Kuliah ttg shock

1. Shock
Oxygen Don’t Go
Where the Blood Won’t Flow
Dita Aditianingsih
Department of Anesthesia and Intensive Care

2. 1960,
shock is hypotension,
CVP
1980-1990
SvO2 parameter hypoperfusion;↓ DO2
>2000;
Shock is imbalance between DO2/VO2
Goal Directed using Cellular parameter; BE,
SvO2, pCO2 gap, Lactate, Gastric Tonometri
2

3. Essentials of Life
• Gas exchange capability of lungs
• Hemoglobin
• Oxygen content
• Cardiac output
• Tissues capability to utilize substrate
• Thermoregulation
Disturbance
Shock 3

4. Definition of Shock
• An acute complex pathophysiologic state of
circulatory dysfunction which results in
inadequate tissue perfusion to meet tissue
demands of oxygen and other nutrients
• An acute clinical syndrome resulting when
cellular dysoxia occurs, leading to organ
dysfunction and failure
• Shock is not a blood pressure diagnosis
SUPPLY < DEMAND 4

5. The Oxygen Transport
Variables
• Oxygen Content [CaO2]
• Oxygen Delivery [DO2]
• Oxygen Uptake [VO2]
• Extraction Ratio [ER]
5

6. 6 steps in oxygen cascade
Oxygenation
Haemoglobin
Cardiac Output
Autoregulation
Distance
Mitochondria
Uptake in the Lung
Carrying capacity
Delivery
Organ distribution
Diffusion
Cellular use
DO2
PaO2
SaO2
Flow rate - ø
O2
ATP = energy
CaO2
VO2
O2ER
6

7. Arterial Oxygen Content
(CaO2)
Hgb 15 gm/100 mL
Hemoglobin
SaO2 97%
Oxygen Saturation
PaO2 100 mmHg
Partial Pressure
O2 bound to Hgb
100 mm Hg
+
O2 in plasma
+
7

8. Oxygen Content
• CaO 2
= (1.34 x Hb x SaO2
) + (0.003 x PaO2
)
amount O2 bound to Hb O2 in plasma
• 1.34 = 1gr og Hb can bind 1.34 ml O2 in sat 100%
• CaO2 = (1.34 x 14 x 0.98) + (0.003 x 100)
• CaO2 = 18.6 ml/dl (ml/dl = vol %; 18.6 vol %)
8

9. Oxygen Delivery
Oxygen Express O2O2O2O2O2O2 O2O2O2O2O2O2
Ca02
CO
DO2=Cardiac Output x Oxygen Content
DO2=(Stroke Volume x Heart Rate) x (1.34 (Hgb x SaO2) + Pa02 x 0.003)
Oxygen delivery is the quantity of oxygen
transported to the body tissue in one minute
9

10. Cardiac Output
• The volume of blood ejected by the heart in one
minute
• Normal CO : 4 – 8 L/min
• Normal CI : 2.5 - 4 L/min/m2 (indexed to BSA)
• CO=Heart Rate x Stroke Volume
• Stroke volume:
– Preload- volume of blood in ventricle
– Afterload- resistance to contraction
– Contractility- force applied
• CO= (Mean arterial pressure (MAP) – CVP)/SVR
10

11. 11
CO=Heart Rate x Stroke Volume
Cardiac Output
Heart Rate
Preload Contractility
Stroke Volume
Afterload
Diastolic Filling Fiber Stretch Contractile Force Ventricular pressure
Ventricular size
Wall thickness
Factors affecting cardiac output. Pathophysiology: Clinical conceprs of disease processes, 1986

12. OXYGEN DELIVERY (DO2)
Cardiac Output (CO) Arterial Oxygen Saturation
(SaO2 or SpO2)
Hemoglobin (Hgb)
Heart Rate (HR) Stroke Volume (SV)
Preload Afterload Contractility
DO2 = CO (L/min/m2) x CaO2 (L/min/m2)
DO2 = (SV x HR) x (1.34 x Hb x SaO2) x 10
DO2 = 3 x (1.34 x 14 x .98) x 10
DO2 = 551 ml/min
(10 dL/L is correction factor for CI in L/min CaO2 in ml/dl) 12

