Clinical Measurements A Quick Guide to...

Clinical Measurements

A Quick Guide to Capnography

Recording and analysisof the CO2 waveformand its use indifferential diagnosis

Prof. B. SmalhoutM.D., Ph.D.

This guide provides convenient views

of a selection of CO2 waveforms,

along with interpretation to explain

their relationship to other routine

physiological monitoring waveforms.

These illustrated waveforms are

semi-schematic diagrams presented

in their ideal shape.

Contents

The CO2 waveformAnalyzing the CO2 waveform 2Important basic rules 4

The CapnogramThe normal capnogram 12Expiratory problems 13Curare capnogram 14Cardiogenic oscillations 15Camel capnogram 16Iceberg capnogram 17Leakage in the respiratory system 18High end-tidal CO2 19Low end-tidal CO2 23

Some disturbances of the respiratory rhythm 26Patient fights the ventilator 32

Differential diagnosisSeven examples with interpretations 35

2

Analyzing the CO2 waveformThe CO2 waveform can be analyzedfor five characteristics:–Height–Frequency–Rhythm–Baseline–Shape

The normal end-tidal value isapproximately: 38 mmHg or 5%etPCO2

• Height depends on the end-tidalCO2 value etPCO2

• Frequency depends on therespiratory rate

• Rhythm depends on the state ofthe respiratory center or on thefunction of the ventilator

• Baseline should be zero • There is only one normal shape

(see page 12)

The CO2 waveform

The waveforms are typicallyrecorded or displayed at twodifferent speeds:

Real-time (high) speed at 12.5mm/sec

Trend (slow) speed at 25 mm/min

3

The CO2 waveform

A sudden drop in CO2 to zero or to a low level always indicates atechnical disturbance or defect:• Spontaneous breathing or

ventilated patients– Kinked ET-tube– CO2 analyzer defective

• Ventilated patients– Total disconnection– Ventilator defective

A sudden change in baseline,sometimes combined withchanges in plateau level,indicates:• Calibration error• CO2 absorber saturated (check

capnograph with room air)• Water drops in analyzer or

condensation in airway adapter

CHECK CAPNOGRAPH !

4

1.

2.

Important basic rules

5


1.

2.

TREND SPEED

TREND SPEED

A sudden decrease in CO2 value(but not to zero) withspontaneous or ventilatedbreathing indicates:• Leakage in the respiratory

system (low airway pressure)• Obstruction (high airway

pressure)

An exponential decrease in CO2

(washout curve) within one ortwo minutes always indicates asudden disturbance in lungcirculation or ventilation:• Circulatory arrest• Embolism• Sudden decrease in blood

pressure• Sudden severe hyperventilation

6


3.

4.

7


3.

4.

TREND SPEED

TREND SPEED

Gradual increase in CO2 forspontaneous or controlledbreathing indicates:• Developing hypoventilation• Absorption of CO2 from

peritoneal cavity (laparoscopy)• Rapidly rising body temperature

Sudden increase in CO2

(spontaneous or controlledventilation):• Injection of sodium bicarbonate• Sudden release of tourniquet

(legs, arms, etc.)• Sudden increase in blood

pressure (e.g., intravenousadrenaline)

8


5.

6.

9


5.

6.

TREND SPEED

TREND SPEED

Gradual upshift in the CO2

baseline and topline can resultfrom:• Saturation of CO2 absorber• Calibration error• Technical error in CO2 analyzer• Increasing dead-space, resulting

in re-breathing• CO2 absorber switched off

Gradual lowering of the end-tidalCO2. The curve retains its normalshape but the height of theplateau falls gradually. In anartificially ventilated patient, thiscan be caused by:• Gradual hyperventilation• Lowering body temperature• Decreasing body or lung

perfusion

10

7.

8.


11


7.

8.

TREND SPEED

TREND SPEED

The normal capnogram

There is only one normal shape.Characteristics:• Rapid increase from P to Q• Nearly horizontal plateau between

Q and R (slightly sloping up to R)• From R rapid decrease to zero• Points P, Q, R, and S appear as

rounded corners. (P, Q, R is theexpiratory phase. R, S, P is theinspiratory phase.)

