Shock

Eric Kaiser M.D.

Rosens Chapter 4 9-7-06 Slides by: Scott Gunderson D.O.

Shock
Transition between life and death Failure to oxygenate & nourish the body adequately Mortality > 20%

Pathophysiology & Biochemistry

Pathophysiology
Shock affects mitochondria first Without oxygen mitochondria convert fuels to lactate lactic acid Failure of the krebs cycle

Oxygen is the final electron accepter to form water

Lactic Acid
Early shock

Skeletal muscle and splanchnic organs 1st affected Lactic acid production

Resuscitation

Pyruvate delivery from glycolysis can overwhelm krebs cycle

Systemic Response
Decreased vascular wall tension increases sympathetic stimulation (blocked in sepsis)

Increased epi, norepi, corticosteroids, renin, and glucagon Increased glycogenolysis and lipolysis

Increased glucose and FFAs to TCA can overwhelm it

Immune Response
Neutrophil and macrophage activation due to hypoxia

Enzymatic organ damage Capillary plugs causing microischemia TNF and Interleukins released

Cardiac Physiology
Contraction created by Ca++, ATP/CP, and troponin C Calcium inflow determines strength of contraction

Inotropics increase Ca++ release in the sarcoplasmic reticulum via -receptors or cAMP

Cardiac Physiology
ATP/CP supply almost entirely from oxidative phosphorylation by mitochondria Complete turnover of ATP/CP every 5-10 beats

Cardiac Physiology
Gregg Phenomenon

Contractile strength decreases with decreased coronary perfusion

Decreased coronary perfusion in shock Decreased workload due to lower SVR Very minimal cardiac ischemia even in severe shock

Cardiac Physiology
Inflammatory actions of TNF, Interleukins, and NO decrease contractility Acidosis can decrease contractility but effect is minimal

Clinical Features & Management

Clinical Features
Frequently no obvious etiology Rapid recognition

H&P, ill appearance, diaphoresis HR and BP not reliable HR/SBP ratio better indicator
Normal is less than 0.8

Urine output is great, but takes time

Normal >1.0 ml/kg/hr

Lactic acid or base deficit

Shock Classification
Rapid, but detailed H&P to direct therapy
Flow diagram

Figure 4-4 in Rosens

Clinical Data
CXR infection, contusions EKG ischemia Glucose CBC anemia, leukocytosis Electrolytes dehydration, GI bleed, acidosis ABG base deficit, acidosis UA dehydration

Management
IV, O2, monitor BP readings every 2-5 minutes

Remember BP reading often underestimates the level of shock until severe

Urine output

>1 cc/kg/min

Management
IV access

Peripheral vs. Central

Most patients OK with one large bore or two smaller bore peripheral IVs CVP pressure may be required for patient with cardiac failure or renal failure Indwelling catheters should be used unless hospital policy states against it in the ED

Volume Replacement
When is the tank full?

Goal CVP slightly elevated of 10-15 cm H2O Must correlate CVP with SBP, urine output, and lactate levels to adequately assess perfusion

Ventilation
Rapid sequence intubation preferred

Ketamine or etomidate are good choices due to minimal cardiovascular depression Intubation protects aspiration, decreases breathing workload, and initial treatment for acidemia High negative pressures in bronchospasm or ARDS can decrease LVEF and positive pressure removes this

Acidosis
Acidosis is a negative inotrope No evidence supports using bicarbonate for treatment Treat with improved ventilation and mild hyperventilation THAM (tris[hydroxymethl]-aminomethane) may be used IV for acidosis reversal

Optimal Hemoglobin
Hemoglobin carries oxygen High hematocrits increase viscosity and cardiac workload Optimal balance is a hemoglobin of 10-12 gm%

Goal-Directed Therapy
Goal directed therapy is the practice of resuscitating to a defined physiologic endpoint

Wedge pressures measures left ventricular filling pressures controversial risk/benefit Lactate clearing index decrease in arterial lactate by 50% in 1 hour and continued efforts until lactate < 2 mM GI tonography permeable balloon in stomach or rectum measuring pH to estimate perfusion
Questionable data supporting

Specific Causes & Treatment

Hemorrhagic Shock
Rapid reduction in blood volume Heart rate and blood pressure responses can be variable No firm conclusion can be made by simply HR and BP readings

Hemorrhagic Shock General Progression

Increased heart rate

Narrowed pulse pressure

Shunting from noncritical organs

Decreased cardiac filling leading to decreased CO

Decreased SBP

Hemorrhagic Shock
Decreased perfusion to splanchnic organs precedes lower BP

Lactic acid production Base deficit

Normal base deficit is greater than -2 mEq/L

After 1/3 of blood volume lost hypotension occurs Acidemia occurs about then as patient cannot create enough respiratory compensation for the lactic acid

Hemorrhagic Shock
Organ injury in resuscitation

Release of activated neutrophils & inflammatory cytokines Distorted balance of vasodilatation vs. vasoconstriction May lead to ARDS, acute tubular necrosis, & centrilobular ischemic liver damage

Consensus Definition
Hemorrhagic Shock 3 classifications

Simple hemorrhage
Bleeding with normal vital signs and base deficit

Hemorrhage with hypoperfusion

Bleeding with base deficit < -5 mmol or persistent HR >100

Hemorrhagic shock
Bleeding with 4 or more of below

Ill appearance or mental status HR >100 RR >22 or PaCO2 <32 Base deficit < -5 or lactate > 4 Urine output < 0.5 cc/kg/hr Hypotension > 20 minutes

