Types and Stages of Shock

Types of Shock

• Hypovolemic shock
• Cardiogenic shock
• Obstructive shock
• Distributive shock

Stages of Shock

• Initial stage: MAP decreased less than 10 mm Hg from baseline, slight increase in heart and respiratory rate, adaptive responses like vascular constriction and increased heart rate
• Nonprogressive stage: Compensatory phase, MAP decreases by 10-15 mm Hg, kidney and hormonal adaptive mechanisms activated, tissue hypoxia in nonvital organs, acidosis
• Progressive stage: Sustained decrease in MAP greater than 20 mm Hg from baseline, vital organs develop hypoxia, life-threatening, immediate intervention needed within 1 hour of onset
• Refractory stage: Too much cell death and tissue damage due to low oxygen reaching tissues, body can no longer respond to interventions, irreversible cell and tissue death

Multiple Organ Dysfunction Syndrome (MODS)

• Metabolites released from dead cells
• Microthrombi formation throughout the body, location depends on specific circumstances of infection and individual's health
• MODS occurs first in liver, heart, brain, and kidneys

Hypovolemic Shock

• Intravascular volume decreased
• MAP stimulates baroreceptors
• SNS stimulation leading to tachycardia and increased contractility, temporarily increasing cardiac output
• Coronary arteries dilate, decreasing blood pressure
• Reduced tissue perfusion

Causes of Hypovolemic Shock

• Hemorrhage
• Dehydration
• Fluid shifts (trauma, burns)

Treatment for Hypovolemic Shock

• Control source of blood loss
• Replenish lost volume
• Colloids (Albumin, Dextran, Hetastarch) to increase serum osmotic pressure
• Crystalloids (Normal Saline, Lactated Ringers) to increase blood pressure
• Blood products (Packed RBCs, Whole Blood) to replace lost blood

Cardiogenic Shock

• Actual heart muscle is unhealthy and pumping is directly impaired.
• Myocardial infarction is the most common cause

Clinical Manifestations of Cardiogenic Shock

• Tachycardia
• Decreased cardiac output
• Low blood pressure
• Narrowing pulse pressure
• Vasoconstriction
• Crackles

Treatment of Cardiogenic Shock

• Beta-adrenergic agonists (Norepinephrine, Dobutamine, Dopamine)
• Dopamine (low dose): dilates renal and mesenteric arteries, increases renal perfusion
• Moderate doses of dopamine: increases heart rate, contractility, and cardiac output.
• High doses: increases vasoconstriction
• Vasodilators: decrease workload, preload, and afterload of the heart (e.g., Nitroprusside, Nitroglycerin)

Mechanical Assist Devices

• Intra-aortic balloon pump (IABP)
• Mobility restricted, pedal pulses

Obstructive Shock

• Caused by problems that impair the ability of the heart muscle to pump effectively
• Caused by: Pulmonary embolism, Cardiac tamponade

Treatment for Obstructive Shock

• Pulmonary Embolism: Heparin, Fibrinolytic therapy (Streptokinase, Alteplase)
• Cardiac Tamponade: Pericardiocenthesis, Pericardial window, drain

Distributive Shock

• Pathogenesis of Septic Shock:
  • Local infection → Systemic infection → SIRS → Sepsis → Organ Failure → Septic Shock → Death

Severe Sepsis

• All tissues have some degree of hypoxia
• Microthrombi formation is extensive
• Amplified systemic inflammatory response
• Anaerobic metabolism continues

Septic Shock

• Most common cause of death in non-cardiac ICUs in the US
• Nosocomial infections are common
• Increased risk with advanced invasive technology, especially in the elderly
• Mortality rate: 40%-85%

Septic Shock: Interventions

• Blood cultures
• Antibiotic therapy (Vancomycin, Aminoglycosides, Penicillins, Cephalosporins)
• Oxygen therapy

Anaphylactic Shock

• Allergic/Antigen-Antibody reaction
• Histamines, Leukotrienes released
• Bronchoconstriction
• Peripheral vasodilation

Treatment for Anaphylactic Shock

• Airway management (bronchodilators, e.g., Albuterol)
• Epinephrine to stabilize mast cells and increase BP
• IV therapy with Normal Saline to increase vascular volume
• Steroids (e.g., Methylprednisolone) to decrease inflammation