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Shock
Pathophysiology, Classification, and
     Approach t M
     A       h to Management  t
Shock

Cardiogenic shock - a major component of the the mortality
      g                  j       p                       y
associated with cardiovascular disease (the #1 cause of U.S.
deaths)
Hypovolemic shock - the major contributor to early mortality
from trauma (the #1 cause of death in those < 45 years of age)
Septic shock - the most common cause of death in American
ICUs (the 13th leading cause of death overall in US)
Shock: Definitions



Kumar and Parrillo (1995) - “The state in which profound and
widespread reduction of effective tissue perfusion leads first to
reversible, and then if prolonged, to irreversible cellular injury.”
Shock: Classification
Hypovolemic shock - due to decreased circulating blood volume in
relation to the total vascular capacity and characterized by a reduction
of diastolic filli pressures
 f di t li filling
Cardiogenic shock - due to cardiac pump failure related to loss of
  y                    y               y
myocardial contractility/functional myocardium or
structural/mechanical failure of the cardiac anatomy and characterized
by elevations of diastolic filling pressures and volumes
Extra-cardiac obstructive shock - due to obstruction to flow in the
cardiovascular circuit and characterized by either impairment of
diastolic filling or excessive afterload
Distributive h k
Di t ib ti shock - caused b l
                            d by loss of vasomotor control resulting i
                                       f        t       t l      lti in
arteriolar/venular dilatation and characterized (after fluid resuscitation)
by increased cardiac output and decreased SVR
Classification of Circulatory Shock
HYPOVOLEMIC
  Hemorrhagic
   •   Trauma
   •   Gastrointestinal
   •   Retroperitoneal
  Fluid depletion (nonhemorrhagic)
   •   External fluid loss
         -   Dehydration
         -   Vomiting
         -   Diarrhea
         -   Polyuria
   •   Interstitial fluid redistribution
         -   Thermal injury
         -   Trauma
         -   Anaphylaxis

  Increased vascular capacitance (venodilatation)
   •   Sepsis
   •   Anaphylaxis
   •   Toxins/drugs
       T i /d

                                     Kumar and Parrillo, 2001
Classification of Circulatory Shock
CARDIOGENIC
  Myopathic
   •   Myocardial infarction (hibernating myocardium)
   •   Left ventricle
  Right ventricle
  Blunt Cardiac Injury (trauma)
  Myocarditis
  Cardiomyopathy
  Post-ischemic myocardial stunning
  Septic myocardial depression
  Pharmacologic
   •   Anthracycline cardiotoxicity
   •   Calcium channel blockers
  M h i l
  Mechanical
   •   Valvular failure (stenotic or regurgitant)
   •   Hypertropic cardiomyopathy
   •   Ventricular septal defect
  Arrhythmic
   •   Bradycardia
   •   Tachycardia                     Kumar and Parrillo, 2001
Classification of Circulatory Shock
EXTRACARDIAC OBSTRUCTIVE
  Impaired diastolic filling (decreased ventricular preload)
    •   Direct venous obstruction (vena cava)
          -   intrathoracic obstructive tumors
    •   Increased intrathoracic pressure
          - Tension pneumothorax
          - Mechanical ventilation (with excessive pressure or volume depletion)
          - Asthma
    •   Decreased cardiac compliance
          - Constrictive pericarditis
          - Cardiac tamponade
   Impaired systolic contraction (increased ventricular afterload)
    •   Right ventricle
          g
          - Pulmonary embolus (massive)
          - Acute pulmonary hypertension
    •   Left ventricle
          - Saddle embolus
          - Aortic dissection
                                     Kumar and Parrillo, 2001
Classification of Circulatory Shock

DISTRIBUTIVE
   Septic (bacterial, fungal, viral, rickettsial)
   Toxic shock syndrome
   Anaphylactic,
   Anaphylactic anaphylactoid
   Neurogenic (spinal shock)
   Endocrinologic
    • Adrenal crisis
    • Thyroid storm
   Toxic (e.g., nitroprusside, bretylium)




                  Kumar and Parrillo, 2001
Shock Hemodynamics

                  CO    SVR     PAOP   EDV
Hypovolemic
Cardiogenic
Obstructive
Ob t ti
  afterload
  preload
Distributive
  pre-resusc
  post-resusc
Hypovolemic Shock


