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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 – PowerPoint PPT presentation

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Title: SHOCK: Classification, Pathophysiology and Approach to Management


1
SHOCK Classification, Pathophysiology and
Approach to Management
  • Darin Stettler D.O.
  • Millcreek Community Hospital
  • Internal Medicine Resident Lectures

2
SHOCK Classification, Pathophysiology and
Approach to Management
Goal The resident will gain a basic
understanding of the shock syndromes and their
Management
3
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.

4
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).

5
Definition
  • The appropriate definition varies with the
    context of its use.

6
Definition
  • Emergency medical personnel
  • A definition that incorporates the typical
    clinical signs of shock, i.e.
  • Arterial hypotension,
  • Tachycardia,
  • Tachypnea,
  • Altered MS,
  • Decreased UOP.

7
Definition
  • Physiologist
  • Shock may be defined by specific hemodynamic
    criteria involving ventricular filling pressures,
  • Venous pressures,
  • Arterial pressures,
  • CO,
  • SVR.

8
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.

9
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)
10
Classification
11
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
12
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).

13
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.

14
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
15
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.
16
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.

17
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.

18
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.

19
Cardiogenic Shock
  • Clinical signs peripheral vasoconstriction,
    oliguria, JVD, S3 and evidence of pulmonary
    edema.
  • The Hemodynamic profile includes CO,
    PAWP, and systemic hypotension.

20
Cardiogenic Shock
Dx CO SVR PWP CVP MVO2 LVMI VSD LVCO nl (Mechanical) RVCOgtLVCO MVR/ RVMI
21
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.

22
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.

23
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.

24
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.

25
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.

26
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.

27
Microbial Factors
  • Gram-Positive
  • Gram-Negative
  • Fungal
  • P. Aeruginosa
  • S. Aureus
  • Peptidoglycans of cw
  • Endotoxin (LPS)
  • Mennan from cw
  • Exotoxin A
  • TSST

28
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

29
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

30
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.
31
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

32
Septic Shock
33
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

34
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
35
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
36
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.

37
  • 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.

38
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

39
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
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