Week 3 - Chapter 20: Shock

Shock Pathogenesis

• Shock is an imbalance between oxygen supply and cellular needs.
• It encompasses a diverse range of life-threatening conditions.
• A common feature is hypoperfusion and impaired cellular oxygen utilization.
• Inadequate cellular oxygenation may stem from decreased cardiac output, maldistributed blood flow, or reduced blood oxygen content.

Shock Causes

• Cardiogenic: Inadequate cardiac output despite sufficient vascular volume.
• Obstructive: Circulatory blockage (e.g., pulmonary embolism, cardiac tamponade) disrupting cardiac output.
• Hypovolemic: Loss of blood volume due to hemorrhage or fluid loss.
• Distributive: Greatly expanded vascular space due to inappropriate vasodilation.

Impaired Tissue Oxygenation

• Impaired oxygen utilization by cells disrupts function, potentially leading to cell death, organ dysfunction, and inflammation.
• Lack of oxygen results in diverse outcomes, including lactate production, cellular swelling, oxygen radical formation, and induction of inflammatory cytokines.
• Cellular hypoxia leads to anaerobic metabolism, free radical production, macrophage induction, and potential reperfusion injury.
• Tumor necrosis factor-α (TNF-α) and interleukin-1 (IL-1) cytokines increase in septic shock.
• They mediate vascular failure and progressive organ damage.
• Increased nitric oxide (NO) synthase activity can lead to excess NO, impacting microcirculation autoregulation, and activating coagulation, which further impacts oxygen debt in tissues.

Compensatory Mechanisms and Stages of Shock

• Shock progresses through compensated, progressive, and refractory stages.
• In the compensatory stage, homeostatic mechanisms maintain adequate tissue perfusion despite reduced cardiac output (CO).
• Sympathetic nervous system (SNS) activation attempts to maintain blood pressure even when cardiac output falls.
• CO and vascular resistance both increase.
• The progressive stage is marked by hypotension and tissue hypoxia.
• Lactate production rises with anaerobic metabolism.
• Organ dysfunction is caused by cellular swelling and death, oxygen-free radicals, inflammatory cytokines, and clotting cascade activation.

Types of Shock

Cardiogenic Shock

• Characterized by low cardiac output (CO), reducing oxygen delivery to tissues and increasing oxygen extraction.
• Therapy focuses on improving CO, reducing workload, and optimizing myocardial oxygen delivery via inotropic, preload-reducing, and afterload-reducing agents; intra-aortic balloon counterpulsation; ventricular assist devices; and, in severe cases, heart transplantation.

Obstructive Shock

• Resulting from mechanical obstructions preventing adequate cardiac filling which reduce stroke volume.
• Common causes include pulmonary embolism, cardiac tamponade, and tension pneumothorax.
• Manifests as right-sided heart failure, necessitating rapid management of the obstruction to prevent cardiovascular collapse.

Hypovolemic Shock

• Results from inadequate circulating blood volume due to hemorrhage, burns, or fluid loss into interstitial spaces.
• External hemorrhage is a frequent cause.
• Low CO and reduced intracardiac pressures trigger SNS activation, causing increased heart rate (HR), vasoconstriction, and increased contractility.
• Therapy involves fluid replacement and controlling the source of volume loss, using colloids and crystalloids, as well as blood products.
• The severity of the shock correlates to the volume of blood loss.

Distributive Shock

• Excessive vasodilation and peripheral blood pooling, reducing preload for the heart.
• Different types: anaphylactic, neurogenic, and septic.

Anaphylactic Shock

• Result of mast cell degranulation triggered by antigens (e.g., medications, insect bites).
• Mast cells release vasodilatory mediators, leading to severe hypotension.
• Treatment includes maintaining airway patency, using epinephrine, bronchodilators, antihistamines, vasopressors, and intravenous (IV) fluids.

Neurogenic Shock

• Resulting from loss of sympathetic activation of arteriolar smooth muscles.
• Caused by medullary depression, or spinal cord injury.
• Treatment includes vasopressors, fluids, elevation of extremities/position changes, and use of pressure stockings as needed.

Septic Shock

• Resulting from a severe systemic inflammatory response to infection (bacteria, fungi).
• Characterized by the release of immune mediators resulting in widespread inflammation.
• The clotting cascade, complement system, and kinin system are triggered leading to widespread inflammation, peripheral vasodilation, hypotension, and maldistribution of blood flow resulting in cellular hypoxia, increased capillary pressure, and edema formation.
• Therapy involves improving blood flow distribution, managing infection with antibiotics, and administering fluids and drugs to improve cardiac/vascular performance.

Assessment and Hemodynamic Monitoring

• Monitoring helps evaluate cardiac output (CO), volume status, and oxygen delivery.
• Techniques include monitoring right atrial pressure, pulmonary artery pressure, left atrial pressure, etc.
• Used to guide management of cardiac preload, afterload, and contractility to optimize CO and minimize workload.

Complications of Shock

• Various complications can result from shock, including:
  • Acute Respiratory Distress Syndrome (ARDS): Characterized by refractory hypoxemia, decreased pulmonary compliance, pulmonary edema, multiple organ failure, not necessarily severe hypoxemia.
  • Disseminated Intravascular Coagulation (DIC): Immune activation of the clotting cascade, leading to microcirculation obstructions that cause ischemic tissue damage. Widespread clot formation consumes platelets and clotting factors. Fibrin degradation products (e.g., D-dimer) increase.
  • Acute Renal Failure (ARF): Kidneys undergo long periods of hypoperfusion; vasoconstriction reduces glomerular blood flow and filtration rates. Associated with acute tubular necrosis (ATN), reduced urinary excretion of waste products (creatinine and urea), possible dialysis requirement.
  • Multiple Organ Dysfunction Syndrome (MODS): When two or more organ systems are affected. It's most commonly caused by sepsis or septic shock. Immune mechanisms become overactive and destructive, cytokines affect the endothelium, recruit neutrophils, and activate inflammation resulting in tissue destruction and organ dysfunction. Inflammatory cytokines cause extensive damage, altering metabolism and recruiting neutrophils while initiating the coagulation cascade, and causing capillary permeability changes.