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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