• Slope of the plateau depends onthe condition of the airways andlung tissue

• End-tidal value is only equivalentto the alveolar CO2 when a nearlyhorizontal plateau is seen

12

Representative capnograms

HIGH SPEED

Expiratory problems

In general, any airway obstructionlimiting expiration.

Possible explanations:• Kinked tube (developing out of a

previously normal shape)• Foreign body• Herniated cuff (developing out of

a previously normal curve)• Bronchospasm• Emphysema• Bronchial asthma

13


HIGH SPEED

“Curare” capnogram*

• Caused by lack of coordinationbetween intercostal muscles anddiaphragm

• Note the cleft in right third of theplateau. CO2 mostly too high. Thedepth of the cleft is proportionalto the degree of muscle paralysis.Seen only in spontaneousrespiration, or when the patientstarts to fight the ventilator

• Also seen in patients with cervicaltransverse lesions

* The expression “curare capnogram” was given at the time thatcurare was a generally accepted muscle relaxant (about 1960).Nowadays, other muscle relaxants are in use, but the shape ofthe capnographic curve in patients who are partially paralyzedis still the same.

14


HIGH SPEED

Cardiogenic oscillations

Caused by the beating of the heartagainst the lungs:• Small tidal volume in combination

with low respiratory rate• At the end of a very long

expiration

Can be caused by a centraldepression of the respiratory systemor by the ventilator running tooslowly.

15


HIGH SPEED

Camel capnogram

• Can be seen in patients in thelateral position on the operatingtable

• During either spontaneous orcontrolled respiration

16


HIGH SPEED

Iceberg capnogram

Caused by a combination of amuscle relaxant and a central actinganalgesic drug (e.g., morphine,fentanyl, etc.):• Mixture of cardiogenic oscillations

and “curare” cleft (see page 14)• No plateau. Low respiratory rate• CO2 higher than normal• Seen only in spontaneous

respiration

17


HIGH SPEED

Leakage in the respiratorysystem

Irregularity mostly in expiratorylimb (see arrows):• Shape and site of this irregularity

depend on the localization andseverity of the leak in theanesthetic system (cuff, valves,tubing, etc.). CO2 could be toohigh due to hypoventilation or too low due to the addition ofleaking air

• Other possible leakage shapes haveto be differentiated from otherdisturbances (e.g., camel curve (seepage 16), etc.)

18


HIGH SPEED

With normal respiratoryrate

Normal plateau but higher thannormal end-tidal CO2. Can be seenin artificially ventilated patients:• When the ventilator is running at

normal respiratory rate but theminute volume is too low

• With primary normal respiratoryrate and minute volume but with arapidly rising body temperature(e.g., in malignant hyperthermia)

19

High end-tidal CO2

A.

HIGH SPEED

With bradypnea

Long plateau but higher thannormal CO2. Respiratorydepression without an attempt tocompensate can be seen: • In cases of high ICP or respiratory

depression due to morphinic-based drugs (e.g., pethidine,fentanyl, etc.)

• In artificially ventilated patients,when the ventilator is runningwith both respiratory rate andminute volume too low

20

High end-tidal CO2

B.

HIGH SPEED

Hypoventilation withtachypnea

Short plateau but higher thannormal end-tidal CO2. Respiratorydepression with an attempt tocompensate by higher respiratoryrate can be caused by:• Volatile anesthetics during

spontaneous respiration (e.g.,halothane, etc.)

• Ventilator running at high rate butwith low tidal volume

21

High end-tidal CO2

C.

HIGH SPEED

Very severe hypoventilation

Very severe hypoventilation (verylow tidal volume) with a highrespiratory rate as an attempt tocompensate. A misleading low levelof CO2 is recorded on thecapnogram. Mostly no properplateau. After thorax compressionor forced exhalation (see arrow),true CO2 value becomes visible:• Can be seen under spontaneous or

controlled breathing• In patients with spontaneous

respiration but with severerespiratory paralysis caused byparalyzed respiratory muscles

• Malfunction of ventilator orleakage in respiratory system

22

High end-tidal CO2

D.