Degree of volume loss
  g                               response
                                     p
• 10% well tolerated (tachycardia)
• 20 - 25% failure of compensatory mechanisms (hypotension, orthostasis,
  decreased CO)  )
• > 40% loss associated with overt shock (marked hypotension, decreased CO,
  lactic acidemia)
Clinical Correlates of Hemorrhage
                        Class I                 ClassII           Class III           Class IV
Blood loss (mL)            > 750               750 - 1500         1500 - 2000           > 2000
Blood loss (% total)      > 15%                 15 - 30%           30 - 40%             > 40%
Pulse rate                 < 100                   > 100             > 120               > 140
Blood pressure            Normal                  Normal               ↓                   ↓
Pulse pressure         Normal or ↑                   ↓                 ↓                   ↓
Orthostasis               Absent                 Minimal            Marked              Marked
Capillary refill          Normal                 Delayed            Delayed             Delayed
Resp rate                 14 - 20                 20 - 30           30 - 40              > 34
UO (mL/hr)                 > 30                   20 - 30            5 - 15               <5
CNS mental status      Slight anxiety          Mild anxiety     Anxious/confused   Confused/lethargic
CI (L/min)
   (     )               ↓ 0-10%                ↓ 20-50%           ↓ 50-75%             ↓ >75%

                           American College of Surgeons, 1989
Hypovolemic Shock

Rate of volume loss and pre-existing cardiac reserve
                        p          g
response:
• Acute 1L blood loss results in mild to moderate hypotension with decreased
  CVP and PWP
• Same loss over longer period may be tolerated without hypotension due to
  increased fluid retention, increased RBC 2,3 DPG, tachycardia, and increased
  myocardial contractility
• Same slow loss in patient with diminished cardiac reserve may cause
  hypotension or shock.
Cardiogenic Shock

#1 cause of in-hospital mortality from Q-wave MI
Requires at least 40% loss of functional myocardium (single MI
or cumulative damage) - stunned, nonfunctional, but viable
myocardium may contribute to post-MI cardiogenic shock
Usually involves left main or left anterior descending obstruction
Historically,
Historically incidence of cardiogenic shock post Q wave MI has
                                            post-Q
run 8 - 20%with mortality 70 - 90% (? reduced incidence with
thrombolytics 4 - 7%)
Cardiogenic Shock

Mortality substantially better for cardiogenic shock due to
surgically remediable lesions:
• aortic valve failure (endocarditis, occasionally prosthetic valve failure or aortic
  dissection)
• papillary muscle rupture (i f
      ill         l         (infarct, post-blunt chest trauma, endocarditis, prosthetic
                                           bl     h               d      di i       h i
  valve failure)
    - ischemic form seen 3 - 7 days post-LAD territory infarct (often preceded by new MR
      murmur)
    - v wave of > 10 mm often seen in PWP trace
• VSD (post-infarct, rarely traumatic)
    - post-infarct seen 3 - 7 days post-LAD occlusion
    - 5 - 10% oxygen saturation step up
                                  step-up
Cardiogenic Shock

RV infarction with cardiogenic shock seen in only 10 - 20%
largest inferior wall MIs
Isolated RV infarcts rare - almost all have some degree of LV
involvement
DX includes cardiac tamponade, restrictive cardiomyopathy,
constrictive pericarditis, and PE - Kussmaul’s sign, p
             p                                   g pulsus
paradoxus, filling pressure equalization may be seen in all
Rx fluids and inotropes rather than pressors
Good prognosis relative to LV infarct + shock
Obstructive Shock

Rate of development of obstruction to blood flow                   response:
• acute, massive PE involving 2 or more lobar arteries and 50% pulmonary bed can
  cause shock (sPAP max 50 mm Hg) but chronic PE can cause > 75% obstruction
  without shock (sPAP 100 + mm Hg)
• acute cardiac tamponade can occur with 150 mL fluid but over 2L can be well
                                                   fluid,
  tolerated if slow accumulation

Similar variability based on presence of pre-existing
cardiopulmonary disease
Distributive Shock


Defining feature: loss of p p
       g                  peripheral resistance
Dominantly septic shock, anaphylactic and neurogenic shock
less common
Clinical form of shock with greatest contribution of other shock
elements - i.e., hypovolemia, cardiac failure
Distributive Shock

Anaphylactic shock: immediate hypersensitivity reaction
    p y                          yp            y
mediated by the interaction of IgE on mast cells and basophils
with the appropriate antigen resulting in mediator cascade
Anaphylactoid reactions involve similar release of mediators
via non-immunologic mechanisms.
Primary mediators include histamine, serotonin, eosinophil
chemotactic factor, and proteolytic enzymes.
Secondary mediators include PAF, b d ki i prostaglandins,
S     d       di t  i l d PAF bradykinin,     t l di
and leukotrienes.
Distributive Shock

