In-depth Notes on Shock and Sepsis

Introduction to Shock and Sepsis

• Shock: Life-threatening syndrome where the circulatory system is unable to provide adequate oxygen to tissues:

  • Results in tissue hypoxia.

  • Potentially leads to organ system failure and death.

  • Critical parameters to assess:

  • Cardiac Output (CO)

  • Oxygen Delivery (DO2)

  • Oxygen Consumption

  • Oxygen Debt

Cardiac Output (CO)

• Defining CO:

  • CO: Volume of blood ejected by the heart per minute.

  • Function of Stroke Volume and Heart Rate (HR).

• Key Terms Related to CO:

  • Preload: Volume of blood in ventricles at end of diastole, indicating fluid volume status.

  • Afterload: Resistance the heart must overcome to eject blood (high afterload makes ejection harder).

  • Contractility: Force of heart's contractions; poor contractility decreases stroke volume and CO.

Oxygen Delivery (DO2)

• DO2: Amount of oxygen delivered to tissues, assessed by evaluating:

  • CO and arterial oxygen content.

• Arterial Oxygen Content includes:

  • Hemoglobin levels

  • Hemoglobin saturation percentage

  • Amount of oxygen dissolved in plasma (PaO2).

Classifications of Shock

1. Hypovolemic Shock:

   • Caused by rapid fluid loss (e.g., trauma, GI bleed).

2. Cardiogenic Shock:

   • Inadequate heart pumping usually from heart attack.

3. Distributive Shock:

   • Resulting from conditions such as sepsis or anaphylaxis that cause vasodilation and low vascular tone.

4. Obstructive Shock:

   • Mechanical barriers to heart filling/emptying, e.g., cardiac tamponade, tension pneumothorax.

Stages of Shock

1. Compensatory Stage:

• Neural Compensation:

  • Baroreceptor detection of hypotension stimulates sympathetic nervous system; increases heart rate, contractility, and blood pressure.

• Endocrine Compensation:

  • Kidneys release renin → Angiotensin I → Angiotensin II (vasoconstrictor) and stimulates aldosterone release, promoting sodium and water retention.

• Chemical Compensation:

  • Chemoreceptors react to low oxygen, causing tachypnea to increase oxygen levels.

2. Progressive Stage:

• Compensatory mechanisms fail; results in profound hypoperfusion, metabolic and respiratory acidosis due to extensive blood shunting.

3. Refractory Stage:

• Irreversible cell death leading to multisystem organ failure; primarily anaerobic metabolism with loss of aerobic metabolism.

System Assessment

CNS:

• Signs of hypoperfusion include restlessness, confusion, lethargy; may lead to coma if untreated.

Cardiovascular:

• Early signs: hypotension, narrowed pulse pressure, tachycardia leading to bradycardia.

• Skin color, peripheral pulse quality, capillary refill as indicators of perfusion status.

Respiratory:

• Tachypnea to combat acidosis, possibly difficulty obtaining pulse oximetry readings due to poor circulation.

Renal:

• Oliguria progressing to anuria; increased creatinine levels indicating renal impairment.

Gastrointestinal:

• Hypoactive bowel sounds, nausea, and vomiting.

Hemodynamic Monitoring

• Arterial Line: Continuous blood pressure display and easy access for blood analysis.

• Pulmonary Artery Catheter: Provides detailed cardiac output/readings on preload, afterload, and contractility.

• Central Venous Catheter: Allows CVP monitoring.

Hypovolemic Shock

• Causes: Acute blood loss, rapid fluid loss (vomiting, diarrhea).

• Pathophysiology: Loss of volume leads to decreased venous return, resulting in decreased stroke volume and cardiac output, causing decreased tissue perfusion.

• Clinical Manifestations: Restlessness, confusion, decreased urine output, poor skin perfusion, metabolic acidosis.

• Management: Focus on airway, breathing, fluid resuscitation, treat underlying causes.

• Nursing Considerations: Regular assessment of vital signs, neurological status, and hemodynamic readings. Monitor laboratory results for ABGs and lactate levels.

Cardiogenic Shock

• Epidemiology: 5%-10% of acute MI patients; high mortality rate.

• Pathophysiology: Decreased cardiac output leading to hypotension and increased myocardial workload.

• Clinical Manifestations: Chest pain, fatigue, decreased output, metabolic acidosis.

• Management: ECG, airway management, emergency revascularization and use of medications like inotropes and vasopressors.

• Nursing Considerations: Monitor neurological status, vital signs, skin response, urine output and teach about disease management.

Obstructive Shock

• Causes: Mechanical barriers (e.g., pulmonary embolism, cardiac tamponade).

• Clinical Manifestations: Hypotension, decreased LOC, tachycardia, poor skin perfusion.

