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Shock
Gordon R. Bernard, M.D.
Division of Allergy, Pulmonary,
and Critical Care Medicine
Vanderbilt University
Overall Objectives
• Understand the pathophysiology of
shock
• Know the types of shock and how
they differ
• Understand th...
Definition
• (Gross, 1882)
“A manifestation of the rude unhinging
of the machinery of life.”
• (Guyton, 1966)
“An abnormal...
Types of Shock
• Hypovolemic
• Loss of blood or plasma
• Cardiogenic
• Myocardial infarction
• Cardiac trauma
• Distributi...
Arterial Resistance
• Controlled by:
• a) Arteriolar tone
• b) Precapillary sphincter
» Control capillary hydrostatic pres...
Blood Pressure = SVR X C.O.
Factors Causing Reduced
Cardiac Output
• A. Reduced venous return
• Hypovolemic shock
• Endotoxic shock
• Anaphylactic sho...
Hemorrhagic shock
• Due to volume loss:
• Blood
• Plasma
• Fluid/electrolyte
• 10% of blood volume can be lost with
minimal hemodynamic effects.
• 20% loss followed by initiation of BP
reduction.
• S...
CORRELATION OF MAGNITUDE OF VOLUME DEFICIT
AND CLINICAL PRESENTATION
Approximate
deficit
Decrease in Blood
Volume Degree S...
Clinical Features
• Sensorium
Anxiety to obtundation
• Weakness or prostration
• Pallor
• Sweating
• Tachycardia
• Thready...
Hypovolemic Shock
First signs are postural drop in pressure
(10 mm) or increase in heart rate
Laboratory Changes
• Hematocrit - No change until dilution occurs
• Blood Gas Studies:
Indicate degree of acid-base distur...
Time Required for
Blood Typing Procedures
Blood Bank Activity Time Required
Release O-negative blood (no 1 minute
testing)...
Compensatory Mechanisms
• To maintain perfusion pressure
• Sympathetic discharge
• Catecholamines increase
• Heart rate an...
• Aim is to effectively perfuse coronary and
carotid arteries.
• Catecholamines produce greater contraction
of precapillar...
Overall Effect:
• Constriction of arterioles and venules
• Increase in central blood volume
• Increase in cardiac output (...
Sympathetic Discharge
• Negative effects if sustained
• Sludging of blood
• Disseminated intravascular coagulation
• Profo...
Late Shock
• Postcapillary sphincter resistance
greater than precapillary
• Therefore, hydrostatic pressure
increased
• In...
Capillary Injury
• Important part of the shock process
• Maybe due to:
• Increased platelet adhesiveness
• Release of vaso...
Shock Lung (ARDS)
• Pulmonary edema
• Alveolar hemorrhage
• Pulmonary vascular congestion
• Loss of surfactant
• Increased...
Hypovolemic Shock
• Control bleeding
• Establish and maintain airway + O2
• Assist ventilation (if necessary)
• Replace vo...
Fluids
• Any fluid can improve perfusion, at least
temporarily
• Only RBC’s carry oxygen
Two generalizations:
Fluids
• Crystalloids (electrolyte solutions)
• Colloids (large molecular weight)
• Red blood cells
Object is to refill th...
Selection of Replacement
Fluid
• Electrolyte solutions (crystalloids)
• Rapidly escape from intravascular
space into the i...
Colloids (large molecules)
• Increase plasma onocotic pressure
• Draw fluid into plasma space
• Remain in circulation long...
Colloid vs Crystalloid Controversy
Choi PTL, et al. Critical Care Med 1999;27:200-10.
Schierhout G, et al. BMJ 1998;316:96...
Cardiogenic Shock
• Myocardial infarction
• Rhythm disturbance
Due to impaired cardiac pumping due to:
CVP Increased
Pulmo...
Cardiogenic Shock
• Systolic BP < 80 mm
• Cardiac Index < 2.1 liters/min/m2
• Urinary output < 20 ml/hr
• Reduced cerebral...
Cardiogenic Shock
• Incidence 15% of M.I.
• Mortality 70-90%
• Usually > 40% of left ventricle
infarcted
Potentially Repairable
Lesions
• Ruptured chordae tendinae
• Intraventricular septal defects
Cardiogenic Shock
PCWP < 18 mmHg PCWP > 18 mmHg
Expand Blood Volume Inotropic drug
Diuretic
Vasodilator
Mechanical Asst.
