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Current Concepts in ICU Management
Barbara McLean, MN, RN, CCRN, CCNS-BC,NP-BC, FCCM
Division of Critical Care
Grady Hospital System, Emory [email protected]
www.barbaramclean.com
mailto:[email protected]://www.barbaramclean.com/http://www.barbaramclean.com/mailto:[email protected] -
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And now.
Patient is now hypotensive and tachycardic
What do you do next?
Hetastarch Dobutamine
Norepinephrine
Amrinone
PRBCS
Dopamine
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What is it.?
First - Recognize type of shock
CI = 6
Hb = 10.5 g/dL
CVP = 17
Second find appropriate treatment
norepinephrine (not dopamine) through a central catheter as
soon as available is the first-choice vasopressor agent to correct
hypotension in septic shock
Critical Care Medicine: 2013
Surviving Sepsis Campaign guidelines for management of severe sepsis and septic shock: Update
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Why identify patients at risk?
Easier management with simplerinterventionsan ounce of prevention.
Prevent further deterioration
Provide time for investigation and treatment
Determine your goals!
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Volume response to treatment?
Appropriate tissue oxygenation?
Is the balance of oxygen delivery and
oxyhemoglobin dissociation adequatetissue
needs?
Is oxygen delivery sufficient?
Are the individual tissues getting the oxygen
they need?
Volume status-would it
help to give fluid? Whattype?
No
Not much
No
Global
Venous O2AG, Lactate
SV
MeasurementTissue O2
Microcirculation
SVV, PPV, SPV
EVLWI
The Present and Future
Adequate
oxygen carryng
(HgB)
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Definitions
The Continuum
SIRS
Sepsis
Severe Sepsis
Septic Shock
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Definition - Sepsis
Sepsis
SIRS PLUS a documented infection
Positive CXR
Positive U/A
Cellulitis /Abscess
Positive Blood Culture
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The Sepsis Continuum: FIRST, identify
A clinical response arisingfrom a nonspecific insult, with2 of the following: T >38oC or 90 beats/min RR >20/min WBC >12,000/mm3 or
10%bands
SIRS with a
presumed
or confirmed
infectiousprocess
Chest 1992;101:1644.
SepsisSIRSSevere
Sepsis
Septic
Shock
Sepsis with
organ failure
Refractory
hypotension
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The McLean-Piedmont Method
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Question?
If we recognized Possible Sepsis Early, treated
IMMEDIATELY with fluids, could we reduce
mortality rate?
Reduce Mortality by 20% system wide
Sepsis most frequent diagnosis associated with
mortality system-wide.
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McLean Model Sepsis: MEWS
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What do these patients have in common?Patient 1 Patient 2 Patient 3
HR 127 133 113
RR 34 28 18
Pa02 70
PaC02 23
Fi02 1.0
PEEP 12Rate 20 ACMV
91
PaC02 35
0.70
PEEP 15Rate 15 SIMV
100
PaC02 39
0.5
PEEP 20Rate 10 SIMV
BPS 80
BPD 55
BPS 80
BPD 40
BPS 100
BPD 60
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Why do we give volume
Increase stroke volume (SV) and cardiacoutput (CO)
Only 50% of patients respond to a fluidchallenge
Cumulative fluid balance may affect outcome
Whether the patient is responsive to fluid ornot?
Optimal strategy of increasing CO and
oxygen delivery
Volume expasion for hemodynamically unstable
patients
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Perel et al. Critical Care 2013, 17:203
The administration of a fluid bolus is done frequently
in the perioperative period to increase the cardiac
output. Yet fluid loading fails to increase the cardiac
output in more than 50% of critically ill and surgicalpatients.
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Cheatham ML. Crit Care Med 2007; 35:1629-30
The Surviving Sepsis Campaign emphasizes the useof CVP as a resuscitation end-point, as suggested bythe work of Rivers et al.
Traditional CVP cannot be used to accurately directresuscitation of the critically ill patients with elevationsin IAP or ITP.
To do so places the patient at risk for under-resuscitation with resultant organ dysfunction, failure,and increased mortality.
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Cumulative fluid balance and mortality
Fluid resuscitation in septic shock: A positive fluid balance and elevated
central venous pressure are associated with increased mortality.
Crit Care Med 2011 Vol. 39, No. 2; John H. Boyd, Jason Forbes, MD; Taka-aki Nakada, Keith R. Walley,James A. Russell,
A more positive fluid balance both early in resuscitation and cumulatively over4 days is associated with an increased risk of mortality in septic shock.
Central venous pressure may be used to gauge fluid balance
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Why do we need dynamic fluid measures
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Pulse Pressure Variation
Pulse pressure variation (PPV) Calculated in the same manner as SVV,
Also predict preload responsiveness well.
A 13% PPV predicts a 15% increase in CO for a 500-mL volume bolus
ANY signal that gives pulse density
REQUIRED Controlled variables
Ventilation
Heart ratePreisman S, Kogan S, Berkenstadt H, Perel A: Predicting fl uid responsivenessin patients undergoing cardiac surgery: functional haemodynamic
parameters including the Respiratory Systolic Variation Test and staticpreload indicators. Br J Anaesth 2005, 95:746-755.
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How I use arterial based cardiac output
Unstable?
Volumeresuscitation
Vasopressors
SV and arterialCardiac output
Unsta
bleonmec
hanical
ventilation?
Assist-control
Fixed PR interval
P/F unstablePatient unstable
SVV, SV and
arterial basedcardiac output
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Lansdorp B, et al. Br J Anaesth. 2012;108(3):395-401.
