3.4 Critical Care, Emergency Nursing & Shock Management

Emergency Nursing Management

Trauma Triage and the Primary/Secondary Survey

Emergency nursing demands rapid prioritization and systematic assessment.

The Primary Survey (ABCDE)

The primary survey is designed to identify and immediately intervene upon life-threatening conditions.

1. Airway with Cervical Spine Immobilization: The highest priority. Assess for patency, vocalization, and obstruction (blood, vomit, foreign bodies). If a cervical spine injury is suspected, use the jaw-thrust maneuver to open the airway rather than the head-tilt/chin-lift. Ensure suction is available and prepare for definitive airway management (endotracheal intubation) if the Glasgow Coma Scale (GCS) is less than 8.
2. Breathing: Assess ventilation and oxygenation. Observe for symmetrical chest expansion, use of accessory muscles, and respiratory rate. Look for paradoxical chest wall movement (flail chest) or tracheal deviation with absent breath sounds (tension pneumothorax, requiring immediate needle decompression). Administer high-flow oxygen.
3. Circulation: Assess pulses (central vs. peripheral), capillary refill, skin color, and temperature. Control external hemorrhage with direct pressure or a tourniquet. Establish two large-bore IVs (14- or 16-gauge) for rapid fluid or blood administration. Administer warmed isotonic crystalloids.
4. Disability: Perform a rapid neurological assessment using the GCS (evaluating eye opening, verbal response, and motor response) and check pupillary size and reactivity. Assess for signs of lateralization indicating intracranial pathology.
5. Exposure/Environmental Control: Completely undress the patient to perform a full assessment of all skin surfaces, checking for hidden injuries. Immediately cover the patient with warm blankets and utilize active warming measures to prevent hypothermia, which exacerbates coagulopathy.

The Secondary Survey

The secondary survey is a head-to-toe evaluation performed only after the primary survey is complete and life threats are addressed. It includes a full set of vital signs, a focused history (AMPLE: Allergies, Medications, Past illness, Last meal, Events), and detailed physical examination.

Mass Casualty Triage (START Method)

In disaster scenarios (Simple Triage and Rapid Treatment), the goal shifts from maximal care for one to the greatest good for the greatest number. Patients are tagged based on their respiratory, perfusion, and mental status.

• Red (Immediate): Life-threatening injuries but treatable with rapid intervention (e.g., tension pneumothorax, massive hemorrhage, airway compromise, respiratory rate >30, delayed capillary refill).
• Yellow (Delayed): Serious but not immediately life-threatening injuries (e.g., stable fractures, large lacerations without massive bleeding). These patients can wait a few hours for care.
• Green (Minor): "Walking wounded." Minor injuries (e.g., sprains, abrasions). These patients can follow commands and walk away from the scene.
• Black (Expectant/Deceased): Deceased or injuries so severe that survival is unlikely even with maximal care (e.g., massive head trauma, no pulse, apnea despite airway repositioning).

Critical Care & Hemodynamic Monitoring

Invasive hemodynamic monitoring is utilized in the ICU to continuously evaluate cardiovascular function, fluid status, and tissue perfusion.

• Central Venous Pressure (CVP): Normal is 2-8 mmHg. It measures right ventricular preload (volume returning to the right heart).
  • Elevated CVP: Indicates fluid overload, right-sided heart failure, or cardiac tamponade.
  • Decreased CVP: Indicates hypovolemia, dehydration, or distributive shock.
• Pulmonary Artery Wedge Pressure (PAWP): Normal is 6-12 mmHg. It measures left ventricular preload and left-sided heart function.
  • Elevated PAWP: Indicates left-sided heart failure, cardiogenic shock, or severe mitral stenosis.
• Cardiac Output (CO): Normal is 4-8 L/min. It represents the volume of blood pumped by the heart per minute (Heart Rate × Stroke Volume).
• Systemic Vascular Resistance (SVR): Normal is 800-1200 dynes/sec/cm⁻⁵. It reflects the afterload or resistance the left ventricle must overcome to eject blood.
  • Elevated SVR: Seen in hypovolemic and cardiogenic shock as a compensatory vasoconstriction response.
  • Decreased SVR: A hallmark of distributive shock (septic, neurogenic, anaphylactic) due to massive vasodilation.
• Mean Arterial Pressure (MAP): Must be ≥ 65 mmHg to ensure adequate organ perfusion. Calculated as [Systolic BP + 2(Diastolic BP)] / 3.

Shock Management

Shock is a complex, life-threatening syndrome characterized by decreased tissue perfusion and impaired cellular metabolism, leading to an imbalance between oxygen supply and demand. If untreated, it progresses to Multiple Organ Dysfunction Syndrome (MODS).