Dobutamine
• ß1 Stimulant
• Mainly inotropic effects
• Probably drug of choice in
cardiogenic shock
Septic Shock
• Endotoxin or other mediator release
• Activation of vasoactive kinins
• Activation of intrinsic coagulation...
Hemodynamics:
• Peripheral resistance fails
• C.O. and HR rise (but not enough)
• BP falls
Therapy for Septic Shock
• General supportive measures
• Specific antibacterial therapy
• Corticosteroids?
• Activated pro...
Recent Randomized Studies
Suggest:
High-dose steroids produce
short-term improvement but no
long-term effects on survival.
Treatment of Shock
Remember: problem is flow, not simply
blood pressure
Aim:
To increase flow through the microcirculation
Vasoconstrictors
• Phenylephrine
• Vasoconstricts
• Elevates blood pressure but increases
myocardial work
• Decrease cardi...
Dopamine
αEffects βEffects Dopaminergic
Low doses
(1-2µg/kg/min)
- - +++
Intermediate doses
(2-10µg/kg/min)
- ++ +++
High ...
Vasopressin in Septic Shock
• Redistributes blood flow
– Away from muscle, skin, gut
– To brain and heart
• High dose: cor...
BP and Vasopressin Levels
After AVP for Septic Shock
0
40
80
120
160
Baseline AVP 0.04
U/min
AVP Off AVP 0.01
U/min
Landry...
TNFTNF
IL-1, 6, 8IL-1, 6, 8
Nitric oxideNitric oxide
OxidantsOxidants
BradykininBradykinin
ThromboxaneThromboxane
Prostagl...
Primary Analysis:Primary Analysis:
28-Day All-Cause Mortality28-Day All-Cause Mortality
24.7
30.8
0
5
10
15
20
25
30
35
Pl...
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Shock Gordon R. Bernard, M.D.

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Transcript of "Shock Gordon R. Bernard, M.D."

  1. 1. Shock Gordon R. Bernard, M.D. Division of Allergy, Pulmonary, and Critical Care Medicine Vanderbilt University
  2. 2. Overall Objectives • Understand the pathophysiology of shock • Know the types of shock and how they differ • Understand the therapeutic approaches to shock
  3. 3. Definition • (Gross, 1882) “A manifestation of the rude unhinging of the machinery of life.” • (Guyton, 1966) “An abnormal state of the circulation in which cardiac output is reduced enough that the tissues of the body are damaged from lack of blood flow.”
  4. 4. Types of Shock • Hypovolemic • Loss of blood or plasma • Cardiogenic • Myocardial infarction • Cardiac trauma • Distributive • e.g., septic shock • Obstructive • Pulmonary embolism
  5. 5. Arterial Resistance • Controlled by: • a) Arteriolar tone • b) Precapillary sphincter » Control capillary hydrostatic pressure • c) Postcapillary sphincter
  6. 6. Blood Pressure = SVR X C.O.
  7. 7. Factors Causing Reduced Cardiac Output • A. Reduced venous return • Hypovolemic shock • Endotoxic shock • Anaphylactic shock • Obstruction to venous return • B. Reduced pumping ability • Cardiogenic shock
  8. 8. Hemorrhagic shock • Due to volume loss: • Blood • Plasma • Fluid/electrolyte
  9. 9. • 10% of blood volume can be lost with minimal hemodynamic effects. • 20% loss followed by initiation of BP reduction. • Sympathetic activity increases. • Vasoconstriction occurs (cerebral and coronary circulation protected).