*P < 0.05
Hemodynamic Variables
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What do these patients have in common?Patient 1 Patient 2 Patient 3
HR 127 133 113RR 34 28 18
Pa02 70
PaC02 23
Fi02 1.0
PEEP 12
Rate 20 ACMV
91
PaC02 35
0.70
PEEP 15
Rate 15 SIMV
100
PaC02 39
0.5
PEEP 20
Rate 10 SIMV
BPS 80
BPD 55
BPS 80
BPD 40
BPS 100
BPD 60
PP 25
SVV 16%
PP 40
SVV 21%
PP 40
SVV 15%
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What are the Limitations of SVV?
Mechanical Ventilation Currently, literature supports the use of
SVV on patients who are 100%mechanically (control mode) ventilatedwith tidal volumes of more than 8cc/kgand fixed respiratory rates.
Spontaneous Ventilation Currently, literature does not support
the use of SVV with patients who arespontaneously breathing.
Arrhythmias Arrhythmias can dramatically affect
SVV. Thus, SVVs utility as a guide for
volume resuscitation is greatest inabsence of arrhythmias.
Updated algorithms actually filter outbeat to beat variability related todysrhythmia (except sustaineddysrhytmias for > 20 secs)
Lose their predictive value underconditions of varying R-R intervals (atrial fibrillation),
tidal volume varies from breath tobreath (with assisted and spontaneousventilation)
McLean Method
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McLean Method
Cardiac
Heart Rate
SV
SVV
PPV
Systolic pressure
EchoOxyhemoglobin
Dissociation
P/F
pPlat
Volume
IOS
PPV
SVV
SV
U/O ml/kg
EchoSV (CV) 02
OxyhemoglobinDissociation
P/F
pPlat
Vascular Tone
Respiratory Rate
PPV
SVV
PPV/SVV
Diastolic pressure
Echo
Oxyhemoglobin
Dissociation
P/F
pPlat
TissueOxyhemoglobin Dissociation ,Anion Gap, Serum C02, Base, pH, Ketones
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What about other information?
With a thermodilution, transpulmonary system, it is
possible to calculate and index:
Intrathoracic blood volume
Pulmonary vascular permeability index
Increased capillary permeability during the first 48 h in
patients with sepsis was associated with a higher mortality
rate during the intensive care unit (ICU) stay than those with
decreased permeability 1, 2
1. Hotchkiss RS, Karl IE (2003) The pathophysiology and treatment of sepsis.N Engl J Med 348: 138150.
2. Abid O, Sun Q, Sugimoto K, Mercan D, Vincent JL (2001) Predictive value of microalbuminuria in medical ICU patients: results of a pilotstudy. Chest 120:19841988.
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What about other information?
With a thermaldilution, transpulmonary system, it is
possible to calculate and index:
Global end diastolic volume
Extravascular lung water
Measurements of extravascular lung water (EVLW) correlate
to the degree of pulmonary edema and have substantial
prognostic information in critically ill patients.
normal EVLW (defined as < 10mL/kg)Martin GS, Eaton S, Mealer M, Moss M. Extravascular lung water in patients with severe sepsis: aprospective cohort study. Crit Care 2005;9:R74
R82.
Kuzkov VV, Kirov MY, Sovershaev MA, et al. Extravascular lung water determined with single transpulmonary thermodilution correlates with the
severity of sepsis-induced acute lung injury. CritCare Med 2006;34:16471653. [
Groeneveld AB, Verheij J. Extravascular lung water to blood volume ratios as measures of permeability in sepsis-induced ALI/ARDS. Intensive Care
Med 2006;32:13151321.
Patroniti N, Bellani G, Maggioni E, Manfio A, Marcora B, Pesenti A. Measurement of pulmonary edema in patients with acute respiratory distresssyndrome. Crit Care Med 2005;33:25472554.
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Transpulmonary vs. Pulmonary Artery Thermodilution
Left heartRight Heart
Pulmonary
CirculationLungs
Body Circulation
PULSIOCATHarterial thermo-
dilution catheter
central venousbolus injection RA
RV
PA
LA
LV
Aorta
Transpulmonary TD (EV 1000, PiCCO) Pulmonary Artery TD (PAC)
In both procedures only part of the injected indicator passes the thermistor.
Nonetheless the determination of CO is correct, as it is not the amount of the detected
indicator but the difference in temperature over time that is relevant!
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Why do we need EVLWI
Diagnosis
Prognosis
Goal to aggressive therapy
Better guide to resuscitation in patients at risk forpulmonary edema (anyone with high permeabilityindex)
Shock or severe sepsisALI
CHF
Monitoring of EVLW
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LPS OA
Pfeiffer UJ et al. Practical applications of fiberoptics in critical care
monitoring. 1990, pp. 114-125
Boldt J. Crit Care Med 2002:6:52-59
Sakka SG et al. Intensive Care Med 2000;26:180-187
Clinical examination, X-ray, CT, blood
Gravimetry
gases
Thermodilution techniques:
thermo-dye dilution,
single transpulmonary thermodilution
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Fluid challenge is a technique in which large amounts of fluids are
administered over a limited period of time under close monitoring to
evaluate the patients response and avoid the development of
pulmonary edema.
More than 50% of the patients with severe sepsis but without ARDS
have increased EVLW, possibly representing sub-clinical lung injury.
Fluid and Hemodynamic Management
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Starling Equation- Kfcapillary filtration coefficient
- PIF interstitial hydrostatic pressure
- pc capillary colloid osmotic pressure
Qf= Kf[(Pc- PIF) s(pc pIF)]- Pc capillary hydrostatic pressure
- s oncotic reflection coefficient
- pIF interstitial colloid oncotic pressure
Fluid and Hemodynamic Management
Pathophysiology:
Increases in capillary hydrostatic pressure Increased membrane permeability
Diminished oncotic pressure gradient
Clinical implications: Reductions in pulmonary capillary hydrostatic pressure/pulmonary
artery occlusion pressure CVP Hemodynamic monitoring to avoid tissue hypoperfusion
Fluid restriction/negative fluid balance
Diuretics
Combination therapy with colloids and furosemide?
l f f l f d f d h h h l
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Mortality as a function of EVLW. Patients were classified into four groups according to their highest EVLW value.