Anaphylactic shock                  Anaphylactoid shock
  insect envenomations                ionic contrast media
  antibiotics (beta-lactams,          protamine
  vancomycin, sulfonamides)           opiates
                                        p
  heterologous serum (anti-toxin,     polysaccharide volume
  anti-sera)                          expanders (dextran,
  blood transfusion                   hydroxyethyl starch)
  immunoglobulins (esp IgA            muscle relaxants
  deficient)                          anesthetics
  Egg-based vaccines
  latex
Hypodynamic Shock: Perfusion

            g      y
Extrinsic regulatory mechanisms dominate in most vascular
beds except brain and heart
Blood flow to other organs decreased via sympathetic
vasoconstrictive effects
Post-resuscitation, perfusion abnormalities may persist for days
(decreased perfusion of brain, kid
(d        d     f i     f b i kidneys, li
                                        liver, splanchnic organs)
                                                 l   h i        )
with potential persistent ischemia
? irreversible hypodynamic shock
Hyperdynamic Shock: Perfusion

Organ blood flow disturbed at higher pressures suggesting a
primary microvascular regulatory defect
Cerebral perfusion decreased by 33% while coronary vascular
resistance is significantly increased in septic shock - i.e.,
                 g        y                p                ,
coronary and cerebral autoregulatory mechanisms are relatively
intact in sepsis
All other vascular beds exhibit similarly decreased vascular
resistance suggesting active vasodilatory process and failure of
extrinsic control mechanisms
Microvascular studies also show aberrant distribution of
perfusion within tissues and organs.
pe us o            ssues a d o ga s
Determinants of Effective Tissue Perfusion

Cardiovascular Performance
               Cardiac Function
               Venous Return
Vascular P f
V     l Performance
Microvascular Function
Oxygen Unloading and Diffusion
Cellular Energy Metabolism
Cardiac Performance

                   Left                Peripheral
   Preload      ventricular            resistance
                                          i t
                   size
                              Stroke                 Arterial
                              volume                p
                                                    pressure
                Myocardial
                                        Cardiac
Contractility      fiber
                                        output
                shortening
                              Heart
                               rate


  Afterload
Organ Blood Flow in Shock

Dependent on maintenance of blood p
  p                               pressure within an
acceptable range
For humans, good overall auto-regulation of blood flow
between 60 - 100 mm Hg
However, experimental data in animals shows brain and heart
have wider ranges while skeletal muscle has a significantly
narrow auto-regulatory range.
Vascular Failure: Potential Causes

1)
 )   Tissue acidosis
2)   Catecholamine depletion and resistance
3)   Endogenous vasoactive substances
4)   Decreased central sympathetic tone
5)   Pathophysiologic it i
     P th h i l i nitric oxide generation
                           id        ti
Microvasculature in Shock


Vessels of 100 to 150 um diameter
Precapillary vs. postcapillary sphincters
Intrinsic control (autoregulation)
• stretch receptors
• chemoreceptors (CO2, H+)

Extrinsic control via autonomic nervous system
Determinants of Effective Tissue Perfusion (cont)

   Oxygen unloading and diffusion
     • Oxyhemoglobin affinity
          - RBC 2, 3 DPG
          - Blood pH
          - Temperature

   Cellular Function
     • Cellular energy generation/substrate utilization
          - Citric acid (Krebs) cycle
               • Oxidative phosphorylation
               • Other energy metabolism pathways



RBC = Red blood cells DPG = Diphosphoglycerate
Mechanisms of Cellular Injury in Shock

1)
 )   Cellular ischemia
2)   Free radical reperfusion injury
3)   Inflammatory mediators (local and circulating)
Physiologic Oxygen Supply Dependency
                on
Oxygen Consumptio




                                                                 Critical Delivery
                                                                    Threshold
O    n




                                              Oxygen Delivery

                            Mizock BA. Crit Care Med. 1992;20:80-93.
Pathologic Oxygen Supply Dependency
                on


                                                                       Pathologic
Oxygen Consumptio



                                                                       Physiologic
O    n




                                              Oxygen Delivery

                            Mizock BA. Crit Care Med. 1992;20:80-93.
Cellular Ischemia in Shock

                        Evidence
Oxygen supply-dependent oxygen consumption
Washout of organic acids (
              g          (from ischemic tissues) in p
                                               ) patients
with sepsis and MODS after vasodilator Rx
Elevated ATP degradation products with decreased
acetoacetate/hydroxybutyrate ratio (suggestive of altered
hepatic mitochondrial redox potential)
Kumar and Parrillo, 2001
Diagnosis and Evaluation