Hemorrhagic Shock Treatment

Several liters of crystalloids in adults Three 20 cc/kg boluses in children If still in shock after bolus start PRBCs at 5-10 cc/kg Blood substitutes possibly in future but not currently advantageous

Hemorrhagic Shock Treatment

Controlling hemorrhage is still always the cornerstone of treatment Immediate surgery if hemorrhage cannot be controlled

In very rare cases inotropics may be beneficial

Septic Shock
Any microbe may cause, but gram negative most common Lipopolysaccharide is a key mediator 1/3 of cases no organism is identified Higher causes recently of gram positive due to

Hospitalized patients Immunocompromised Indwelling catheters Increasing drug resistance

Septic Shock
3 major effects

Hypovolemia
Relative due to increased venous capacitance Absolute due to GI loss, diaphoresis, tachypnea

Cardiovascular depression
Depression due to inflammatory mediators

Systemic inflammation
Capillary leak causing ARDS in up to 40%

Consensus Definition
SIRS

Two or more of the following

Temperature > 38 C or <36 C Heart rate > 90 Respiratory rate > 20 resp/min or PaCO2 <32 WBC > 12,000, < 4,000, or >10% bands

Septic Shock

Severe sepsis with hypotension unresponsive to fluid resuscitation and perfusion abnormalities

Septic Shock Treatment

Ventilatory support

Decrease respiratory workload and correct hypoxia

Increase ventricular filing 20-25 cc/kg crystalloids followed by 5-10 cc/kg colloids Used to keep Hct at 30-35% if needed

Fluids

Blood

Septic Shock Treatment

Antibiotics

If focus identified
Use clinical experience

If no focus identified
Semisynthetic PCN with -lactamase inhibitor with an aminoglycoside and vancomycin Imipenem-cilastatin good monotherapy choice Antifungal in immunocompromised

Septic Shock Treatment

Vasopressors

Dopamine
Most common first line agent and a bad idea Remove from you armamentarium

Norepinephrine
Start 0.5-1 g/min and titrate to response Excellent first choice; well studied

Dobutamine
Start 5 g/kg/min Hypotension unresponsive to vasopressors and IVF.

Cardiogenic Shock
Pump failure Results when more than 40% of myocardium damaged Similar circulatory and metabolic changes to hemorrhagic shock May also be due to a PE

Consensus Definitions
Cardiogenic

Cardiac failure
Evidence of impaired cardiac outflow including dyspnea, tachycardia, rales, edema, or cyanosis

Cardiogenic shock
Cardiac failure plus four of below criteria

Ill appearance or mental status HR >100 RR >22 or PaCO2 <32 Base deficit < -5 or lactate > 4 Urine output < 0.5 cc/kg/hr Hypotension > 20 minutes

Cardiogenic Shock Treatment

Ventilatory support

Often needed in pulmonary edema or if respiratory failure imminent Avoid barbiturates, morphine, propofol and benzodiazepines
Negative inotropic effects Fentanyl, ketamine and etomidate much better choices

Cardiogenic Shock Treatment

Ionotropics/vasopressors

Dobutamine and Milrinone are agents of choice Amrinone (Replaced by Milrinone) Milrinone
Similar to amrinone Load at 50 g/kg (Consider half loading dose) Infuse at 0.375 - 0.75 g/kg/min Be prepared for hypotension

Cardiogenic Shock Treatment

Intraaortic balloon pump

When all pharmacologic therapy is failing

Requires appropriate facility and ICU/CCU Improves cardiac output by 30%

Cardiogenic Shock Treatment

Myocardial infarction causing cardiogenic shock

Management not significantly different than another MI accept additional management

Ventilatory support as needed Treat dysrhythmias Inotropic support Aspirin Heparin PTCA vs. thrombolytics

Cardiogenic Shock Treatment

Pulmonary Embolism

Ventilatory support IV fluids Norepinephrine Thrombolytics (systemic vs. intra-arterial) Possis catheter Surgical embolectomy at few centers

Anaphylactic Shock
IgE mediated response to an allergen Mast cells release histamine Histamine causes
Smooth muscle relaxation Bronchial contraction Capillary leak

Anaphylactic Shock Treatment

Epinephrine

1 cc of 1:10,000 IV infused slowly and watch response 5 mg in 500 cc NS at 10 cc/hr thereafter

May titrate to response

Use even with coronary artery disease if hypotensive

Anaphylactic Shock Treatment

Corticosteroids

Decrease immune response Methylprednisolone 125mg IV Hydrocortisone 5-10 mg/kg IV

Antihistamines

Diphenhydramine 0.5 mg/kg IV Cimetidine 2-5 mg/kg IV Famotidine

Intubation if needed

Neurogenic Shock
CNS cord lesions above T1

Heart gets unopposed vagal simulation Bradycardia and hypotension

Atropine

First line therapy

Neurogenic Shock Treatment

Volume expansion

Confirm by CVP and BP

Vasopressors

Ephedrine
10 mg IV bolus good for 3-4 hours

Phenylephrine
100-180 g/min IV until stable

Summary
Early recognition of shock and early treatment is key Do not rely solely on a HR and BP to determine their status

Aggressive and goal directed therapy have proven to decrease mortality

References
Jones, Alan E., & Kline, Jeffrey A. (2006). Shock. In Marx, John A., Hockberger, Robert S., & Walls, Ron M. (Eds.). Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Pg. 41-56. Mosby.