13. Oxygen Uptake
• Oxygen uptake is the final destination of oxygen
transport and represents the oxygen suply for
tissue metabolism
• The Fick Equation:
Oxygen Uptake is Cardiac Output multiply by the
difference between arterial and venous Oxygen
Content :
• VO2 = CO x [(CaO2 - CvO2)]
13

14. Oxygen Uptake
14

15. Oxygen Uptake
• The Fick Equation:
• VO2 = CO x (CaO2 - CvO2)
• VO2 = CO x [(1.34 x Hb) x (SaO2 - SvO2) x 10]
• VO2 = 3 x [ (1.34 x 14) x (.98 - .73) x 10 ]
• VO2 = 3 x [ 46 ]
• VO2 = 140 ml/min/m2
• Normal VO2: 110 - 160 ml/min/m2
15

16. Oxygen Content
• M, 35 yo, multiple trauma
• Pulse 126x/min, BP 164 / 70, RR 26
• Hb = 12
• Hct = 36
• ABG’s: pH 7.38 / PaO2 100 / PaCO2 32 / 96 % Sat
• Oxygen Content:
• CaO2 = (1.34 x Hb x SaO2)
• CaO2 = 1.34 x 12 x 0.96 = 15.4 ml O2/100 dl blood
16

17. Oxygen Delivery
• M, 35 th, multiple trauma
• Pulse 126 BP 164 / 72 RR 26
• Hb/Ht = 12/36
• ABG’s: pH 7.38 / PaO2 100 / PaCO2 32 / 96 % Sat
• CO = 4.8 (CI = 2.1)
• Oxygen Delivery:
• DO2 = CO x CaO2 x 10
• DO2 = 4.8 x 15.4 x 10 = 739.2 ml O2/min
17

18. Oxygen Uptake
• Laki2, 35 th, multiple trauma
• Pulse 126 BP 164 / 72 RR 26
• Hb/Hct = 12/36
• ABG’s: pH 7.38 / PaO2 100 / PaCO2 32 / 96 % Sat
• CO 4.8 (CI 2.1)
• SvO2 56 %
• Oxygen Uptake:
• VO2 = CO x (CaO2 - CvO2)
• VO2 = CO x [(1.34 x Hb) x (SaO2 - SvO2) x 10]
• VO2 = 4.8 x [ 1.34 x 12 x 0.4 x 10] = 308.7 ml O2/min
18

19. Extraction Ratio
• Extraction Ratio is a fraction of oxygen taken from yang
diambil capillary bed
• O2ER: ratio between Oxygen Uptake to Oxygen Delivery
• Normal Extraction is 22 - 32 %
• O2ER = VO2 / DO2 x 100
• O2ER = 134 (n) / 324 (↓) x 100
• O2ER = 41 % (↑)
• atau 1-SvO2 = if SvO2 59% --O2ER = 41%
• Questions:
1. ER = 16 %, ?
2. ER = 42 %, ?
19

20. Normal value
Basal metabolisme :
• CO 4-8 l/min (CI 2.5-4 l/min/m2)
• DO2 470-600 ml/min
• VO2 170-250 ml/min
• O2ER < 30%
20

21. PaO2 P50
(13) (3.5) Hb(150g/l)
SaO2(97%) CaO2(200ml/l)
COt(5l/min)
Diffusion of oxygen in tissues
Cappilary
Arterial
(13)
Venous
(5.3)
Interstitial
(5.3-2.7)
Intracellular
(2.7-1.3)
Mitochondria
(1.3-0.7)
Oxygen
Consumption
(250 ml/min)
Carbon
Dioxide
production
(200 ml/min)
Oxygen
return
(750 ml/min)
Qt5(5 l/min)
Cvo2(150 ml/min)
P50
PVO2
(5.3)
PAO2
(14)
Shunt
(2-3%)
PiO2 humidified
(20)
SVO2 (75%)
Hb(150 g/l)
Minute volume
(5 l/min)
Oxygen
Delivery
(1000 ml/l)
Heart and lungs
Shunt
(2-3%)
O2ER = 25%
In Normal Physiological State
21