Sakka S G et al. Chest 2002;122:2080-2086
2002 by American College of Chest Physicians
R l i hi b l h d i d l d f i d l di i d i d
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Relationship between pulmonary hydrostatic pressure and lung edema formation under normal conditions and increased
permeability.
Calfee C S , Matthay M A Chest 2007;131:913-920
2007 by American College of Chest Physicians
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Stroke
Volume
00
Cardiac Ouput Maximization
Cardiac Output Optimization Concept
EVLWLarge increase in EVLW
for small increase CO
OptimalPreload
Preload
EVLW tifi f l d
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ELWI = 7 ml/kg
ELWI = 8 ml/kgELWI = 14 ml/kg
ELWI = 19 ml/kg
Extravascular lung
water index
(ELWI)
normal range:3 7 ml/kg
EVLW as a quantifier of lung edema
R l f EVLW A t
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ELWI (ml/kg)
> 21
n = 5414 - 21
n = 1007 - 14
n = 174
< 7
n = 45
Mortality(%)
10
00
n = 373*p = 0.002
20
30
40
50
60
7080
Sturm J in: Lewis, Pfeiffer (eds): Practical Applications of Fiberoptics in
Critical Care Monitoring, Springer Verlag Berlin - Heidelberg - NewYork
1990, pp 129-139
The amount of extravascular lung water is a predictor for mortality in the intensivecare patient
ELWI (ml/kg)
4 - 6
30
0
Mortality (%)
20
n = 81
40
50
60
70
80
6 - 8 8 - 10 10 -12
12 - 16 16 - 20 > 20
90
100
Sakka et al , Chest 2002
Relevance of EVLW Assessment
R l f EVLW A t
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Intensive Care
days
Mitchell et al, Am Rev Resp Dis 145: 990-998, 1992
Volume management guided by EVLW can significantly reduce time on ventilation and
ICU length of stay in critically ill patients, when compared to PCWP oriented therapy,
Ventilation Days
PAC Group
n = 101* p 0,05
PAC GroupEVLW Group EVLW Group
22 days 15 days9 days 7 days
* p 0,05
Relevance of EVLW Assessment
.
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2008 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins. 5
Extravascular lung water in sepsis-associated acute
respiratory distress syndrome: indexing with
predicted body weight improves correlation with
severity of illness and survival.
Phillips CR; Chesnutt MS; Smith SM
Critical Care Medicine. 36(1):69-73, 2008 Jan.
Figure 3. Receiver operator characteristic curves for
extravascular lung water indexed to predicted body
weight (EVLWp), dead space-tidal volume fraction
(Vd/Vt), extravascular lung water (EVLW), and Pao2/Fio2
for mortality with sensitivity vs. 1-specificity for
identification of nonsurvivors. The areas under the
curves were 0.988 +/- 0.019, 0.869 +/- 0.112, 0.851 +/-
0.113, and 0.643 +/- 0.137 for EVLWp, Vd/Vt, EVLW, and
Pao2/Fio2, respectively.
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2010 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins. 6
Extravascular lung water indexed to predicted body
weight is a novel predictor of intensive care unit
mortality in patients with acute lung injury.
Craig TR; Duffy MJ; Shyamsundar M; McDowell C;
McLaughlin B; Elborn JS; McAuley DF
Critical Care Medicine. 38(1):114-20, 2010 Jan.
Figure 2. Receiver operator characteristic (ROC) curves
for extravascular lung water indexed to predicted
(EVLWp) and actual body weight (EVLWa) for mortality.
The area under the curve (95% confidence interval [CI])
for EVLWp (0.8; CI, 0.6-0.9) was larger than for EVLWa
(0.7; CI, 0.5-0.9), but there was no statistically significant
difference between these two areas (p = .12).
EVLW predicting mortality
EVLW as Predictor
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2010 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins. 3
Extravascular lung water indexed to predicted body
weight is a novel predictor of intensive care unit
mortality in patients with acute lung injury.
Craig TR; Duffy MJ; Shyamsundar M; McDowell C;
McLaughlin B; Elborn JS; McAuley DF
Critical Care Medicine. 38(1):114-20, 2010 Jan.
Figure 1. A, Actual extravascular lung water (EVLWa) is
increased in non-intensive care unit (ICU) survivors
compared with ICU survivors. The median EVLWa was
16.4 (10.8-21.8) for non-ICU survivors and 10.5 (8.7-14.5)
for ICU survivors *p = .0278 Mann-Whitney U test. B,
predicted extravascular lung water (EVLWp) is increased
in non-ICU survivors compared with ICU survivors. The
median EVLWp was 17.5 (15.3-21.4) for non-ICU
survivors and 10.6 (9.5-15.4) for ICU survivors. *p = .0029
Mann-Whitney U test.
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What am I looking for?
Indices of hypovolemia: SVV > 13%
volume loading should decrease SVV. If not
Stop fluid administration
Inotropic support initiated
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What is the arterial tone?
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What is the arterial tone?
Hypotension
Relationship between PPV/SVV
Better relationship of elastance /vascular tone than
SVR
No assumption regarding volume distribution
Physics calculation
PP reflects variance
SV more regarding EF
PP/SV normal 1.2-2
What is the arterial tone?
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What is the arterial tone?
