Shock – Types, Causes, Signs, and Treatments

Types of Shock:

1.  Hypovolemic Shock:

• • Definition: Low blood volume (hypo-volemic).
  • Causes:
    • Blood loss due to hemorrhage.
    • Fluid loss from severe burns or extensive inflammation.
    • Fluid shift into interstitial spaces (edema) during inflammation, burns, or peritonitis.
    • Dehydration, especially in athletes during heat exposure or lack of acclimatization.
  • Mechanism:
    • Reduced blood volume decreases preload.
    • Leads to poor cardiac output.
    • Heart compensates by increasing sympathetic activity, causing vasoconstriction and raising blood pressure.  Eventually not able to fully compensate and….
  • Effects:
    • Organs receive insufficient oxygen and nutrients.
    • If untreated, causes organ failure.
  • Treatment:
    • Restoring blood volume via IV fluids or blood transfusions.

2.  Cardiogenic Shock:

• • Cause: Heart’s muscle dysfunction.
  • Common causes:
    • Myocardial infarction (heart attack).
    • Arrhythmias that impair contraction.
    • Valvular damage
    • Dissected aorta
    • Cardiac tamponade (fluid in pericardium compressing the heart).
    • Poor ventricular filling (e.g., severe heart damage).
  • Impact:
    • The weakened heart cannot pump blood effectively, leading to decreased stroke volume, low cardiac output and organ hypoperfusion.
  • Treatment:
    • Address underlying causes (e.g., revascularization, arrhythmia control).
    • Supportive therapies to boost cardiac function.

3.  Obstructive Shock:

• • Cause: Physical obstruction in blood flow.
  • Examples:
    • Pulmonary embolism (blockage in lungs).
    • Cardiac tamponade (fluid compresses the heart).
    • Severe aortic or pulmonary artery stenosis (narrowing).
  • Impact:
    • Limit blood flow into or out of the heart.
    • Reduce cardiac output and tissue perfusion.
  • Treatment:
    • Remove or bypass the obstruction (e.g., pericardiocentesis, thrombolysis).

4.  Vasogenic (Distributive) Shock:

• • Cause: Excessive vasodilation causing severe hypotension.
  • Types:
    • Anaphylactic shock: Allergic reaction with massive histamine release causing vasodilation.
    • Septic shock: Infection triggers widespread inflammation and vasodilation.
    • Neurogenic shock: Neuronal impairment (e.g., spinal cord injury) reduces sympathetic tone on blood vessels, and blood vessel dilate.
    • Diabetic shock (hypoglycemia): Severe hypoglycemia causes nervous system failure, resulting in reduced sympathetic tone on blood vessels and vasodilation.
  • Effects:
    • No pressure or flow to tissues, organs become hypoxic.
    • Brain and neurons suffer from lack of oxygen, leading to dizziness, confusion, loss of consciousness, brain death.
  • Signs:
    • Weak, rapid pulse.
    • Anxiety, restlessness, tachycardia.
    • Cool, clammy skin (except in sepsis, where fever may be present).
    • Confusion, dizziness
    • Organ dysfunction (including kidney failure, liver damage and signs of brain hypoxia).
    • Signs of hypoxia: headache, fatigue, decreased responsiveness, coma.
  • Treatment:
    • Epinephrine in anaphylactic shock.
    • Antibiotics in septic shock.

Signs and Symptoms:

• Early: Anxiety, restlessness, tachycardia.
• Progression:
  • Hypotension (low blood pressure).
  • Cold, clammy skin due to vasoconstriction.
  • Decreased urine output.
  • Weak or rapid pulse.
  • Confusion, dizziness, weakness, fatigue.
  • Organ failure (kidneys, liver, lungs, brain) in late stages.
  • Signs of hypoxia, acidosis, and cell death.

Organ Damage & Fatal Outcomes:

• Sluggish blood flow leads to clots.
• Emboli can cause organ infarction (brain, kidney, lungs).
• Metabolic acidosis occurs from anaerobic respiration and lactic acid buildup.
• Kidney failure: due to ischemia and necrosis, with accumulation of waste products (urea, creatinine).

All these effects can lead to multi-organ failure and death if untreated.

Body’s Compensations Mechanisms:

• Neural (sympathetic):
  • Increased heart rate.
  • Venoconstriction to maintain preload.
• Endocrine:
  • Renin-angiotensin-aldosterone system (RAAAS):
    • Kidneys secrete renin → angiotensin II causes vasoconstriction and stimulates aldosterone and ADH secretion.
    • Aldosterone and ADH retains salt and water, increasing blood volume.
  • Antidiuretic hormone (ADH): increases water reabsorption.

Effects: Maintain blood pressure initially but worsens fluid overload if prolonged.

Treatment Strategies and Emergency Response:

1. Hypovolemic Shock:
   • Stop bleeding if present.
   • Restore blood volume with IV fluids or blood transfusions.
2. Anaphylactic Shock:
   • Administer epinephrine (epi-pen).
   • Give antihistamines and anti-inflammatories.
   • Maintain airway and provide oxygen.
3. Septic Shock:
   • Treat underlying infection with antibiotics.
   • Use vasoconstrictors if blood vessels are dilated excessively.
   • Provide oxygen and supportive care.
4. Other supportive measures:
   • Oxygen therapy to maximize oxygen delivery.
   • Vasoactive drugs to restore blood pressure in vasodilatory shock (e.g., vasocontrictors such as epinephrine).
   • Keep patient comfortable and monitor vital signs.

Emergency Response:

• Call 911 immediately.
• Control bleeding and hypoxia.
• Provide fluids, medications, and airway management as needed.
• Can be fatal if not treated.

Summary:

Shock involves inadequate blood flow from various causes: volume loss (hypovolemic), heart failure (cardiogenic), obstructions (obstructive), or abnormal vessel dilation (vasogenic). Treatment centers on restoring blood volume, removing obstructions, and reversing vasodilation, depending on the type. Early recognition and intervention are crucial to prevent organ failure and death.

Shock is a life-threatening condition caused by various mechanisms disrupting blood flow and oxygen delivery. Early recognition, resuscitation, and targeted treatment of the underlying cause are critical to prevent organ failure and death. Proper supportive care, including oxygen and fluids, is essential in managing all types of shock.

Summary Table: