Introduction to Shock

Is All Shock Alike?

Barbie J. Barrett MD, FACEP Associate Professor Department of Surgery Division of Emergency Medicine Stanford University and Medical Center Palo Alto, California U.S.A.

Central Venous Pressure Training for MD

RN Education on SCVO2

Sepsis Class for Paramedical Providers

Definition
Shock is an imbalance between tissue oxygen supply and demand, resulting in inadequate tissue perfusion.

- Shock may be present in the face of a: high, low or normal blood pressure High or Low Cardiac Output (CO) High or Low Systemic Volume Resistance (SVR)

Hypotension is a drop in systolic blood pressure of > 40-50 mm HG from baseline.

Systolic < 90 mm Hg MAP < 65 mm Hg

The Surviving Sepsis Campaign recommends maintaining MAP at > 65.

PERFUSION is crucial
Normal blood pressure may not equate to good flow

ARDS Adult Respiratory Distress Syndrome CA O2 Arterial Oxygen Content CO Cardiac Output EGDT Early Goal Directed Therapy

MAP Mean Arterial Pressure MODS Multi-organ Dysfunction Syndrome PAC Pulmonary Artery Catheter

ScvO2
SvO2 SIRS

Central Venous Oxygen Saturation

Mixed Venous Oxygen Saturation Systemic Inflammatory Response Syndrome Systemic Vascular Resistance Tissue Utilization of Oxygen Ventilatory Oxygen Consumption

SVR
TO2 VO2

TO2 crit Critical Oxygen Uptake to Supply

Classification by Etiology
Cardiogenic
Myocardial Dysrrhythmia Congenital Heart Disease (Duct Dependent)

Hypovolemic
Hemorrhage Serum/Plasma loss Drugs

Distributive
Anaphylactic Neurogenic Septic

Obstructive
Pneumothorax, Tamponade, Dissection

Dissociative
Heat, CO, Cyanide Endocrine

The Chain of Survival

Early Detection

Early and Rapid Intervention

Appropriate Disposition

Improved Outcomes

Right Atrium (RA) or CVP

Indicates preload Crude example of fluid volume Normal 2 8 mmHg

Right Ventricle (RV)

Normal systolic 15 25 mmHg Normal diastolic 08 mmHg

Pulmonary Artery (PA)

Normal systolic 15 25 mmHg Normal diastolic 8 15 mmHg PAD correlates with the filling pressure of the left heart

Pulmonary Capillary Wedge Pressure (PCWP)

Sees what is in front of it left side of heart Normal 8 12 mmHg

Mortality
Septic Shock 30% - 45% (1 month mortality) Cardiogenic 60% - 90% Hypovolemic 30% - 40%
Grater than 1 million cases of shock are seen in Emergency Departments annually
EGDT = Early Goal Directed Therapy

Pathophysiology
Oxygen supply and demand imbalance Conversion from aerobic to anaerobic metabolism

Lactic acidosis due to both appropriate and inappropriate response

 Cellular
Major third space fluid loss
Capillary Leak Fluid & Electrolyte Imbalance
Diarrhea, Sweat, Vomit

Vasodilation due to excessive activation of macrophages, neutrophils Pro inflammatory mediators

Prostanoids, Nitric Oxide Kinins and Pyrogens

Pathophysiology
Vascular Hyporeactivity
Adrenocortical Disruption Decreased Response to Catecholamines

Cardiac Profound Myocardial Depression

Excess Nitric Oxide Release of Myocardial Depressant Factors

Pathophysiology
Resultant Systemic Physiology -Cell Death -End Organ Dysfunction

MODS = Multiorgan Dysfunction Sydrome

Identifying Acute Organ Dysfunction as a Marker of Severe Sepsis

CNS: Altered consciousness Confusion Respiratory: Tachypnea PaO2 PaO2/FiO2 ratio Hepatic: Jaundice, Liver enzymes Albumin Cardiovascular: Tachycardia Hypotension Altered CVP + PAOP Renal: Oliguria Anuria Creatinine Hematologic: Platelets PT/INR, aPTT Protein C D-dimer Metabolic: Metabolic acidosis Lactate level Lactate clearance
Balk RA, Crit Care Clin, 2000-16.337.352 Keipell RM Crit Care Nurs Clin North Am 2003-15.27.34

Physiology
Characterized by three stages
Preshock (warm shock, compensated shock, cryptogenic shock) Shock End organ dysfunction

Physiology
Compensated shock
Low preload shock tachycardia, vasoconstriction, mildly decreased BP Low afterload (distributive) shock peripheral vasodilatation, hyperdynamic state

