlorhexidine–alcohol skin preparation, maximal sterile-barrier precautions, sterile ultrasound cover and dedicated transducer.
  • Transparent dressing with date/time; inspect insertion site at least once per shift.
  • Daily line-necessity check—catheter-related bloodstream infection risk rises steeply after day 4–5; remove or resite where feasible.

Complications and Mitigation

Category Incidence Prevention/Management
Mechanical failure / haematoma 6–28 % Ultrasound, <3 attempts, compression 5 min
Thrombosis / digital ischaemia 0.1–0.5 % Small catheter, limb perfusion checks, remove if blanching
Catheter-related infection 0.15 per 1000 catheter-days Strict asepsis, minimise dwell time
Haemorrhage / line disconnection <1 % Locking connectors, alarms, securement device
Nerve injury (median, radial) Rare Use ultrasound to visualise nerve, avoid multiple passes

Arterial Pressure Waveform Interpretation

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  • Components: rapid systolic upstroke → peak systolic → dicrotic notch (aortic valve closure) → diastolic runoff → end-diastolic pressure.
  • Peripheral amplification: from aorta to radial the systolic rises (~5–20 mm Hg), diastolic falls; MAP remains constant.
  • Dynamic response errors:
    • Underdamped–tall, narrow peaks, overshoot SBP, wide pulse pressure.
    • Overdamped–blunted upstroke, loss of dicrotic notch, underestimated SBP.
  • Troubleshooting: remove air/clots, shorten tubing (<120 cm), ensure 300 mm Hg flush pressure, replace kinked catheter/tubing.

Special Situations

  • Paediatrics/neonates: ultrasound guidance markedly improves success; 24 G radial or posterior tibial preferred.
  • Cardiac bypass/vasopressor use: dual radial + femoral lines detect radial–central gradient.
  • Prone ventilation/major burns: secure limb padding, consider dorsalis pedis.
  • South African context: higher prevalence of HIV, diabetes and peripheral vascular disease—ultrasound enhances safety, and resource-adjusted protocols should balance cost with reduction in complications and cannulation time.

Normal ABG on Room Air

  • pH: 7.40
  • pCO2: 40 mmHg
  • HCO3: 24 mEq/L
  • Normal O2: > 80 mmHg
  • Normal Anion Gap (AG): 12 ± 2

Steps to Interpret Acid-Base Disturbances

1. Adequate Oxygenation?

  • Normal O2: > 80 mmHg
  • Possible Hypoxemia: Consider if pO2 is less than expected.

2. Define the Acid-Base Disturbance

  • pH < 7.35: Acidemia
    • Metabolic Acidosis: Gain of acid or loss of HCO3⁻
    • Respiratory Acidosis: Hypoventilation, increased pCO2
  • pH > 7.45: Alkalemia
    • Metabolic Alkalosis: Gain of HCO3⁻ or loss of acid
    • Respiratory Alkalosis: Hyperventilation, decreased pCO2

3. Identify the Primary Process

  • Metabolic Acidosis:

    • Acute: HCO3⁻ < 24 mEq/L with corresponding pCO2 compensation
    • Chronic: Same pattern but over longer duration
  • Respiratory Acidosis:

    • Acute: Elevated pCO2 with minimal change in HCO3⁻
    • Chronic: Elevated pCO2 with compensatory increase in HCO3⁻
  • Metabolic Alkalosis:

    • Acute: HCO3⁻ > 24 mEq/L with compensatory increase in pCO2
    • Chronic: Same pattern but over longer duration
  • Respiratory Alkalosis:

    • Acute: Decreased pCO2 with minimal change in HCO3⁻
    • Chronic: Decreased pCO2 with compensatory decrease in HCO3⁻

4. Compensatory Mechanisms

A. Metabolic Disorders

  1. Metabolic Acidosis (Winter’s formula)
  • pCO2 expected=(1.5×[HCO3−])+8  ±  2(mmHg)
  1. Metabolic Alkalosis
  • pCO2 expected=(0.7×[HCO3−])+20(mmHg)

B. Respiratory Disorders

ΔPCO₂ = (measured PCO₂ – 40 mmHg).

