Shock

Oxygen Don’t Go
Where the Blood Won’t Flow

Dita Aditianingsih
Department of Anesthesia and Intensive Care
 1960,
shock is hypotension,
CVP

1980-1990
SvO2 parameter hypoperfusion;↓ DO2

>2000;
Shock is imbalance between DO2/VO2

Goal Directed using Cellular parameter; BE, 2

SvO2, pCO2 gap, Lactate, Gastric Tonometri
 Essentials of Life
• Gas exchange capability of lungs
• Hemoglobin
• Oxygen content
• Cardiac output
• Tissues capability to utilize substrate
• Thermoregulation
Disturbance

Shock 3
 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

 The Oxygen Transport
Variables

• Oxygen Content [CaO2]

• Oxygen Delivery [DO2]
• Oxygen Uptake [VO2]
• Extraction Ratio [ER]

5
 6 steps in oxygen cascade
O2
Uptake in the Lung Oxygenation PaO2
CaO2
Carrying capacity Haemoglobin SaO2 DO2

Delivery Cardiac Output Flow rate - ø

Organ distribution Autoregulation

VO2
Diffusion Distance
O2ER

Cellular use Mitochondria

ATP = energy 6
 Arterial Oxygen Content
(CaO2)
100 mm Hg

Hgb 15 gm/100 mL SaO2 97% PaO2 100 mmHg

Hemoglobin Oxygen Saturation

+ Partial Pressure

O2 bound to Hgb + O2 in plasma

7
 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
 Oxygen Delivery
Oxygen delivery is the quantity of oxygen
transported to the body tissue in one minute

Oxygen Express O2O2O2O2O2O2 O2O2O2O2O2O2

CO Ca02

DO2=Cardiac Output x Oxygen Content

DO2=(Stroke Volume x Heart Rate) x (1.34 (Hgb x SaO2) + Pa02 x 0.003)

9
 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
 CO=Heart Rate x Stroke Volume

Cardiac Output

Heart Rate Stroke Volume

Preload Contractility Afterload

Diastolic Filling Fiber Stretch Contractile Force Ventricular pressure

Ventricular size
Wall thickness
11
Factors affecting cardiac output. Pathophysiology: Clinical conceprs of disease processes, 1986
 OXYGEN DELIVERY (DO2)

Cardiac Output (CO) Arterial Oxygen Saturation Hemoglobin (Hgb)

(SaO2 or SpO2)

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
 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
Oxygen Uptake

14
 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
 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
 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
 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
 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
 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
In Normal Physiological State
Oxygen
PaO2 P50 SaO2(97%) CaO2(200ml/l)
Delivery
(13) (3.5) Hb(150g/l) COt(5l/min) (1000 ml/l)

PiO2 humidified Diffusion of oxygen in tissues

(20) Cappilary
Heart and lungs
Arterial Venous
(13) (5.3)
Interstitial Oxygen
Shunt
Shunt O2ER = 25% (5.3-2.7) Consumption
Minute volume (2-3%)
(2-3%) (250 ml/min)
(5 l/min) Intracellular
(2.7-1.3) Carbon
Dioxide
production
Mitochondria (200 ml/min)
(1.3-0.7)
PAO2
(14)
PVO2 P50 SVO2 (75%) Oxygen
(5.3) Hb(150 g/l) Qt5(5 l/min) return
Cvo2(150 ml/min) (750 ml/min)

21
 In Shock or
Catabolic State
O2ER ↑↑

DO2 ↓↓ SvO250%

22
In Shock or Catabolic State
Oxygen
Hypoxemia Oxygen
PaO2 P50 SaO2(97%) CaO2(200ml/l) Delivery
Anemia Delivery
(13) (3.5) Hb(150g/l)
Hypotension COt(5l/min) ↓↓ml/l)
(1000