Pathophysiology
Shock
Initial signs of end organ dysfunction Tachycardia Tachypnea Metabolic acidosis Oliguria Cool and clammy skin

Physiology
End Organ Dysfunction Progressive irreversible dysfunction Oliguria or anuria Progressive acidosis, CO Agitation, obtundation, coma Patient death

Shock Pathways
Distributive
Decreased SVR
Myocardial Dysfunction

Cardiogenic
Myocardial Damage

Obstructive
Pericardial Tamponade

Hypovolemic
Hemorrhage

~% Uncompensated Blood Flow Maldistribution ~% Compensated High or Normal Cardiac Output

Reduced Filling
Reduced Systolic Function

Reduced Preload

Low Cardiac Output

Decreased MAP Shock

DEATH

Physical Examination
Vitals Temperature may be or normal. General Pale, Weak HEENT Dry Mucous Membranes, Pale Conjunctiva Neck Weak or Absent Carotid Pulses Cardiovascular Usually Tachycardia Late Bradycardia Exception Athletes, Beta-blockers, Intra-abdominal Hemorrhage Hypoglycemia Cardiovascular drugs

Physical Examination
Respiratory Tachypnea Dead Space Bronchospasm Adult Respiratory Distress Syndrome (ARDS) Abdomen ILEUS low flow state GI Bleed Pancreatitis Acute Cholecystitis Mesenteric Ischemia

Physical Examination
Extremities Pulses Look for effusions, tracks, infections, septic joints, line infection,

Skin Pale Cyanosis Acrocyanosis Diaphoretic Capillary Refill Altered Temperature

Physical Examination
GU Genitourinary (Trauma, Blood Loss) Oliguria Polyuria NeuroAltered Mental Status Cord Signs Loss of cardiac sympathetic tone Paralysis Meningismus Psyche Agitation

Obtundation

Hypovolemic Shock
Hypovolemic Shock is an acute intravascular volume loss Results from decreased preload

Etiology Hemorrhage, Trauma, GI Bleed, and Ruptured Aneurysm Fluid loss Burns, Diabetic Ketoacidosis Diabetic Insipidus, Vomiting, and Diarrhea

Cardiogenic Shock
Cardiogenic Shock is decreased cardiac output (CO) despite adequate volume.

Cardiogenic Shock is the leading cause of death in acute myocardial infarction.

Cardiogenic Shock
Etiology Myocardial Infarction Cardiomyopathy Dysrhythmia Mechanical CHF (Congestive Heart Failure) Valve Contusion Extra cardiac (obstructive)

Cardiogenic Shock
Artioventricular valves Tricuspid and Mitral
During diastole, the valves serve as a conduit from atria to ventricles

Semilunar Valves Pulmonic and Aortic

After the end of systole, high pressure drops with the pulmonary artery and aorta, causing retrograde flow thus filling the aortic and pulmonary cusps with blood and snapping them shut. Aortic valve is the valve most frequently replaced

Cardiogenic Shock
Clinical features
Distended Neck Veins Weak or Absent Pulse Arrhythmia often Tachycardia Pulsus Paradoxus (if tamponade)

Distributive Shock
Distributive Shock is a metabolic derangement that impairs cellular respiration, due to severe decrease in SVR

Vasodilation reduces after load. May be found with cardiac output (CO).

Bacteremia
Pancreatiits

Infection
Fungemia

SEPSIS`

SIRS

Parisitemia

Trauma

Viremia
Other

Burns

Other
Bone et al Chest 1992

Sepsis: Defining a Disease Continuum

Septic Shock

Lactic Acid < 4

Bone RC et al. Chest 1992, 101:1644-1655

Distributive Shock
Neurogenic / High Spinal Loss of cardiac sympathetic tone Heart rate Vascular dilitation Warm skin

Distributive Shock
Systemic Inflammation Pancreatitis Burns Biliary
Toxic Shock Syndrome

Toxic Reactions (transfusion, drugs)

Do not confuse spinal shock with neurogenic shock.

