Wednesday, September 3, 2025

Critical Care Medicine Part 1&2

Critical Care Medicine – Study Notes (Part 1)

Oxygen Content & Delivery

Physiologic Goal

  • Oxygen’s end-point: mitochondrial ATP production.

  • Hypoxemia/desaturation → ↓ ATP, failure of membrane integrity → apoptosis/necrosis.

Oxygen Gradient

  • Required across all steps: atmosphere → alveoli → arterial blood → tissues → mitochondria.

Oxygen Transport

  • Carried mostly by hemoglobin, with a small dissolved fraction.

O₂ Content Formula:

CaO2=(1.34×Hgb×SaO2)+(0.003×PaO2)CaO₂ = (1.34 \times Hgb \times SaO₂) + (0.003 \times PaO₂)

  • Hemoglobin & saturation = main determinants.

  • PaO₂ contributes little.

Hemoglobin–Oxygen Binding

  • Influenced by p50 (~26 mmHg).

  • Right shift (↑ p50, ↓ affinity): acidosis, ↑ temperature, ↑ CO₂, ↑ 2,3-DPG.

  • Left shift (↓ p50, ↑ affinity): alkalosis, ↓ temperature, ↓ CO₂, ↓ 2,3-DPG.

Oxygen Delivery (DO₂)

DO2=CaO2×CO×10DO₂ = CaO₂ \times CO \times 10

  • Cardiac output × oxygen content (×10 for unit correction).

  • DO₂ is what matters clinically.

Oxygen Consumption (VO₂)

  • Normal ≈ 250 mL/min (varies).

  • Measured by direct or indirect calorimetry (metabolic cart).

Fick Principle:

CO=VO2CaO2CvO2CO = \frac{VO₂}{CaO₂ - CvO₂}

  • Must use oxygen content, not just saturation.

  • Errors: using venous saturation instead of content.

VO₂ increased by: sepsis, hyperthyroidism, seizures, shivering, fever, malignant hyperthermia.
VO₂ decreased by: anesthesia, neuromuscular blockade, hypothyroidism, hypothermia.

Mechanical Ventilation

Non-Invasive Ventilation

  • BiPAP: improves both ventilation (↑ IPAP) and oxygenation (↑ EPAP).

  • CPAP: improves oxygenation only; classically for cardiogenic pulmonary edema.

  • Contraindications: altered mental status, vomiting/aspiration risk, bowel obstruction, gastroparesis.

  • High-flow nasal cannula (HFNC) increasingly replacing CPAP.

Ventilatory Cycle

  • Trigger → Inspiratory flow → Cycle → Expiration.

  • Triggers: machine, pressure, flow.

  • Cycling: volume, time, flow, or pressure.

Ventilation Modes

  • Volume Control: constant tidal volume; variable pressures.

  • Pressure Control: constant pressure; variable tidal volume.

  • Assist Control (AC): minimum set rate + patient-triggered breaths.

  • SIMV: mandatory breaths + spontaneous breaths (may add pressure support).

  • Pressure Support: fully patient-driven; no backup rate (except apnea safety mode).

Key Pressures

  • Peak Inspiratory Pressure (PIP): resistance + compliance.

  • Plateau Pressure: compliance only (measured during inspiratory pause).

  • Interpretation:

    • High PIP, normal plateau → resistance problem.

    • High PIP & plateau → compliance problem.

PEEP (Positive End-Expiratory Pressure)

  • Prevents alveolar derecruitment.

  • Improves oxygenation but ↑ intrathoracic pressure → ↓ venous return.

  • Overdistension risk if too high.

ARDS (Acute Respiratory Distress Syndrome)

  • Non-cardiogenic pulmonary edema due to inflammatory injury of alveolo-capillary membrane.

  • Heterogeneous distribution in lungs.

  • Causes: pneumonia, aspiration, trauma, burns, pancreatitis, sepsis.

  • CXR: bilateral infiltrates, diffuse.

No curative treatment.

  • Focus = treat underlying cause + supportive care.

  • Lung-protective ventilation:

    • Low tidal volume (6 mL/kg IBW).

    • Plateau pressure < 30 cmH₂O.

    • Avoid volutrauma/barotrauma.

  • Inhaled nitric oxide: may transiently improve oxygenation, but no mortality benefit. Rescue use only.

Infection Control in Critical Care

Precautions

  • Standard: baseline for all patients.

  • Contact: gown/gloves.

  • Droplet: surgical mask.

  • Airborne: N95, negative pressure.

Ventilator-Associated Pneumonia (VAP)

  • From microaspiration around ETT cuff.

  • Organisms differ from community pneumonia.

  • Specialized ETTs may help but limited mortality impact.

VAP Prevention Bundle:

  • Daily sedation breaks / awakening trials.

  • Early extubation.

  • Stress ulcer prophylaxis.

  • DVT prophylaxis.

  • Chlorhexidine oral care.

Central Line–Associated Bloodstream Infection (CLABSI)

  • Caused by poor insertion or maintenance.

  • Prevention Bundle:

    • Hand hygiene.

    • Full barrier precautions (cap, gown, mask, sterile gloves, full drape).

    • Chlorhexidine skin prep.

    • Daily assessment & prompt removal when no longer needed.

    • Antimicrobial discs/occlusive dressings reduce risk.

