Introduction to Shock

Is All Shock Alike?

Introduction to Shock

Is All Shock Alike?

Barbie J. Barrett MD, FACEPAssociate Professor

Department of Surgery Division of Emergency Medicine

Stanford University and Medical CenterPalo Alto, California U.S.A.

Barbie J. Barrett MD, FACEPAssociate Professor

Department of Surgery Division of Emergency Medicine

Stanford University and Medical CenterPalo Alto, California U.S.A.

Central Venous Pressure Training for MD

RN Education on SCVO2RN Education on SCVO2

Sepsis Class for Paramedical Providers

Sepsis Class for Paramedical Providers

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)

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)

Definition

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.

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 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 Central Venous Oxygen Saturation

SvO2 Mixed Venous Oxygen Saturation

SIRS Systemic Inflammatory Response Syndrome

SVR Systemic Vascular Resistance

TO2 Tissue Utilization of Oxygen

TO2 crit Critical Oxygen Uptake to Supply

VO2 Ventilatory Oxygen Consumption

Classification by EtiologyClassification by Etiology

• Hypovolemic– Hemorrhage– Serum/Plasma loss– Drugs

• Distributive– Anaphylactic– Neurogenic– Septic

• Cardiogenic– Myocardial– Dysrrhythmia– Congenital Heart

Disease (Duct Dependent)

• 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 CVPRight Atrium (RA) or CVP

• Indicates preload• Crude example of

fluid volume• Normal 2 – 8

mmHg

Right Ventricle (RV)Right Ventricle (RV)

• Normal systolic 15 – 25 mmHg

• Normal diastolic 0 – 8 mmHg

Pulmonary Artery (PA)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)

Pulmonary Capillary Wedge Pressure (PCWP)

• “Sees” what is in front of it left side of heart

• Normal 8 – 12 mmHg

MortalitySeptic 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

MortalitySeptic 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

Oxygen supply and demand imbalance

Conversion from aerobic to anaerobic metabolism

Lactic acidosis due to both appropriate and inappropriate response

Oxygen supply and demand imbalance

Conversion from aerobic to anaerobic metabolism

Lactic acidosis due to both appropriate and inappropriate response

Pathophysiology

• 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

PathophysiologyResultant Systemic Physiology

- Cell Death- End Organ Dysfunction

MODS = Multiorgan Dysfunction Sydrome

Identifying Acute Organ Dysfunction as a Marker of Severe Sepsis

Identifying Acute Organ Dysfunction as a Marker of Severe Sepsis

Cardiovascular:TachycardiaHypotension

Altered CVP + PAOP

Renal:OliguriaAnuria

Creatinine

Hematologic: Platelets

PT/INR, aPTT Protein C D-dimer

Hepatic:Jaundice, Liver

enzymes Albumin

CNS:Altered

consciousnessConfusion

Respiratory: Tachypnea

PaO2

PaO2/FiO2ratio

Metabolic: Metabolic acidosis Lactate level

Lactate clearance

Balk RA, Crit Care Clin, 2000-16.337.352Keipell 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 Cardiogenic Obstructive Hypovolemic

DecreasedSVR

Blood FlowMaldistribution

Shock

Decreased MAP

Low Cardiac Output

Myocardial Dysfunction

Myocardial Damage

Pericardial Tamponade

Hemorrhage

Uncompensated

Compensated ReducedSystolicFunctionHigh or Normal

Cardiac Output

Reduced Filling

Reduced Preload

DEATH

Physical ExaminationVitals – Temperature may be or normal.General – Pale, Weak HEENT – Dry Mucous Membranes, Pale ConjunctivaNeck – Weak or Absent Carotid PulsesCardiovascular –

Usually TachycardiaLate BradycardiaException – Athletes, Beta-blockers,

Intra-abdominal Hemorrhage HypoglycemiaCardiovascular drugs

Physical Examination

Respiratory –Tachypnea Dead SpaceBronchospasmAdult Respiratory Distress Syndrome (ARDS)

Abdomen – ILEUS – low flow stateGI BleedPancreatitisAcute CholecystitisMesenteric Ischemia

Physical Examination

Extremities – Pulses Look for effusions, tracks,

infections, septic joints, line infection,

Skin – Pale Cyanosis Acrocyanosis Diaphoretic Capillary Refill Altered Temperature

Physical ExaminationGU – Genitourinary (Trauma, Blood Loss)

OliguriaPolyuria

Neuro-Altered Mental StatusCord SignsLoss of cardiac sympathetic toneParalysisMeningismus

Psyche –

Agitation Obtundation

Hypovolemic Shock Hypovolemic Shock is an acute intravascular volume loss

Results from decreased preload

EtiologyHemorrhage, Trauma,GI Bleed, and Ruptured Aneurysm

Fluid lossBurns, Diabetic KetoacidosisDiabetic Insipidus, Vomiting, andDiarrhea

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

EtiologyMyocardial InfarctionCardiomyopathyDysrhythmiaMechanical

CHF (Congestive Heart Failure)

ValveContusion

Extra cardiac (obstructive)

Cardiogenic ShockCardiogenic 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 VeinsWeak or Absent PulseArrhythmia often TachycardiaPulsus 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).

Infection

Other

Burns

Trauma

Pancreatiits

Fungemia

Parisitemia

Viremia

Other

SIRS

Bacteremia

SEPSIS`

Bone et al Chest 1992

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

Sepsis: Defining a Disease Continuum

Septic Shock

Lactic Acid < 4

Distributive ShockDistributive Shock

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

Distributive Shock

Systemic InflammationPancreatitis BurnsBiliary

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

AddisonianMyxedema

Anaphylactic Reaction vs

Anaphylactoid Reaction

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

AnaphylaxisAnaphylaxis

• Vasodilatation• Increased vascular permeability• Bronchoconstriction• Increased mucus production• Increased inflammatory mediators

recruitment to sites of antigen interaction

AnaphylaxisAnaphylaxis

• Immediate response• Cutaneous manifestations

– urticaria, erythema, pruritis, angioedema

• Respiratory compromise– stridor, wheezing, bronchorrhea, resp. distress

• Circulatory collapse– tachycardia, vasodilation, hypotension

Clinic Presentation

Obstructive ShockObstructive Shock is extra cardiac obstruction to blood flow.

Tension pneumothoraxCardiac tamponade Pulmonary embolusAortic stenosis

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

Dissociative Shock

Heat

Carbon Monoxide

Cyanide

Endocrine

EvaluationSimultaneous differential diagnosis thinking occurs in tandem with your treatment.

Targeted History & PhysicalWhat type(s) of shock am I dealing with?

Full Laboratory Protocols & EvaluationWhat would you order? (don’t forget pregnancy)What Cultures would you obtain?

EvaluationEvaluation

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

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)

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

Early Goal-Directed Therapy

Pearls and Pitfalls

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.

Don’t miss tension pneumothorax.

Does the patient have a pneumothorax after your CVP (central venous pressure) line placement?

Precise diagnosis is often delayed but immediate treatment is essential.

Don’t miss cardiac tamponade in your cancer/dialysis patients.

Pearls and Pitfalls

Isolated intracranial injuries do not cause shock.

Call for help.

Don’t assume there is only one cause for shock.

Keep your code/resuscitation bay warm blood loss will cause hypothermia.

Does the patient arrive with any preexisting lines that may be infected.

Check and recheck lines, monitors and infusions

Up to 30% of shock patients can have adrenal insufficiency

Is All Shock Alike?

ReferencesReferences

– 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. Tintinalli’s 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.