  10. 10. CORRELATION OF MAGNITUDE OF VOLUME DEFICIT AND CLINICAL PRESENTATION Approximate deficit Decrease in Blood Volume Degree Signs ml % 0 – 500 0 – 10 None None 500 – 1200 10 - 25 Mild (Compromised) Slight tachycardia Postural blood pressure changes Mild peripheral vasoconstriction 1200 – 1600 25 – 15 Moderate Thready pulse, 100-120 beats/min Blood pressure 90-100 mmHg systolic Marked vasocontriction Diaphoresis Anxiety, restlessness Decreased urinary output 1600-2500 16 – 60 Severe Thready pulse > 120 beats/min Blood pressure <60 mmHg systolic Marked vasocontriction Obtundation No urinary output Shock
  11. 11. Clinical Features • Sensorium Anxiety to obtundation • Weakness or prostration • Pallor • Sweating • Tachycardia • Thready pulse • Hypotension • Tachypnea
  12. 12. Hypovolemic Shock First signs are postural drop in pressure (10 mm) or increase in heart rate
  13. 13. Laboratory Changes • Hematocrit - No change until dilution occurs • Blood Gas Studies: Indicate degree of acid-base disturbance and lactic acidosis (anaerobic metabolism) • Electrolytes and Renal Function Tests: Important baseline information • Blood - Type and crossmatch • Urine Output - Monitor continuously Initial:
  14. 14. Time Required for Blood Typing Procedures Blood Bank Activity Time Required Release O-negative blood (no 1 minute testing) Issue type specific blood (group 15 minutes and type recipient’s blood) Carry out saline and albumin 30 minutes cross-matches Finish complete crossmatch (regroup, 45 minutes retype, carry out saline, Coombs, and albumin crossmatches, screen recipient’s blood)
  15. 15. Compensatory Mechanisms • To maintain perfusion pressure • Sympathetic discharge • Catecholamines increase • Heart rate and contractility increased • Afferent arterioles in vascular beds constrict • Peripheral resistance • Venous capacitance vessels constricted • Increase in venous return
  16. 16. • Aim is to effectively perfuse coronary and carotid arteries. • Catecholamines produce greater contraction of precapillary sphincter than postcapillary sphincter. • Therefore, cappilary hydrostatic pressure is reduced. • In early stages of shock this is important in pulling fluid into the intravascular space and increasing blood volume (Hct reduced).
  17. 17. Overall Effect: • Constriction of arterioles and venules • Increase in central blood volume • Increase in cardiac output (circulates the available blood more rapidly) • Draws interstitial fluid into intravascular space
  18. 18. Sympathetic Discharge • Negative effects if sustained • Sludging of blood • Disseminated intravascular coagulation • Profound acidosis • Tissue hypoxia-cell death • Acidosis, metabolites and hypoxia relax precapillary sphincter more than post capillary sphincter.
  19. 19. Late Shock • Postcapillary sphincter resistance greater than precapillary • Therefore, hydrostatic pressure increased • Interstitial edema produced
  20. 20. Capillary Injury • Important part of the shock process • Maybe due to: • Increased platelet adhesiveness • Release of vasoactive materials • Leads to further loss of plasma volume. • Also, if in pulmonary bed may contribute to shock lung.
  21. 21. Shock Lung (ARDS) • Pulmonary edema • Alveolar hemorrhage • Pulmonary vascular congestion • Loss of surfactant • Increased lymph flow
  22. 22. Hypovolemic Shock • Control bleeding • Establish and maintain airway + O2 • Assist ventilation (if necessary) • Replace volume • Acid-base correction Therapy
  23. 23. Fluids • Any fluid can improve perfusion, at least temporarily • Only RBC’s carry oxygen Two generalizations:
  24. 24. Fluids • Crystalloids (electrolyte solutions) • Colloids (large molecular weight) • Red blood cells Object is to refill the vascular compartment. Choice:
  25. 25. Selection of Replacement Fluid • Electrolyte solutions (crystalloids) • Rapidly escape from intravascular space into the interstitium. Therefore, short-lived volume expansion.