PiO2 humidified Diffusion of oxygen in tissues

(20) Cappilary
Heart and lungs
Cellular
Arterial Venous
Hypoxia(13) (5.3)
Interstitial Oxygen
Oxygen
Shunt
Shunt O2ER = 50% (5.3-2.7) Consumption
Minute volume (2-3%)
(2-3%) Consumption
(250 ml/min)
(5 l/min) Intracellular ↑↑
(2.7-1.3) Carbon
Dioxide
production
Mitochondria (200 ml/min)
(1.3-0.7)
PAO2
(14)
PVO2 P50 Oxygen
(5.3) SVO2 ↓↓50%) Qt5(5 l/min) return
Cvo2(150 ml/min) ↓↓

23
 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

 Organ failure and
(late) Septic Shock
O2ER ↓↓ O2 is available but cells are unable to
extract oxygen = Dysoxia

DO2 N/↓ SvO2 90%

25
In Organ Failure and (late) Septic Shock
Hyperdynamic
Oxygen
Oxygen
PaO2 P50 SaO 2(97%)
Circulation CaO2(200ml/l) Delivery
Delivery
(13) (3.5) Hb(150g/l) COt(5l/min) N/↓ml/l)
(1000

PiO2 humidified Diffusion of oxygen in tissues

(20) Cellular / Cappilary
Heart and lungs
Arterial Venous
Mitochondrial
(13) (5.3)
dysfunction
Interstitial Oxygen
Oxygen
Shunt
Shunt (5.3-2.7) Consumption
Minute volume (2-3%)
(2-3%) O2ER ↓10% Consumption
(250 ml/min)
(5 l/min) Intracellular ↓↓
(2.7-1.3) Carbon
Dioxide
production
Mitochondria (200 ml/min)
(1.3-0.7)
PAO2
(14)
PVO2 P50 Oxygen
(5.3) SVO2 ↑↑90% Qt5(5 l/min) return
Cvo2(150 ml/min) ↑↑

26
 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
VO2-DO2 relationship

Shock Sepsis,
hyperthermia,
agitation,
stress surgery

Rest, sedation,
Hypothermia

28
Supply dependent oxygen
consumption curve High Risk Surgery
Critical DO2 Values
INCREASED METABOLIC STATE
(High-risk Surgical Patients)
OXYGEN CONSUMPTION (VO2)

Shock oxygen need

NORMAL PHYSIOLOGIC STATE

SUPRANORMAL DO2  ↑ Preload, inotropik, tranfusion

OXYGEN DELIVERY (DO2)

29
 Stages of shock
• Pre-shock
• Shock
• End-organ dysfunction

30
 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
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
 Assessment of Circulation
Early Late
Early Late

Heart rate Tachycardia Tachycardia/ End-organ: Decreased Very decreased

Bradycardia Skin cap refill cap refill
Blood Normal Decreased
pressure Brain Irritable, Lethargic,
Peripheral Warm/Cool Cool restless unresponsive
circulation Decreased/ Decreased
Increased pulses Kidneys Oliguria Oliguria, anuria
pulses
 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
 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
 Classification of Shock

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

37
 Shock classifications
Physiologic variable Preload Pump function Afterload Tissue perfusion

Pulmonary Mixed venous

Systemic vascular
Clinical measurement capillary wedge Cardiac output oxygen Lactate
resistance
pressure, CVP saturation

Hypovolemic

Cardiogenic

Distributive
Septic Early

Septic Late

Neurogenic

Obstructive

38
39
 Stages of Shock

↓DO2 = ↓Hb, ↓SaO2 or ↓CO

Microcirculation Macrocirculation

SvO2
Micro and macro compensatory response s
to maintain BP and VO2 still normal

O2 Extraction

Lactate
Hypoperfusion begins: best time for intervention like
supranormal DO2 or decreased VO2 (demand) ASAP
too late for intervention: hypotension
and cell damage was already occured 40
41
 Macrocirculation
Upstream endpoints

42
 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
 Microcirculation
Downstream endpoints

44
 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
 Stratification level of illness
by base deficits
Stratification Base deficit
Mild 2 – 5 mmol/L
Moderate 6 – 14 mmol/L
Severe > 14 mmol/L

• Base deficit can be misleading in cause of

hyperchloremic acidosis, citrat from blood
products

46
 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
 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
 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
 SvO2-ScvO2 Superior vena cava