Anesthesia Keyword Review – Critical Care (Part 2 of 2)

Topics Covered

  • Shock states

  • Sepsis

  • Resuscitation & fluids

  • Nutrition

  • Burns

  • Drowning

Shock States

Definition

  • Circulatory shock = syndrome of reduced tissue perfusion.

  • Not just hypotension → key problem = inadequate capillary blood flow to supply O₂ + glucose for ATP production.

  • Result: electrolyte imbalance → cell membrane pump failure → ischemia → infarction → necrosis.

Mortality

  • Still very high.

  • Septic or cardiogenic shock: mortality may reach ~50%.

Phases of Shock

  1. Reversible/Early Shock

    • Reflexes (macro/microvascular + cellular + immunologic) try to preserve cardiac output & arterial pressure.

    • Organ dysfunction absent or minimal.

  2. Late Shock

    • Perfusion of heart/major organs begins to fail.

    • Organ dysfunction becomes obvious.

    • Not a sharp cutoff; continuum.

  3. Irreversible/Terminal Shock

    • Vasomotor dysfunction, loss of arteriolar tone.

    • Paradoxical ↑ central venous tone (pathologic).

    • Ischemia → infarct → necrosis.

Types of Shock

  • Distributive (hyperdynamic)

    • ↑ Cardiac output.

    • ↓ SVR.

    • ↑ Mixed venous saturation.

    • ↓ Wedge pressure.

    • Ex: Septic shock.

  • Hypovolemic

    • ↓ CO, ↑ SVR.

    • ↓ Mixed venous saturation.

    • ↓ Wedge pressure.

  • Cardiogenic

    • ↓ CO, ↑ SVR.

    • ↓ Mixed venous saturation.

    • ↑ Wedge pressure.

  • Obstructive

    • ↓ CO, ↑ SVR.

    • ↓ Mixed venous saturation.

    • ↑ Wedge pressure.

Sepsis & Septic Shock

  • Distributive shock subtype.

  • Pathophysiology: dysregulated host immune response, pro-inflammatory imbalance.

  • Genetics: influence severity/outcome.

  • Early recognition = survival.

  • Treat septic shock like a code (time-critical).

Definitions

  • Sepsis definitions evolving (Sepsis-3 replaced SIRS-based).

  • Still: infection → systemic inflammation → sepsis → septic shock (hypotension + tissue malperfusion).

Management Principles

  • Initial resuscitation: aggressive fluids + vasopressors if needed.

  • Antibiotics: broad spectrum within 1 hour of symptom onset.

    • Blood cultures first if possible (then urine → lung).

    • De-escalate once pathogen identified.

  • Source control: drain abscess, remove infected hardware.

  • Fluids:

    • Crystalloids preferred (no consistent advantage to colloids).

    • May require 10–14 L/24 hrs early.

    • Remove excess fluid aggressively by day 2–3.

  • Hemodynamic goals: MAP ≥ 65 mmHg.

  • Vasopressors:

    • 1st line = norepinephrine.

    • Add vasopressin to reduce norepi dose.

    • Rescue = epinephrine.

  • Inotropes:

    • Dobutamine if myocardial dysfunction + low CO.

    • Avoid supraphysiologic oxygen delivery goals.

  • Steroids:

    • Consider if refractory to catecholamines.

    • Watch for hyperglycemia.

Resuscitation Fluids

Crystalloids vs Colloids

  • No mortality difference overall.

  • Colloids (albumin) indicated in specific conditions:

    • Cirrhosis + SBP (spontaneous bacterial peritonitis).

    • Hepatorenal syndrome.

    • Large-volume paracentesis.

  • Hydroxyethyl starches (HES): avoided (coagulopathy, AKI risk).

Crystalloids

  • Options: D5W, ½NS, NS, LR, Plasma-Lyte.

  • Electrolyte content varies.

  • Balanced solutions (LR, Plasma-Lyte) preferred for large resuscitation.

Nutrition in Critical Care

  • Enteral (preferred) over TPN when possible.

    • Improves mortality, ↓ infection, ↓ ventilator days.

  • TPN (yellow bag): hypertonic glucose, amino acids, electrolytes, vitamins, lipids.

    • Indications: short gut, high-output fistula, prolonged obstruction or ileus.

    • Complications: infection (CLABSI), liver dysfunction, cholelithiasis, refeeding syndrome, hyperglycemia.

  • Caloric needs: ~25 kcal/kg/day (↑ in burns, trauma, sepsis).

  • Protein needs: 1.5–2 g/kg/day (↑ in burns, trauma, AKI).

Burns

  • Cause massive inflammation and fluid loss.

  • Airway management:

    • Intubate early if facial soot, singed nasal hairs, mouth burns → prevent airway edema obstruction.

  • Fluid resuscitation: Parkland formula (starting point, not absolute).

  • Neuromuscular blockade considerations:

    • Succinylcholine contraindicated after 24–48 hrs (risk hyperkalemia).

    • Resistance to non-depolarizers possible.

Drowning

  • Primary cause of death: hypoxemia from aspiration.

  • Even if rescued: risk of ARDS, inflammation.

  • Hypothermia common (even in non-arctic water).

  • Cardiogenic shock possible (↑ CVP/wedge with immersion).

  • Always evaluate for secondary injuries (trauma → spinal cord injury, internal lacerations).

No comments:

Post a Comment

On Crocodiles

1. What Crocodiles Actually Eat Crocodiles are obligate carnivores . Their diet includes: Fish Birds Mammals Reptiles Carrion (dead animals)...