Shock Lecture Notes

Introduction to Shock

• Shock is described as "a momentary pause in the act of death" (John Collins Warren, 1885) and "the manifestation of the rude unhinging of the machinery of life" (Samuel Gross, 1862).
• Physiological or circulatory shock is different from psychological or emotional shock.
• Shock is a life-threatening condition where the circulatory system fails to deliver enough oxygen to all body parts, leading to death without proper treatment.

Why Shock Kills

• Inadequate tissue perfusion leads to impaired cellular metabolism.
• Perfusion is the circulation of blood through different organs and tissues.
• Adequate blood flow equals adequate perfusion, while inadequate flow equals inadequate perfusion (hypoperfusion), which defines shock.

Physiology of Perfusion

• Circulatory perfusion depends on three key components:
  • Pump (the heart)
  • Container (blood vessels)
  • Fluid (blood volume)
• Adequate blood flow requires:
  1. A well-functioning heart
  2. An adequate amount of circulating blood
  3. Intact blood vessels able to adjust blood flow

Pathophysiology of Shock

• Reduced perfusion triggers:
  • Neuroendocrine response
  • Cytokine response
  • Redistribution of flow to vital organs
  • Ischemia of non-vital organs
  • Flow maldistribution within organs
  • Dysoxia and multiple organ failure

Stages of Shock

• Compensated Shock
  • Perfusion is maintained by the body's defense mechanisms.
  • The sympathetic response is activated.
  • Blood is shunted to vital organs.
  • Blood pressure is normal or elevated.
  • Cellular ischemic phase occurs.
  • Decreased O_2 delivery causes cells to switch from aerobic to anaerobic metabolism, leading to lactic acid buildup and slowed cellular activity.
  • Pre-capillary sphincters close, causing stagnation and coagulation of blood.
  • Post-capillary sphincters also close.
• Decompensated Shock
  • The body's defense mechanisms struggle to maintain perfusion.
  • Body cells are profoundly hypoxic.
  • The body cannot maintain systemic blood pressure.
  • Capillary Stagnation Phase:
    • Lactic acid buildup in cells leaks into capillaries, stimulating the opening of pre-capillary sphincters, which allows stagnated/clotted blood to move into the capillaries.
    • Cell function drops dramatically.
    • Continued closure of post-capillary sphincters causes pressure changes that lead to fluid shifts into the capillaries, dropping circulating blood volume.
• Irreversible Shock
  • The body's defense mechanisms fail to maintain perfusion.
  • Cellular ischemia and necrosis progress to end-organ failure.
  • Death is imminent despite intervention.
  • Capillary Washout Phase:
    • Cell functions cease, and cells die from lack of O_2.
    • Large accumulations of acid force the opening of capillary sphincters, causing sludge, clots, and acid to circulate throughout the body.
    • Organ function fails from profound acidosis and hypoxia.

Types of Shock

• Hypovolemic: diminished blood volume.
• Cardiogenic: inefficient myocardial function.
• Neurogenic: peripheral vasodilation causing decreased resistance and increased pooling.
• Septic.
• Others: anaphylactic, endocrinal, and obstructive shock.

Shock Combinations

• Patients can develop a combination of shock types. For example, a trauma patient may experience:
  • Bleeding leading to hypovolemic shock.
  • Hemopericardium leading to obstructive shock.
  • Cord injury leading to neurogenic shock.