Venous O2 saturasi Right atrium

SvO2 (65%)
ScvO2 (>70%) Pulmonary artery

• 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
 If SvO2 decreases, it
means that DO2 is not
high enough to meet
tissue needs VO2

1. This might be due

ScvO2 inadequate DO2
(poor saturation,
anemia, low
cardiac output)
2. It might be due to
increased tissue
consumption VO2
(fever, shivering,
agitation, exercise,
thyrotoxicosis)
51
 If SvO2 increases
combine with rising
lactate levels indicate
ScvO2 tissues are unable to
extract oxygen (dysoxia)

This can be seen in

such things as septic
shock, cyanide toxicity ,
carbon monoxide,
shunt, etc

52
Monitoring O2 transport and
tissue oxygenation

Reinhart K. Monitoring O2 transport and tissue oxygenation in ctitically ill

patint. 1989 , 195-211 53
 (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

54
Abramson D, et al. Lactate clearance and survival following injury. J Trauma 1993
 Hyperlactatemia

↑ Lactate production ↓ Lactate clearance

Anaerobic Aerobic -Impaired liver function

-Decrease liver blood flow

-Tissue hypoxia -Endogenous production

/hypoperfusion -Inflammation mediated
-Increased metabolisme - accelerated glycolysis
- inhibition of pyruvate
dehydrogenase

Intensive Care Med 2003 ; 29 : 699 55

56
Weil MH. Defining hemodynamic instability. Braunwald E (ed ) Heart disease571998
Blood Lactate Clearance

Nguyen et al. Crit Care Med 2004 58

Serum Lactate

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

59
 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
60
hypoxia. Crit Care Med 30
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
 (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
Management of Shock

63
 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
 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
 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
 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
 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
Management of various Preload and
Cardiac Output states

Preload Low Normal High

(CVP,PCWP)
Cardiac
output
Low Optimise fluid, then Inotropes Inotropes, vasodilator,
Consider inotropes diuretics
Normal Optimise fluid Monitor Monitor, consider
vasodilators, diuretics
High Optimise fluid Monitor Monitor, consider
vasodilators, diuretics

69
Frank Starling curve

Represents optimal preload

in the normal heart.

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.
70
 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
 Properties of Vasopressors
Arterial
Drug HR Contractility constriction
Dobutamine + +++ -

Dopamine ++ ++ ++

Epinephrine +++ +++ ++

Norepinephrine ++ ++ +++

Phenylephrine 0 0 +++

Amrinone + +++ --

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
72
 Monitoring response to therapy
• All patients require close monitoring
• Evidence of deterioration merits a prompt,
through reevaluation

73
 Assessment of adequate
tissue perfussion

Clinical Global Regional /Organ

Parameter Parameter Specific Parameter

Mental status Gastric

Temperature Hemodynamic :
DO2-VO2 tonometry
Capillary refill Cardiac Ouput: SV, HR
SvO2-ScVO2 Sublingual
Urine output Preload: CVP,PCWP,
Serum Lactate capnometry
GEDI
Base Deficit Near-infrared
Contractility : CFI
A-V pCO2 gap Spectroscopy
Afterload : MAP, SVR

Macrocirculation Microcirculation 74
 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
 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
 Control of septic focus
• Prompt identification and treatment of
infectious source are critical and definitive
• Previously fluid and vasoactive agents
treatments are supportive

77
 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
 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
 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

80
EBL Based on Patient’s Initial
Presentation
ATLS 2008

81
Assessment of Shock
Cardiogenic
Yes shock

Quantitative
Yes shock ↓ Q Cardiac problem Hemorrhagic
Yes Shock

No Hypovolemia Hemorrhage

Inadequate DO2 with ↓ VO2 and ↑ lactate Hypovolemic

No
↓ Scvo2 → Low cardiac ouput ? shock Fluid
losses (gut,
Hypoxemia kidney, fever)
Yes ↓ SaO2

Acute
respiratory Microciculation Failure
No (inflammation,
failure
Yes anaphylaxis, sepsis)
Distributive shock
No ↑ Scv02, ↓ ERO2 ↑CO2 gap
Cytopathic dysoxia
No (poisoning, sepsis,
cell death)

