Shock

Oxygen Dont Go
Where the Blood Wont Flow

Dita Aditianingsih
Department of Anesthesia and Intensive Care
Cipto Mangunkusumo Hospital University of
indonesia

1971
Swan Ganz
Hemodynamic parameter
CO, SV, SVR

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,

Essentials of Life
Gas exchange capability of
lungs
Hemoglobin
Oxygen content
Cardiac output
Tissues capability to utilize
substrate
Disturbanc
e
Thermoregulation

Shock

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

SUPPLY < DEMAND

4

The Oxygen
Transport Variables

Oxygen Content [CaO2Supp

]
Oxygen Delivery [DO2]ly
Oxygen Uptake [VO2]
Dema
Extraction Ratio [ER] nd

6 steps in oxygen cascade

O2
Uptake in the Lung

Oxygenation

PaO2

Carrying capacity

Haemoglobin

SaO2

Delivery
Organ
distribution
Diffusion

Cellular use

Cardiac Output

CaO2
DO2

Flow rate -

Autoregulation
Distance

VO2
O2ER

Mitochondria

ATP = energy

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

CO

O2O2O2O2O2O2

O2O2O2O2O2O2

Ca02

DO2=Cardiac Output x Oxygen Content

DO2=(Stroke Volume x Heart Rate) x (1.34 (Hgb x SaO 2) + Pa02 x 0.003)

OXYGEN DELIVERY
(DO2)
Cardiac Output
(CO)
Heart Rate
(HR)

Preload

DO2 =
DO2 =
x 10

Arterial Oxygen
Saturation
(SaO2 or SpO2)

Hemoglobin
(Hgb)

Stroke Volume
(SV)

Afterload

Contractility

CO (L/min/m2) x CaO2 (L/min/m2)

(SV x HR) x (1.34 x Hb x SaO2)

(10 dL/L is correction factor for CI in L/min CaO 2 in ml/dl)

Arterial Oxygen Content

(CaO2)
100 mm Hg

Hgb 15 gm/100 mL

SaO2 97%

Hemoglobin

Oxygen Saturation

O2 bound to
Hgb

PaO2 100 mmHg

Partial Pressure

+ O2 in
plasma

Cardiac Output
The volume of blood ejected by the
heart in one minute
Normal CO : 4 8 L/min
CO=Heart Rate x Stroke Volume
Stroke volume:

Preload- volume of blood in ventricle

Afterload- resistance to contraction
Contractility- force applied
10

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)]

12

Oxygen Uptake

13

Extraction Ratio
Extraction Ratio is a fraction of
oxygen taken from yang capillary
bed
O2ER: ratio between Oxygen Uptake
to Oxygen Delivery
Normal Extraction is 22 - 32 % (25%)
O2ER = VO2 / DO2 x 100
Or 1-SvO2 = if SvO2 70% --O2ER =
30%
14

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%

15

16

Microcirculation
Downstream endpoints

17

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 .
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
Calculated using the arterial blood gas as follows
Base Deficit = -[(HCO3) - 24.8 + (16.2)(pH - 7.4)]
18

Stratification level of illness

by base deficits
Stratification
Mild
Moderate
Severe

Base deficit
2 5 mmol/L
6 14 mmol/L
> 14 mmol/L

Base deficit can be misleading in

cause of hyperchloremic
acidosis, citrat from blood
products
19

Mixed Venous Oxygen Saturation

SvO2-ScvO2
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
20

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
Its an oxygen saturation of the blood
goes back to the heart

21

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)
22

SvO2ScvO2

Venous O2
saturasi
SvO2 (65%)
ScvO2 (>70%)

Superior vena
cava
Right atrium
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
23

Monitoring O2 transport
and tissue oxygenation

Reinhart K. Monitoring O2 transport and tissue oxygenation

in ctitically ill patint. 1989 , 195-211
24

(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
Lactate
normalization
:
prognostic
factor
for survival
24 hours survived
24-48 hours 25% mortality
> 48% hours did not normalized
86% mortality

25

Abramson D, et al. Lactate clearance and survival following injury.