Hypotension, volume responsiveness
PP/SV normal 1.2- 1.5
< 0.9 indicates vasoconstriction, SVV > 13%
Volume
< 0.9 indicates vasoconstriction, SVV 1.5 indicates vasodilation, SVV>13% Volume
vasopressor
Pinsky, personal communication ESICM 2011
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Variation from Ventilation
SVV, PPV, and SPV are created by tidal volume-induced changes in venous return.
presumes a constant R-R interval and aremeasured from diastole to systole
+ pressure ventilation causes changes in venousreturn, which is accentuated in hypovolemicpatients
take advantage of the swings in venous return inorder to determine the fluid responsiveness ofhypotensive patients
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Crit Care Med. 2002 Jun;30(6):1210-3.Use of a peripheral perfusion index derived from the
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Use of a peripheral perfusion index derived from the
pulse oximetry signal as a noninvasive indicator of
perfusion.
..the variation of the peripheral perfusion index in healthyadults and related it to the central-to-toe temperaturedifference and capillary refill time in critically ill patients afterchanges in clinical signs of peripheral perfusion.
Poor peripheral perfusion was defined as a capillary refill time>2 secs and central-to-toe temperature difference > or = 7degrees C. Peripheral perfusion index and arterial oxygensaturation were measured by using the Philips MedicalSystems Viridia/56S monitor.
The distribution of the peripheral perfusion index was skewedand values ranged from 0.3 to 10.0, median 1.4 (innerquartile range, 0.7-3.0).
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Use of a peripheral perfusion index derived from the pulseoximetry signal as a noninvasive indicator of perfusion
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oximetry signal as a noninvasive indicator of perfusion
Alexandre Pinto Lima, MD; Peter Beelen, RN; Jan Bakker,
MD, PhD
Changes in the peripheral perfusion index reflect
changes in the core-to-toe temperature difference.
Therefore, peripheral perfusion index measurements
can be used to monitor peripheral perfusion incritically ill patients. (Crit Care Med 2002;
30:12101213)
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Cli i l U f PI
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Clinical Uses for PI
Below 1.4, PI indicates poor perfusion
The PI is unique for each patient and the trend is
what is important!
EGDT
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EGDT
SVV
PI
PLR
S i it ti 2013 id li
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Sepsis resuscitation: 2013 guidelines
Serum lactate measured Blood cultures obtained before antibiotics administered
Improve time to broad-spectrum antibiotics 45 mins
Initial empiric therapy include 1 or more drugs with activityagainst ALL likely pathogens (bacterial and or fungal or viral)
Reassessed daily to optimize activity, prevent development ofresistance, reduce toxicity, and reduce costs
Surviving Sepsis Campaign Management Guidelines Committee. Crit Care Med 2013
Diagnosis
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Diagnosis
Before the initiation of antimicrobial therapy, at least two
blood cultures should be obtained At least one drawn percutaneously
At least one drawn through each vascular access device if inserted longer
than 48 hours
Other cultures such as urine, cerebrospinal fluid, wounds,respiratory secretions or other body fluids should be
obtained as the clinical situation dictates
Other diagnostic studies such as imaging and sampling
should be performed promptly to determine the source andcausative organism of the infection
may be limited by patient stabilityWeinstein MP. Rev Infect Dis 1983;5:35-53
Blot F. J Clin Microbiol 1999; 36: 105-109.
Th ti St t i i S i
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Therapeutic Strategies in Sepsis
Optimize Organ Perfusion
Expand effective blood volume.
Hemodynamic monitoring.
Early goal-directed therapy. 16% reduction in absolute risk of in-house mortality.
39% reduction in relative risk of in-house mortality.
Decreased 28 day and 60 day mortality. Less fluid volume, less blood transfusion, less vasopressor
support, less hospital length of stay.
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What about this one.?
64 year old with severe sepsis (not septic shock) Infection
Acute onset fever, chills, cough
RML and RLL infiltrates
SIRS Criteria Tachycardia, tachypnea, leukocytosis with shift
Organ dysfunction
Renal, pulmonary Hypotension
NOT refractory to fluid bolus (yet)
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Corticosteroids in Sepsis:
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Corticosteroids in Sepsis:
refractory hpotension
**first measure the serum lactate
Look for cryptic shock
Physiologic doses
Replacement
Stress dose
Pharmacologic doses
Anti-inflammatory
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Why do we need ScV02?
Understanding Tiss e O gen
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Understanding Tissue Oxygen
Tissue Oxygenation The single MOST important issue is tissue oxygenation.
All physiologic components are designed to maintain
balanced tissue oxygen consumption (demand). What are the components of Oxygen Consumption?
Oxygen delivery
Metabolic demand at the cellular level
Blood flow through the capillary
Ability to dissociate oxygen from hemoglobin
Understanding Tissue Oxygen
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Understanding Tissue Oxygen
Tissue Oxygenation There are two mechanisms designed to meet oxygen
consumption (demand)
Increase oxygen delivery Increase the release (dissociation) of oxygen fromhemoglobin
In the best of critical situations, both delivery and
dissociation increase to maintain cells failure of one mechanism will be supported by
compensation by the other
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Understanding Tissue Oxygen
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Understanding Tissue Oxygen
Components of Oxygen Delivery
1. Cardiac Output = Heart rate x stroke volume 2. Total hemoglobin (02 carrying capacity)
3. Saturation of hemoglobin First line compensatory mechanism ( patient)
Increase the heart rate and stroke volume to increasedelivery when cells are hyper metabolic and/or when oxygenis not functionally dissociating from its transporter,hemoglobin.
Is cardiac output responsive to intravascular
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p p
fluid loading?