22. In Shock or
Catabolic State
DO2 ↓↓
O2ER ↑↑
SvO250%
22

23. PaO2 P50
(13) (3.5) Hb(150g/l)
SaO2(97%) CaO2(200ml/l)
COt(5l/min)
Diffusion of oxygen in tissues
Cappilary
Arterial
(13)
Venous
(5.3)
Interstitial
(5.3-2.7)
Intracellular
(2.7-1.3)
Mitochondria
(1.3-0.7)
Oxygen
Consumption
(250 ml/min)
Carbon
Dioxide
production
(200 ml/min)
Oxygen
return
↓↓
Qt5(5 l/min)
Cvo2(150 ml/min)
P50
PVO2
(5.3)
PAO2
(14)
Shunt
(2-3%)
PiO2 humidified
(20)
SVO2 ↓↓50%)
Minute volume
(5 l/min)
Oxygen
Delivery
(1000 ml/l)
Heart and lungs
Shunt
(2-3%)
O2ER = 50%
In Shock or Catabolic State
Hypoxemia
Anemia
Hypotension
Oxygen
Delivery
↓↓
Oxygen
Consumption
↑↑
Cellular
Hypoxia
23

24. In Shock or Catabolic State
• If SvO2 decreases, it means that DO2 is
not high enough to meet tissue needs VO2
1. This might be due to inadequate DO2
(poor saturation, anemia, low cardiac
output)
2. Or, it might be due to increased tissue
extraction VO2 (fever, shivering,
thyrotoxicosis, agitation, exercise, etc.)
DO2 < VO2 24

25. Organ failure and
(late) Septic Shock
DO2 N/↓
O2ER ↓↓
SvO2 90%
O2 is available but cells are unable to
extract oxygen = Dysoxia
25

26. PaO2 P50
(13) (3.5) Hb(150g/l)
SaO2(97%) CaO2(200ml/l)
COt(5l/min)
Diffusion of oxygen in tissues
Cappilary
Arterial
(13)
Venous
(5.3)
Interstitial
(5.3-2.7)
Intracellular
(2.7-1.3)
Mitochondria
(1.3-0.7)
Oxygen
Consumption
(250 ml/min)
Carbon
Dioxide
production
(200 ml/min)
Oxygen
return
↑↑
Qt5(5 l/min)
Cvo2(150 ml/min)
P50
PVO2
(5.3)
PAO2
(14)
Shunt
(2-3%)
PiO2 humidified
(20)
SVO2 ↑↑90%
Minute volume
(5 l/min)
Oxygen
Delivery
(1000 ml/l)
Heart and lungs
Shunt
(2-3%) O2ER ↓10%
In Organ Failure and (late) Septic Shock
Oxygen
Delivery
N/↓
Oxygen
Consumption
↓↓
Cellular /
Mitochondrial
dysfunction
26
Hyperdynamic
Circulation

27. Organ failure and
(late) Septic Shock
• Increases in SvO2 combined with rising
lactate levels indicate tissues are unable to
extract oxygen
• This can be seen in such things as septic
shock, cyanide toxicity, carbon monoxide,
methemoglobin.
• Might also indicate hypothermia, shunt,
inotrope excess, etc.
27

28. VO2-DO2 relationship
Sepsis,
hyperthermia,
agitation,
stress surgery
Shock
Rest, sedation,
Hypothermia
28

29. OXYGEN DELIVERY (DO2)
OXYGEN
CONSUMPTION
(VO2)
NORMAL PHYSIOLOGIC STATE
INCREASED METABOLIC STATE
(High-risk Surgical Patients)
Critical DO2 Values
Supply dependent oxygen
consumption curve High Risk Surgery
Shock
SUPRANORMAL DO2  ↑ Preload, inotropik, tranfusion
oxygen need
29

30. Stages of shock
• Pre-shock
• Shock
• End-organ dysfunction
30

31. Stages: Pre-shock
• Warm or compensated shock
• Regulatory mechanisms are able to compensate
for diminished perfusion
• Low-preload:
– Tachycardia
– Peripheral vasoconstriction
– Decrease in blood pressure
• Low-afterload:
– Peripheral vasodilation
– Hyperdynamic state
31

32. One should not discount
the value of a good
physical examination,
despite of all the interest lab values, non
invasive or invasive monitoring device to
determine the adequacy of tissue
perfusion
32