Hyperlactate
mia
Lactate
production
Anaero
bic
-Tissue hypoxia
/hypoperfusion
-Increased
metabolisme

Lactate
clearance
Aerob
ic

-Impaired liver
function
-Decrease liver
blood flow

-Endogenous
production
-Inflammation
mediated
- accelerated
glycolysis
- inhibition of
pyruvate
Intensive Care Med 2003 ;
dehydrogenase
29 : 699

26

27

Weil MH. Defining hemodynamic instability. Braunwald E (ed )28

Heart disease 1998

Blood Lactate Clearance

Nguyen et al. Crit Care

Med 2004

29

Classification of Shock
Hypovolemic

dehydration,burns,
hemorrhage

Distributive

septic, anaphylactic,
spinal

Compensated

Uncompensated

Cardiogenic
-

Myocardial infarction
myocarditis,dysrhythmia

Obstructive

tamponade,pneumothorax

organ perfusion is
maintained
Circulatory failure
with end organ
dysfunction

Irreversible

Irreparable loss
of essential
organs
30

Stages of shock
Pre-shock
Shock
End-organ dysfunction

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
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

33

Assessment of Circulation in
Shock

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
35

In Normal Physiological
PaO
P
SaO (97%)
State
2

(13)

PiO2 humidified
(20)

(3.5)

Hb(150g/l)

Heart and lungs

Shunt
Shunt
(2-3%)
(2-3%)

Minute volume
(5 l/min)

PAO2
(14)

50

PVO2
(5.3)

P50

O2ER

SVO2 (75%)
Hb(150 g/l)

CaO2(200ml/l)
COt(5l/min)

Oxygen
Delivery
(1000 ml/l)

Diffusion of oxygen in tissues

Cappilary
Arterial
Venous
(13)
(5.3)
Interstitial
Oxygen
= 25% (5.3-2.7)
Consumption
Intracellular
(250 ml/min)
(2.7-1.3)
Carbon
Dioxide
Mitochondria
production
(1.3-0.7)
(200 ml/min)
Qt5(5 l/min)
Cvo2(150 ml/min)

Oxygen
return
(750 ml/min)
36

In Shock or
Catabolic State
O2ER

DO2

SvO250%
37

In Shock or Catabolic
Hypoxemia
PaO
P
SaO (97%)
State
Anemia
2

(13)

PiO2 humidified
(20)

50

(3.5)

Hb(150g/l)
Hypotension

Heart and lungs

Shunt
Shunt
(2-3%)
(2-3%)

Minute volume
(5 l/min)

CaO2(200ml/l)
COt(5l/min)

Diffusion of oxygen in tissues

Cappilary
Cellular
Arterial
Venous
Hypoxia
(13)
(5.3)
Interstitial
Oxygen
Oxygen
O2ER = 50% (5.3-2.7)
Consumption
Consumption
Intracellular
(250
ml/min)
(2.7-1.3)

Mitochondria
(1.3-0.7)
PAO2
(14)

PVO2
(5.3)

P50

Oxygen
Oxygen
Delivery
Delivery
ml/l)
(1000

SVO2 50%)

Qt5(5 l/min)
Cvo2(150 ml/min)

Carbon
Dioxide
production
(200 ml/min)

Oxygen
return

38

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 <

39

Organ failure and

(late) Septic Shock
O2ER

DO2 N/

O2 is available but cells are unable to

extract oxygen = Dysoxia

SvO2 90%
40

In Organ Failure and (late)

Hyperdynamic
Septic Shock
PaO
P
SaO (97%)
CaO (200ml/l)
2

(13)

PiO2 humidified
(20)

2
Circulation

50

(3.5)

Hb(150g/l)

Heart and lungs

Shunt
Shunt
(2-3%)
(2-3%)

Minute volume
(5 l/min)

COt(5l/min)

Diffusion of oxygen in tissues

Cappilary
Cellular /
Arterial
Mitochondrial
Venous
(13)
(5.3)
dysfunction
Interstitial
Oxygen
Oxygen
(5.3-2.7)
Consumption
O2ER 10%
Consumption
Intracellular
(250
ml/min)
(2.7-1.3)

Mitochondria
(1.3-0.7)
PAO2
(14)

PVO2
(5.3)

P50

Oxygen
Oxygen
Delivery
Delivery
N/ml/l)
(1000

SVO2 90%

Qt5(5 l/min)
Cvo2(150 ml/min)

Carbon
Dioxide
production
(200 ml/min)

Oxygen
return

41

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.

