7/4/2015 of care for a patient with altered tissue perfusion. –integrate lactate levels, base...

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7/4/2015 1 Leanna R. Miller, RN, MN, CCRN – CSC, PCCN CMC, CEN, CNRN, NP Education Specialist LRM Consulting Nashville, TN Optimizing Outcomes in Shock Behavioral Objectives Evaluate the effect of therapeutics on the delivery of oxygen to the cells. Correlate physical signs and symptoms, diagnostic studies, and hemodynamic alterations to develop a plan of care for a patient with altered tissue perfusion. Integrate lactate levels, base excess, and oxygen deliver and consumption parameters into clinical decision making and selection of therapeutic modalities. Optimizing Outcomes in Shock Definition tissue perfusion that is inadequate to maintain normal metabolic and nutritional functions if unresolved, progresses to an irreversible state that results in multisystem organ failure & death Optimizing Outcomes in Shock

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7/4/2015

1

Leanna R. Miller, RN, MN, CCRN – CSC, PCCN – CMC, CEN, CNRN, NP

Education Specialist LRM Consulting

Nashville, TN

Optimizing Outcomes in Shock

• Behavioral Objectives

– Evaluate the effect of therapeutics on the delivery

of oxygen to the cells.

– Correlate physical signs and symptoms, diagnostic

studies, and hemodynamic alterations to develop a

plan of care for a patient with altered tissue

perfusion.

– Integrate lactate levels, base excess, and oxygen

deliver and consumption parameters into clinical

decision making and selection of therapeutic

modalities.

Optimizing Outcomes in Shock

Definition

tissue perfusion that is inadequate to maintain normal metabolic and nutritional functions

if unresolved, progresses to an irreversible state that results in multisystem organ failure & death

Optimizing Outcomes in Shock

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Introduction

12% to 18% of patients

presenting initially in severe

shock have increased

mortality or morbidity

related to secondary organ

failure

Optimizing Outcomes in Shock

Optimizing Outcomes in Shock

Clinical Signs of Shock

Preterminal Stages

severe hypotension

agonal respirations

thready pulse

tachy or bradydysrhythmias

Optimizing Outcomes in Shock

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• Vital Signs

• Hemodynamic Parameters

• Global Indices

• Organ Specific Indices

Parameters Used to Assess Shock

Optimizing Outcomes in Shock

Assessing Shock

• Majority of patients are still in compensated shock even though VS, CI, UO & SvO2 have returned to normal

• 80% of trauma patients with normal BP showed signs of hypoperfusion to non vital organs

Optimizing Outcomes in Shock

Assessing Shock

• 85% has increased lactate and

decreased SvO2 even though HR,

BP, UO were normal

• Compensatory mechanisms mask

true organ perfusion

Optimizing Outcomes in Shock

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Shock Index

HR / systolic blood pressure

inversely related to LVSW

abnormal > 0.9

application: persistently abnormal

shock index in patient with normal

VS suggests need for more

invasive monitoring

Rady (1992) Resuscitation 23:227 - 234

Optimizing Outcomes in Shock

most important

parameter in the

care of a critically ill

patient is delivery of

oxygen to the cells

Optimizing Outcomes in Shock

CO X CaO2 X 10

CaO2 = Hgb x SaO2 x 1.38

Normal 900 - 1100 mL/min

DO2I = 360 - 550 mL/min/m2

Optimizing Outcomes in Shock

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oxygen consumption

CO x (SaO2 - SvO2) Hgb x 1.38 x 10

VO2 = 220 - 290 mL/min

VO2I = 108 - 165 mL/min/m2

Optimizing Outcomes in Shock

normally VO2 is

25% of DO2

Optimizing Outcomes in Shock

Optimizing Outcomes in Shock

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SvO2 or ScvO2

–SaO2

–Hgb

–CO

–VO2

Optimizing Outcomes in Shock

O2 Extraction Ratio

amount of oxygen extracted from blood as it passes through the tissues

(CaO2 - CvO2 )/ CaO2

values > 0.30 abnormal

> 0.35 serious

normal 22% to 27%

Optimizing Outcomes in Shock

> 0.35

–increased VO2

–decreased DO2

–both

Optimizing Outcomes in Shock

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Supranormal Values

CI 4.5 L/min/m2

DO2I 600 L/min/m2

VO2I 170 mL/min/m2

Optimizing Outcomes in Shock

inadequate pulmonary

gas exchange

inadequate CO

inadequate oxygen

carrying capacity

Optimizing Outcomes in Shock

Optimizing Outcomes in Shock

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conditions and activities

that alter demand and

consumption

Optimizing Outcomes in Shock

critically low DO2

vasodilated state

vaso-obstructed state

diffusion distances

affinity of Hgb for O2

Optimizing Outcomes in Shock

increased extraction

once extraction maximized

– consumption is dependent

on delivery

demand > consumption =

O2 debt

Optimizing Outcomes in Shock

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volume

inotropes

vasoactive drugs

reassess peripheral

circulation

Therapeutics

Optimizing Outcomes in Shock

Identify potentially inadequate

DO2 states

–clinical evidence of shock

–SvO2 < 60%

–O2ER > 30%

Optimizing Outcomes in Shock

Identify pathological

flow dependency state

• DO2 with fluids

or inotrope

• recalculate VO2

• VO2 > 10-20

L/m2

Optimizing Outcomes in Shock

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ensure accurate parameters

index to body size

eliminate sources of error

use parameters with < 5-10% variance

Calculations of O2 Delivery & Consumption

Optimizing Outcomes in Shock

calculate actual VO2

estimate potential VO2

(look at factors that

demand)

O2 Supply / Demand Determinants

Optimizing Outcomes in Shock

[email protected]