33. Assessment of Circulation
Early Late
Heart rate Tachycardia Tachycardia/
Bradycardia
Blood
pressure
Normal Decreased
Peripheral
circulation
Warm/Cool
Decreased/
Increased
pulses
Cool
Decreased
pulses
Early Late
End-organ:
Skin
Decreased
cap refill
Very decreased
cap refill
Brain Irritable,
restless
Lethargic,
unresponsive
Kidneys Oliguria Oliguria, anuria

34. Stages: shock
• Usually occur with:
– Loss of 20-25% of effective blood volume
– Fall in cardiac index to ≤ 2.5 L/min/M2
– Activation of mediators of the sepsis syndrome
• Compensatory mechanisms become
overwhelmed, resulting in:
– Tachycardia
– Tachypnea
– Metabolic acidosis
– Oligouria
– Cool, clammy skin
34

35. End-organ dysfunction
• End organ dysfunction:
– reduced urine output
– altered mental status (agitation, obtundation and
coma)
– poor peripheral perfusion
• Metabolic dysfunction:
– acidosis
– altered metabolic demands
• Mutiple organ system failure which leads to
death
35

36. Classification of Shock
• Hypovolemic
– dehydration,burns,
hemorrhage
• Distributive
– septic, anaphylactic, spinal
• Cardiogenic
- Myocardial infarction
myocarditis,dysrhythmia
• Obstructive
– tamponade,pneumothorax
• Compensated
– organ perfusion is
maintained
• Uncompensated
– Circulatory failure
with end organ
dysfunction
• Irreversible
– Irreparable loss of
essential organs
36

37. 37
Mechanisms of Shock

38. Shock classifications
Physiologic variable Preload Pump function Afterload Tissue perfusion
Clinical measurement
Pulmonary
capillary wedge
pressure, CVP
Cardiac output
Systemic vascular
resistance
Mixed venous
oxygen
saturation
Lactate
Hypovolemic
Cardiogenic
Distributive
Septic Early
Septic Late
Neurogenic
Obstructive
38

39. 39

40. 40
Microcirculation Macrocirculation
Stages of Shock
↓DO2 = ↓Hb, ↓SaO2 or ↓CO
SvO2
O2 Extraction
Lactate
too late for intervention: hypotension
and cell damage was already occured
Micro and macro compensatory response s
to maintain BP and VO2 still normal
Hypoperfusion begins: best time for intervention like
supranormal DO2 or decreased VO2 (demand) ASAP

41. 41

42. Macrocirculation
Upstream endpoints
42

43. Supranormal resuscitation
• In the 1970s, Shoemaker et al. reviewed the
physiologic patterns in surviving and
nonsurviving shock patients
• They observed that survivors had significantly
increased oxygen delivery, oxygen consumption,
and cardiac index values
• Oxygen delivery DO2 ≥600 mL/minute/m2,
• Oxygen consumption VO2≥170 mL/minute/m2
• Cardiac index CI ≥4.5 L/minute/m2
43

44. Microcirculation
Downstream endpoints
44

45. Base Deficit
• Base deficit is defined as the amount of base in
millimoles required to increase 1 liter of whole blood
to the predicted pH based on the PaCO2 .
• Calculated using the arterial blood gas as follows Base
Deficit = -[(HCO3) - 24.8 + (16.2)(pH - 7.4)]
• In shock states, the base deficit may serve as a
surrogate marker for anaerobic metabolism and
subsequent lactic acidosis if metabolic acidosis is the
primary disorder and not a compensatory response.
• It is superior to pH secondary to the many
compensatory mechanisms in place to normalize pH
45

46. Stratification level of illness
by base deficits
• Base deficit can be misleading in cause of
hyperchloremic acidosis, citrat from blood
products
Stratification Base deficit
Mild 2 – 5 mmol/L
Moderate 6 – 14 mmol/L
Severe > 14 mmol/L
46

47. Mixed Venous Oxygen Saturation
• Critically ill patients, Gattinoni resuscitated patients
to one of three hemodynamic goals included a
cardiac index between 2.5 and 3.5 L/minute/m2,
cardiac index >4.5, L/minute/m2, and SvO2 ≥70%
• Rivers' study of severe sepsis/septic shock patients
where reaching SvO2 ≥70% within 6 hours of
resuscitation improved survival
47