  26. 26. Colloids (large molecules) • Increase plasma onocotic pressure • Draw fluid into plasma space • Remain in circulation longer than crystalloids • Raise interstitial onocotic pressure • May cause pulmonary edema e.g. Dextran, Albumin, Hetastarch, P.P.F. But When they escape from circulation, e.g., through damaged capillaries:
  27. 27. Colloid vs Crystalloid Controversy Choi PTL, et al. Critical Care Med 1999;27:200-10. Schierhout G, et al. BMJ 1998;316:961-4. Lowe 1977 0.68 Lucas 1978 0.07 Butros 1979 2.22 Virgillo 1979 1.07 Moss 1981 2.43 Goodwin 1983 0.27 Modic 1983 1.08 Rackow 1983 1.23 Shires 1983 1.0 Metildi 1984 0.82 Sade 1985 1.83 Karanko 1987 2.37 Davidson 1991 1.0 London 1992 0.22 Pocka 1994 0.90 Overall 0.97 1 100.10.01 100 Favors Crystalloid Favors Colloid
  28. 28. Cardiogenic Shock • Myocardial infarction • Rhythm disturbance Due to impaired cardiac pumping due to: CVP Increased Pulmonary Capillary Wedge increased
  29. 29. Cardiogenic Shock • Systolic BP < 80 mm • Cardiac Index < 2.1 liters/min/m2 • Urinary output < 20 ml/hr • Reduced cerebral perfusion (Confusion Obtundation)
  30. 30. Cardiogenic Shock • Incidence 15% of M.I. • Mortality 70-90% • Usually > 40% of left ventricle infarcted
  31. 31. Potentially Repairable Lesions • Ruptured chordae tendinae • Intraventricular septal defects
  32. 32. Cardiogenic Shock PCWP < 18 mmHg PCWP > 18 mmHg Expand Blood Volume Inotropic drug Diuretic Vasodilator Mechanical Asst.
  33. 33. Dobutamine • ß1 Stimulant • Mainly inotropic effects • Probably drug of choice in cardiogenic shock
  34. 34. Septic Shock • Endotoxin or other mediator release • Activation of vasoactive kinins • Activation of intrinsic coagulation system • Increasing capillary permeability • Decreased peripheral vascular resistance • Disseminated intravascular coagulation • Mortality 40-50% Causing
  35. 35. Hemodynamics: • Peripheral resistance fails • C.O. and HR rise (but not enough) • BP falls
  36. 36. Therapy for Septic Shock • General supportive measures • Specific antibacterial therapy • Corticosteroids? • Activated protein C
  37. 37. Recent Randomized Studies Suggest: High-dose steroids produce short-term improvement but no long-term effects on survival.
  38. 38. Treatment of Shock Remember: problem is flow, not simply blood pressure Aim: To increase flow through the microcirculation
  39. 39. Vasoconstrictors • Phenylephrine • Vasoconstricts • Elevates blood pressure but increases myocardial work • Decrease cardiac output • Decrease tissue perfusion • Rarely used except in anesthesia for management of drug induced vasodilation α1-Agonists
  40. 40. Dopamine αEffects βEffects Dopaminergic Low doses (1-2µg/kg/min) - - +++ Intermediate doses (2-10µg/kg/min) - ++ +++ High doses +++ +++ +++
  41. 41. Vasopressin in Septic Shock • Redistributes blood flow – Away from muscle, skin, gut – To brain and heart • High dose: coronary vasoconstriction • Antidiuretic effect • Inexpensive • No proven effect on ultimate outcome
  42. 42. BP and Vasopressin Levels After AVP for Septic Shock 0 40 80 120 160 Baseline AVP 0.04 U/min AVP Off AVP 0.01 U/min Landry DW, et al. Circulation 1997;95:1122-5. Landry DW, et al. Crit Care Med 1997;25:1279-82. SBP N=10 SBP (mmHg) or AVPlevel(pg/mL)
  43. 43. TNFTNF IL-1, 6, 8IL-1, 6, 8 Nitric oxideNitric oxide OxidantsOxidants BradykininBradykinin ThromboxaneThromboxane ProstaglandinsProstaglandins LeukotrienesLeukotrienes EnzymesEnzymes ComplementComplement TNFsr IL-TNFsr IL- 1ra1ra PGE2PGE2 IL-6 IL-IL-6 IL- 1010 Tissue FactorTissue Factor TNFTNF IL-1IL-1 IL-6IL-6 IL-8IL-8 TNFTNF IL-1IL-1 IL-6IL-6 IL-8IL-8 VIIIaVIIIa VaVa TAFITAFI PAI-1PAI-1 Inhibition ofInhibition of FibrinolysisFibrinolysis ThrombinThrombin APCAPC APCAPC APCAPC APCAPC APCAPC APCAPC APCAPC
  44. 44. Primary Analysis:Primary Analysis: 28-Day All-Cause Mortality28-Day All-Cause Mortality 24.7 30.8 0 5 10 15 20 25 30 35 Placebo Drotrecogin Alfa (Activated) Mortality 2-sided P value 0.005 Relative risk reduction 19.4% Increase in odds of survival 38.1% N=840 N=850 Bernard GR, et al. N Engl J Med 2001;344:699-709.
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