82
 Vincent protocol, 2005
SVO2

Normal Low
(≥79%) (<70%)

Do nothing
SaO2 Low SaO2 Normal (95%)
pCO2 (Hypoxemia) (↑ O2ER)
gap Oxgen therapy
↑ PEEP
Cardiac Output PLR

High Low
(>2.5 L/min/m2) (<2.5 L/min/m2)

Hemoglobin PAOP SVV

>8 g/dL <8 g/dL >18 mm Hg <18 g/dL

Stress, anxiety, pain Anemia Myocardial Hypovolemia
(High VO2) dysfunction

Analgesic Blood
Dobutamine Fluid challenge
Sedation transfusion

84
Pinsky MR, Vincent JL: Let us use the PAC correctly and only when we need it. Crit Care Med 2005;33:1119-1122
 Pearce protocol, 2005

85
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
Glucose Control
Hemofiltration

86
Textbook of critical care, Vincent JL, 2010
EARLY GOAL-DIRECTED THERAPY IN THE TREATMENT OF
SEVERE SEPSIS AND SEPTIC SHOCK

87
RIVERS E. N Engl J Med, Vol. 345, No 19, 2001
Static : CVP, PAOP
Volumetric : PAC, PICCO,
LidCO
Echocardiographic : Echo,
TEE
Dynamic : SVV, PPV, PLR

<6

Proposed tools for a refined early goal-

directed therapy (EGDT) algorithm,88
modified from Rivers et.al
 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

Trachea Optimization of DO2

(Goal Directed Therapy)

Alveolus
Vasodilator and low dose inotropes

Arterial blood
Future agents?

Microcirculation

Mitochondria

89
Jhanji S, Pearse RM The use of early intervention to prevent postoperative complications Current Opinion in Critical Care 2009, 15:349–354
 Trauma/hemorrhage
Hypovolemic Shock Elevated lactate
Management Supplemental O2 ± ETI with
mech ventilation (if necessary) Begin fluid resuscitation (initial bolus
Target SaO2 of ≥ 95%
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

Filling pressure
<8 mmHg Insert CVP or
Fluid boluses PA Cath

*If PAC is used a mixed venous Os sat is an Filling pressure

acceptable surrogate, and 65% would be the > 8 mmHg
target < 70%
Dobutamine/
ScvO2*
Dopamine

< 70%
MAP < 65
Vasopressor (norepinephrine or MAP
dopamine prefered)
MAP ≥ 65

NO
ALL Goals
achieved?

90
Hypovolemic shock; Parillo and Delinger, Critical Care Medicine Textbook, 2008
91
 Clinical signs: Shock, hypoperfusion, congestive heart failure, acute pulmonary edema
Most likely major underlying disturbance

Hypovolemia Arrythmia
Low output –
Administer Cardiogenic shock Bradycardia Tachycardia
-Fluid
-Blood transfusion Brady-tachycardia
-Cause-specific intervenstions guideline
-Consider vasopressors Check Blood Pressure

Systolic >100 Systolic 70-100 Systolic 70-100 Systolic <70 mmHg,

mmHg mmHg, no symptoms mmHg, with with symptoms of
of shock symptoms of shock shock

Nitroglycerine Dobutamine Dopamine Norepinephrine

10-20mcg/min IV 2-20mcg/kg/min IV 5-20mcg/kg/min IV 0,01-2mcg/kg/min IV

Further diagnostics Further therapeutics

consideration : consideration :
-PA catheter -IABP
-Echocardiography -Reperfusion/revascularization
92
-Angiography for MI
 Conclusion
Hypotension and level of consciousness
are a late marker of hypoperfusion

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

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
 1960,
shock is hypotension,
CVP

1980-1990
Thank You
SvO2 parameter hypoperfusion;↓ DO2

any question?

>2000;
Shock is imbalance between DO2/VO2

Goal Directed using Cellular parameter; BE, 95

SvO2, pCO2 gap, Lactate, Gastric Tonometri