48. SvO2 (mixed venous) –
ScvO2 (central venous oxygen
saturation)
• SvO2-ScvO2 levels could reflect the adequacy of
O2 delivery DO2 to the tissue in relation to
global tissue O2 demands VO2
• SvO2-ScvO2 reflects the amount of oxygen left
after utilized by the tissue
• It’s an oxygen saturation of the blood goes back
to the heart
48

49. SvO2 / ScvO2:
• Modified Fick Equation for SvO2 :
• SvO2 = SaO2 - (VO2/[CO x 1.38 x Hgb])
• SvO2 is derived from :
- SaO2
- Oxygen consumption (VO2)
- Cardiac output (CO)
- Hemoglobin (Hb)
• In daily practice SvO2 is measured (not calculated)
49

50. Venous O2 saturasi
SvO2 (65%)
ScvO2 (>70%)
Superior vena cava
Right atrium
Pulmonary artery
SvO2-ScvO2
• SvO2 is measured in pulmonary artery and
reflect the venous oxygen saturation of the
whole body
• ScvO2 is measured in superior vena cava or
right atrium and reflects the venous oxygen
saturation majority of brain and upper body
• Average SvO2 5-13% lower than ScvO2
50

51. ScvO2
If SvO2 decreases, it
means that DO2 is not
high enough to meet
tissue needs VO2
1. This might be due
inadequate DO2
(poor saturation,
anemia, low
cardiac output)
2. It might be due to
increased tissue
consumption VO2
(fever, shivering,
agitation, exercise,
thyrotoxicosis)
51

52. ScvO2
If SvO2 increases
combine with rising
lactate levels indicate
tissues are unable to
extract oxygen (dysoxia)
This can be seen in
such things as septic
shock, cyanide toxicity ,
carbon monoxide,
shunt, etc
52

53. Reinhart K. Monitoring O2 transport and tissue oxygenation in ctitically ill
patint. 1989 , 195-211
Monitoring O2 transport and
tissue oxygenation
53

54. (Arterial) Lactate
• Level lactate at initial and response to fluid
resuscitation, can be predictive value
• Normal level is < 2 mmol/L
• Time needed to normalize serum lactate level
is an important prognostic factor for survival
Lactate normalization :
24 hours → survived
24-48 hours → 25% mortality
> 48% hours did not normalized → 86% mortality
Abramson D, et al. Lactate clearance and survival following injury. J Trauma 1993
54

55. Hyperlactatemia
↑ Lactate production ↓ Lactate clearance
Anaerobic Aerobic -Impaired liver function
-Decrease liver blood flow
-Tissue hypoxia
/hypoperfusion
-Increased metabolisme
-Endogenous production
-Inflammation mediated
- accelerated glycolysis
- inhibition of pyruvate
dehydrogenase
Intensive Care Med 2003 ; 29 : 699 55

56. 56

57. Weil MH. Defining hemodynamic instability. Braunwald E (ed ) Heart disease 1998
57

58. Blood Lactate Clearance
Nguyen et al. Crit Care Med 2004 58

59. Serum Lactate
Aduen, et al. JAMA 1994;272:1678-1685
59

60. A-V pCO2 gap
• Changes (↑) venous CO2 is the ratio between
the waste product of aerobic metabolism
(VCO2) and its clearance by flow
• P(v-a)CO2 could be considered as a marker of
adequacy of venous blood flow to remove
the total CO2 produced by the peripheral
tissues.
Neviere R et al(2002) Small intestine intramucosal PCO2 and microvascular blood flow during hypoxic and ischemic
hypoxia. Crit Care Med 30
60

61. Increased P(v-a)CO2
was mainly related to
the decrease in cardiac
output as P(v-a)CO2
was increased in
ischemic hypoxia but
not in hypoxic hypoxia
or mitochondrial
dysfunction (energy
failure at O2
dependency)
61

62. (A-v)pCO2 gap Critical Ilness
• In ICU resuscitated patients, targeting only ScvO2
may not be sufficient to guide therapy.
• When the 70% ScvO2 goal value is reached, the
presence of a P(cv-a)CO2 larger than 6 mmHg might
be a useful tool to identify patients who still remain
inadequately resuscitated.
Vallee F et al. Central venous-to-arterial carbon dioxide difference: an additional target
for goal-directed therapy in septic shock? Intensive Care Med 2008 62