• Management: Treat underlying cause, supportive therapies including fluids and vasopressors.

Distributive Shock

1. Neurogenic Shock:

   • Caused by spinal cord injury; presents with warm, dry skin and bradycardia.

2. Septic Shock:

   • Due to infection causes systemic inflammatory response leading to vasodilation.

   • Early management is crucial; employ the 'Hour 1' bundle of care - blood work, cultures, and timely antibiotics.

Sepsis and Septic Shock

• Epidemiology: 437 cases/100,000 with high mortality in ICU settings.

• Pathophysiology: Host response failure to infection causing systemic issues.

• Clinical Signs: Spectrum from tachycardia and fever to hypotension and altered mental status.

• Management: Emphasis on prevention and rapid response with antibiotics and fluid resuscitation.

• Evaluate Outcomes: Monitor vital signs, hemodynamic response, and tissue perfusion.

Classifications of Shock

1. Hypovolemic Shock:

   • Causes: Rapid fluid loss can occur due to trauma, gastrointestinal (GI) bleeding, severe dehydration from vomiting or diarrhea. Inadequate intake or excessive loss leads to reduced blood volume.

   • Pathophysiology: Decreased circulating volume results in diminished venous return to the heart, leading to reduced stroke volume and cardiac output. Tissues become hypoperfused, causing metabolic acidosis due to inadequate oxygen delivery.

   • Clinical Manifestations: Patients may present with restlessness, confusion, decreased urine output (oliguria), poor skin perfusion (cool, clammy skin), and may exhibit symptoms of metabolic acidosis (e.g., increased respiratory rate).

   • Management: Focus on maintaining airway and breathing, aggressive fluid resuscitation with crystalloids or blood products, and addressing the underlying cause of fluid loss (control of hemorrhage, treat GI losses).

   • Nursing Considerations: Regular assessment of vital signs (HR, BP), neurological status (level of consciousness), and hemodynamic readings (CVP, MAP). Monitor laboratory results for arterial blood gases (ABGs) and lactate levels to evaluate metabolic status.

2. Cardiogenic Shock:

   • Epidemiology: Occurs in 5%-10% of acute myocardial infarction (MI) cases; associated with a high mortality rate (up to 70% if untreated).

   • Pathophysiology: Impaired cardiac output results from the heart's inability to pump effectively, which leads to hypotension and compensatory mechanisms that increase myocardial oxygen demand yet fail to improve perfusion.

   • Clinical Manifestations: Chest pain, fatigue, decreased urine output, altered mental status, and signs of poor perfusion (such as cold extremities and altered skin color). Patients may demonstrate signs of metabolic acidosis due to lactic acid build-up.

   • Management: Immediate ECG monitoring, airway management, emergency revascularization procedures (angioplasty, thrombolytics), and medications like inotropes to enhance contractility and vasopressors to increase systemic vascular resistance.

   • Nursing Considerations: Continuous monitoring of neurological status, vital signs, skin changes, urine output; educate patients on disease processes and self-management post-stabilization.

3. Distributive Shock:

   • Classification: Includes neurogenic, septic, and anaphylactic shock.

   • Neurogenic Shock:

     • Cause: Often results from spinal cord injury leading to loss of sympathetic tone.

     • Clinical Manifestations: Observed with warm, dry skin, bradycardia, and hypotension due to vasodilation. Patients may not compensate with tachycardia due to impaired sympathetic response.

     • Management: Maintain spinal alignment, intravenous fluid management, and administration of vasopressors to restore vascular tone.

   • Septic Shock:

     • Pathophysiology: Resulting from overwhelming infection and systemic inflammatory response syndrome (SIRS), leading to vasodilation and relative hypovolemia despite adequate or high cardiac output.

     • Clinical Signs: Patients may present with fever, tachycardia, varying levels of consciousness, hypotension, and possibly cool, mottled extremities.

     • Management: Emphasize prevention strategies and rapid response; initiate the 'Hour 1' bundle of care for sepsis, which includes ordering blood work, obtaining cultures, administering broad-spectrum antibiotics, and aggressive fluid resuscitation with crystalloids.

   • Anaphylactic Shock:

     • Cause: Severe allergic reaction due to exposure to allergens (e.g., medications, food).

     • Clinical Manifestations: Rapid onset of symptoms such as urticaria, angioedema, respiratory distress, and hypotension.

     • Management: Immediate administration of epinephrine, antihistamines, and corticosteroids; establish airway and provide supplemental oxygen as needed.

4. Obstructive Shock:

   • Causes: Mechanical obstruction impedes cardiac filling or ejection; includes conditions such as pulmonary embolism, cardiac tamponade, or tension pneumothorax.

