Types of Shock in Medicine

Shock

• Shock is hypoperfusion to tissues, leading to hypotension, impaired tissue perfusion, and cellular hypoxia.
• The initial hypoxic and metabolic effects of hypoperfusion cause only reversible cellular injury.
• However, persistent shock causes irreversible tissue injury and can result in the patient's death.

Types of Shock

• Cardiogenic shock: Failure of the heart's pumping mechanisms. This is typically due to myocardial infarction, ventricular rupture, arrhythmia, cardiac tamponade, or pulmonary embolism.
• Hypovolemic shock: Inadequate blood or plasma volume. Common causes include hemorrhage, fluid loss (e.g., vomiting, diarrhea, burns, or trauma).
• Septic shock: Overwhelming microbial infections (e.g., endotoxic shock, gram-positive septicemia, fungal sepsis, or superantigens). This causes peripheral vasodilation, endothelial activation/injury, leukocyte-induced damage, disseminated intravascular coagulation (DIC), and cytokine cascades.
• Neurogenic shock: Loss of vascular tone and peripheral pooling of blood; less common. It can be caused by anesthetic accidents or spinal cord injuries.
• Anaphylactic shock: Systemic vasodilation and increased vascular permeability due to an immunoglobulin E hypersensitivity reaction.

Pathogenesis of Septic Shock

• Septic shock has a mortality rate of 25% to 50%.
• Most cases are caused by endotoxins, commonly lipopolysaccharides (LPS) produced by gram-negative bacilli.
• Free LPS attaches to a circulating LPS-binding protein, forming a complex that attaches to a specific receptor (CD14) on monocytes, macrophages, and neutrophils.
• This results in profound activation and production of potent cytokines, such as IL-1 and TNF.
• These cytokines then act on endothelial cells, causing additional cytokine production (e.g., IL-6 and IL-8), inducing adhesion molecules, and widespread endothelial injuries and activation. Consequently, systemic leukocyte adhesion and diffuse alveolar capillary damage occur in the lungs.
• Further, cytokine activation can lead to DIC.
• The combined effects of widespread vasodilation, myocardial pump failure, and DIC cause multiorgan system failure, impacting the liver, kidneys, central nervous system, and others.

Stages of Shock

• Initial (nonprogressive) stage: Reflex compensatory mechanisms are activated to maintain vital organ perfusion.
• Progressive stage: If the underlying causes are not addressed, shock progresses to widespread tissue hypoxia, which initiates anaerobic glycolysis, leading to substantial lactic acid production. This results in lactic acidosis which lowers the tissue pH and reduces the effectiveness of the vasomotor response.
• Irreversible stage: Severe cellular and tissue injury causes widespread effects, making survival impossible even if the hemodynamic issues are addressed.

Early Phase of Shock

• Various neurohumoral mechanisms maintain cardiac output and blood pressure in the early phase of shock.
• These mechanisms include baroreceptor reflexes, catecholamine release, renin-angiotensin axis activation, antidiuretic hormone release, and generalized sympathetic stimulation.
• The net effect is tachycardia, peripheral vasoconstriction, and renal fluid conservation.

Clinical Course of Shock

• In hypovolemic and cardiogenic shock, patients exhibit hypotension, weak rapid pulse, tachypnea, and cool, clammy, cyanotic skin.
• In contrast, septic shock may involve warm, flushed skin due to peripheral vasodilation.

Morphological Changes

• Cellular and tissue changes in shock are hypoxic injuries caused by hypoperfusion and microvascular thrombosis.

• Shock is characterized by organ system failure; morphological changes are notably obvious in the brain, heart, kidneys, adrenal glands, and gastrointestinal tract.

• Fibrin thrombi commonly observed in kidney glomeruli.

• Acute tubular necrosis, oliguria, anuria, and electrolyte disturbances are often present in the kidneys.

• Focal mucosal hemorrhage and necrosis can appear in the gastrointestinal tract.

• Lungs are generally not affected in hypovolemic shock but may be affected by diffuse alveolar damage (shock lung) in other types of shock, such as sepsis or trauma.