42

Shock classifications
Physiologic variable

Preload

Clinical measurement

Pulmonary
capillary wedge
pressure, CVP

Pump function

Afterload

Cardiac output

Systemic vascular
resistance

Tissue perfusion
Mixed venous
oxygen
saturation

Lactate

Hypovolemic

Cardiogenic

Distributive
Septic Early
Septic Late

Neurogenic

Obstructive

43

Stages of Shock

Sh
oc
kDy
so
x

ia

DO2 = Hb, SaO2 or

CO
Microcirculation Macrocirculation

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

O2 Extraction

Lactate
too late for intervention:
hypotension and cell
damage was already

Hypoperfusion begins: best time for

intervention like increase DO2 or
decreased VO2 (demand) ASAP
44

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
45

EBL Based on Patients Initial

Presentation
ATLS 2008

46

Assessment of
Shock
Ye
s

Quantitat
ive shock
Q

Ye
s
Cardiac
problem

No
Inadequate DO2 with VO2 and
lactate
Scvo2 Low cardiac ouput ?
Hypoxemi
Ye
a
s
SaO2
No

Cardiog
enic
shock

Ye
s
Hypovole
mia

Acute
respirat
ory
failure

No

Distributive
shock
Scv02, ERO2

Hemorrha
ge

No

Ye
s

CO2
gap

No

Hemorrha
gic
Shock

Hypovolemi
c shock
Fluid losses
(gut,
kidney,
fever)

Microciculation
Failure
(inflammation,
anaphylaxis,
sepsis)
Cytopathic
dysoxia
(poisoning,
sepsis, cell
death)

47

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
48

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
DO2
Tissue Oxygenation measurement :
normal Serum Lactate levels dan
Scvo2

49

1971
Swan Ganz
Hemodynamic parameter
CO, SV, SVR

1960,
shock is
hypotension, CVP

1980-1990
SvO2 parameter hypoperfusion;
DO2

Thank You

>2000;
Shock is imbalance between
DO2/VO2

Goal Directed using Cellular

parameter; BE, SvO2, pCO2 gap,

50

51

60

Macrocirculation
Upstream endpoints

61

Scv
O2

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
63
consumption

Scv
O2

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

64

Serum Lactate

Aduen, et al. JAMA 1994;272:16781685

65

Management of Shock

69

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

70

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
71

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, PRBCs and vasopressors to achieve
these goals depending on patients intravascular
volume, cardiac status and severity of shock

72

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
73

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

74

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

75

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
76
pressure (LVEDP) is a measure

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
77

Properties of
VasopressorsArterial
HR

Contractili
ty

constricti
on

Dobutamin
e

+++

Dopamine

++

++

++

Epinephrine

+++

+++

++

Norepineph
rine

++

++

+++

Phenylephri
ne

+++

Drug

Amrinone
+
+++
-Useful in patients who fail to reach adequate blood
pressures despite adequate volume resuscitation
Useful in patients who develop cardiogenic pulmonary
edema
78
Vasopressin can be used in patients refractory to first-

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

79

Assessment of adequate
tissue perfussion

Clinical
Parame
ter
Mental
status
Temperatu
re
Capillary
refill
Urine
output

Global
Parameter

Hemodynamic :
Cardiac Ouput:
SV, HR
Preload:
CVP,PCWP,
GEDI
Contractility :
CFI
Afterload : MAP,

Macrocirculat
ion

DO2-VO2
SvO2ScVO2
Serum
Lactate
Base
Deficit
A-V pCO2
gap

Regional
/Organ Specific
Parameter

Gastric
tonometry
Sublingual
capnometry
Nearinfrared
Spectrosco
py

Microcirculati
on

80

Monitoring response to
therapy
Monitoring parameters:
Respiratory: PaO2/FiO2 ratio
Renal: urine output, creatinine
Hematologic: platelet counts
CNS: Glascow coma scale
Hepatobiliary: bilirubin, LFTs
CV: blood pressure, arterial lactate
GI: ileus, blood in NG aspirate
81

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)
82

Control of septic focus

Prompt identification and
treatment of infectious source
are critical and definitive
Previously fluid and vasoactive
agents treatments are
supportive

