SHOCK: Classification, Pathophysiology and Approach to Management Darin Stettler D.O. Millcreek Community Hospital Internal Medicine Resident Lectures.

SHOCK: SHOCK: Classification, Pathophysiology and Classification, Pathophysiology and

Approach to ManagementApproach to Management

Darin Stettler D.O.

Millcreek Community Hospital

Internal Medicine Resident Lectures

SHOCK: SHOCK: Classification, Pathophysiology and Classification, Pathophysiology and

Approach to ManagementApproach to Management

Goal:

The resident will gain a basic understanding of the shock syndromes and their Management

SHOCK: SHOCK: Classification, Pathophysiology and Classification, Pathophysiology and

Approach to ManagementApproach to Management

Objectives:

The resident will:

1. Identify the various classifications of shock.

2. Describe the hemodynamic profile associated with each class of shock.

3. Explain the Pathophysiology and mechanisms of cellular injury associated with shock.

4. Discuss the Management and therapy involved in the treatment of shock.

BackgroundBackground

Shock is one of the most frequent physiologic entities encountered by intensive care physicians.

Despite continued investigation into the syndrome, mortality from the shock states remains high (35%).

DefinitionDefinitionThe appropriate definition varies with the

context of its use.

DefinitionDefinition

Emergency medical personnel A definition that incorporates the typical

clinical signs of shock, i.e. Arterial hypotension, Tachycardia, Tachypnea, Altered MS, Decreased UOP.

DefinitionDefinition

PhysiologistShock may be defined by specific

hemodynamic criteria involving ventricular filling pressures,

Venous pressures, Arterial pressures, CO, SVR.

DefinitionDefinition

PhysicianA syndrome in which profound and

widespread reduction of effective tissue perfusion leads first to reversible, and then if prolonged, to irreversible cellular injury.

Determinants of Effective Tissue Determinants of Effective Tissue PerfusionPerfusion

Cardiac Function Local Oxygen unloading and Diffusion Preload Oxyhemoglobin affinity Afterload RBC 2,3 DPG Contractility pHHeart rate TemperatureVenous return (RAP)Vascular compliance

Distribution of CO Cellular Energy Generation & Use Intrinsic/ extrinsic regulation Citric acid Cycle Autonomic Vascular resistance Oxidative phosphorylation pathwayExogenous vasoactive agents Other energy metabolism pathways– ATP utilization

Microvascular Function Pre/post capillary sphincter functionCapillary endothelial integrityMicrovascular obstruction (fibrin, platelets, WBC)

ClassificationClassification

H Y P O V O L E M IC S H O C KH e m orrh ag ic

trau m aN on -H e m o rrh ag ic

C A R D IO G E N ICM I

M echa n ica lA r rh ythm ic

E X T R A C A R D IA C O B S T R U C T IV EC a rd ica c T am po na de

T e ns io n P ne um oth oraxE m b o lus : sa dd le , P E

D IS T R IB U T IV ES ep tic

A n ap hy lac ticN eu rog en ic

S H O C K

Obstructive Cardiogenic Hypovolemic Distributive

MI hemorrhage sepsis

Diastolic vs Systolic myocardial damage preload myocardial

Function depression

Systolic & Diastolic diastolic filling S & D

Function function

CO SVR

SVR CO

MAP

Maldistribution

SHOCK of flow

MODS

Hypovolemic ShockDue to a decreased circulating blood volume

in relation to total vascular capacity.

May be due to dehydration, internal/external hemorrhage, GI fluid losses (D/V), urinary losses (diuretics, renal dysfunction), decreased vascular permeability (sepsis), venodilation (drugs, spinal).

Hypovolemic Shock

NOTE: significant blood volume may be shed in the absence of any clinical sings

General manifestations include cold, clammy skin from SNS stimulation and peripheral hypoperfusion.

Decreased UOP and Tachycardia may be the only objective clinical abnormality.

Hypovolemic Shock Class I Class II Class III Class IV

Blood loss ml <750 750-1,500 1,500-2,000 >2,000

Blood loss % <15% 15-30% 30-40% >40%

Pulse rate <100 >100 >120 >140

BP nml nml decreased decreased

Pulse Pressure nml/Inc decreased decreased decreased

CRT nml decreased decreased decreased

Respiratory rate 14-20 20-30 30-40 >35

UOP ml/hr 30+ 20-30 5-15 negligible

Mental Status sl anxious anxious confused lethargic

Fluid Replacement crystalloid crystalloid crystalloid +blood

Hypovolemic ShockHemodynamic ProfileHemodynamic Profile

Diagnosis CO SVR PWP CVP MVO2

Hypovolemic

Shock

Note: Filling pressures appear normal if hypovolemia occurs in the setting of base line myocardial compromise.

Hypovolemic Shock Hypovolemic shock is more than a simple

mechanical response to loss of volume.

It involves a dynamic process of competing adaptive and maladaptive responses at each stage of development.