63. Management of Shock
63

64. Therapeutic priorities
• Supportive measures to treat hypoxemia,
hypotension and impaired tissue oxygenation
• Distinguish between sepsis and SIRS
(systemic inflammatory response syndrome)
so medical/surgical treatment of the source
of infection can be started
• Assess for adequate tissue perfusion
64

65. Initial management
• Resuscitation
– Assess airway, respiration and perfusion
– Supplemental O2 should be given to all patients
– Intubation often required to protect airway,
decrease demand
– Mechanical ventilation often needed due to
development of lung injury or ARDS
65

66. Initial management
• Monitoring of tissue perfusion
– Hypotension is typically present
– Prompt volume resuscitation and restoration of perfusion
pressure can limit end organ damage
– Consider arterial catheterization if restoration of perfusion
pressure is expected to be a protracted process
• Restoration of tissue perfusion
– CVP 8 - 12
– MAP > 65
– Urine output > 0.5 ml/kg/hr
– ScvO2 > 70%
– Can use IV fluids, PRBC’s and vasopressors to achieve these
goals depending on patient’s intravascular volume, cardiac
status and severity of shock
66

67. Initial management
• IV fluids
– Rapid, large volume infusions are usually indicated
– Should be given in well-defined, rapidly infused
boluses
– CHF is the primary contraindication
– Assess volume status, tissue perfusion, blood
pressure, and for pulmonary edema before/after
each bolus
– Colloids have not been proven to have any
advantage over crystalloids
67

68. Initial management
• May repeat IV fluid boluses until:
– Blood pressure, tissue perfusion and oxygen delivery are
acceptable
– PAWP > 18
– Development of pulmonary edema
– Note that septic patients can develop pulmonary edema with
relatively normal wedge pressures
• IV fluids: how much?
– Central venous catheters can be used to monitor central
venous pressures
– Can also be used to estimate mixed venous oxygen content
– Lactate level
– pCO2 gap
68

69. Management of various Preload and
Cardiac Output states
Preload
(CVP,PCWP)
Low Normal High
Cardiac
output
Low
Normal
High
Optimise fluid, then
Consider inotropes
Optimise fluid
Optimise fluid
Inotropes
Monitor
Monitor
Inotropes, vasodilator,
diuretics
Monitor, consider
vasodilators, diuretics
Monitor, consider
vasodilators, diuretics
69

70. Frank Starling curve
Frank-Starling curves showing the effect
of positive and negative inotropy.
Stroke Volume is a measure of
contractility, where normal stroke
volume is approximately 70 mls.
Left ventricular end diastolic pressure
(LVEDP) is a measure of preload.
Represents optimal preload
in the normal heart.
70

71. Initial management
• Vasopressors
– Second-line agents
– Useful in patients who fail to reach adequate blood
pressures despite adequate volume resuscitation
– Also useful in patients who develop cardiogenic
pulmonary edema
– Dopamine and Norepinephrine recommended and first-
choice drugs
– Phenylephrine (pure a-adrenergic) can be useful when
tachycardia or arrythmia due to b-adrenergic activity
becomes problematic
– Vasopressin can be used in patients refractory to first-
choice agents
71

72. Properties of Vasopressors
Drug HR Contractility
Arterial
constriction
Dobutamine + +++ -
Dopamine ++ ++ ++
Epinephrine +++ +++ ++
Norepinephrine ++ ++ +++
Phenylephrine 0 0 +++
Amrinone + +++ --
72
Useful in patients who fail to reach adequate blood pressures despite
adequate volume resuscitation
Useful in patients who develop cardiogenic pulmonary edema
Vasopressin can be used in patients refractory to first-choice agents

73. Monitoring response to therapy
• All patients require close monitoring
• Evidence of deterioration merits a prompt,
through reevaluation
73

74. Assessment of adequate
tissue perfussion
Clinical
Parameter
Global
Parameter
Regional /Organ
Specific Parameter
Mental status
Temperature
Capillary refill
Urine output
Hemodynamic :
Cardiac Ouput: SV, HR
Preload: CVP,PCWP,
GEDI
Contractility : CFI
Afterload : MAP, SVR
DO2-VO2
SvO2-ScVO2
Serum Lactate
Base Deficit
A-V pCO2 gap
Gastric
tonometry
Sublingual
capnometry
Near-infrared
Spectroscopy
Macrocirculation Microcirculation 74