Assumes that venous return and LV preload are theprimary determinants of cardiac output (StarlingsLaw of the Heart)
Assumes low LV end-diastolic volume (EDV) equalspreload-responsiveness
Attempts to assess EDV through surrogatemeasures CVP, Ppao, LV end-diastolic area, RV EDV, intrathoracic
blood volume
Sepsis management: 2013
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Sepsis management: 2013
Dobutamine
patients with cardiac dysfunction (filling pressures,
cardiac output OR clinical signs of hypoperfusion after
restoration of BP with volume resuscitation Do NOT use strategy to increase Cardiac index to
predetermined supranormal level
Surviving Sepsis Campaign Management Guidelines Committee. Crit Care Med 2013
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Understanding Tissue Oxygen
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Understanding Tissue Oxygen
Oxygen dissociation as a compensatory response Shifts in the bound oxygen mean that there is a
change in the way oxygen is
Taken up by the hemoglobin molecule at the alveolar level(Sa02) Depends on the partial pressure of alveolar gas (PA02)
Released related to the partial pressure of capillary oxygen(Pa02, Pcap02)
Capillary oxygen depends on the tissue oxygen (Pti02)
Tissue oxygen goes down when cells are hypermetabolic and/or thedelivery is inadequate
Venous Oxygenation Patterns
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Pv02
Sv02
Scv02
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Targeting Mixed Venous Saturation
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Targeting Mixed Venous Saturation
few studies have specifically targeted resuscitationto a mixed venous saturation of >70%
prospective, randomized trial in adults:
treatment to a mixed venous saturation >70% did notreduce mortality compared with therapy targeting a normal
CI
(Gattinoni et al NEJM1995)
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But
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But
Sa02 is pre-cell reservoir: 95-100%
Sv02 is globalpost cell left over: 60-80%
Scv02 is part ial(upper extremities) post
cell left over: 65-85%
Tissue Oxygenation
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Tissue Oxygenation
overwhelmed compensatory mechanisms and lowSvO2 tissue hypoxia and lactate ----Vincent JL, DeBacker D. Oxygen transport the oxygen delivery controversy.
Intensive Care Med 2004; 30:19901996
drop in SvO2 or ScvO2does not necessarily mean
tissue hypoxia occurs!
What do these patients have in common?
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What do these patients have in common?Patient 1 Patient 2 Patient 3
HR 127 133 113
RR 34 28 18
Pa02 70
PaC02 23
Fi02 1.0
PEEP 12
Rate 20 ACMV
91
PaC02 35
0.70
PEEP 15
Rate 15 SIMV
100
PaC02 39
0.5
PEEP 20
Rate 10 SIMV
BPS 80
BPD 55
BPS 80
BPD 40
BPS 100
BPD 60
Sv02 45% Sv02 70% Sv02 65
AG 34 AG 41 AG 13
LA 6.1 LA 7.2 LA 2.8
PP 25
SVV 16%
PP 40
SVV 21%
PP 40
SVV 15%
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SCVO2 : 49%
CVP 8 cm H2O SBP 73 mmHg
Lactate > 12
Glucose 950
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Scv02 tells us about compensation, but
acidosis measures tell us about adequacy!
The Oxygenation Profile
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The Oxygenation Profile
Acid-Base Disturbances Are common in critical patients
May be complex or mixed
Are often confusing Requires accurate analysis to facilitate appropriate
treatment
Focus on Metabolic Acidosis
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The Oxygenation Profile
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yg
Cells: Producer
Produces acid duringmetabolism: acid transported ascarbonic acid
Tissue acids increase in insulindeficiency states
Tissue acids increase in tissuehypoxia states
Cells: Regulate pH Acidosis: acid (H+) uptake in
exchange for potassium releaseprovides buffer effect andpromotes intracellularhypokalemia
Alkalosis: acid (H+) release in
exchange for potassium uptakeprovides buffer effect andpromotes intracellularhyperkalemia
Kidney: Regulator Major volume and
electrolyte regulator Acid regulator Base regulator
Lung: Acid regulator Rate and depth of
breaths depends on thecarbonic acid and
therefore the pH
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Response to increase in acid H+
and related acid pH
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and related acid pH
H+pH C02
mL/DL mmHgAcidcontent
Compensation in attempts to sustain Tissue Oxygen
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Sv02
Normal toHighWithPersistentLactic
Acidosis
Pv02
p p yg
Cells do not
need it!
OR
Cells need it
but cannot
get it!
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Anion Gap
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Anion gapis a concept used to estimate electrolyte (anions & cation)
levels in the serum and {measures or estimates the , sic} conditionsthat influence them (Tabers Cyclopedic Medical Dictionary, 2005).
Normal Anion Gap = (Na+) - (Cl- + HCO3-) = 12 (+/- 2)
Positive charged ions and negative charged ions are relatively equalin normal physiology. In vivo physiology all equal!
The measured ions (lab analysis) are represented by Na+, Cl- andHC03
- (or total serum C02), the external measured gap of 12 (+/- 2)is considered acceptable
Na+(Cl - + HCO3
-)
Anion GapAnion Gap = (Na+) - (Cl- + HCO3-)
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p ( ) ( )
When there is an increase in unmeasured ions, there will be a gapbetween the + and measures
A gap of > 20 implies a metabolic increase in acid production.
Lactic Acid and Ketoacid donate H+ .
H+ binds to HC03 and/or Cl changing the charge
HC03 and/or Cl
The gap between + and gets wide
Na+ constant
(Cl - + HCO3 -) : light on the negatives
(Lactic acid or ketones donated H+) heavy on the positives
Anion Gap
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Used to confirm type of metabolic acidosis with ABG
Used to diagnose metabolic acidosis without ABG
Affected by:
albumin (for each 1 gm decrease in albumin , add three points to
gap) hyperchloremia (usually from fluid resuscitation)
High Cl- causes decrease in available HC03-
High Cl- binds to H+ HCl
Cannot compensate because is not a compound that can be blown off
Metabolic acidosis with normal gap: non-gap acidosis
most commonly occurs in hyperchloremia
EGDT
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SVV
PI
PLR
Base
Bicarb
AG
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So what about lactate?