HIGH SPEED

With normal respiratoryrate

With normal respiratory rate andplateau but a lower than normalend-tidal CO2. Can be observed inartificially ventilated patients:• When the ventilator runs with a

normal rate but the minutevolume is too high

• Who are in shock• With normal respiratory rate and

tidal volume but with a low bodytemperature

Can also be seen in patients withspontaneous respiration when theyare compensating a metabolicacidosis.

23

Low end-tidal CO2

A.

HIGH SPEED

With bradypnea

With bradypnea but a lower thannormal end-tidal CO2 and a longplateau in:• Artificially ventilated patient when

the ventilator is running at a lowrate and a high minute volume

• In patients with spontaneousrespiration with:– Damage to the central nervous

system (e.g., the so-called centralneurogenic hyperventilation)

– A low body temperature andrespiratory depression caused byanalgesics

24

Low end-tidal CO2

B.HIGH SPEED

With tachypnea

With tachypnea but a lower thannormal end-tidal CO2 and shortplateau:• In patients on artificial ventilation

when the ventilator is running athigh rate and with a high minutevolume

• In patients with spontaneousrespiration who are:– In pain– Trying to compensate a

metabolic acidosis– Hypoxic

• In some cases of centralneurogenic hyperventilation

• In severe shock conditions

25

Low end-tidal CO2

C.HIGH SPEED

Some disturbances of therespiratory rhythm

Cheyne-Stokes respiration

Only seen with spontaneousrespiration. Cardiac oscillations(indicated by the arrows) after everyrespiratory group.• Can be seen in cases of severe

cerebral arteriosclerosis, braindamage, intoxication, etc.

26

Heaving respiration

Can be seen in some patients as atransition condition betweenCheyne-Stokes and normalbreathing.• Only seen with spontaneous

respiration. The tidal volumechanges regularly, hence thewaving characteristic of the upperlimit on the capnographic trendrecording.


27

Gasping respiration

• Very low respiration rate (2-6/min)

• CO2 mostly higher than normal• Often cardiogenic oscillations

after every capnographic curve (see arrows)

Seen in very severe respiratorydepression or in dying patients

28


Very irregular or chaoticrespiration

• No regularity• All curves differ in size, shape, and

height. Average CO2 level abovenormal

Seen in severe cerebral damage

29


Sighing respiration

• A regular pattern with regularintervals interrupted by a deepsigh (indicated by arrows)

• Physiological in babies, smallchildren, and very old peopleduring sleep or when under ananesthetic

• Pathological in young people andadults when deep sighs are morefrequent than once in 5 minutes.An indication of brain damage

• Average CO2 level can be normal,high, or lower than normal

30


31

A.

B.

Can also be seen in ventilatedpatients when the ventilator has anintermittent deep sigh mechanism.In normal lungs, the deep sigh CO2

level is lower than average (A). Incases of obstructive lung disease, thedeep sigh level will be higher thanaverage (B).


When a patient starts to breathe againstthe ventilator (A), the regular pattern ofthe capnogram is interrupted. Therespiratory activity of the patientincreases quickly. The end-tidal CO2

rises slightly due to the increasingmetabolism of the contractingrespiratory muscles.

Capnogram created by the ventilator (B).

Capnogram created through theattempted spontaneous respiration ofthe patient (C).• During an anesthetic this capnogram

indicates that another dose of musclerelaxant should be given to the patient

32

Patient fights the ventilator

Note:Combinations of the waveformsdiscussed up to this point are alwayspossible. Results depend on theclinical condition of the patient andthe technical status of theinstrumentation used.