Hypovolemic Shock

• Most common type of shock.
• A person can lose up to 0.5 liter (1 pint) of blood without significant effect.
• After losing 2 liters (3.5 pints), shock symptoms become apparent.
• Losing 3 liters (5 pints) of blood (half the body's normal capacity) leads to the end stages of shock, including loss of consciousness and heart failure.
• Causes:
  • Blood Loss (Hemorrhagic):
    • Traumatic hemorrhage
    • Non-traumatic hemorrhage (e.g., vomiting blood, vaginal bleeding, melena)
  • Fluid Loss (Dehydration):
    • External (e.g., vomiting, diuresis, sweating)
    • Internal (e.g., pancreatitis, peritonitis, bowel obstruction)
• Clinical Presentation:
  • Pulse: weak and rapid
  • BP: hypotension (low blood pressure) – a late sign!
  • Breathing: shallow and rapid
  • Skin: pale, cool, and clammy
  • Mouth: thirst and dry
  • Mental State: early restlessness & anxiety, then late confusion & loss of consciousness
• First Aid:
  • Check (A,B,C): airway, breathing, and circulation
  • Place the person in the shock position: elevate the legs about 12 inches
  • Provide first aid for any wounds or injuries
  • Keep the person warm and comfortable
  • Loosen tight clothing
  • Apply the pneumatic anti-shock garment if possible
  • DO NOT:
    • Elevate the head
    • Give the person anything by mouth
    • Move the person with a suspected spinal injury
    • Wait for symptoms to worsen before calling for medical help
• Treatment:
  • IV Fluid Infusion (venous access):
    1. Crystalloids: e.g., 1000-2000 cc Lactated Ringer over one hour
    2. Blood: after proper matching
    3. Colloids: e.g., plasma, albumin, dextran
  • Oxygen Therapy (Face mask):
    1. Face mask with high O_2 concentration
    2. Endotracheal intubation
    3. Mechanical Ventilation
  • Pain Relief:
    1. Adequate IV Analgesia
    2. Immobilization of fractures early
  • Inotropic Agents:
    1. Used if adequate IV fluids and oxygenation fail to improve the situation
    2. DUPAMINE & DOPUTAMINE are used to improve cardiac contractility
• Monitoring:
  • Vital signs: pulse, BP, temp., and RR
  • Urine output
  • CVP (central venous pressure)
  • ECG
  • Blood gases
  • Laboratory tests

Cardiogenic Shock

• Causes:
  1. Acute myocardial infarction
  2. Arrhythmias
  3. Massive pulmonary embolism
  4. Cardiac tamponade
  5. Myocarditis
• Clinically: Characterized by congested neck veins and elevated CVP.

Neurogenic Shock

• Causes:
  • Cervical or high thoracic spinal cord injury
  • General or spinal anesthesia
  • Drugs: barbiturates, sympathetic blocking agents
• Pathophysiology: Sympathetic denervation inhibits vasomotor signals, causing widespread peripheral vasodilation and hypotension.
• Clinical Presentation:
  • Three classic signs:
    1. Bradycardia: more prominent when injury above T3 (affects sympathetic stimulation of the heart)
    2. Hypotension: secondary to vasodilation
    3. Warm skin: due to peripheral vasodilation (causing venous pooling, similar to septic shock)
  • Additional signs:
    4. Loss of vasomotor tone in periphery
    5. Areflexia below the level of injury
    6. Hypothermia
    7. Warm, dry, flushed skin
• Neurogenic Shock (Vasovagal Attack):
  • Simplest type of neurogenic shock.
  • Due to unpleasant events or severe pain.
  • May follow trauma to the larynx, epigastrium, or testis.
  • Excessive vagal stimulation causes bradycardia (slow heart) and widespread splanchnic dilatation (blood pooling).
  • Treatment: Lie the patient flat with leg elevation, IV fluids & Vasopressor drugs.

Anaphylactic Shock

• Due to antigen-antibody reaction causing rupture of mast cells and release of large amounts of Histamine, resulting in widespread vasodilation.
• Antigens may be drugs (e.g., antibiotics like Penicillin) or plasma.
• Associated signs are bronchospasm, laryngospasm, and cutaneous signs.
• Treatment: Antihistaminics, steroids, fluids, and respiratory support.

Septic Shock

• Causes:
  1. Severe bacterial sepsis leading to toxins.
  2. Gram-negative bacilli are the most common.
  3. Immune suppression such as HIV & steroids.
• Clinical Presentation: Similar to hypovolemic shock, except:
  1. The skin is warm due to fever.
  2. CVP is elevated.
• Prognosis: Up to 90% mortality.