   • Clinical Manifestations: Patients may show signs of hypotension, decreased level of consciousness, tachycardia, and exhibit poor skin perfusion highlighting reduced cardiac output.

   • Management: Treatment focuses on resolving the underlying obstruction (e.g., decompression in tension pneumothorax or removal of a thrombus in pulmonary embolism).

   • Nursing Considerations: Monitor vital signs, assess peripheral perfusion, manage patient discomfort, and prepare for possible surgical interventions if necessary.

Classifications of Shock

1. Hypovolemic Shock:

   • Causes: Rapid fluid loss can occur due to trauma, gastrointestinal (GI) bleeding, severe dehydration from vomiting or diarrhea. Inadequate intake or excessive loss leads to reduced blood volume.

   • Pathophysiology: Decreased circulating volume results in diminished venous return to the heart, leading to reduced stroke volume and cardiac output. Tissues become hypoperfused, causing metabolic acidosis due to inadequate oxygen delivery.

   • Clinical Manifestations: Patients may present with restlessness, confusion, decreased urine output (oliguria), poor skin perfusion (cool, clammy skin), and may exhibit symptoms of metabolic acidosis (e.g., increased respiratory rate).

   • Management: Focus on maintaining airway and breathing, aggressive fluid resuscitation with crystalloids or blood products, and addressing the underlying cause of fluid loss (control of hemorrhage, treat GI losses).

   • Nursing Considerations: Regular assessment of vital signs (HR, BP), neurological status (level of consciousness), and hemodynamic readings (CVP, MAP). Monitor laboratory results for arterial blood gases (ABGs) and lactate levels to evaluate metabolic status.

2. Cardiogenic Shock:

   • Epidemiology: Occurs in 5%-10% of acute myocardial infarction (MI) cases; associated with a high mortality rate (up to 70% if untreated).

   • Pathophysiology: Impaired cardiac output results from the heart's inability to pump effectively, which leads to hypotension and compensatory mechanisms that increase myocardial oxygen demand yet fail to improve perfusion.

   • Clinical Manifestations: Chest pain, fatigue, decreased urine output, altered mental status, and signs of poor perfusion (such as cold extremities and altered skin color). Patients may demonstrate signs of metabolic acidosis due to lactic acid build-up.

   • Management: Immediate ECG monitoring, airway management, emergency revascularization procedures (angioplasty, thrombolytics), and medications like inotropes to enhance contractility and vasopressors to increase systemic vascular resistance.

   • Nursing Considerations: Continuous monitoring of neurological status, vital signs, skin changes, urine output; educate patients on disease processes and self-management post-stabilization.

3. Distributive Shock:

   • Classification: Includes neurogenic, septic, and anaphylactic shock.

   • Neurogenic Shock:

     • Cause: Often results from spinal cord injury leading to loss of sympathetic tone.

     • Clinical Manifestations: Observed with warm, dry skin, bradycardia, and hypotension due to vasodilation. Patients may not compensate with tachycardia due to impaired sympathetic response.

     • Management: Maintain spinal alignment, intravenous fluid management, and administration of vasopressors to restore vascular tone.

   • Septic Shock:

     • Pathophysiology: Resulting from overwhelming infection and systemic inflammatory response syndrome (SIRS), leading to vasodilation and relative hypovolemia despite adequate or high cardiac output.

     • Clinical Signs: Patients may present with fever, tachycardia, varying levels of consciousness, hypotension, and possibly cool, mottled extremities.

     • Management: Emphasize prevention strategies and rapid response; initiate the 'Hour 1' bundle of care for sepsis, which includes ordering blood work, obtaining cultures, administering broad-spectrum antibiotics, and aggressive fluid resuscitation with crystalloids.

   • Anaphylactic Shock:

     • Cause: Severe allergic reaction due to exposure to allergens (e.g., medications, food).

     • Clinical Manifestations: Rapid onset of symptoms such as urticaria, angioedema, respiratory distress, and hypotension.

     • Management: Immediate administration of epinephrine, antihistamines, and corticosteroids; establish airway and provide supplemental oxygen as needed.

4. Obstructive Shock:

   • Causes: Mechanical obstruction impedes cardiac filling or ejection; includes conditions such as pulmonary embolism, cardiac tamponade, or tension pneumothorax.

   • Clinical Manifestations: Patients may show signs of hypotension, decreased level of consciousness, tachycardia, and exhibit poor skin perfusion highlighting reduced cardiac output.

   • Management: Treatment focuses on resolving the underlying obstruction (e.g., decompression in tension pneumothorax or removal of a thrombus in pulmonary embolism).

   • Nursing Considerations: Monitor vital signs, assess peripheral perfusion, manage patient discomfort, and prepare for possible surgical interventions if necessary.