SHOCK: Classification, Pathophysiology and Approach to Management

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SHOCK Classification, Pathophysiology and
Approach to Management

• Darin Stettler D.O.
• Millcreek Community Hospital
• Internal Medicine Resident Lectures

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SHOCK Classification, Pathophysiology and
Approach to Management
Goal The resident will gain a basic
understanding of the shock syndromes and their
Management
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SHOCK Classification, Pathophysiology and
Approach to Management

• Objectives
• The resident will
• Identify the various classifications of shock.
• Describe the hemodynamic profile associated with
  each class of shock.
• Explain the Pathophysiology and mechanisms of
  cellular injury associated with shock.
• Discuss the Management and therapy involved in
  the treatment of shock.

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Background

• 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).

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Definition

• The appropriate definition varies with the
  context of its use.

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Definition

• Emergency medical personnel
• A definition that incorporates the typical
  clinical signs of shock, i.e.
• Arterial hypotension,
• Tachycardia,
• Tachypnea,
• Altered MS,
• Decreased UOP.

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Definition

• Physiologist
• Shock may be defined by specific hemodynamic
  criteria involving ventricular filling pressures,
• Venous pressures,
• Arterial pressures,
• CO,
• SVR.

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Definition

• Physician
• A syndrome in which profound and widespread
  reduction of effective tissue perfusion leads
  first to reversible, and then if prolonged, to
  irreversible cellular injury.

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Determinants of Effective Tissue Perfusion
Cardiac Function Local Oxygen unloading and Diffusion Preload Oxyhemoglobin affinity Afterload RBC 2,3 DPG Contractility pH Heart rate Temperature Venous return (RAP) Vascular compliance Distribution of CO Cellular Energy Generation Use Intrinsic/ extrinsic regulation Citric acid Cycle Autonomic Vascular resistance Oxidative phosphorylation pathway Exogenous vasoactive agents Other energy metabolism pathways ATP utilization Microvascular Function Pre/post capillary sphincter function Capillary endothelial integrity Microvascular obstruction (fibrin, platelets, WBC)
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Classification
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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
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Hypovolemic Shock

• Due 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).

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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.

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Hypovolemic Shock
Class I Class II Class III Class IV Blood loss ml lt750 750-1,500 1,500-2,000 gt2,000 Blood loss lt15 15-30 30-40 gt40 Pulse rate lt100 gt100 gt120 gt140 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 gt35 UOP ml/hr 30 20-30 5-15 negligible Mental Status sl anxious anxious confused lethargic Fluid Replacement crystalloid crystalloid crystalloid blood
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Hypovolemic Shock
Hemodynamic 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.
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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.

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Cardiogenic 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.

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Cardiogenic 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.

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Cardiogenic Shock

• Clinical signs peripheral vasoconstriction,
  oliguria, JVD, S3 and evidence of pulmonary
  edema.
• The Hemodynamic profile includes CO,
  PAWP, and systemic hypotension.

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Cardiogenic Shock
Dx CO SVR PWP CVP MVO2 LVMI VSD LVCO nl (Mechanical) RVCOgtLVCO MVR/ RVMI
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Cardiogenic Shock

• Optimal cardiac performance in pts with impaired
  myocardium may occur at higher than normal PWP
  (20-24)
• Pts should not be Dx with Cardiogenic Shock
  unless hypotension (MAPlt65), and CI lt 2.2,
  coexist with a PWP of gt 18.

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Cardiogenic 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.

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Obstructive Shock
Obstruction to normal CO and diminished system
perfusion

• 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 (gt 2 lobar arteries with gt 50
  occlusion), acute P-HTN, aortic dissection
  saddle embolus.

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Obstructive Shock
Hemodynamic Profile
Similar to other low output shocks with decreased
CI, SVI, MVO2, Lactate.

• 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.

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Distributive 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.

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Septic 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 ICUs across the country
  25-60. It is primarily nosocomial.
• Thought to be initiated by an exaggerated host
  inflammatory response to certain pathogens.

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Microbial Factors

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

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

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Inflammatory 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

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Inflammatory Mediators

• Stimulates TNF, IL-6,8, PAF, Leukotrienes, T-A2,
  prostaglandins,
• 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

• IL-1

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Hemodynamic 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.
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Organ 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

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Septic Shock
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Treatment

• To effectively combat septic shock, clinicians
  should use an integrated treatment approach
• Eradicate the microorganism
• Provide ICU life support
• Neutralize microbiological toxins
• Modulate host inflammatory response

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Immediate Goals

• Hemodynamic Support
• Optimization of O2 Delivery
• Reversal of Organ System Dysfunction

• MAP gt 60mmhg, PWP15-18 (inc. with Cardiogenic
  shock) CIgt2.1L/m, (cardiac Obstructive)
  CIgt4.0L/m, (septic hemorrhagic)
• Hgb gt 10, SaO2 gt 92, MVO2gt60mmHg
• Normalization of lactate (lt2.2)
• Reverse Encephalopathy Maintain UOP gt 0.5cc/kg/hr

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 level
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Vasopressors Inotropic Support
Pressor Dose B1 A1 B2 Dopa Indicaiton mcg/kg/min MAPlt60, PWPgt12-15 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
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Additional 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.

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• Case One
• A 66 y/o white male, who was diagnosed with a
  myocardial infarction 4 days ago suddenly
  develops dyspnea, fatigue, and orthopnea. You
  notice he has marked JVD and pulses paradoxus on
  exam. Which Hemodynamic profile would you expect
  to see in this patient?
• Increased and equalized right and left
  ventricular diastolic pressures, PADP, CVP, and
  PWP.
• Decreased SVR with an increased CO.
• Increased SVR with an Increased CO.
• Decreased PWP and a Decreased CVP.

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Case Two

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

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Case Three

• A 19 y/o male arrives in the Emergency Department
  following a auto-pedestrian accident. He is
  anxious and confused. Heart rate is 125, BP
  84/60. Respirations are 30. His skin is cool and
  clammy with CRTgt5 seconds. You diagnose him with
  Hypovolemic shock. Which class of Hypovolemic
  shock would best explain his situation?
• Class I
• Class II
• Class III
• Class IV
• Class V