Ch14 Shock

Overview of Shock and Sepsis

• Shock: A life-threatening syndrome where the circulatory system cannot supply adequate oxygen to tissues, leading to tissue hypoxia.

  • Consequences: May result in organ system failure and death.

  • Critical Assessment Metrics:

    • Cardiac output (CO)

    • Oxygen delivery (DO2)

    • Oxygen consumption

    • Oxygen debt

Cardiac Output

• Definition: Amount of blood ejected by the heart per minute.

  • Calculated as a function of stroke volume and heart rate (HR).

• Preload: Blood volume in the ventricles at the end of diastole.

  • Significance: Indicates patient’s fluid volume status.

Factors Affecting Cardiac Output

• Afterload: Resistance the ventricle faces to eject blood.

  • Increased afterload complicates blood ejection.

• Contractility: Strength of heart contractions.

  • Poor contractility results in decreased stroke volume and cardiac output.

Oxygen Delivery

• Oxygen Delivery (DO2): Amount of oxygen sent to tissues.

• Assessment: Evaluated through cardiac output and arterial oxygen content.

  • Includes hemoglobin levels, saturation percentage, and dissolved oxygen (PaO2).

Classifications of Shock

1. Hypovolemic Shock:

   • Result of rapid fluid loss reducing circulating volume.

   • Causes include trauma or severe GI bleeding.

2. Cardiogenic Shock:

   • Inadequate heart pumping, often from a heart attack.

3. Distributive Shock:

   • Occurs due to poor vascular tone (sepsis, anaphylaxis).

4. Obstructive Shock:

   • Caused by barriers to heart filling/emptying (e.g., cardiac tamponade).

Stages of Shock

Compensatory Stage

• Neural Compensation:

  • Baroreceptors trigger sympathetic nervous system leading to catecholamine release, increasing HR and contractility.

  • Causes vasoconstriction, reallocating blood to vital organs.

• Endocrine Compensation:

  • Kidneys release renin leading to angiotensin production which promotes vasoconstriction and fluid retention.

• Chemical Compensation:

  • Hypoxia triggers hyperventilation (tachypnea).

Progressive Stage

• Compensatory Mechanism Failure: Inability to maintain adequate blood pressure; leads to worsened acidosis.

• Shunting to Vital Organs: Low perfusion leading to potential organ damage.

Refractory Stage

• Conditions: Continuous inadequate blood supply, resulting in cell death and multi-organ failure.

• Irreversible state due to loss of aerobic metabolism.

Assessment by Organ System

• CNS: Indicators include restlessness, confusion, potential progress to coma due to low oxygen.

• Cardiovascular: Signs of hypotension, narrow pulse pressure, tachycardia that may shift to bradycardia.

• Respiratory: Tachypnea, metabolic acidosis impact on breathing.

• Renal: Oliguria leading to anuria, increased creatinine levels.

• Gastrointestinal: Hypoactive bowel sounds, nausea, vomiting.

Hemodynamic Monitoring

• Methods to assess cardiac function:

  • Arterial line: Continuous BP display, easy access for sample collection.

  • Pulmonary artery catheter: Monitors variables affecting cardiac output.

Hypovolemic Shock

• Causes: Blood loss (trauma, GI bleeding), rapid fluid losses (vomiting, burns).

• Pathophysiology: Leads to decreased stroke volume and cardiac output due to loss of volume.

• Clinical Manifestations: Confusion, low urine output, cold clammy skin, weak pulses.

• Management:

  • Medical: Optimize oxygenation, fluid resuscitation, identify and treat causes.

  • Nursing: Ongoing assessments, patient vitals monitoring, and necessary lab tests.

Cardiogenic Shock

• Epidemiology: Occurs in 5-10% of acute MI patients, with a 50% mortality rate.

• Pathophysiology: Results in decreased cardiac output with increased myocardial oxygen demand.

• Clinical Signs: Chest pain, decreased LOC, weak pulses.

• Management: Emergency interventions and hemodynamic support.

Obstructive Shock

• Causes: Mechanical barriers impairing heart filling (e.g., pulmonary embolism).

• Clinical Features: Decreased consciousness, cool skin, chest pain.

• Management: Immediate treatment of underlying cause, oxygen support.

Distributive Shock

Neurogenic Shock

• Caused by sympathetic system disruption leading to hypotensive conditions.

Anaphylactic Shock

• Severe allergic reactions with widespread vasodilation.

Sepsis/Septic Shock

• Epidemiology: High occurrence with significant mortality rates, especially in older populations in ICUs.

• Pathophysiology: Deregulated response to infections, leading to pro-inflammatory responses and vascular changes.

• Management: Emphasis on prevention, rapid identification, and comprehensive management plans following established guidelines.