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