The iceberg capnogram is anexample of a combinationwaveform. (see page 17)

33

Differential diagnosisCorrect interpretation of the manypossible capnographic curves canonly be achieved by comparisonwith other parameters recordedsimultaneously. This makes adifferential diagnosis possible.Useful parameters for this purposeare:– ECG/heart rate– Blood pressure (direct or indirect)– Body temperature– Plethysmogram (taken from the

earlobe or finger)– PaCO2

– PaO2

– Airway pressure– Central venous pressure– Acid-base status

35

Differential diagnosis

Exa

mp

le 1

– E

CG

: dis

appe

ars,

no

hear

t rat

e–

Plet

h: b

ecom

es a

stra

ight

line

– B

lood

pre

ssur

e: d

rops

– C

apno

gram

: no

chan

ge

Inte

rpre

tati

on:

Tech

nica

l def

ect w

hen

the

vita

l sig

ns m

onit

or (E

CG

, ple

th, b

lood

pres

sure

) and

the

capn

ogra

ph a

re se

para

te in

stru

men

ts.

Pati

ent i

s not

in d

ange

r. W

itho

ut p

rope

r cir

cula

tion

a n

orm

al c

apno

gram

is n

ot p

ossi

ble.

36

38

Exa

mp

le 2

– C

ontr

olle

d re

spir

atio

n, te

mpe

ratu

re 3

7°C

– E

CG

: nor

mal

– Pl

eth:

nor

mal

– B

lood

pre

ssur

e: c

onst

ant

– C

apno

gram

: rap

id d

ecre

ase

in C

O2

Pos

sibl

e in

terp

reta

tion

s:–

Con

sider

able

leak

age i

n th

e res

pira

tion

syst

em.

PAT

IEN

T IN

DA

NG

ER

– Te

chni

cal d

istu

rban

ce in

cap

nogr

aph.

Pat

ient

not

in d

ange

r

Dif

fere

ntia

l dia

gnos

is:

– C

heck

air

way

pre

ssur

e–

Che

ck ca

pnog

raph

with

ow

n ex

pira

tory

air (

alw

ays a

roun

d 38

mm

Hg

or 5

%)

40

Exa

mp

le 3

– E

CG

: inc

reas

ed h

eart

rate

, occ

asio

nal P

VC

s–

Plet

h: d

imin

ishi

ng a

mpl

itud

e an

d ir

regu

lari

ties

in a

mpl

itud

e–

Blo

od p

ress

ure:

incr

easi

ng–

Cap

nogr

am: C

O2le

vel r

ises

Pos

sibl

e in

terp

reta

tion

s:–

Adr

enal

ine

into

xica

tion

(e.g

., lo

cal a

nest

hesi

a)–

Eff

ect f

rom

man

ipul

atin

g a

pheo

chro

moc

ytom

a–

Eff

ect f

rom

pai

nful

stim

ulus

– Pa

tien

t aw

akes

– PA

TIE

NT

PO

SS

IBLY

IN

DA

NG

ER

41

PV

Cs

42

Exa

mp

le 4

– E

CG

: asy

stol

e, a

fter

som

e PV

Cs

– Pl

eth:

dim

inis

hing

am

plit

ude

deve

lopi

ng in

to a

stra

ight

line

– B

lood

pre

ssur

e: d

rops

to ze

ro–

Cap

nogr

am: w

asho

ut c

urve

. Val

ue d

rops

tow

ards

zero

but

hol

ds a

t ale

vel o

f sev

eral

mm

Hg

Inte

rpre

tati

on:

Thi

s com

bina

tion

is ty

pica

l for

car

diac

arr

est e

ven

thou

gh th

ere

can

still

be so

me

elec

tric

al a

ctiv

ity

in th

e E

CG

.

