14. SHOCK

Shock is a life-threatening condition where the body fails to supply enough blood and oxygen to vital organs. It is defined as systolic blood pressure below 90 mmHg, or a sudden drop of 40 mmHg from baseline, with signs of poor tissue perfusion despite fluids. Shock leads to cellular hypoxia, organ failure, and if untreated, death.

Types of Shock

1. Hypovolemic Shock

Occurs when there is a major loss of blood or plasma volume. Common causes include:

  • Acute bleeding
  • Severe dehydration (vomiting, diarrhea)
  • Burns
  • Excessive diuretic use
  • Acute pancreatitis

2. Cardiogenic Shock

Caused by failure of the heart to pump blood effectively.

Due to poor emptying:

  • Myocardial infarction
  • Cardiomyopathy
  • Heart rupture or papillary muscle rupture
  • Arrhythmias

Due to poor filling:

  • Cardiac tamponade (fluid around heart)

Due to obstruction:

  • Pulmonary embolism
  • Ball-valve thrombus
  • Tension pneumothorax
  • Dissecting aortic aneurysm

3. Septic Shock

Triggered by severe infections, especially Gram-negative bacteria (E. coli, Klebsiella, Proteus, Pseudomonas). Gram-positive infections can also cause it.

4. Other Variants

  • Traumatic shock: Blood loss + fluid leakage into injured tissues.
  • Neurogenic shock: Loss of sympathetic tone due to spinal cord injury or spinal anesthesia.
  • Hypoadrenal shock: Due to adrenal insufficiency; body cannot respond to stress.

General Pathogenesis

All types of shock share three major problems:

  • Reduced effective blood volume (actual loss or poor cardiac output).
  • Low oxygen delivery causing tissue hypoxia.
  • Inflammatory mediators released during injury worsen cell damage.

1. Reduced Circulating Volume

Occurs from actual blood loss (hypovolemic shock) or reduced cardiac output (cardiogenic/septic shock).

2. Impaired Oxygenation

Low blood flow → low oxygen delivery → cellular injury and dysfunction.

3. Release of Inflammatory Mediators

Cytokines like TNF-α and IL-1 worsen vasodilation, capillary leakage, and cellular damage.

Specific Pathogenesis

Hypovolemic Shock

Results in:

  • Low cardiac output
  • Low blood pressure
  • Fast heart rate
  • Low urine output
  • Altered mental state

Severity depends on blood loss:

  • <1000 mL: compensated
  • 1000–1500 mL: mild
  • 1500–2000 mL: moderate
  • >2000 mL: severe

Cardiogenic Shock

Left ventricular failure → reduced cardiac output → tissue hypoperfusion.

Leads to:

  • Pulmonary edema (fluid in lungs)
  • Severe breathlessness
  • Hypotension

Septic Shock

Triggered by endotoxins from Gram-negative bacteria or toxins from Gram-positive bacteria.

Key mechanisms:

  • Macrophage activation: Endotoxin binds CD14 → release of TNF-α, IL-1.
  • Neutrophil recruitment: Causes free radical injury.
  • Excess nitric oxide: Vasodilation → hypotension.
  • Complement activation: Causes microthrombi.
  • Histamine release: Increases capillary permeability.
  • Kinin system: Produces bradykinin → vasodilation.

Results in warm skin, vasodilation, fluid leakage, inflammatory edema, and risk of DIC.

Stages of Shock

1. Non-Progressive Stage (Compensated)

Body activates protective mechanisms to maintain blood flow:

  • Sympathetic activation → tachycardia, vasoconstriction
  • Renin-angiotensin system → sodium/water retention
  • Increased respiratory rate
  • Fluid movement from tissues to blood

If blood loss is <10%, compensation works. If >30–40%, cells start irreversible injury.

2. Progressive Stage

Compensation fails → tissue hypoxia worsens → metabolic acidosis.

Consequences:

  • Reduced vasomotor tone
  • Increased clotting
  • Cell swelling due to pump failure
  • Organ dysfunction (kidney, liver, lungs, heart)

3. Irreversible Stage

Prolonged hypoxia → cellular death → organ failure → death.

Management of Shock

Hypovolemic Shock

  • Fluid resuscitation (crystalloids)
  • Blood transfusion if needed
  • Treat underlying cause (bleeding, dehydration, burns)

Cardiogenic Shock

  • Treat MI or arrhythmia
  • Inotropes to improve cardiac output
  • Manage pulmonary edema

Distributive / Anaphylactic Shock

  • Give fluids
  • Adrenaline (drug of choice)
  • Antihistamines, steroids

Obstructive Shock

  • Treat cause (pneumothorax, cardiac tamponade, pulmonary embolism)

Septic Shock

  • Broad-spectrum antibiotics
  • IV fluids
  • Vasopressors (noradrenaline)
  • Control source of infection

Detailed Notes:

For PDF style full-color notes, open the complete study material below:

Share your love