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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,
SvO2, pCO2 gap, Lactate, Gastric Tonometri
2
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
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
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
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 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
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
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
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
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
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
In Shock or
Catabolic State
DO2 ↓↓
O2ER ↑↑
SvO250%
22
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
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
DO2 N/↓
O2ER ↓↓
SvO2 90%
O2 is available but cells are unable to
extract oxygen = Dysoxia
25
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
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
Sepsis,
hyperthermia,
agitation,
stress surgery
Shock
Rest, sedation,
Hypothermia
28
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
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
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
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
– 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
Mechanisms of Shock
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
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
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
• 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
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
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
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
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
Reinhart K. Monitoring O2 transport and tissue oxygenation in ctitically ill
patint. 1989 , 195-211
Monitoring O2 transport and
tissue oxygenation
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
Abramson D, et al. Lactate clearance and survival following injury. J Trauma 1993
54
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
Weil MH. Defining hemodynamic instability. Braunwald E (ed ) Heart disease 1998
57
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
hypoxia. Crit Care Med 30
60
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
(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
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
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
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
Monitoring response to therapy
• All patients require close monitoring
• Evidence of deterioration merits a prompt,
through reevaluation
73
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
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
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
EBL Based on Patient’s Initial
Presentation
ATLS 2008
81
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
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
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
Textbook of critical care, Vincent JL, 2010
86
Glucose Control
Hemofiltration
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
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
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
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
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
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
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
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

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Shock Kuliah Residen.pptx

  • 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
  • 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
  • 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
  • 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
  • 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
  • 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
  • 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