PA

TIE

NT

IN

MO

RT

AL

DA

NG

ER

43

PV

Cs

44

Exa

mp

le 5

– EC

G: t

achy

card

ia, S

T d

epre

ssio

n. O

r bra

dyca

rdia

with

very

low

blo

od p

ress

ure

– Pl

eth:

dec

reas

e in

am

plit

ude

– B

lood

pre

ssur

e: d

ecre

ases

– C

apno

gram

: dro

ps in

par

alle

l wit

h bl

ood

pres

sure

Pos

sibl

e in

terp

reta

tion

s:–

Seve

re b

lood

loss

– Se

vere

cir

cula

tory

col

laps

e th

roug

h ot

her c

ause

s:–

Ana

phyl

acti

c sh

ock

– C

ardi

ac m

alfu

ncti

on–

Ove

rdos

e of

cer

tain

car

dio-

depr

essi

ng d

rugs

(e.g

., ha

loth

ane

or

barb

itur

ates

)–

PAT

IEN

T I

N D

AN

GE

R

46

Exa

mp

le 6

– E

CG

: no

chan

ges.

Som

etim

es b

rady

card

ia d

evel

ops

– Pl

eth:

rapi

d in

crea

se in

am

plit

ude

– B

lood

pre

ssur

e: ra

pid

decr

ease

, rem

ains

low

– C

apno

gram

: no

sign

ifica

nt c

hang

e

Pos

sibl

e in

terp

reta

tion

s:–

Eff

ect o

f neu

role

ptic

dru

gs (e

.g.,

Dro

peri

dol)

, alp

ha-b

lock

er o

rga

nglio

n bl

ocke

rs o

r ane

sthe

tic

drug

s–

Indu

ctio

n of

ane

sthe

sia

Blo

od p

ress

ure

decr

ease

s due

to v

asod

ilata

tion

. Per

fusi

on im

prov

ed.

Pati

ent i

s not

in d

ange

r as l

ong

as th

e ca

pnog

ram

rem

ains

unc

hang

ed.

48

Exa

mp

le 7

– E

CG

: rem

ains

unc

hang

ed a

t fir

st a

lthou

gh h

ypox

ic c

hang

es m

ay o

ccur

afte

r a fe

w m

inut

es w

ith

PVC

s–

Plet

h: d

evel

ops i

nto

an a

lmos

t str

aigh

t lin

e (o

ften

wit

hin

ten

seco

nds)

T

his m

ay b

e pr

eced

ed b

y a

broa

deni

ng o

f the

reco

rd fo

r a fe

w se

cond

s–

Blo

od p

ress

ure:

falls

wit

hin

thir

ty se

cond

s (of

ten

to a

ver

y lo

w le

vel)

– C

apno

gram

: fal

ls w

ithin

one

min

ute

(oft

en to

a v

ery

low

leve

l of e

tCO

2)

Inte

rpre

tati

on:

Larg

e pu

lmon

ary

embo

lism

(oft

en a

ir e

mbo

lism

). R

ecov

ery

is u

sual

lygr

adua

l. Ev

en a

fter

a sm

all a

ir e

mbo

lism

, whi

ch is

not

life

-thr

eate

ning

,th

e ca

pnog

ram

doe

s not

retu

rn to

its o

rigi

nal l

evel

for a

t lea

st fi

ve to

ten

min

utes

.

PA

TIE

NT

IN

SE

VE

RE

DA

NG

ER

49

PV

Cs

Author:Prof. B. Smalhout, M.D., Ph.D.Professor of AnesthesiologyUniversity Hospital Utrecht The Netherlands

Other Publications• Atlas of Capnography

Smalhout/KalendaKerckebosch - ZeistThe Netherlands

• The Suffocating ChildSmalhout/VaughanBoehringer-IngelheimGermany

Philips MedicalSystems is partof Royal [email protected]: +31 40 27 64 887

Philips Medical Systems3000 Minuteman RoadAndover, MA 01810-1085(800) 934-7372

© Koninklijke PhilipsElectronics N.V. 2004All rights are reserved.Reproduction in wholeor in part is prohibitedwithout the priorwritten consent of thecopyright holder.

Philips Medical SystemsNederland B.V. reservesthe right to makechanges in specificationsand/or to discontinue anyproduct at any timewithout notice orobligation and will not beliable for anyconsequences resultingfrom the use of thispublication.

4522 981 93901/862SEP 2004

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