75. Monitoring response to therapy
• Monitoring parameters:
– Respiratory: PaO2/FiO2 ratio
– Renal: urine output, creatinine
– Hematologic: platelet counts
– CNS: Glascow coma scale
– Hepatobiliary: bilirubin, LFT’s
– CV: blood pressure, arterial lactate
– GI: ileus, blood in NG aspirate
75

76. Monitoring response to therapy
• Detection of tissue hypoxia
– Arterial lactate concentration is the most useful measure of
tissue perfusion
• Treatment of tissue hypoxia
- If arterial lactate concentrations fail to fall with
adequate transfusion, cardiac output must be
increased
- Further IV fluid therapy can be given
- Dobutamine can be given when arterial pressures are
adequate to tolerate vasodepression
(after phenylephrine/norepinephine has been added if
needed)
76

77. Control of septic focus
• Prompt identification and treatment of
infectious source are critical and definitive
• Previously fluid and vasoactive agents
treatments are supportive
77

78. Control of septic focus
• Identification of septic focus:
– Blood cultures (2 sets, aerobic and anaerobic)
– Urine Gram stain and culture
– Sputum in a patient with productive cough
– Intra-abdominal collection in post-operative patients
• Investigational methods:
– Elevated serum procalcitonin, CRP,
– Diff count
– Chest xray
– Ultrasound, Ct Scan
78

79. Control of septic focus
• Eradication of infection
– Potentially infected foreign bodies (vascular access
devices)
– Percutaneous or surgical drainage of abscesses
– Soft-tissue debridement or amputation if necessary
• Antimicrobial regimen
– Should be started promptly after cultures have been
obtained
– Time to initiation of treatment has been shown to be
the strongest predictor of mortality
– Appropriate antibiotic selection has been shown to
decrease mortality
79

80. 80
Optimization perioperative oxygen
delivery using guideline
(Goal-Directed Therapy = GDT)
• General guideline using invasive device (Vincent )
• Perioperative guideline (Pearce protocol)
• Severe sepsis- septic shock guideline ( EGDT -
Rivers)
• Hipovolemic guideline (Parillo)
• Tranfusion guideline in trauma

81. EBL Based on Patient’s Initial
Presentation
ATLS 2008
81

82. 82
Inadequate DO2 with ↓ VO2 and ↑ lactate
↓ Scvo2 → Low cardiac ouput ?
Quantitative
shock ↓ Q
Yes
No
Acute
respiratory
failure
Cardiogenic
shock
Cardiac problem
Hypovolemia
Yes
No Hemorrhage
Yes
No
Hemorrhagic
Shock
Hypovolemic
shock Fluid
losses (gut,
kidney, fever)
Microciculation Failure
(inflammation,
anaphylaxis, sepsis)
Cytopathic dysoxia
(poisoning, sepsis,
cell death)
Yes
No
Yes
No
Hypoxemia
↓ SaO2
Distributive shock
↑ Scv02, ↓ ERO2 ↑CO2 gap
Assessment of Shock

83. SVO2
Hemoglobin
>8 g/dL
Stress, anxiety, pain
(High VO2)
<8 g/dL
Anemia
Analgesic
Sedation
Blood
transfusion
PAOP
>18 mm Hg
Myocardial
dysfunction
<18 g/dL
Hypovolemia
Dobutamine Fluid challenge
Cardiac Output
High
(>2.5 L/min/m2)
Low
(<2.5 L/min/m2)
SaO2 Low
(Hypoxemia)
SaO2 Normal (95%)
(↑ O2ER)
Normal
(≥79%)
Low
(<70%)
Do nothing
Oxgen therapy
↑ PEEP
Vincent protocol, 2005
Pinsky MR, Vincent JL: Let us use the PAC correctly and only when we need it. Crit Care Med 2005;33:1119-1122
PLR
SVV
pCO2
gap
84