                          Clinical Signs
Primary diagnosis - tachycardia, tachypnea, oliguria,
encephalopathy (confusion), peripheral hypoperfusion
(mottled, poor capillary refill vs. hyperemic and warm),
hypotension
Differential DX:
   JVP - hypovolemic vs. cardiogenic
   Left S3, S4, new murmurs - cardiogenic
   Right heart failure - PE, tamponade
     g                      ,    p
   Pulsus paradoxus, Kussmaul’s sign - tamponade
   Fever, rigors, infection focus - septic
Diagnosis and Evaluation

                         Laboratory
Hgb, WBC, platelets
PT/PTT
Electrolytes, arterial blood gases
BUN, Cr
Ca, Mg
Serum lactate, SVO2
      lactate
ECG
Diagnosis and Evaluation

                  Invasive Monitoring
Arterial pressure catheter
CVP monitoring
Pulmonary artery catheter (+/- RVEF, oximetry)
SVO2 / ScVO2
DO and VO
       2
      2           2
A Clinical Approach to Shock
          Diagnosis and Management
              Initial Diagnostic Steps
CXR
Abdominal views*
CT scan abdomen or chest*
Echocardiogram*
Pulmonary perfusion scan*
A Clinical Approach to Shock
            Diagnosis and Management
                  Initial Therapeutic Steps
Admit to intensive care unit (ICU)
Venous access (1 or 2 wide-bore catheters)
                 (                       )
Central venous catheter
Arterial catheter
EKG monitoring
Pulse oximetry
Hemodynamic support (MAP < 60 mmHg)
• Fluid challenge
• Vasopressors for severe shock unresponsive to fluids
       p                             p
A Clinical Approach to Shock
             Diagnosis and Management

      Diagnosis Remains Undefined or
         g
 Hemodynamic Status Requires Repeated Fluid
        Challenges of Vasopressors
Pulmonary Artery Catheterization
• Cardiac output
• Oxygen delivery
• Filling pressures

Echocardiography
• Pericardial fluid
• Cardiac function
• Valve or shunt abnormalities
A Clinical Approach to Shock
                 Diagnosis and Management
                       Immediate Goals in Shock
Hemodynamic support                                 MAP > 60mmHg
                                                    PAOP = 12 - 18 mmHg
                                                    Cardiac Index 2.2 L/min/m
                                                    C di I d > 2 2 L/ i / 2
Maintain oxygen delivery                            Hemoglobin > 10 g/dL
                                                    Arterial saturation > 92%
                                                    Supplemental oxygen and
                                                    mechanical ventilation
Reversal of oxygen dysfunction                      Decreasing lactate (< 2 2 mM/L)
                                                                            2.2
                                                    Maintain urine output
`                                                   Reverse encephalopathy
                                                    Improving renal, liver function tests
                                                      p     g       ,
          MAP = mean arterial pressure; PAOP = pulmonary artery
          occlusion pressure.
A Clinical Approach to Shock
             Diagnosis and Management

                     Hypovolemic Shock
Rapid replacement of blood, colloid, or crystalloid
Identify
Id if source of blood or fl id l
              f bl d fluid loss:
•   OR
•   Endoscopy/colonoscopy
•   Angiography
•   CT/MRI scan
•   Other
A Clinical Approach to Shock
                Diagnosis and Management
                           Cardiogenic Shock
                                 g
LV infarction
•   Intra-aortic balloon pump (IABP)
•   Cardiac angiography
•   Revascularization
     - angioplasty
     - coronary bypass

RV infarction
•   Fluid and inotropes with PA catheter monitoring

Mechanical b
M h i l abnormality
               lit
•   Echocardiography
•   Cardiac cath
•   C     ti
    Corrective surgery
A Clinical Approach to Shock
              Diagnosis and Management
             Extra-
             Extra-cardiac Obstructive Shock
Pericardial tamponade
• pericardiocentesis
  p
• surgical drainage (if needed)

Pulmonary embolism
•   heparin
•   ventilation/perfusion lung scan
•   pulmonary angiography
•   consider:
     - thrombolytic therapy
     - embolectomy at surgery
A Clinical Approach to Shock
               Diagnosis and Management
                          Distributive Shock
Septic shock
•   Identify site of infection and drain, if possible
•   Antimicrobial agents (key rules)
•   ICU monitoring and support with fluids, vasopressors, and inotropic agents
•   EGDT (Rivers, 2001)
            (Rivers
•   Surviving Sepsis Guidelines (CCM, 2007)
•   Goals:
     - SV02 > 70%
     - improving organ function
     - decreasing lactate levels
Fluid Therapy