Optimizing Outcomes in Shock

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delivery needs to

by at least same

percentage as demand

O2 Supply / Demand Determinants

Optimizing Outcomes in Shock

Global Indicators of Perfusion

• SvO2, ScvO2

• Serum lactate

• Base Excess

• End Tidal CO2 monitoring

(PETCO2)

Optimizing Outcomes in Shock

60 – 75%

75 – 80%

SvO2

ScvO2

Optimizing Outcomes in Shock

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Optimizing Outcomes in Shock

Problems with SvO2, ScvO2

• reflects venous blood O2 saturation from entire body – not organ specific

• invasive monitoring

• does not reflect actual cellular utilization

Optimizing Outcomes in Shock

may be or normal in

presence of hypoxia

not reliable reflection

of tissue hypoxia

reliable indicator of

tissue perfusion

Lactate Levels

Optimizing Outcomes in Shock

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indirect measure of

oxygen debt

time to normalization is

predictive of outcome

more helpful if used as

trend

Lactate Levels

Optimizing Outcomes in Shock

liver is efficient at

metabolizing lactate

acute alcohol intoxication

affects lactate metabolism

liver injury will slow lactate

clearance

Lactate Levels

Optimizing Outcomes in Shock

arterial more precise

normal < 1 mEq/L

> 3 - 4 mEq/L significant hypoperfusion – associated with higher mortality

will decrease 5 - 10% / hr when appropriate therapy used

Lactate Levels

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Lab Studies – Base Excess

Normal value: - 2 to + 2

reflects the extent to which the body buffers have been exhausted

rapidity of normalizing base deficit decreases morbidity & mortality

Optimizing Outcomes in Shock

Lab Studies – Base Excess

values

- 2 to – 5 mild

- 6 to – 15 moderate

- 16 or higher severe

global indicator

trending is best use of info

more prognostic if used with lactate

Optimizing Outcomes in Shock

PETCO2

• PETCO2 reflects carbon dioxide

at end expiration

• Normal is 35 – 45 mmHg

• PaCO2 – PETCO2 gradient is

2 – 5 mmHg

• PaCO2 is usually higher

• Inverse relationship with VE

– VE, PETCO2

– VE, PETCO2

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Assessment of Blood Flow

• in systemic blood flow

pulmonary blood flow

• PETCO2 is decreased

• Shock

– PETCO2

• Cardiac Arrest

– Absent or very low PETCO2

• ROSC

– Return to normal PETCO2

Optimizing Outcomes in Shock

Tonometry

pHi

early warning of inadequate splanchnic tissue oxygenation

low pH = poor prognosis (consistently < 7.3)

Optimizing Outcomes in Shock

StO2

• near infrared light illuminates

tissue

• light scatters and is absorbed

differently by oxygenated and

deoxygenated hemoglobin in

the microcirculation

• light returns to sensor and is

analyzed and displayed as %

StO2

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StO2

Optimizing Outcomes in Shock

StO2

.75 - .90

Optimizing Outcomes in Shock

O2 demands are 30-50%

triggers systemic inflammatory

response

Trauma

Optimizing Outcomes in Shock

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Hgb/Hct < 11/33 is associated with delivery-dependence

mortality if therapeutic targets reached < 12 - 24 hours

Trauma

Optimizing Outcomes in Shock

CI > 4.5

DOI2 700

VOI2 170

Trauma

Optimizing Outcomes in Shock

46 - year old male

– motor vehicle crash

– injuries: aortic disruption, severe bilateral pulmonary contusions, bilateral rib fractures, splenic fracture

– traumatic shock due to injuries

Case Study

Optimizing Outcomes in Shock

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Which hemodynamic

findings are abnormal?

Case Study

Optimizing Outcomes in Shock

HR 52

BP 122/64/82

CVP 10

Case Study

Optimizing Outcomes in Shock

HR 52

BP 122/64/82

CVP / PAOP 10/11

CI 4.6

RVSWI / LVSWI 17/61

PAP 46/22/32

Case Study

Optimizing Outcomes in Shock

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EDV / EDVI 237/107

EF 60%

O2ER 26.8

SvO2 .74

DO2 / DO2I 1603/722

VO2 / VO2I 430/194

Case Study

Optimizing Outcomes in Shock

ABGs (.40 FiO2)

pH 7.31

pCO2 42

pO2 157

SaO2 .99

HCO3 20.8

SvO2 74%

P/F ratio 314.0

Case Study

Optimizing Outcomes in Shock

Lab Values

Hgb 12.1

Hct 31.0

Magnesium 1.7

Lactate 5.1

Base Excess -5.1

StO2 72%

Case Study

Optimizing Outcomes in Shock

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Does this patient need

further resuscitation?

Case Study

Optimizing Outcomes in Shock

• 33 yr with GSW to chest

• 4 units of PRBC due to Hct of 27

• SVO2 – 70 after blood administration

• StO2 – 80%

• Lactate 1.2

• Does he need further treatment?

StO2 and Hemodynamic Monitoring

Optimizing Outcomes in Shock

StO2 and Hemodynamic Monitoring

• 48 yr with GSW to head

• Levophed at 50 mcg

• BP 114/74

• StO2 – 91

• Lactate – 5.2

• Does he need further treatment?

–What BP is really needed

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Lactate Base Excess ScvO2 StO2

Early Early Delayed Early

Global Global Global Organ Specific

Invasive Invasive Invasive Non-invasive

Intermittent Intermittent Continuous Continuous

Delayed Info Delayed Info Real – time Real – time

Multiple

Variables

Multiple

Variables

Multiple

Variables

Specific

Requires additional info to direct appropriate interventions

Optimizing Outcomes in Shock

Optimizing Outcomes in Shock

Optimizing Outcomes in Shock