Surgical Critical Care: Shock
Shock
Definition
- Shock: Cellular/Tissue Hypoxia from Reduced Oxygen Delivery, Increased Oxygen Consumption or Inadequate Oxygen Utilization
- Generally Caused by Circulatory Failure with Hypotension
- Can Present with Hypertension in Certain Cases
4 Classifications of Shock
- Distributive Shock – Severe Peripheral Vasodilation (50% – Most Common Cause)
- Septic Shock
- Systemic Inflammatory Response Syndrome (SIRS)
- Neurogenic Shock
- Anaphylactic Shock
- Endocrine Shock (Addisonian/Adrenal Crisis)
- Drug/Toxin-Induced Shock
- Cardiogenic Shock – Cardiac Etiology Causing Reduced Cardiac Output (14%)
- Hypovolemic Shock – From Reduced Intravascular Volume (31%)
- Hemorrhagic Shock
- Non-Hemorrhagic Hypovolemic Shock
- Obstructive Shock – Extra-Cardiac Etiology of Cardiac Pump Failure (1%)
Mortality
- Distributive Shock: 20-50%
- Septic Shock: 40-50%
- Neurogenic Shock: 13-23%
- Endocrine Shock (Addisonian/Adrenal Crisis): 6%
- Cardiogenic Shock: 50-75% (Highest Risk)
- Hypovolemic Shock: 20-37%
Hemodynamic Changes & Differentiation
Preload
(PCWP) |
Contractility
(CO/CI) |
Afterload
(SVR) |
SvO2 | VC | |
Distributive Shock | ↓ | ↑1 | ↓ | – | – |
Septic | ↓ | ↑ | ↓ | ↓/↑2 | ↑ |
Neurogenic | ↓ | ↓ | ↓ | ↓ | – |
Cardiogenic Shock | ↑↑3 | ↓ | ↑ | ↓ | – |
Hypovolemic Shock | ↓ | ↓ | ↑ | ↓ | ↓ |
Obstructive Shock | ↓4 | ↓ | ↑ | ↓ | – |
- 1: Distributive Shock Generally Causes Increased CO/CI Except in Neurogenic Shock Where it is Decreased
- 2: Septic Shock Caused Decreased SvO2 Early Due to Increased Oxygen Consumption & Then Increased SvO2 Later Due to Decreased End-Oxygen Utilization (Not Impaired Perfusion)
- 3: Cardiogenic Shock Due to Right Ventricular Failure Causes Decreased PCWP
- 4: Obstructive Shock Due to Pericardial Tamponade Causes Paradoxically Increased PCWP Due to External Compression Despite Decreased Left-Sided Preload
Distributive Shock
Causes of Distributive Shock
- Septic Shock
- Neurogenic Shock
- Anaphylactic Shock
- Endocrine Shock (Addisonian/Adrenal Crisis)
- Drug/Toxin-Induced Shock
Septic Shock
- Definition: Shock Caused by Infection with a Dysregulated Host Response & Organ Dysfunction
- Most Common Cause of Distributive Shock
- *See Surgical Critical Care: SIRS & Sepsis
Systemic Inflammatory Response Syndrome (SIRS) Induced Shock
- Definition: Shock Caused by a Profound Inflammatory Response
- Can Be Infectious (Sepsis) or Noninfectious (Pancreatitis, Burns, etc.)
- *See Surgical Critical Care: SIRS & Sepsis
Neurogenic Shock
- Definition: Shock Caused by a Loss of Sympathetic Tone from Severe TBI or Spinal Cord Injury
- Seen in Spinal Injuries Above the T6 Level
- Incidence:
- Cervical Spine Injury: 19.3%
- Thoracic Spine Injury: 7%
- Presentation:
- Hypotension
- Bradycardia
- Extremities Remain Warm from Vasodilation
- Flushed Skin
- May See Priapism from Vasodilation
- Treatment: IV Fluids (#1) & Vasopressors
- Vasopressor Choice:
- Norepinephrine (Preferred)
- Phenylephrine – May Cause Reflex Bradycardia
- Goal MAP > 85 for 5-7 Days – Little Actual Data to Support
- Vasopressor Choice:
Anaphylactic Shock
- Definition: Shock from a Severe Allergic Reaction
- Mediated by IgE with a Massive Histamine-Mediated Vasodilation
- Most Common Cause:
- Children: Foods
- Adults: Insect Venom (Wasps & Bees)
- Treatment: Epinephrine (Most Important) & IV Fluids
- Epinephrine Dose: IM 0.3-0.5 mg of 1 mg/mL (1:1,000)
- Repeat Every 5-15 Minutes
- Possible Adjuncts:
- Antihistamines (Diphenhydramine)
- Corticosteroids
- Albuterol for Bronchospasms
- Epinephrine Dose: IM 0.3-0.5 mg of 1 mg/mL (1:1,000)
Endocrine Shock (Addisonian/Adrenal Crisis)
- Definition: Shock Caused by Insufficient Adrenal Hormone Production
- *See Endocrine: Adrenal Insufficiency
Drug/Toxin-Induced Shock
- Definition: Shock Drugs or Toxins
- Causes:
- Drug Overdoses
- Transfusion Reactions
- Bites (Snakes, Spiders & Insects)
- Heavy-Metal Poisoning (Iron & Arsenic)
- Cyanide
Cardiogenic Shock
Causes of Cardiogenic Shock
- Cardiomyopathy