Crystalloids
  y
• Lactated Ringer’s solution
• Normal saline

Colloids
• Hetastarch
• Albumin

Packed red blood cells
Infuse to physiologic endpoints
Fluid Therapy

Correct hypotension first (g
         yp               (golden hour)
                                      )
Decrease heart rate
Correct hypoperfusion abnormalities
Monitor for deterioration of oxygenation
Therapy: Resuscitation Fluids

Crystalloid vs. colloid
  y
Optimal PWP 10 - 12 vs. 15 - 18 mm Hg

20 mL/kg fluid challenge in hypovolemic or septic shock with
re challenges
re-challenges of 5 - 10 mL/kg
100 - 200 mL challenges in cardiogenic
shock

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shock

  • 1. Shock Pathophysiology, Classification, and Approach t M A h to Management t
  • 2. Shock Cardiogenic shock - a major component of the the mortality g j p y associated with cardiovascular disease (the #1 cause of U.S. deaths) Hypovolemic shock - the major contributor to early mortality from trauma (the #1 cause of death in those < 45 years of age) Septic shock - the most common cause of death in American ICUs (the 13th leading cause of death overall in US)
  • 3. Shock: Definitions Kumar and Parrillo (1995) - “The state in which profound and widespread reduction of effective tissue perfusion leads first to reversible, and then if prolonged, to irreversible cellular injury.”
  • 4. Shock: Classification Hypovolemic shock - due to decreased circulating blood volume in relation to the total vascular capacity and characterized by a reduction of diastolic filli pressures f di t li filling Cardiogenic shock - due to cardiac pump failure related to loss of y y y myocardial contractility/functional myocardium or structural/mechanical failure of the cardiac anatomy and characterized by elevations of diastolic filling pressures and volumes Extra-cardiac obstructive shock - due to obstruction to flow in the cardiovascular circuit and characterized by either impairment of diastolic filling or excessive afterload Distributive h k Di t ib ti shock - caused b l d by loss of vasomotor control resulting i f t t l lti in arteriolar/venular dilatation and characterized (after fluid resuscitation) by increased cardiac output and decreased SVR
  • 5. Classification of Circulatory Shock HYPOVOLEMIC Hemorrhagic • Trauma • Gastrointestinal • Retroperitoneal Fluid depletion (nonhemorrhagic) • External fluid loss - Dehydration - Vomiting - Diarrhea - Polyuria • Interstitial fluid redistribution - Thermal injury - Trauma - Anaphylaxis Increased vascular capacitance (venodilatation) • Sepsis • Anaphylaxis • Toxins/drugs T i /d Kumar and Parrillo, 2001
  • 6. Classification of Circulatory Shock CARDIOGENIC Myopathic • Myocardial infarction (hibernating myocardium) • Left ventricle Right ventricle Blunt Cardiac Injury (trauma) Myocarditis Cardiomyopathy Post-ischemic myocardial stunning Septic myocardial depression Pharmacologic • Anthracycline cardiotoxicity • Calcium channel blockers M h i l Mechanical • Valvular failure (stenotic or regurgitant) • Hypertropic cardiomyopathy • Ventricular septal defect Arrhythmic • Bradycardia • Tachycardia Kumar and Parrillo, 2001
  • 7. Classification of Circulatory Shock EXTRACARDIAC OBSTRUCTIVE Impaired diastolic filling (decreased ventricular preload) • Direct venous obstruction (vena cava) - intrathoracic obstructive tumors • Increased intrathoracic pressure - Tension pneumothorax - Mechanical ventilation (with excessive pressure or volume depletion) - Asthma • Decreased cardiac compliance - Constrictive pericarditis - Cardiac tamponade Impaired systolic contraction (increased ventricular afterload) • Right ventricle g - Pulmonary embolus (massive) - Acute pulmonary hypertension • Left ventricle - Saddle embolus - Aortic dissection Kumar and Parrillo, 2001
  • 8. Classification of Circulatory Shock DISTRIBUTIVE Septic (bacterial, fungal, viral, rickettsial) Toxic shock syndrome Anaphylactic, Anaphylactic anaphylactoid Neurogenic (spinal shock) Endocrinologic • Adrenal crisis • Thyroid storm Toxic (e.g., nitroprusside, bretylium) Kumar and Parrillo, 2001
