Shock Sections

Pathogenesis of Shock

• Shock: Insufficient delivery of oxygenated blood to the microcirculation.
• Common factor among all types of shock is hypoperfusion and impaired cellular oxygen utilization.
• Results in tissue hypoxia and cellular dysfunction/death and stimulates inflammatory reactions.
• Characterization:
  • O2 Supply less than O2 Demand
  • Impaired tissue oxygenation
  • Inflammation
  • Cell death
  • Vascular dysregulation

Shock at a Cellular Level

• Shock at the cellular level involves a cascade of events:
  • Pump failure, hypovolemia, and vasodilation lead to impaired tissue oxygenation.
  • Cellular hypoxia results in:
    • Anaerobic metabolism
    • Lactic acidosis
    • Free radical production
    • Inhibition of the $Ca^{2+}$ pump, leading to increased intracellular $Ca^{2+}$.
    • Inhibition of the $(Na^+ - K^+)$ pump, leading to hydropic swelling.
    • Impaired membrane integrity and release of enzymes, ultimately causing cell death.
  • The cellular dysfunction stimulates:
    • Macrophage induction and release of cytokines.
    • Vascular dysregulation and activation of coagulation.
    • Recruitment of neutrophils.

Compensatory Mechanisms

• Compensatory mechanisms are triggered to help maintain arterial blood pressure despite a fall in cardiac output.
• Attempt to restore adequate perfusion pressure.
• Mechanisms:
  • Baroreceptors
  • RAAS (Renin-Angiotensin-Aldosterone System)

Types of Shock

• Cardiogenic
• Hypovolemic
• Obstructive
• Distributive
  • Septic
  • Anaphylactic
  • Neurogenic

Cardiogenic Shock

• Result of ventricular dysfunction.
• Causes:
  • Usually result of severe ventricular dysfunction associated with MI (Myocardial Infarction).
  • Other causes: cardiomyopathy, papillary muscle rupture, congenital heart defects.
• Low cardiac output due to high left ventricular diastolic filling pressure.
• High left ventricular preload leads to movement of fluid from the pulmonary vascular beds into the pulmonary interstitial space, resulting in interstitial pulmonary edema → alveolar pulmonary edema.
• Compensation makes things much worse by increasing the preload and the afterload.
• Clinical Manifestations:
  • SNS (Sympathetic Nervous System) increases the heart rate and vascular resistance to maintain blood pressure even though cardiac output has decreased.
  • Peripheral vasoconstriction produces cool, clammy skin.
  • Auscultation of the lungs reveals coarse crackles resulting from pulmonary edema.

Hypovolemic Shock

• Circulating blood volume inadequate to perfuse tissues.
• Result of internal or external volume losses.
• $\downarrow$ Intravascular volume → $\downarrow$ Venous return → $\downarrow$ CO (Cardiac Output) → $\downarrow$ $O_2$ → Cell Injury
• Blood volume loss leads to low blood volume circulating and low venous return, resulting in reduced preload and CO.
• Low intracardiac pressures (low preload) lead to SNS activation = elevated HR, vasoconstriction, increased contractility.

Obstructive Shock

• Filling of the left ventricle is physically impeded, preventing effective cardiac filling and stroke volume.
• Causes:
  • Pulmonary embolism
  • Cardiac tamponade
  • Tension pneumothorax
• Signs and symptoms similar to cardiogenic shock.
• Treatment:
  • Identify and remove the obstruction.

Distributive (Vasodilatory) Shock

• Characterized by excessive vasodilation and peripheral pooling of blood.
• Extreme vasodilation impedes venous return.
• Not enough blood to fill the circulatory system.
• Blood flow decreases.
• Less blood is returned to the heart – preload drops.
• Less blood is circulated to the body.
• Widespread Vasodilation leads to VERY low Resistance and $\downarrow$ $O<em>2$ - Blood moving too fast to unload $O</em>2$, resulting in Cell inadequately perfused.
• Three forms:
  • Septic Shock
    • Most common
    • Due to infection
  • Anaphylactic Shock
    • Allergic reaction
  • Neurogenic Shock
    • Neurological

Septic Shock

• Organism is most-often gram-negative bacterium, but gram-positive bacterium and fungi are also causative.
• Predisposition: invasive lines, catheters, surgery, immunosuppressive therapy.
• Inflammatory response to infection in immunocompromised individual.
  • Complement cascade
  • Coagulation cascade
  • Kinin cascade- Bradykinin→ vasodilation
  • Histamine release by mast cells
• Causes systemic signs of inflammation:
  • Fever, increased respiration, respiratory alkalosis, vasodilation, warm flushed skin
• Late stage: CO drops and organ ischemia occurs
• Progression:
  • Suspected or confirmed infection → Systemic inflammatory response → Diffuse endothelium disruption and impaired microvascular function → Severe sepsis with organ dysfunction (Hypotension, hypoxemia, oliguria, metabolic acidosis, thrombocytopenia) → Septic Shock

Anaphylactic Shock

• Systemic response to inflammatory mediators released in Type I hypersensitivity.
• Involves antigen/immunoglobulin E (IgE) antibody reaction on the surface of mast cells and basophils.
• Allergic reaction leading to Low Blood Pressure
• Histamine, acetylcholine, kinins, leukotrienes, and prostaglandins all cause vasodilation.
• Acetylcholine, kinins, leukotrienes, and prostaglandins all cause bronchoconstriction.

Neurogenic Shock

• Failure of the baroreceptor response.
• Depression of the vasomotor center in the medulla.
• Interruption of sympathetic fibers from spinal cord.
• Due to trauma, spinal anesthesia, drug overdose.
• Damaged central nervous system leading to Low Blood Pressure.

Complications of Shock

• Acute lung injury/respiratory distress syndrome
• Acute kidney injury
• Gastrointestinal complications
• Disseminated intravascular coagulation
• Multiple organ dysfunction syndrome (MODS) - progressive organ dysfunction (2 or more) not involved in the disorder that resulted in the ICU admission.
  • The most frequent cause of death in the noncoronary intensive care unit.
  • Mortality rates vary from 30-100%.
  • Mechanism not known.