- Myocardial Infarction (Most Common Cause)
- Severe CHF Exacerbation
- Myocardial Confusion
- Myocarditis
- Advanced Septic Shock
- Drug-Induced
- Arrhythmia
- Mechanical
- Valve Pathology (Insufficiency, Rupture or Stenosis)
- Atrial Myxoma
Treatment
- Primary Treatment: Vasopressors
- Vasopressor Choice:
- Norepinephrine (Preferred)
- Dobutamine (*Historically the Agent of Choice but Newer Evidence Shows Increased Risk of Arrhythmia & Trend to Increased Mortality)
- Vasopressor Choice:
- Avoid Aggressive IV Fluid Resuscitation – Can Cause Pulmonary Edema
- May Require an Initial IV Fluid Bolus to Maintain Preload
- Myocardial Infarction Specifics:
- Emergent Percutaneous Coronary Intervention (PCI) or Coronary Artery Bypass Graft (CABG)
- Fibrinolytic Therapy if Unable to Undergo PCI/CABG
- Mechanical Circulatory Support:
- Intra-Aortic Balloon Pump (IABP)
- Should Not be Used Routinely
- General Indications:
- Severe Mechanical Defects (Mitral Regurgitation or Ventricular Septal Defects)
- Rapid Deterioration
- Extracorporeal Membrane Oxygenation (ECMO)
- *See Surgical Critical Care: Mechanical Circulatory Support
- Intra-Aortic Balloon Pump (IABP)
Hypovolemic Shock
Causes of Hypovolemic Shock
- Hemorrhagic Shock
- Trauma
- GI Bleeding
- Vascular Rupture (AAA)
- Obstetric Hemorrhage
- Non-Hemorrhagic Hypovolemic Shock
- Dehydration
- GI Loss (Vomiting, Diarrhea or External Drainage)
- Skin Loss (Burns or Heat Stroke)
- Renal Loss (Excessive Diuresis or Salt-Wasting Nephropathy)
- Third-Space Losses (Bowel Obstruction, Operations, Crush Injury, Cirrhosis, etc.)
Hormones in Hypovolemia
- Early Hormones:
- Epinephrine & Norepinephrine (Adrenergic) – Vasoconstriction, Increased Contractility & Increased Heart Rate
- Late Hormones:
- Renin (Kidney) – RAAS Vasoconstriction & Water Resorption
- ACTH (Pituitary) – Increases Cortisol
- ADH (Pituitary) – Water Resorption
Fluid Responsiveness
- Definition: Assessment if Blood Pressure Will Respond to an IV Fluid Bolus
- Assessment:
- Fluid Challenge
- Test: Patient Given a 500 cc Bolus of Fluid as Fast as Possible (Around 10 Minutes)
- Passive Leg Raise
- The Most Well Validated Test of Fluid Responsiveness
- Test: Patient Placed Supine & Legs Passively Raised to 45 Degrees
- Quickly Returns a Reservoir of Venous Blood into Central Circulation in 30-90 Seconds
- Positive Results: 10% Increase in Cardiac Output or Stroke Volume
- Surrogate Measure without a Pulmonary Artery Catheter: 10% Increase in Pulse Pressure on Arterial-Line
- Fluid Challenge
- Stroke Volume Variation (SVV)
- SVV (%) = (Maximum SV – Minimum SV) / Average SV
- Measured Using a FloTrac/Vigileo System
- Normal Values: 10-13%
- < 10% Unlikely to Be Volume Responsive
- > 13-15% Likely to Be Volume Responsive
- Accurately Measured Only if on Controlled Mechanical Ventilation & In Normal Sinus Rhythm
- Use Contraindicated if Having Arrhythmias or Spontaneous Ventilation (Irregular Nature of Spontaneous Breaths Causes Variation)
- Poor Discriminators Not to be Used:
- Central Venous Pressure (CVP) Measurement
- Mean Arterial Pressure (MAP) Alone
- Chest X-Ray
- IVC Diameter
Hemorrhagic Shock
Non-Hemorrhagic Hypovolemic Shock
- First Vital Sign Changes:
- Increased Diastolic Blood Pressure
- Narrowed Pulse Pressure
- Physical Exam Findings:
- Dry Mucous Membranes
- Decreased Skin Turgor
- Low Jugular Venous Pressure
- Treatment: IV Fluids
- Crystalloids Preferred Over Colloids if Not Due to Hemorrhage
- Most Accurate Sign of Adequate Fluid Resuscitation: Urine Output
Obstructive Shock
Causes of Obstructive Shock
- Pulmonary Vascular Obstruction – Right Heart Fails to Create Enough Pressure to Overcome Elevated Pulmonary Vascular Resistance
- Pulmonary Embolism
- Pulmonary Hypertension
- Venous Air Embolism
- High-PEEP Ventilation
- Mechanical Obstruction – Decreased Venous Return to Right Heart or Right Ventricular Filling
- Tension Pneumothorax
- Tension Hemothorax
- Pericardial Tamponade
- Abdominal Compartment Syndrome
Treatment
- Primary Treatment: Correction of Underlying Cause