  • 9. Shock Hemodynamics CO SVR PAOP EDV Hypovolemic Cardiogenic Obstructive Ob t ti afterload preload Distributive pre-resusc post-resusc
  • 10.
  • 11. Hypovolemic Shock Degree of volume loss g response p • 10% well tolerated (tachycardia) • 20 - 25% failure of compensatory mechanisms (hypotension, orthostasis, decreased CO) ) • > 40% loss associated with overt shock (marked hypotension, decreased CO, lactic acidemia)
  • 12. Clinical Correlates of Hemorrhage Class I ClassII Class III Class IV Blood loss (mL) > 750 750 - 1500 1500 - 2000 > 2000 Blood loss (% total) > 15% 15 - 30% 30 - 40% > 40% Pulse rate < 100 > 100 > 120 > 140 Blood pressure Normal Normal ↓ ↓ Pulse pressure Normal or ↑ ↓ ↓ ↓ Orthostasis Absent Minimal Marked Marked Capillary refill Normal Delayed Delayed Delayed Resp rate 14 - 20 20 - 30 30 - 40 > 34 UO (mL/hr) > 30 20 - 30 5 - 15 <5 CNS mental status Slight anxiety Mild anxiety Anxious/confused Confused/lethargic CI (L/min) ( ) ↓ 0-10% ↓ 20-50% ↓ 50-75% ↓ >75% American College of Surgeons, 1989
  • 13. Hypovolemic Shock Rate of volume loss and pre-existing cardiac reserve p g response: • Acute 1L blood loss results in mild to moderate hypotension with decreased CVP and PWP • Same loss over longer period may be tolerated without hypotension due to increased fluid retention, increased RBC 2,3 DPG, tachycardia, and increased myocardial contractility • Same slow loss in patient with diminished cardiac reserve may cause hypotension or shock.
  • 14. Cardiogenic Shock #1 cause of in-hospital mortality from Q-wave MI Requires at least 40% loss of functional myocardium (single MI or cumulative damage) - stunned, nonfunctional, but viable myocardium may contribute to post-MI cardiogenic shock Usually involves left main or left anterior descending obstruction Historically, Historically incidence of cardiogenic shock post Q wave MI has post-Q run 8 - 20%with mortality 70 - 90% (? reduced incidence with thrombolytics 4 - 7%)
  • 15. Cardiogenic Shock Mortality substantially better for cardiogenic shock due to surgically remediable lesions: • aortic valve failure (endocarditis, occasionally prosthetic valve failure or aortic dissection) • papillary muscle rupture (i f ill l (infarct, post-blunt chest trauma, endocarditis, prosthetic bl h d di i h i valve failure) - ischemic form seen 3 - 7 days post-LAD territory infarct (often preceded by new MR murmur) - v wave of > 10 mm often seen in PWP trace • VSD (post-infarct, rarely traumatic) - post-infarct seen 3 - 7 days post-LAD occlusion - 5 - 10% oxygen saturation step up step-up
  • 16. Cardiogenic Shock RV infarction with cardiogenic shock seen in only 10 - 20% largest inferior wall MIs Isolated RV infarcts rare - almost all have some degree of LV involvement DX includes cardiac tamponade, restrictive cardiomyopathy, constrictive pericarditis, and PE - Kussmaul’s sign, p p g pulsus paradoxus, filling pressure equalization may be seen in all Rx fluids and inotropes rather than pressors Good prognosis relative to LV infarct + shock
  • 17. Obstructive Shock Rate of development of obstruction to blood flow response: • acute, massive PE involving 2 or more lobar arteries and 50% pulmonary bed can cause shock (sPAP max 50 mm Hg) but chronic PE can cause > 75% obstruction without shock (sPAP 100 + mm Hg) • acute cardiac tamponade can occur with 150 mL fluid but over 2L can be well fluid, tolerated if slow accumulation Similar variability based on presence of pre-existing cardiopulmonary disease
  • 18. Distributive Shock Defining feature: loss of p p g peripheral resistance Dominantly septic shock, anaphylactic and neurogenic shock less common Clinical form of shock with greatest contribution of other shock elements - i.e., hypovolemia, cardiac failure
  • 19. Distributive Shock Anaphylactic shock: immediate hypersensitivity reaction p y yp y mediated by the interaction of IgE on mast cells and basophils with the appropriate antigen resulting in mediator cascade Anaphylactoid reactions involve similar release of mediators via non-immunologic mechanisms. Primary mediators include histamine, serotonin, eosinophil chemotactic factor, and proteolytic enzymes. Secondary mediators include PAF, b d ki i prostaglandins, S d di t i l d PAF bradykinin, t l di and leukotrienes.