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Lactate Levels
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Utility of a single high initial lactate have been debated poor sensitivity and specificity
Lactate clearance is a better predictor of mortality
Lac-time: time it takes to clear 10% of lactate
Time to clear < 24 hours , improves survival in Severe sepsis Lac-time also directly correlated with number of organ failures
One lactate (lactic acid ) level is not as predictive orevaluative as a series over 24 hours ( i.e., Q6H)
1. Bakker, J., Coffernils, M., Leon, M., Vincent, J.L. (1991). Blood lactate levels are superior to oxygen-derived variables in predicting
outcomes in human patient shock. Chest, 99, 956-962.
2. Bakker, J., Gris, P., Coffernils, M., Kahn R.J., Vincent, J.L. (1996). Serial blood lactate levels can predict the development of multiple
organ failure following septic shock. Am J Surg, 171(2), 221-226.
3. Nguyen, H.B., Rivers, E.P., Knoblich, B.P., et al. (2004). Early lactate clearance is associated with improved outcome in severe
sepsis and septic shock. Crit Care Med, 32(8), 1637-1642.
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LACTIC ACID TABLE
What do these patients have in common?
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Patient 1 Patient 2 Patient 3
HR 127 133 113
RR 34 28 18
Pa02 70
PaC02 23
Fi02 1.0
PEEP 12Rate 20 ACMV
91
PaC02 35
0.70
PEEP 15Rate 15 SIMV
100
PaC02 39
0.5
PEEP 20Rate 10 SIMV
BPS 80
BPD 55
BPS 80
BPD 40
BPS 100
BPD 60
Sv02 45% Sv02 70% Sv02 65
AG 34 AG 41 AG 13
LA 6.1 LA 7.2 LA 2.8
EGDT
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SVV
PI
PLR
Base
Bicarb
AG
LA
A-V PCO2 Gradient (DPCO2)
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Can the PCO2 gradient between arterial andvenous blood gas samples (DPCO2) represent
adequacy of perfusion?
A-V PCO2Gradient (PCO2)
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PCO2 = PvCO2 PaCO2 The PCO2 is an index to identify the critical
oxygen delivery point (VO2/DO2).
The critical oxygen delivery point is whenconsumption (VO2) is dependent on delivery (DO2)
A-V PCO2 Gradient (PCO2)
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critical oxygen delivery point is associated with anabrupt increase of blood lactate levels and a
significant widening in PCO2
Since CO2 is 20x more soluble in aqueous solutions
than O2, it is logical that PCO2 may serve as an
excellent measurement of adequacy of perfusion.
Comparison ofPCO2 and SvO2
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Key Points : SvO2 may reflect the metabolic rate and oxygen
consumption
PCO2 and/or serial lactate levels and clearancemay reflect the adequacy of tissue perfusion
Definitions of ETC02
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Capnometry is the measurement of expired CO2 and provides anumeric display of CO2 tension in mm Hg or % CO2
Capnograph is the measuring instrument
Capnography is the graphic representation of expired CO2 over
time
Capnography
End-tidal CO2 concentration is close to arterial PaCO2 levels
Inversely Indicates the adequacy of alveolar ventilation Capnogram is the waveform displayed by the capnograph
PaCO2 vs. PeTCO2
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PaCO2= Partial Pressure of Carbon Dioxide inarterial blood gases
The PaCO2 is measured by drawing the ABGs,
which also measure the arterial pH If ventilation and perfusion are stable PaCO2
should correlate to PetCO2
Capnograms
Normal
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Zero baseline Rapid, sharp uprise
Alveolar plateau
Well-defined end-tidalpoint
Rapid, sharp downstroke
AB Deadspace
BC Dead space and alveolar gasCD Mostly alveolar gas
D End-tidal point
DE Inhalation
Interpretation of ETCO2
Excellent correlation between
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Excellent correlation betweenETCO2 and cardiac output
when cardiac output is low. When cardiac output is nearnormal, then ETCO2 correlateswith minute volume.
Only need to ventilate as oftenas a load of CO2 molecules
are delivered to the lungs andexchanged for 02 molecules.
Clinical applications
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Endotracheal intubation Etiologies of hypocapnea/hypercapnea
Cardiopulmonary resuscitation
Respiratory problems
V/Q mismatch
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Capnography & Pulse Oximetry
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CO2: Relects ventilation
Detects apnea and
hypoventilation immediately
Should be used with pulseoximetry
O2 Saturation: Reflects oxygenation
30 to 60 second lag in
detecting apnea or
hypoventilation Should be used with
capnography
ACLS:WaveformCapnography
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2010AmericanHeartAssociation.Allrightsreserved.
p g p y After intubation, exhaled carbon dioxide
is detected, confirming tracheal tubeplacement.
Highest value at end-expiration.
ETCO2 & Cardiac Resuscitation
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Non-survivorsAverage ETCO2: 4-10 mmHg
Survivors (to discharge)Average ETCO2: >30 mmHg
ETCO2 & Cardiac Resuscitation
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If patient is intubated and pulmonary ventilation isconsistent with bagging, ETCO2 will directly reflect
cardiac output
Flat waveform can establish PEA Increasing ETCO2 can alert to return of spontaneous
circulation
Configuration of waveform will change withobstruction
Capnograms
Normal
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Zero baseline Rapid, sharp uprise
Alveolar plateau
Well-defined end-tidalpoint
Rapid, sharp downstroke
AB DeadspaceBC Dead space and alveolar gas
CD Mostly alveolar gas
D End-tidal point
DE Inhalation of CO2 free gas
Physiology
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Relationship between CO2 and RR
RR CO2 Hyperventilation
RR CO2 Hypoventilation
What is this?
