SHOCK!!

Justin Bright, M.D.

Emergency Physicians of NW Ohio February 20, 2013

The Plan For Today

• • • • • Define shock – What it means physiologically – The different types of shock Discuss treatment modalities Discuss ways we handle shock in our ED Make this fun and interesting Reward you with chocolate

What is Shock?

• • • • Circulatory insufficiency that creates imbalance between oxygen supply and demand Global tissue hypoperfusion Causes metabolic acidosis Left untreated, progresses to end organ failure

Why Is Shock A Big Deal?

• • • People in shock are the most critically ill patients in our ED – Shock = “actively trying to die” 30-45% of septic shock patients, and 60 90% of cardiogenic shock patients die within 1 month of presentation Quick decision making and adequate treatment can prolong life

Pathophysiology

• • Systemic oxygen delivery is a result of arterial O2 content (CaO2) and cardiac output (CO) A normal Hgb molecule contains 4 O2 molecules – Tissue takes one O2 (25%), leaving 75% O2 content returning to the heart in venous circulation

Hemoglobin Molecule

Compensation

• • When there is a supply/demand imbalance, the body attempts to compensate – Pumps out more blood (increased CO) – Extracts more O2 (decreases SVO2) When compensation fails, the body switches over to anaerobic metabolism – Increases lactate levels in the blood

More Compensation

• • • • Arteriolar vasoconstriction to redistribute blood flow Constriction of venous capacitance vessels to increase VR Release of catacholamines Release of ADH and activation of renin angiotensin system

What’s Happening At The Cellular Level?

• • • • ATP gets depleted – Na/K ATPase can no longer function – Pump dysfunction causes cellular edema Cells become less responsive to stress hormones Lyosymes get released Cellular integrity is lost and cells rupture – Hemoconcentration, hyperkalemia, hyponatremia, prerenal azotemia, loss of glycemic control, lactic acidosis

General Management Plan

• The ABCDE’s of shock – A: airway management – B: reduce work of breathing – C: insure adequate circulation – D: adequate oxygen delivery – E: achieving endpoints of resuscitation

What Are The Types of Shock?

• • • • Septic Shock Cardiogenic Shock Hypovolemic Shock Distributive Shock – Anaphylaxis – Neurogenic shock

What Is Septic Shock?

• • Sepsis is a systemic inflammatory response to infection This major inflammatory response leads to – Depression of cardiac activity – Large scale vasodilation – Increased metabolic consumption

Septic Shock

• Where are the most common sites of infection?

– Chest – Abdomen – Urinary Tract

Clinical Features of Septic Shock

• Constitutional – Hyperthermia or hypothermia – Tachycardia – Wide pulse pressure – MS changes – tachypnea • Cardiovascular – Hypotension that does not respond well to fluids – Cardiac depression • Due to coronary hypoperfusion with resultant cardiac ischemia

Clinical Features of Septic Shock

• • Renal – Acute renal failure Pulmonary – SS is the most common cause of ARDS – Significant, non-cardiogenic pulmonary edema • • Hematologic – Neutropenia, thrombocytopenia, DIC Endocrine – Hyperglycemia, even in the non-diabetic – Poor glycemic control in critical patients is correlated with a much poorer outcome

Septic Shock

• Back in the olden days – Patients in septic shock would sit in the ER for hours waiting for a bed – They’d get some fluids – Maybe some antibiotics – Then they’d go the ICU and die

Take A Moment….

• …To Bow Down To The ER God

The Gist of EGDT

• • • • • While the patient is sitting in the ED, you optimize treatment early There are well defined optimization end points Patient goes to the ICU….

….and they live!

Most of the time

Why EGDT is a Big Deal

• • • • It has received the most buzz, and produced the most significant change in EM practice in the 21 st century Clinical data shows it significantly improves patient outcomes Two of our attendings trained under Dr. Rivers We are good, but not great at EGDT

What Does EGDT entail?

• • • • • • Filling up the tank Insuring adequate MAP Insuring adequate SVO2 Reducing work of breathing, which reduces metabolic demand Giving pressure support as needed Giving antibiotics

EGDT

• How do we reduce work of breathing?

– Oxygenation by NRB – Very low threshold for intubation

Filling Up The Tank

• • • • Septic shock causes major vasodilation Typically will give fluid bolus with minimal BP response How do we know we’ve given enough fluids?

Central venous pressures (CVP) – Done off a central line – Goal is between 8-12 mmHg

What About The SVO2 and the MAP?

• • To increase the SVO2, blood transfusion is often necessary – A goal is SVO2 of 70% To increase the MAP, pressure support medications are often needed – Goal is a MAP between 65 and 90

Pressors in Septic Shock

• • • Dopamine – Increases heart rate and blood pressure Levophed (norepinephrine) – Increases blood pressure without affecting HR Dobutamine – Increases HR without really affecting BP

Antibiotics

• • Blood cultures obtained before antibiotics if possible Antibiotics given empirically – Will depend on patient comorbidities and history – Ideally will cover against both gram+ and gram- bacteria

So How Will It All Go Down?

• Labs ordered – CBC – Lytes – Blood culture – UA – Coaggs – ABG – Lactate – Blood type and cross • • Studies – CXR or AAS Procedures – Central line – A-line – Foley – Intubation

What Do These Pictures Have In Common?