  • 20. Distributive Shock Anaphylactic shock Anaphylactoid shock insect envenomations ionic contrast media antibiotics (beta-lactams, protamine vancomycin, sulfonamides) opiates p heterologous serum (anti-toxin, polysaccharide volume anti-sera) expanders (dextran, blood transfusion hydroxyethyl starch) immunoglobulins (esp IgA muscle relaxants deficient) anesthetics Egg-based vaccines latex
  • 21. Hypodynamic Shock: Perfusion g y Extrinsic regulatory mechanisms dominate in most vascular beds except brain and heart Blood flow to other organs decreased via sympathetic vasoconstrictive effects Post-resuscitation, perfusion abnormalities may persist for days (decreased perfusion of brain, kid (d d f i f b i kidneys, li liver, splanchnic organs) l h i ) with potential persistent ischemia ? irreversible hypodynamic shock
  • 22. Hyperdynamic Shock: Perfusion Organ blood flow disturbed at higher pressures suggesting a primary microvascular regulatory defect Cerebral perfusion decreased by 33% while coronary vascular resistance is significantly increased in septic shock - i.e., g y p , coronary and cerebral autoregulatory mechanisms are relatively intact in sepsis All other vascular beds exhibit similarly decreased vascular resistance suggesting active vasodilatory process and failure of extrinsic control mechanisms Microvascular studies also show aberrant distribution of perfusion within tissues and organs. pe us o ssues a d o ga s
  • 23. Determinants of Effective Tissue Perfusion Cardiovascular Performance Cardiac Function Venous Return Vascular P f V l Performance Microvascular Function Oxygen Unloading and Diffusion Cellular Energy Metabolism
  • 24. Cardiac Performance Left Peripheral Preload ventricular resistance i t size Stroke Arterial volume p pressure Myocardial Cardiac Contractility fiber output shortening Heart rate Afterload
  • 25. Organ Blood Flow in Shock Dependent on maintenance of blood p p pressure within an acceptable range For humans, good overall auto-regulation of blood flow between 60 - 100 mm Hg However, experimental data in animals shows brain and heart have wider ranges while skeletal muscle has a significantly narrow auto-regulatory range.
  • 26. Vascular Failure: Potential Causes 1) ) Tissue acidosis 2) Catecholamine depletion and resistance 3) Endogenous vasoactive substances 4) Decreased central sympathetic tone 5) Pathophysiologic it i P th h i l i nitric oxide generation id ti
  • 27. Microvasculature in Shock Vessels of 100 to 150 um diameter Precapillary vs. postcapillary sphincters Intrinsic control (autoregulation) • stretch receptors • chemoreceptors (CO2, H+) Extrinsic control via autonomic nervous system
  • 28. Determinants of Effective Tissue Perfusion (cont) Oxygen unloading and diffusion • Oxyhemoglobin affinity - RBC 2, 3 DPG - Blood pH - Temperature Cellular Function • Cellular energy generation/substrate utilization - Citric acid (Krebs) cycle • Oxidative phosphorylation • Other energy metabolism pathways RBC = Red blood cells DPG = Diphosphoglycerate
  • 29. Mechanisms of Cellular Injury in Shock 1) ) Cellular ischemia 2) Free radical reperfusion injury 3) Inflammatory mediators (local and circulating)
  • 30. Physiologic Oxygen Supply Dependency on Oxygen Consumptio Critical Delivery Threshold O n Oxygen Delivery Mizock BA. Crit Care Med. 1992;20:80-93.
  • 31. Pathologic Oxygen Supply Dependency on Pathologic Oxygen Consumptio Physiologic O n Oxygen Delivery Mizock BA. Crit Care Med. 1992;20:80-93.
  • 32. Cellular Ischemia in Shock Evidence Oxygen supply-dependent oxygen consumption Washout of organic acids ( g (from ischemic tissues) in p ) patients with sepsis and MODS after vasodilator Rx Elevated ATP degradation products with decreased acetoacetate/hydroxybutyrate ratio (suggestive of altered hepatic mitochondrial redox potential)
  • 33.
  • 34.
  • 36.
  • 37.
