4.1 Cardiopulmonary Resuscitation & Shock

Cardiopulmonary Resuscitation & Shock

In critical care and emergency medicine, cardiopulmonary resuscitation (CPR) and shock management represent the cornerstones of acute life support. A structured, evidence-based approach to the patient in cardiac arrest or circulatory collapse is vital for optimizing survival and neurological outcomes.

Basic Life Support (BLS) and Advanced Cardiovascular Life Support (ACLS) Protocols

High-Quality Cardiopulmonary Resuscitation (CPR)

High-quality CPR is the single most critical determinant of survival in cardiac arrest. The Dubai Health Authority (DHA) adopts protocols aligned with international guidelines, emphasizing:

1. Compression Rate: 100 to 120 compressions per minute.
2. Compression Depth: At least 2 inches (5 cm) but not exceeding 2.4 inches (6 cm) in adults.
3. Chest Recoil: Allowing complete chest wall recoil after each compression to permit ventricular filling; avoiding leaning on the chest.
4. Minimizing Interruptions: Pauses in chest compressions must be kept under 10 seconds (e.g., during rhythm checks or shock delivery).
5. Ventilation Ratio: 30 compressions to 2 ventilations in a non-intubated patient. Once an advanced airway is placed, compressions are continuous, and ventilations are delivered at a rate of 1 breath every 6 seconds (10 breaths per minute).
6. Quantitative Waveform Capnography: Recommended to monitor CPR quality and detect Return of Spontaneous Circulation (ROSC). A PETCO2 reading < 10 mmHg indicates inadequate chest compressions, warranting optimization of technique. A sudden, sustained increase in PETCO2 to > 35-40 mmHg is a highly reliable indicator of ROSC.

ACLS Algorithms: Shockable vs. Non-Shockable Rhythms

The immediate management of cardiac arrest depends on the cardiac rhythm identified during the brief rhythm check:

• Shockable Rhythms (Ventricular Fibrillation [VF] and Pulseless Ventricular Tachycardia [pVT]):

  • The priority is immediate, unsynchronized defibrillation (120-200 J biphasic, or 360 J monophasic).
  • Resume chest compressions immediately after the shock without checking the pulse or rhythm.
  • Establish IV/IO access. Administer Epinephrine 1 mg IV/IO every 3 to 5 minutes, typically initiated after the second shock.
  • If VF/pVT persists after the second shock, administer antiarrhythmics: Amiodarone (300 mg IV/IO bolus first dose, followed by 150 mg for the second dose) or Lidocaine (1.0-1.5 mg/kg first dose, then 0.5-0.75 mg/kg).

• Non-Shockable Rhythms (Asystole and Pulseless Electrical Activity [PEA]):

  • The priority is high-quality CPR and early administration of Epinephrine (1 mg IV/IO as soon as access is established, repeated every 3 to 5 minutes).
  • Defibrillation is not indicated and can be harmful.
  • Search diligently for reversible causes (the 5 H's and 5 T's).

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Pathophysiology and Classification of Shock

Shock is defined as a state of systemic tissue hypoperfusion resulting from an imbalance between oxygen supply and demand. This leads to cellular hypoxia, anaerobic metabolism, lactic acidosis, and eventually multiorgan dysfunction syndrome (MODS). Shock is classified into four main categories based on the underlying hemodynamic profile:

1. Hypovolemic Shock

Hypovolemic shock results from a critical loss of intravascular volume.

• Etiology: Hemorrhage (trauma, GI bleed), non-hemorrhage fluid loss (severe vomiting, diarrhea, burns, diabetic ketoacidosis).
• Hemodynamics: Characterized by a low central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP), reduced cardiac output (CO), and a compensatory increase in systemic vascular resistance (SVR) via sympathetic activation.
• Management: Immediate volume replacement. In non-hemorrhagic shock, initiate isotonic crystalloids (e.g., Balanced Salt Solutions or Normal Saline) at 30 mL/kg. In hemorrhagic shock, restrict crystalloids to prevent coagulopathy ("dilutional coagulopathy") and prioritize early administration of blood products (packed red blood cells, fresh frozen plasma, platelets) in a 1:1:1 ratio.
• Ultrasound Assessment: Bedside point-of-care ultrasound (POCUS) is invaluable in shock assessment. In hypovolemic shock, ultrasound reveals a hyperdynamic, underfilled left ventricle and a collapsible inferior vena cava (IVC) with respiratory variation > 50%.

2. Cardiogenic Shock

Cardiogenic shock is characterized by primary myocardial pump failure leading to inadequate tissue perfusion despite adequate intravascular volume.

• Etiology: Acute myocardial infarction (most common), severe myocarditis, valvular dysfunction, end-stage cardiomyopathy, or arrhythmias.
• Hemodynamics: Elevated CVP and PCWP (due to venous congestion), low CO, and elevated SVR (compensatory vasoconstriction).
• Management: Avoid aggressive fluid administration, which worsens pulmonary edema. Optimize oxygenation. Pharmacological support focuses on inotropes like Dobutamine (first-line) to increase contractility, and vasopressors like Norepinephrine if severe hypotension is present. Definitive management requires addressing the underlying cause (e.g., urgent percutaneous coronary intervention for myocardial infarction).
• Ultrasound Assessment: Demonstrates impaired left ventricular contractility, a dilated, non-collapsible IVC, and B-lines on lung ultrasound (indicative of pulmonary edema).

3. Distributive Shock

Distributive shock is caused by severe systemic vasodilation, resulting in relative hypovolemia despite normal blood volume.

• Septic Shock: A subset of sepsis with circulatory and cellular/metabolic abnormalities.
  • Hemodynamics: Low CVP/PCWP, low SVR (due to inflammatory vasodilation), and a normal or high CO (hyperdynamic state in early phases).
  • Management: Obtain blood cultures before administering broad-spectrum antibiotics (within 1 hour of recognition). Administer 30 mL/kg of isotonic crystalloids. If hypotension persists despite fluid resuscitation, initiate Norepinephrine as the first-line vasopressor to maintain a Mean Arterial Pressure (MAP) >= 65 mmHg.
• Anaphylactic Shock: A severe, life-threatening systemic hypersensitivity reaction.
  • Hemodynamics: Low CVP/PCWP, low SVR.
  • Management: First-line therapy is intramuscular Epinephrine (0.3-0.5 mg of 1:1000 dilution in the anterolateral thigh) administered immediately. IV fluids, antihistamines (H1 and H2 blockers), and corticosteroids are adjunctive.
• Neurogenic Shock: Caused by loss of sympathetic vascular tone, typically due to high-cervical or thoracic spinal cord injury.
  • Hemodynamics: Low CVP, low SVR, and low CO accompanied by bradycardia (due to unopposed vagal tone; a key distinguishing feature).

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Vasopressors and Fluids in Resuscitation

The selection of vasoactive agents and fluids must be tailored to the specific shock etiology:

• Fluid Choice: Isotonic crystalloids (Lactated Ringer's or Plasma-Lyte) are preferred over 0.9% Normal Saline for large-volume resuscitation to prevent hyperchloremic metabolic acidosis. Colloids (such as albumin) are reserved for specific situations (e.g., volume resuscitation in patients requiring large amounts of crystalloids), while starch-based colloids are contraindicated due to risk of acute kidney injury.