Hypovolemic Shock

• • Due to deficiency in intravascular volume 3 different categories – Hemorrhage • Trauma, surgery, GI bleeding – Intravascular volume loss • Gastroenteritis, burns, diabetes insipidus, heat stroke – Interstitial loss • Burns, sepsis, nephrotic syndrome, bowel obstruction, ascities

Treatment of Hypovolemic Shock • • ABC’s Volume expansion – Repetitive bolus and re-assessment – If no hemodynamic improvement after 2-3 boluses, patient should get blood products

Cardiogenic Shock

• • Decreased cardiac output producing inadequate tissue perfusion despite adequate or excessive circulating volume Causes – Massive AMI causing LV dysfunction – Depression of cardiac contractility • • • CHF, sepsis, contusion – Obstruction of forward flow Stenosis, myxoma, HCOM – Regurgitation of LV output Valve deficiency

What Will We Order?

• Studies – EKG – CXR – Cardiac echo • Labs – Chest-O – BNP – lactate

Clinical Findings in Cardiogenic Shock • • • • • Tachypnea Cool, mottled extremities Significant peripheral edema JVD Cardiac murmurs

Treatment of Cardiogenic Shock

• • • ABC’s Central line and a-line If due to AMI – Heparin, ASA, cath lab

Hypotension in Cardiogenic Shock • • Excessive fluid administration is contraindicated – Problem is not volume, its that there’s no means to push the blood around Very small fluid challenges (250 cc)

Pressure Support in Cardiogenic Shock • • Dobutamine and milrinone are your friends – Increase contractility – Can’t use if SBP < 90 because have vasodilatory properties Dopamine alone is bad news  cardiac workload too much increases – Has been shown to work well when used in conjunction with dobutamine

Cardiogenic Shock

• What do these patient’s need more than anything – Reperfusion with a quickness • Cath lab is better than thrombolytics • Intraaortic balloon pump helps by decreasing afterload and decreases cardiac work

Distributive Shock

• • Anaphylaxis Neurogenic

Anaphylaxis

• • • • A severe systemic hypersensitivity reaction Multisystem involvement May include airway compromise and significant hypotension Caused by a massive release of a cascade of inflammatory mediators from mast cells and basophils

Risk Factors for Anaphylaxis

• • • Those with severe asthma or previous history of anaphylaxis are at risk for fatal or near-fatal anaphylactic episodes Recurrence risks are not 100% – 40-60% for insect stings – 20-40% for radiocontrast – 10-20% for penicillin Atopic individuals are NOT considered to be at any greater risk

Clinical Features of Anaphylaxis

• • • • • • Diffuse uticaria and angioedema Nausea/vomiting Bronchospasm Conjunctivitis and rhinorrhea Hypotension Symptoms tend to occur within 60 minutes of exposure

Anaphylaxis Pathophysiology

• • • • Mast cell and basophil degranulation and mediator release Causes IgE mediated reaction Complement activation Process requires a previous exposure

So What Do We Do About It?

• • • ABC’s Single most important step is administration of epinephrine Decontamination/removal of offending agent

Epinephrine

• • • Research shows epi is underused in anaphylaxis Start by giving epi bolus (0.1mg) IV – If refractory, then given epi drip at 1-4 mcg/min if Sx less severe, can give IM epinephrine

After Epi….

• • • • Fluids for hypotension Steroids (Solumedrol 125mg IV) Antihistamines – Benadryl (50mg IV) is a H1 blocker – Pepcid (20mg IV) is a H2 blocker • H2 blockers are controversial, but our attendings tend to use them  won’t harm patient, might help Albuterol + Atrovent nebulizers for bronchospasm

• • •

Neurogenic Shock

Occurs after acute spinal cord injury Causes disruption of sympathetic chain – Leaves unopposed vagal tone (PNS) – Causes hypotension and bradycardia Neurogenic shock is NOT the same as spinal shock – Spinal shock resolves within 48 hours and is due to swelling around the spinal cord

Neurogenic Shock

• • • Predominantly due to blunt cord injury Most common causes – MVC – Falls – Sports injury C-spine is most commonly affected area

Primary vs. Secondary Cord Injury • • Primary – Caused by initial traumatic event – Compression, laceration, or stretching of the cord Secondary – Occurs over days to weeks – Cord ischemia – Importance is that presentation can change • An initial incomplete cord injury can evolve into a complete cord injury

Clinical Features of Neurogenic Shock • • • • • Generally hypotensive Warm, dry skin – Patient has lost ability to redirect blood from periphery to the core organs Bradycardia Hypothermia The higher the injury, the more severe – More likely to disrupt sensory and motor tracts – Injuries C5 and higher are going to impact patient’s capacity to breathe on his/her own

Treatment of Neurogenic Shock

• • • ABCDE’s – A = airway AND c-spine protection Neurosurgery gets involved early Use of steroids is controversial and neurosurgeon dependant

The Moral of the Story

Type Hypovolemic Preload PCWP i Cardiac Output Syst Resist i h SvO2 i Cardiogenic Distributive h n i h h i i h

We’re Done!

• Any questions or comments?