ICU Manangement 8-28 - Copy (2)

7/29/2019 ICU Manangement 8-28 - Copy (2)

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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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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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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


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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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


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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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



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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



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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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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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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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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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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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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



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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


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

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