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What is this?
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ABNORMALITIES
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Gradual Hyperventilation Decreasing temp
Gradual in volume
Sudden increase in ETCO2 Sodium bicarb
administration
Release of limb tourniquet
Gradual increase Fever
Hypoventilation
Increased baseline
Rebreathing Exhausted CO2 absorber
USES
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MetabolicAssess energy expenditure
Cardiovascular
Monitor trend in cardiac output Can use as an indirect Fick method, but actual numbers
are hard to quantify
Measure of effectiveness in CPR Diagnosis of pulmonary embolism: measure gradient
PULMONARY USES
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Effectiveness of therapy in bronchospasm Monitor PaCO2-PetCO2 gradient Worsening indicated by rising Phase III without plateau
Find optimal PEEP by following the gradient. Should
be lowest at optimal PEEP. Can predict successful extubation.
Dead space ratio to tidal volume ratio of >0.6 predicts failure.Normal is 0.33-0.45
Limited usefulness in weaning the vent when patient isunstable from cardiovascular or pulmonary standpoint
Confirm ET tube placement
Circulation and Metabolism
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Capnography Is A Direct Measurement OfVentilation
Indirectly Measures Metabolism And Circulation
Increased Metabolism : Increase The Production OfCarbon Dioxide: Increasing The PetC02
Decrease In Cardiac Output Lowers PulmonaryPerfusion: Decrease Delivery Of Carbon Dioxide To
The Pulmonary Capillaries: Results In DecreaseThe PetC02
V/Q Mismatch
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If ventilation or perfusion are unstable, aVentilation/Perfusion (V/Q) mismatch can occur
Alters the correlation between PaC02 and PetCO2
V/Q mismatch can be caused by blood shunting atelectasis (perfusing unventilated lung area)
dead PE or Hypovolemia
PetCO2 Values
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Ventilation Normal 30 45 mmHg
(PaC02within 10 mmHg)
Hypoventilation > 45 mmHg Hyperventilation < 35 mmHg
HypoPerfusion ETC02 is significantly
lower than PaC02
PaC02 high Pay close attention!
Ventilation Perfusion Match
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Critically ill patients often have rapidly changingdead space and V/Q mismatch
Higher rates and smaller TV can increase theamount of dead space ventilation
High mean airway pressures and PEEP restrictalveolar perfusion, leading to falsely decreasedreadings
Low cardiac output will decrease the reading MUST compare blood and exhaled C02
CO2 Physiology a-ADCO2
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Normally 2-3mmHg. Adults < 10 mmHg Widened if
Incomplete alveolar emptying
Poor sampling
High VQ abnormalities (normal 0.8), seen with PE,hypovolemia, arrest, lateral decubitus
Decreased with shunt
a-ADCO2 small Causes: Atelectasis, mucus plug, right mainstem ETT
PaCO2-PetCO2 gradient
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PetCO2 is usually less Difference depends on the number of
underperfused alveoli
Decreased cardiac output will increase the gradient The gradient can be negative when healthy lungs
are ventilated with high TV and low rate
Case in point
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PetC02 = 20 mmHg Hypoventilation is assumed
PaC02 is 76 mmHg
What is the gradient?
Is ventilation the problem?
Is perfusion the problem?
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The conventional view serves to protect us from
the painful job of thinking.
John Kenneth Galbraith (1908-2006)
Limited Role of Pulse Oximetry in Assessing
Ventilation
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Normal SaO2 determined by PaO2 If patient hypoventilates, PaCO2 increases and will
drive PaO2 downward in direct proportion to PaCO2increase
If PaCO2 increases by 10, PaO2 will decrease by 10
If PaO2 is 90, will decrease to 80 mm Hg SaO2 will decrease from 98 to 97.
Oximeter is not sensitive to rises in PaCO2
When oxygen therapy is added or increased, rise inPaCO2 is completely obscured
Capnography & Pulse Oximetry
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CO2: Relects ventilation
Detects apnea and
hypoventilation immediately
Should be used with pulseoximetry
O2 Saturation: Reflects oxygenation
30 to 60 second lag in
detecting apnea or
hypoventilation Should be used with
capnography
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Case Example of Limited Role of Oximetry in
Hypoventilation
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PaO2 95 80 99
SpO2 .98 .96 .98
FIO2 RA RA .30
PetCO2 39 54 60pH 7.38 7.25 7.23
A 56 year old man admitted to the outpatient procedure area for a follow-up
colonoscopy. The patient had a colonoscopy 3 years earlier where a pre
cancerous polyp was removed. During this procedure, the physician elects
t P f l i t d f Mid l d t it id li i ti d
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to use Propofol instead of Midazolam due to its more rapid elimination and
shorter recovery time. Twenty minutes into the procedure, you note the
PetCO2 listed below. What would your actions be based on this
information?
P RR BP SpO2 PetCO2
Admission 72 12 132/72 100 37
5 minutes into procedure 76 10 128/70 100 42
20 minutes into procedure 73 10 134/78 100 48
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Final Case. Case 4
A 44 yr old male admitted to MICU with unknown fever, SOB,
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Pulse RR NIBP SpO2 PetCO
2
Meds
Pre extubation 114 44 132/64 98 34 2 mg Midazolam,
50 mcg/Fentanyl
Extubated 102 38 138/60 97 33 5 mg bolus
Gtt to 4 mg Midazolam,Gtt to 100 mcg/Fentanyl
Post
reintubation
and
sedation
76 12 128/88 99 47
y , ,
hypoxemia. pH 7.34, PaCO2 38, PaO2 44, SpO2 .78. He is
intubated, IMV 12/44. Extubates himself, is reintubated.