83

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
84

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
85

Optimization perioperative
perioperative oxygen
oxygen
Optimization
delivery
using guideline
guideline
delivery using
(Goal-Directed Therapy = GDT)
General guideline
guideline using
using invasive
invasive device
device
General
(Vincent ))
(Vincent
Perioperative guideline
guideline (Pearce
(Pearce protocol)
protocol)
Perioperative
Severe sepsissepsis- septic
septic shock
shock guideline
guideline (( EGDT
EGDT
Severe
-Rivers)
-Rivers)
Hipovolemic guideline
guideline (Parillo)
(Parillo)
Hipovolemic
Tranfusion guideline
guideline in
in trauma
trauma
Tranfusion
86

Vincent protocol, 2005

SVO2
Low
(<70%)

Normal
(79%)

Do nothing

pCO
2
gap

SaO2 Normal (95%)

( O2ER)

SaO2 Low
(Hypoxemia)

Oxgen therapy
PEEP

Cardiac Output

High
(>2.5 L/min/m2)

PL
R
Low
(<2.5 L/min/m2)

Hemoglobin
>8 g/dL
Stress, anxiety, pain
(High VO2)

Analgesic
Sedation

PAOP
<8 g/dL
Anemia

Blood
transfusion

>18 mm Hg
Myocardial
dysfunction

Dobutamine

SV
V
<18 g/dL
Hypovolemia

Fluid challenge
88

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

89

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
Hemofiltrati
on
Textbook of critical care, Vincent JL, 2010

90

EARLY GOAL-DIRECTED THERAPY IN THE TREATMENT OF SEVERE SEPSIS

AND SEPTIC SHOCK

91
RIVERS E. N Engl J Med, Vol. 345, No

Static : CVP, PAOP

Volumetric : PAC,
PICCO,
LidCO
Echocardiographic :
Echo,
TEE
Dynamic : SVV, PPV,
PLR

<6

Proposed tools for a refined

early goal-directed therapy
92
(EGDT) algorithm, modified

Oxygen
Oxygen Delivery
Delivery Cascade
Cascade indicating
indicating the
the
potensial
potensial therapies
therapies to
to optimize
optimize oxygen
oxygen
delivery
delivery to
to the
the tissues
tissues
to
to prevent
prevent further
further complications
complications
O2 and Airway maintenance
CPAP or Ventilation

Pa
P
aO
O
2
2

Trachea

Optimization of DO2
(Goal Directed Therapy)
Alveolus

Vasodilator and low dose inotropes

Arterial blood
Future agents?
Microcirculation

Mitochondria

93
Jhanji S, Pearse RM The use of early intervention to prevent postoperative complications Current

Hypovolemic
Shock
Management

Supplemental O2 ETI
with mech ventilation
(if necessary)
Target SaO2 of 95%

Fluid boluses
*If PAC is used a mixed venous Os
sat is an acceptable surrogate,
and 65% would be the target

Dobutamine/
Dopamine

Vasopressor
(norepinephrine or
dopamine prefered)

Trauma/hemorrh
age
Elevated lactate
Begin fluid resuscitation
(initial bolus of at least 20
ml/kg crystalloid, to be
continued with colloids, red
cell concentrates and
SBP remainsfactors
< 90
coagulation

Filling
pressure
<8 mmHg

<
70%

MAP <
65

mmHg or
MAP remains < 65
mmHg;
lactate does not fall
Insert
CVP or PA
Cath

Filling
pressure
> 8 mmHg
ScvO2*
<
70%
MAP
MAP
65
ALL Goals
achieved?

Hypovolemic shock; Parillo and Delinger, Critical Care

N
O
94

95

Clinical signs: Shock, hypoperfusion, congestive heart failure,

acute pulmonary edema
Most likely major underlying disturbance

Hypovole
mia
Administer
-Fluid
-Blood transfusion
-Cause-specific
intervenstions
-Consider vasopressors

Systolic
>100
mmHg

Low output
Cardiogenic
shock
Check Blood
Pressure

Systolic 70-100
mmHg, no
symptoms of
shock

Nitroglyceri
ne
1020mcg/min
IV
Further

Dobutamine
220mcg/kg/min
IV

diagnostics
consideration :
-PA catheter
-Echocardiography
-Angiography for MI

Systolic 70100 mmHg,

with
symptoms of
shock
Dopamine
520mcg/kg/min
IV

Arrythm
ia
Bradycar Tachycar
dia
dia
Bradytachycardia
guideline

Systolic <70
mmHg, with
symptoms of
shock
Norepinephrine
0,012mcg/kg/min IV

Further therapeutics
consideration :
-IABP
-Reperfusion/revascula
rization

96