While volume replacement is always a necessary component of treatment, a series of inflammatory mediators, CV, and organ responses are initiated that supersede the initial insult in driving further injury.

Cardiogenic ShockCardiogenic Shock

The underlying defect is PUMP Failure.

Most commonly due to ischemic myocardial injury- requires 40% nonfunctional myocardium.

Usually involves Anterior MI with Left Main or proximal LAD occlusion.

Cardiogenic ShockCardiogenic Shock

Incidence of shock after AWMI is 8-20%.

Unless the lesion is amenable to surgical correction, mortality rates can exceed 75%.

Other causes: cardiomyopathy, AS, aortic dissection, MS, AR/MR, VSD, Atrial Myxoma, dysrhythmias.

Cardiogenic ShockCardiogenic Shock

Clinical signs: peripheral vasoconstriction, oliguria, +JVD, S3 and evidence of pulmonary edema.

The Hemodynamic profile includes CO, PAWP, and systemic hypotension.

Cardiogenic ShockCardiogenic Shock

Dx CO SVR PWP CVP MVO2

LVMI

VSD LVCO nl (Mechanical) RVCO>LVCO

MVR/

RVMI

Cardiogenic ShockCardiogenic Shock

Optimal cardiac performance in pt’s with impaired myocardium may occur at higher than normal PWP (20-24)

Pt’s should not be Dx with Cardiogenic Shock unless hypotension (MAP<65), and CI < 2.2, coexist with a PWP of > 18.

Cardiogenic Shock TxCardiogenic Shock Tx

Stabilize BP with vasopressors (LV), Inotropes (RV), and fluids as tolerated.

Tx pulmonary congestion with diuretics and venodilators.

Institute mechanical ventilation, if needed.Place IABP.Restore NSR.Assess candidacy for angioplasty/bypass or

other surgical repair.

Obstructive ShockObstructive Shock

Directly impair diastolic filling of the RV.

Indirectly impair RV filling by obstructing venous return.

Increased ventricular afterload.

Pericardial Tamponade, constrictive pericarditis.

Tension Pneumothorax Intrathoracic tumors.

Massive PE (> 2 lobar arteries

with > 50% occlusion), acute P-HTN, aortic dissection & saddle embolus.

Obstruction to normal CO and diminished system perfusionObstruction to normal CO and diminished system perfusion

Obstructive ShockObstructive Shock

Tension Pneumothorax, Intrathoracic tumors.

Cardiac Tamponade.

Constrictive pericarditis.

Massive PE.

Saddle embolus/aortic dissection.

CI, SVR +JVD.

Increased and equalized RV & LV diastolic pressures, PAD, CVP, PWP .

RV & LV diastolic pressures and within 5 mmHg of each other.

RV failure with PA & CVP and normal PWP.

PWP, BP signs of LVF.

Hemodynamic ProfileHemodynamic ProfileSimilar to other low output shocks with decreased CI, SVI, MVO2, Lactate.

Distributive ShockDistributive Shock The defining feature is loss of peripheral vascular

resistance, characterized by SVR or Capacitance.

Septic shock---most common form.

Anaphylactic shock---IgE mediated release of mediators from tissue mast/basophils.

Neurogenic Shock---loss of peripheral vasomotor control, from spinal injury, or similar phenomenon of vasovagal syncope sometimes associated with SAB.

Septic ShockSeptic Shock

Septic shock is an immediate life-threatening syndrome initiated by microorganisms, their toxins, or both, that have invaded the bloodstream.

Septic shock is the most common cause of non cardiac death in ICU’s across the country 25%-60%. It is primarily nosocomial.

Thought to be initiated by an exaggerated host inflammatory response to certain pathogens.

Microbial FactorsMicrobial Factors

Gram-Positive Gram-Negative Fungal P. Aeruginosa S. Aureus

Peptidoglycans of cw Endotoxin (LPS) Mennan from cw Exotoxin A TSST

Inflammatory MediatorsInflammatory Mediators

TNF Stimulates IL-1,6,8, PAF, Prostaglandin's

Activates coagulation pathway and compliment system

Increases permeability Produces fever Depresses cardiac myocyte

contractility Decreases arterial pressure,

SVR, EF, Increases CO

Inflammatory MediatorsInflammatory Mediators

IL-1

Stimulates TNF, IL-6,8, PAF, Leukotrienes, T-A2, prostaglandin’s,

Promotes PMN cell activation and accumulation

Increased endothelial procoagulant activity

Depresses cardiac myocyte contractility.

Produces fever. Promotes adhesion of endothelial

cells Activates T & B cells

Hemodynamic ProfileHemodynamic Profile

Dx CO SVR PWP CVP MVO2

Septic

Shock

The hyperdynamic circulatory state ( CO and SVR) is dependant on fluid resuscitation. Prior to giving fluids, a hypodynamic circulation is typical..