84. Pearce protocol, 2005
Pearse RM, Dawson D, Fawcett J, et al: Early goal-directed therapy after major surgery reduces complications and duration of hospital stay. Crit Care 2005;9:687-693
85

85. Textbook of critical care, Vincent JL, 2010
86
Glucose Control
Hemofiltration

86. EARLY GOAL-DIRECTED THERAPY IN THE TREATMENT OF
SEVERE SEPSIS AND SEPTIC SHOCK
RIVERS E. N Engl J Med, Vol. 345, No 19, 2001
87

87. Proposed tools for a refined early goal-
directed therapy (EGDT) algorithm,
modified from Rivers et.al
<6
Static : CVP, PAOP
Volumetric : PAC, PICCO,
LidCO
Echocardiographic : Echo,
TEE
Dynamic : SVV, PPV, PLR
88

88. Oxygen Delivery Cascade indicating the
potensial therapies to optimize oxygen
delivery to the tissues
to prevent further complications
O2 and Airway maintenance
CPAP or Ventilation
Optimization of DO2
(Goal Directed Therapy)
Vasodilator and low dose inotropes
Future agents?
Trachea
Alveolus
Arterial blood
Microcirculation
Mitochondria
Jhanji S, Pearse RM The use of early intervention to prevent postoperative complications Current Opinion in Critical Care 2009, 15:349–354
89

89. Begin fluid resuscitation (initial bolus
of at least 20 ml/kg crystalloid, to be
continued with colloids, red cell
concentrates and coagulation factors
SBP remains < 90 mmHg or
MAP remains < 65 mmHg;
lactate does not fall
Insert CVP or
PA Cath
Fluid boluses
ScvO2*
MAP
ALL Goals
achieved?
Supplemental O2 ± ETI with
mech ventilation (if necessary)
Target SaO2 of ≥ 95%
Dobutamine/
Dopamine
Vasopressor (norepinephrine or
dopamine prefered)
< 70%
Filling pressure
<8 mmHg
MAP < 65
MAP ≥ 65
NO
Hypovolemic shock; Parillo and Delinger, Critical Care Medicine Textbook, 2008
Filling pressure
> 8 mmHg
< 70%
*If PAC is used a mixed venous Os sat is an
acceptable surrogate, and 65% would be the
target
90
Trauma/hemorrhage
Elevated lactate
Hypovolemic Shock
Management

90. 91

91. Clinical signs: Shock, hypoperfusion, congestive heart failure, acute pulmonary edema
Most likely major underlying disturbance
Hypovolemia
Low output –
Cardiogenic shock
Arrythmia
92
Administer
-Fluid
-Blood transfusion
-Cause-specific intervenstions
-Consider vasopressors Check Blood Pressure
Bradycardia Tachycardia
Brady-tachycardia
guideline
Systolic >100
mmHg
Systolic 70-100
mmHg, no symptoms
of shock
Systolic 70-100
mmHg, with
symptoms of shock
Systolic <70 mmHg,
with symptoms of
shock
Nitroglycerine
10-20mcg/min IV
Dobutamine
2-20mcg/kg/min IV
Dopamine
5-20mcg/kg/min IV
Norepinephrine
0,01-2mcg/kg/min IV
Further diagnostics
consideration :
-PA catheter
-Echocardiography
-Angiography for MI
Further therapeutics
consideration :
-IABP
-Reperfusion/revascularization

92. Conclusion
1. The level of arterial pressure is not a reliable
indicator of circulatory performance and
tissue perfusion
2. Tissue hypoperfusion may be present despite
normal levels of blood pressure as blood flow
is redirected toward more vital organs
Hypotension and level of consciousness
are a late marker of hypoperfusion
93

93. End Points of Resuscitation:
• Restoration of normal vital signs
• Adequate Urine output
– 0.5 - 1.0 cc/kg/hr
• Adequate Cardiac Index
• Normalization of Oxygen delivery DO2I
• Tissue Oxygenation measurement : normal
Serum Lactate levels dan Scvo2
94

94. 1960,
shock is hypotension,
CVP
1980-1990
SvO2 parameter hypoperfusion;↓ DO2
>2000;
Shock is imbalance between DO2/VO2
Goal Directed using Cellular parameter; BE,
SvO2, pCO2 gap, Lactate, Gastric Tonometri
Thank You
any question?
95