  1. Respiratory Acidosis
    • Acute:
      Δ[HCO3−]=0.1×ΔpCO2⟹
      (HCO3−)exp=24+0.1×(pCO2−40)
    • Chronic:
      Δ[HCO3−]=0.35×ΔpCO2⟹
      (HCO3−)exp=24+0.35×(pCO2−40)
  2. Respiratory Alkalosis
    • Acute
      Δ[HCO3−]=0.2×(40−pCO2)⟹
      (HCO3−)exp=24−0.2×(40−pCO2)
    • Chronic:
      Δ[HCO3−]=0.35×(40−pCO2)⟹
      (HCO3−)exp=24−0.35×(40−pCO2)

5. Calculate Anion Gap (AG)

  • AG: Na⁺ – (Cl⁻ + HCO3⁻)
    • Normal AG: 12 ± 2
    • High AG: Presence of unmeasured anions

6. Normal AG Metabolic Acidosis (NAGMA)

  • Causes:
    • GI Losses of HCO3⁻ (Diarrhea)
    • Renal Tubular Acidosis (RTA)

7. High AG Metabolic Acidosis (HAGMA)

  • Causes: Accumulation of acids like lactate or ketones, renal failure, toxins.

8. Compensation and Mixed Disorders

  • Winter’s Formula for Metabolic Acidosis: Expected pCO2 = 1.5 × (HCO3⁻) + 8 ± 2
  • Delta-Delta (Δ/Δ) Ratio: Used to identify mixed disorders

Metabolic Acidosis Considerations

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Winter’s Formula

PCO2=(1.5×HCO3)+8

  • Interpretation:
    • If measured PCO2 > calculated PCO2: Concurrent respiratory acidosis is present.
    • If measured PCO2 < calculated PCO2: Concurrent respiratory alkalosis is present.

Delta Gap (Δ gap)

Δgap=AG−12+HCO3

  • Interpretation:
    • If Δ gap < 22 mEq/L: Concurrent non-gap metabolic acidosis exists.
    • If Δ gap > 26 mEq/L: Concurrent metabolic alkalosis exists.

MUDPILES (High Anion Gap Metabolic Acidosis – HIGMA)

  • M: Methanol
  • U: Uremia
  • D: Diabetic ketoacidosis
  • P: Paraldehyde
  • I: Infection, In therapy
  • L: Lactic acidosis
  • E: Ethanol, ethylene glycol
  • S: Salicylates (aspirin)

Causes of Normal Anion Gap Metabolic Acidosis (NAGMA)

  • Excessive administration of 0.9% normal saline
  • Gastrointestinal losses: Diarrhea, ileostomy, neobladder, pancreatic fistula
  • Renal losses: Renal tubular acidosis
  • Drugs: Acetazolamide

Lactic Acidosis

Definition and Types

  • Lactic Acidosis: Elevated blood lactate levels > 2 mmol/L
    • Type A: Impaired oxygen delivery (e.g., shock, hypoxia)
    • Type B: Impaired oxygen utilization (e.g., mitochondrial dysfunction)
    • Type D: Bacterial overgrowth

Pathophysiology

  • Anaerobic Glycolysis: Pyruvate converted to lactate when oxygen is scarce
  • Lactate Clearance: Liver and kidneys play major roles

Causes of Increased Lactate Production

  • Hypoxia: Decreased oxygen delivery (e.g., cardiac arrest, sepsis)
  • Increased Oxygen Demand: Exercise, seizures
  • Impaired Clearance: Liver disease, renal failure

Treatment Approaches

  • Address Underlying Cause: Oxygen delivery, removal of toxins
  • Supportive Measures: IV fluids, bicarbonate in severe cases

Respiratory Acidosis Considerations

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Increased CO2 Production

  • Malignant hyperthermia
  • Hyperthyroidism
  • Sepsis
  • Overfeeding

Decreased CO2 Elimination

  • Intrinsic pulmonary disease: Pneumonia, ARDS, fibrosis, edema
  • Upper airway obstruction: Laryngospasm, foreign body, OSA
  • Lower airway obstruction: Asthma, COPD
  • Chest wall restriction: Obesity, scoliosis, burns
  • CNS depression: Anesthetics, opioids, CNS lesions
  • Decreased skeletal muscle strength: Myopathy, neuropathy, residual effects of neuromuscular blocking drugs
  • Rarely, an exhausted soda–lime or incompetent one-way valve in an anesthesia delivery system can contribute to respiratory acidosis.

Respiratory Alkalosis

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Metabolic Alkalosis

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Links


References:

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Summaries:
ICU OP- ABG
ICU One pager Acid base
ICU One pager Lactic acidosis)
Acid/base


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