  • 38. Diagnosis and Evaluation Clinical Signs Primary diagnosis - tachycardia, tachypnea, oliguria, encephalopathy (confusion), peripheral hypoperfusion (mottled, poor capillary refill vs. hyperemic and warm), hypotension Differential DX: JVP - hypovolemic vs. cardiogenic Left S3, S4, new murmurs - cardiogenic Right heart failure - PE, tamponade g , p Pulsus paradoxus, Kussmaul’s sign - tamponade Fever, rigors, infection focus - septic
  • 39. Diagnosis and Evaluation Laboratory Hgb, WBC, platelets PT/PTT Electrolytes, arterial blood gases BUN, Cr Ca, Mg Serum lactate, SVO2 lactate ECG
  • 40. Diagnosis and Evaluation Invasive Monitoring Arterial pressure catheter CVP monitoring Pulmonary artery catheter (+/- RVEF, oximetry) SVO2 / ScVO2 DO and VO 2 2 2
  • 41. A Clinical Approach to Shock Diagnosis and Management Initial Diagnostic Steps CXR Abdominal views* CT scan abdomen or chest* Echocardiogram* Pulmonary perfusion scan*
  • 42. A Clinical Approach to Shock Diagnosis and Management Initial Therapeutic Steps Admit to intensive care unit (ICU) Venous access (1 or 2 wide-bore catheters) ( ) Central venous catheter Arterial catheter EKG monitoring Pulse oximetry Hemodynamic support (MAP < 60 mmHg) • Fluid challenge • Vasopressors for severe shock unresponsive to fluids p p
  • 43. A Clinical Approach to Shock Diagnosis and Management Diagnosis Remains Undefined or g Hemodynamic Status Requires Repeated Fluid Challenges of Vasopressors Pulmonary Artery Catheterization • Cardiac output • Oxygen delivery • Filling pressures Echocardiography • Pericardial fluid • Cardiac function • Valve or shunt abnormalities
  • 44.
  • 45.
  • 46.
  • 47. A Clinical Approach to Shock Diagnosis and Management Immediate Goals in Shock Hemodynamic support MAP > 60mmHg PAOP = 12 - 18 mmHg Cardiac Index 2.2 L/min/m C di I d > 2 2 L/ i / 2 Maintain oxygen delivery Hemoglobin > 10 g/dL Arterial saturation > 92% Supplemental oxygen and mechanical ventilation Reversal of oxygen dysfunction Decreasing lactate (< 2 2 mM/L) 2.2 Maintain urine output ` Reverse encephalopathy Improving renal, liver function tests p g , MAP = mean arterial pressure; PAOP = pulmonary artery occlusion pressure.
  • 48. A Clinical Approach to Shock Diagnosis and Management Hypovolemic Shock Rapid replacement of blood, colloid, or crystalloid Identify Id if source of blood or fl id l f bl d fluid loss: • OR • Endoscopy/colonoscopy • Angiography • CT/MRI scan • Other
  • 49. A Clinical Approach to Shock Diagnosis and Management Cardiogenic Shock g LV infarction • Intra-aortic balloon pump (IABP) • Cardiac angiography • Revascularization - angioplasty - coronary bypass RV infarction • Fluid and inotropes with PA catheter monitoring Mechanical b M h i l abnormality lit • Echocardiography • Cardiac cath • C ti Corrective surgery
  • 50. A Clinical Approach to Shock Diagnosis and Management Extra- Extra-cardiac Obstructive Shock Pericardial tamponade • pericardiocentesis p • surgical drainage (if needed) Pulmonary embolism • heparin • ventilation/perfusion lung scan • pulmonary angiography • consider: - thrombolytic therapy - embolectomy at surgery
  • 51. A Clinical Approach to Shock Diagnosis and Management Distributive Shock Septic shock • Identify site of infection and drain, if possible • Antimicrobial agents (key rules) • ICU monitoring and support with fluids, vasopressors, and inotropic agents • EGDT (Rivers, 2001) (Rivers • Surviving Sepsis Guidelines (CCM, 2007) • Goals: - SV02 > 70% - improving organ function - decreasing lactate levels
  • 52. Fluid Therapy Crystalloids y • Lactated Ringer’s solution • Normal saline Colloids • Hetastarch • Albumin Packed red blood cells Infuse to physiologic endpoints
  • 53. Fluid Therapy Correct hypotension first (g yp (golden hour) ) Decrease heart rate Correct hypoperfusion abnormalities Monitor for deterioration of oxygenation
  • 54. Therapy: Resuscitation Fluids Crystalloid vs. colloid y Optimal PWP 10 - 12 vs. 15 - 18 mm Hg 20 mL/kg fluid challenge in hypovolemic or septic shock with re challenges re-challenges of 5 - 10 mL/kg 100 - 200 mL challenges in cardiogenic