1. Hypovolemic Shock

Caused by an absolute loss of intravascular volume (e.g., hemorrhage, severe dehydration, massive burns, vomiting/diarrhea).

• Pathophysiology: Decreased venous return leads to decreased preload (low CVP/PAWP), decreased stroke volume, and ultimately decreased cardiac output. The body compensates by increasing SVR (vasoconstriction) and heart rate.
• Clinical Signs: Tachycardia, hypotension, tachypnea, cool/clammy skin, decreased urine output (<30 mL/hr), altered mental status.
• Nursing Interventions:
  • Prioritize ABCs and maximize oxygenation.
  • Execute specific fluid resuscitation protocols: Administer rapid IV fluids (crystalloids like 0.9% NS or Lactated Ringer's) via two large-bore IVs.
  • If hemorrhagic, administer blood products (PRBCs, FFP, platelets) in a balanced ratio (often 1:1:1) to prevent dilutional coagulopathy.
  • Continuously monitor urine output, MAP, and lactate levels as indicators of tissue perfusion.

2. Cardiogenic Shock

Caused by severe impairment of the heart's pumping ability, most commonly due to a massive anterior Myocardial Infarction or severe heart failure.

• Pathophysiology: Decreased contractility leads to severely decreased cardiac output and increased pulmonary pressures (high PAWP). SVR is high due to compensatory vasoconstriction.
• Clinical Signs: Tachycardia, hypotension, tachypnea, crackles in lungs (pulmonary edema), cyanosis, narrowed pulse pressure.
• Nursing Interventions:
  • Fluid Restriction: Do NOT aggressively give fluids, as it exacerbates pulmonary edema.
  • Inotropes: Administer Dobutamine or Milrinone to increase myocardial contractility without significantly increasing heart rate.
  • Vasopressors: Use cautiously to support blood pressure if profound hypotension exists.
  • Vasodilators: Administer Nitroglycerin (if BP tolerates) to decrease preload and afterload.
  • Prepare the patient for mechanical circulatory support, such as an Intra-Aortic Balloon Pump (IABP) or ventricular assist device.

3. Distributive Shock

Characterized by massive vasodilation, causing relative hypovolemia despite normal total body fluid volume. SVR is uniquely decreased in distributive shock.

Septic Shock A dysregulated host response to infection leading to systemic inflammation, massive vasodilation, and increased capillary permeability.

• Pathophysiology: Endotoxins trigger an inflammatory cascade, resulting in low SVR, initially high or normal CO (hyperdynamic phase), followed by low CO.
• Sepsis Bundle (Within 1 Hour):
  1. Measure lactate level (re-measure if initial is > 2 mmol/L).
  2. Obtain blood cultures PRIOR to administering antibiotics.
  3. Administer broad-spectrum antibiotics.
  4. Begin rapid administration of 30 mL/kg crystalloid for hypotension or lactate ≥ 4 mmol/L.
  5. Apply vasopressors (Norepinephrine is the first-line agent) if hypotensive during or after fluid resuscitation to maintain MAP ≥ 65 mmHg.

Anaphylactic Shock A severe, life-threatening Type I hypersensitivity allergic reaction.

• Pathophysiology: Massive release of histamine causes systemic vasodilation and increased capillary permeability.
• Clinical Signs: Stridor, wheezing, angioedema, hives, severe hypotension, sense of impending doom.
• Interventions:
  • IM Epinephrine (0.3 to 0.5 mg, 1:1000) is the absolute priority medication (causes bronchodilation and vasoconstriction).
  • Maintain the airway; prepare for early intubation if angioedema is severe.
  • Administer IV fluids, antihistamines (Diphenhydramine), H2 blockers (Famotidine), and corticosteroids (Methylprednisolone) to blunt the delayed immune response.

Neurogenic Shock Caused by spinal cord injury (usually above T5), resulting in a loss of sympathetic tone.

• Pathophysiology: Interruption of sympathetic nervous system pathways prevents vasoconstriction and compensatory tachycardia.
• Clinical Signs: Unique among shock states—presents with hypotension and BRADYCARDIA. Skin may be warm, dry, and flushed initially due to vasodilation.
• Interventions:
  • Spine immobilization and airway management.
  • Cautious fluid resuscitation to restore intravascular volume.
  • Administer vasopressors (e.g., Phenylephrine or Norepinephrine) to restore vascular tone.
  • Administer Atropine for severe, symptomatic bradycardia, or prepare for transcutaneous pacing.