Distributive Shock
Anaphylaxis & Anaphylactoid (Know the difference) Widespread vasodilatation due to release of histamine. Endocrine Addisonian Myxedema

Anaphylactic Reaction vs Anaphylactoid Reaction

Anaphylactic
Previous exposer/sensitisation
Mediated by specific IgE antibodies Common reaction to contrast media

Anaphylactoid
No prior exposure necessary No IgE antibody involved Common reaction to invenomations/insect, Nuts, Shell fish, Pharmaceuticals, Latex

Histamine known responsible agent for most of manifestations

Anaphylaxis
Vasodilatation Increased vascular permeability Bronchoconstriction Increased mucus production Increased inflammatory mediators recruitment to sites of antigen interaction

Anaphylaxis
Clinic Presentation
Immediate response Cutaneous manifestations
urticaria, erythema, pruritis, angioedema

Respiratory compromise
stridor, wheezing, bronchorrhea, resp. distress

Circulatory collapse
tachycardia, vasodilation, hypotension

Obstructive Shock
Obstructive Shock is extra cardiac obstruction to blood flow.
Tension pneumothorax Cardiac tamponade Pulmonary embolus Aortic stenosis

Can two or three different types of shock exist in one patient?

Dissociative Shock
Heat
Carbon Monoxide Cyanide Endocrine

Evaluation
Simultaneous differential diagnosis thinking occurs in tandem with your treatment. Targeted History & Physical What type(s) of shock am I dealing with?

Full Laboratory Protocols & Evaluation What would you order? (dont forget pregnancy) What Cultures would you obtain?

Evaluation
Other Studies / Imaging
EKG = Electrocardiogram) FAST = Focused Assessment with Sonography in Trauma CT = Computerized Tomography ECHO = Echocardiogram LP = Lumbar Puncture (if appropriate)

Evaluation
Monitoring Vital signs including capnography Urine output CVP Central Venous Pressure Rectal probe Arterial line Pulmonary Artery (PA) catheterization

Suspected etiology will direct studies.

Index of 2008 Recommendations

Initial resuscitation (first 6 hours) Diagnosis Antibiotic therapy Source identification and control Fluid therapy Vasopressors Inotropic therapy Steroids Recombinant human activated protein C (rhAPC) Blood production administration
Mechanical ventilation of sepsis induced acute lung injury ALI/ARDS (acute respiratory distress syndrome) Sedation, analgesia, and neuromuscular blockade in sepsis Glucose control Renal replacement Bicarbonate therapy Deep vein thrombosis (DVT) prophylaxis Stress ulcer prophylaxis Consideration for limitation of support

Dellinger RP, et al. Crit Care Med. 2008,36:296-327. (Updated 36:1394-1396)

Early Goal-Directed Therapy

N Engl J Med 2001; 345(19):1368-1377

Pearls and Pitfalls

Precise diagnosis is often delayed but immediate treatment is essential. There is no single test that is diagnostic for sepsis. Young healthy patients may crash quickly due to their abilities to compensate initially.

Obtain pregnancy testing on all females of child bearing age.

Dont miss tension pneumothorax. Does the patient have a pneumothorax after your CVP (central venous pressure) line placement? Dont miss cardiac tamponade in your cancer/dialysis patients.

Pearls and Pitfalls

Call for help. Check and recheck lines, monitors and infusions

Does the patient arrive with any preexisting lines that may be infected.
Up to 30% of shock patients can have adrenal insufficiency

Isolated intracranial injuries do not cause shock.

Keep your code/resuscitation bay warm blood loss will cause hypothermia. Dont assume there is only one cause for shock.

Is All Shock Alike?

References
Dellinger R, Carlet JM, Masur H, et al. Surviving sepsis campaign guidelines for management of severe sepsis and septic shock. Crit Care Med 2004; 32(3): 858-873. Dellinger R, Levy M, Carlet J, et al. Surviving sepsis campaign: International guidelines for management of severe sepsis and septic shock. Crit Care Med 2008;36(1):296-327. Morris E, Light RB, Garber GE. Identifying patients with severe sepsis who should not be treated with drotrecogin alfa (activated). Am J Surgery 2002; 184: 19S-24S. Nguygen HB, Rivers EP, Knoblich BP, et al. Early lactate clearance is associated with improved outcome in severe sepsis and septic shock. Crit Care Med 2004: 32(8): 1637-1642) Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med 2001;345(19):13681377. Ruble, Cheryl RN, MICN, Alameida, Rich MD. Sepsis Workshop. 2011. Mills/Pensula Medical Center Sherwin RL, M.D. Shock. Wayne State University. July 18th 2006. Presentation Tintinalli JE. Tintinallis Emergency Medicine, A comprehensive Study Guide 7th ed. McGrawHill Med 2011. (165-182, 222-240, 1003-1014) Vanhorebeek I, Van den Berghe G. The neuroendocrine response to critical illness is a dynamic process. Crit Care Clin 2006; 22: 1-15.