Organ System DysfunctionOrgan System Dysfunction CNS

Heart

Pulmonary Renal GI

Hepatic

Hematological Metabolic

Encephalopathy (ischemic or septic) Cortical necrosis

Tachy/Bradycardia, SVT, Ventricular ectopy, Myocardial ischemia

Acute Respiratory Failure, ARDS. Pre-renal failure, ATN Ileus, Erosive gastritis, Pancreatitis,

Acalculous cholecystitis, Transluminal translocation of bacteria/Endotoxin

Ischemic hepatitis, Shock Liver DIC, dilutional thrombocytopenia Hyperglycemia early, Hyopglycemia late

hypertriglyceridemia

Septic ShockSeptic Shock

TreatmentTreatment

To effectively combat septic shock, clinicians should use an integrated treatment approach

Eradicate the microorganismProvide ICU life supportNeutralize microbiological toxinsModulate host inflammatory response

Immediate GoalsImmediate Goals Hemodynamic Support

**

Optimization of O2 Delivery

Reversal of Organ System Dysfunction

MAP > 60mmhg, PWP=15-18 (inc. with Cardiogenic shock) CI>2.1L/m, (cardiac & Obstructive)

CI>4.0L/m, (septic & hemorrhagic)

Hgb > 10, SaO2 > 92%, MVO2>60mmHg

Normalization of lactate (<2.2)

Reverse Encephalopathy Maintain UOP > 0.5cc/kg/hr

** Although CI is increased, perfusion may not be effective if it does not reach the tissue, ** Although CI is increased, perfusion may not be effective if it does not reach the tissue, or there is a defect in substrate utilization at the subcellular levelor there is a defect in substrate utilization at the subcellular level

Vasopressors & Inotropic SupportVasopressors & Inotropic Support

Pressor Dose B1 A1 B2 Dopa Indicaiton mcg/kg/min MAP<60, PWP>12-15

Dopamine 1-10 ++ + ++ +++ or normal CO

10-20 +++ +++ + 0

NorEpi 2-10 +++ ++++ 0 0 Dopamine failure

Phenylephrine 2-200 0 ++++ 0 0 Dysrhythmias

EPI 1-8 ++++ ++++ ++ 0 CO, NorEpi Failure

Dobutamine 1-10 ++++ + ++ 0 CO, & NE Tx

Additional PointsAdditional Points

New therapies for septic shock have been directed at specific bacterial toxins (endotoxin), and endogenous proinflamatory mediators like TNF, IL-1.

However, clinical trials have not established additional safety of better outcomes with this therapy.

Case OneCase One

A 66 y/o white male, who was diagnosed with a myocardial A 66 y/o white male, who was diagnosed with a myocardial infarction 4 days ago suddenly develops dyspnea, fatigue, and infarction 4 days ago suddenly develops dyspnea, fatigue, and orthopnea. You notice he has marked JVD and pulses orthopnea. You notice he has marked JVD and pulses paradoxus on exam. Which Hemodynamic profile would you paradoxus on exam. Which Hemodynamic profile would you expect to see in this patient?expect to see in this patient?

1.1. Increased and equalized right and left ventricular diastolic Increased and equalized right and left ventricular diastolic pressures, PADP, CVP, and PWP.pressures, PADP, CVP, and PWP.

2.2. Decreased SVR with an increased CO.Decreased SVR with an increased CO.

3.3. Increased SVR with an Increased CO.Increased SVR with an Increased CO.

4.4. Decreased PWP and a Decreased CVP.Decreased PWP and a Decreased CVP.

Case TwoCase Two

A 32 y/o white female recently had a subarachnoid block in A 32 y/o white female recently had a subarachnoid block in the O.R. prior to having a total knee replacement. She the O.R. prior to having a total knee replacement. She suddenly becomes confused, anxious and vomits prior suddenly becomes confused, anxious and vomits prior to passing out. Her BP is found to be 56/28 manually. to passing out. Her BP is found to be 56/28 manually. Which classification of shock would best describe this Which classification of shock would best describe this event?event?

1.1. HypovolemicHypovolemic

2.2. CardiogenicCardiogenic

3.3. ObstructiveObstructive

4.4. DistributiveDistributive

Case ThreeCase Three

A 19 y/o male arrives in the Emergency Department following a A 19 y/o male arrives in the Emergency Department following a auto-pedestrian accident. He is anxious and confused. Heart auto-pedestrian accident. He is anxious and confused. Heart rate is 125, BP 84/60. Respirations are 30. His skin is cool rate is 125, BP 84/60. Respirations are 30. His skin is cool and clammy with CRT>5 seconds. You diagnose him with and clammy with CRT>5 seconds. You diagnose him with Hypovolemic shock. Which class of Hypovolemic shock would Hypovolemic shock. Which class of Hypovolemic shock would best explain his situation?best explain his situation?

1.1. Class IClass I

2.2. Class IIClass II

3.3. Class III Class III

4.4. Class IVClass IV

5.5. Class VClass V