Sedation is increased. RR decreases to 12. .What is the effect
of sedation on ventilation?
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Now a case.
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ARDSnet
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ARDSNetventilationRR35,Vt=5ml/kgPBW
plateaupressure~33
PaO2/FiO262with18PEEP100%O2APRV
PaO2/FiO286
Fluid balance 3 7 lit
Vitals..
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Hypotension, tachycardia, high normal CVP,hypoxemia, fluid long
60ml/hr
82
0mlUrine output
PaO2/FiO2
10 mmHg
1.0
CVP
FiO2
95 128HR
Fluid balance
Blood Pressure
+ 3.7 liters
135/80 82/38
What would you do?
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Fluid load, decreased urine output, high normalCVP in shock
Vasopressors?
Inotropes? Fluids?
Transpulmonary thermodilutionmeasurements
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CI
SVRI
GEDVI
SVVEVLWI
=
=
=
==
2.7 L/min/m2
825 dyne.cm.sec-5/m2
550 ml/m2(800-1000)
18-20% (13%)19 ml/kg
Septic,drybutwithseverepulmonaryedema
Gave 500 ml bolus of NS
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MAPCVP
CI
SVRI
GEDVI
SVV
EVLWI
= 55 mmHg= 10mmHg
= 3.2 L/min/m2
= 950 dyne.cm.sec-5/m2
= 625 ml/m2(800-1000)
= 16% (13%)
= 19 ml/kg
No change in lung water so given 2 additionalboluses
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MAP = 76 mmHg
12 hours later on norepinephrine
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MAP = 76 mmHg
CI = 4.1 L/min/m2
SVRI = 1250 dyne.cm.sec-5/m2
Fluid balance + additional 3.2 liters in ARF
GEDVI = 1100 ml/m2(800-1000)
PPV = 9% (
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CO
Preload
Large decrease in EVLWfor small decrease preload
The Case for Measuring EVLW in ARDS
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Can drown with only 200-300 ml extra lung water Want to know precisely what is happening to lung
water with resuscitative and therapeuticinterventions
CXR, oxygen need, severity of injury LIS, areimprecise determinates of the amount of pulmonaryedema
No correlation to PaOP, CVP or fluid balance withlung water
The case for measuring EVLW
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EVLW predicts mortality in ARDS EVLW predicts progression to ALI in patients at risk
EVLW driven protocols only approach shown to
improve mortality
What do these patients have in common?
Patient 1 Patient 2 Patient 3
HR 127 133 123
RR 34 28 21
Pa02 70
P C02 23
91
P C02 35
100
P C02 39
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PaC02 23
Fi02 1.0
PEEP 12
Rate 20 ACMV
PaC02 35
0.70
PEEP 15
Rate 15 SIMV
PaC02 39
0.5
PEEP 20
Rate 10 SIMV
BPS 80
BPD 55
BPS 80
BPD 40
BPS 80
BPD 60
Sv02 45% Sv02 70% ( levo 10 mgms) Sv02 58
AG 34 AG 41 AG 23
LA 6.1 LA 7.2 LA 4.8
SVV 16% SVV 21% SVV 15%
EVLWI 11% / SV 62Would you give fluid?
What type
EVLWI 15% /41Would you give fluid?
What type
EVLWI 17%/ 41Would you give fluid?
What type?
Post fluid EVLWI 13%/
SV 75/ SVV 12%
Post fluid EVLWI
16%/64/SVV 16%
Post fluid 22%/ 40/SVV 14%
How I use arterial based cardiac output
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Unstable?
Volumeresuscitation
Vasopressors
SV and arterialCardiac output
Unstableo
nmechanical
ventilation?
Assist-control
Fixed PR interval
P/F unstable
Patient unstable
SVV, SV andarterial basedcardiac output
UnstableandP
/Fdecreasing
+/-ACS
Central line,femoral arterialline with sensor
Continuousarterial basedcardiac output
Intemittent Icedinjectate forEVLW
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Physiological Truth
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There is no such thing as aNormal Cardiac Output
Cardiac output is either
Adequate to meet the metabolic demands
Inadequate to meet metabolic demands
Absolute values can only be used as minimal
levels below which some tissue beds areunder perfused
Conclusions Regarding Different Monitors
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Hemodynamic monitoring becomes more effectiveat predicting cardiovascular function when
measured using performance parameters CVP and arterial pulse pressure (PP) variations predict
preload responsiveness
ScvO2, SvO2 predict the adequacy of oxygen transport
Summary and Key Points
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EVLW as a valid measure for the extravascular watercontent of the lungs is the only parameter forquantifying lung edema available at the bedside.
Blood gas analysis and chest x-ray do not reliablydetect and measure lung edema
CVP and PaOP do not predict who will respond to fluidand when enough is enough
ScV02 reveals depth of compensation, LA and AG
reflect adequacy It all adds up to better management!
Case Presentation 2
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ScV02: 54%, HR 128, RR 26 22% SVV what now?
PP/SV 0.8 . Vasoconsticted or dilated?
Next?
Volume responsive!
Case Presentation 2
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SVV 15% PP/SV 1.8
Sv02 50%
Next?
Vasopressor
Case Presentation 2
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SVV 20% PP/SV 0.8
Sv02 80%
Next?
Volume inotrope dilator
Goals for cardiocirculatory therapy
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ScvO2 >70% or SvO2 >65% MAP (mean arterial pressure) >65 mmHg
Cardiac Index >2.0 l/min/m2
CVP 815 mmHg (dependent on ventilation mode) SVV < 13 %
PAOP 1215 mmHg
Diuresis >0.5 ml/kgBW/h Lactate
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Before I came here I wasconfused about this
subject. Having listened
to your lecture I am still
confused. But on ahigher level.
-Enrico Fermi