questions??

TheBa Assessm Monitoring

t%

When to rely on what the monitor tells you vs. the patient

s medical technology continues to

advance and assessment tools

become smaller, cheaper and more

practical for use in the field, we

are faced with the challenge of

determining where these tools fit within our

overall pafienf assessmenf.

In trying to emphasize the imporfance ot

a proper physical exam, it is often said that

paramedics must "treat the patient and not the

monitor."This conventional wisdom is beginning

to change, with one exampie being STEMi bypass

programs that involve altering patient care based

largely on what is seen on the cardiac monitor.

Furthermore, the 2010 American Heart

Association guidelines recommend against

routine supplemental oxygen tor acute coronary

syndrome because ot the risks that are naw recog-

nized and likely result in part trom tree radical

formation. Specifically, supplemental oxygen is

not recommended tor patients who are not short

ot breath, have an oxygen saturation ot at least

94%, and are not showing signs ot heart tailure

ar shock.i

This increasing emphasis on these previously

downplayed assessment tindings requires a shift

in our thinking where we will need to. at times,

trust our monitor.

In a discussion with colleagues around this

shift in thinking, it was suggested the monitor is

a good tool, but you never want to be the para-

medic who withholds oxygen trom a patient wha is

cyanotic based on a high oxygen saturation levei.

Having heard so many times about treating

the patient and not the monitor, everyone seemed

to agree. It certainly sounded iike a nice idea,

but it is one that must be caretuiiy assessed. We

must tirst exclude trom the discussion any poten-

tial issues with the quality ot the reading being

obtained. For this, it is important that we examine

the plethysmograph or pieth waveform from the

oxygen saturation probe.

The most important component ot this

wavetorm tor our purposes is the a

tude, which would be low if there is pi

signal strength, Assuming there is

good wavetorm and the monitor i

tunctioning properly, what would

cause a patient to preserit with

centrai cyanosis but also a high

oxygen saturation? This ques-

tion is more difficult to answer,

but taking the time to work

through the possibilities is

an interesting exercise.

We should begin

by briefly reviewing

the normal physi-

ology and essen-

tial components

ot respiration and

oxygénation.

This begins with

having adequate

levels of oxygen in

ambient air. Normally

air consists ot mainly

nitrogen with approxi'

EMSWORLD.com

PATIENT M O N I T O R I N G

mately 21 % oxygen.The movement of the

diaphragm is responsible for decreasing

pressure in the chest so that air travels

down the pressure gradient and enters

the lungs.

Upon reaching the aiveoii where gas

exchange takes place, it is essential there

is sufficient surface area of thin respiratory

membranes for gas exchange to take piace.

Fick's Law reminds us of the importance

of these membranes being thin and not

obstructed by fluid. The pulmonary capil-

laries must be adequately perfused with

hemoglobin-rich blood that can enter the

lungs and become saturated with oxygen.

Finally, there must be sufficient circula-

tion of blood to deliver oxygen to tissues.

Deficiencies in any of these components

can leave a patient without adequate

oxygénation.

It you were to ask what would cause a

patient to present with central cyanosis as

well as an erroneously high oxygen satu-

ration, the tirst answer that you wiil likely

receive is carbon monoxide poisoning. If

we consider for a moment what causes

cyanosis, we can quickly see how this will

not be true. Cyanasis is due to deoxyhemo-

globin, but in carbon monoxide poisoning,

the hemogiobin is bound, just not to

oxygen. This lack of deoxyhemoglobin

and the presence of carboxyhemoglobin,

means patients with carbon monoxide

poisoning do not normally present with

cyanosis.'

Another answer to this question is

that patients with anemia may appear

cyanotic but have a high oxygen saturation.

To assess this possibility, we must recall

that cyanosis is due to the deoxygenated

hemoglobin. Patients with anemia have

low ieveis of hemoglobin, so they actually

may never become cyanotic because they

cannot have a high enough concentration

ot deoxygenated hemoglobin in their blood

to display the blue color.'' Even when their

overall oxygen levels are decreasing, their

oxygen saturation levels may remain high

since the small amount of hemoglobin they

have will be saturated.This is a worthwhile

consideration when interpreting oxygen

saturation readings, but it does not meet

the type of patient we are trying to find.

At the other end ot the spectrum, a

patient with polycythemia could have

cyanosis with only mild hypoxia." Because

these patients have so much hemoglobin

available, it may not all be saturated under

normal conditions. Since the pulse oxim-

eter is measuring the saturation of hemo-

globin, the readings will be lower despite

an otherwise normal arterial oxygen

content. While this patient wouid have a

low oxygen saturation along with cyanosis,

it wouid not normally be due to hypoxemia.

This is another interesting consideration

when interpreting oxygen saturation, but

it is not what we are trying to find.

If none of these will cause a patient

with cyanosis to present with a falsely

high oxygen saturation, maybe something

with the reading, rather than the patient's

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PATIENT M O N I T O R I N G

condifion, could cause fhis. Nail polish,

dirfy fingers, poor perfusion and motion

arfifact are all possibilifies we mighf

considerThese should all be identifiable in

fhe oxygen saturation waveform (the pleth

waveform),^ which should make fhe astute

clinician skeptical of a pofenfiaily unreli-

able reading. Specifically, poor perfusion or

signal strength will be indicated by a low

amplitude waveform while mofion artifact

will appear as a jagged waveform with a

wandering baseline.

Another possibility worfh considering,

which also involves poor perfusion, is

Raynaud's phenomenon. A tuil descrip-

tion of this condition is beyond the scope

of fhis discussion, buf if involves episodic

excessive vasoconsfriction in fhe fingers

and toes in response to stress or cold.

This is normally symmefrical and can

lead fo cyanosis in the affected area.'

Given the poor peripheral perfusion, fhe

oxygen saturation waveform is also likely

fo be poor. Even if pertusion was sufficienf

for a reliable reading, the oxygen satura-

tion would be expected fo be low, corre-

sponding appropriately to the peripheral

cyanosis. Since that would involve cyanosis

presenting wifh a low oxygen safuration,

that is nof whaf we are looking for.

Let us consider for a moment that f here

was fhe uncommon pafienf wifh unilateral

Raynaud's. It you placed the oxygen safura-

tion probe on the unaffected side, you may

obtain a high oxygen safurafion reading on

the monitor along with peripheral cyanosis

in fhe pafienfs other hand.This is close but

not quite fhe pafienf we are seeking, since

the initiai question was about a patient with

central cyanosis and a high oxygen satura-

tion.The spirit of fhe question also related

to inappropriately withholding supplemental

oxygen trom someone who needed it, so we

will need to continue our search.

After working through all ot these possi-

bilifies, we are forced fo shift our search

toward more obscure conditions.This leads

us to mefhemogiobinemia, which is an

uncommon condition that mosf of us are

nof familiar wifh. Hemoglobin normally

confains iron in fhe reduced, or terrous,

form (Fe^*). In fhis torm, hemogiobin can

combine wifh oxygen to transport if fo fhe

fissues. If fhe hemoglobin loses an elec-

tron and the iron becomes oxidized to fhe

ferric form (Fe^+), if is no longer capable of

oxygen fransport.This form of hemoglobin

is called methemoglobin.'

Under normal conditions,some hemo-

globin is continually being converted fo

methemoglobin, buf this is kept to around

1 % by specialized enzyme systems.

Cyfochrome b5 reducfase is the most

imporfanf of fhese.^ The precise mecha-

nisms are beyond the scope of fhis article,

but these enzyme systems are able fo

reduce the iron (Fe *̂) back to the funcfional

form (Fe2+).When these systems are nof

functioning, or fheir capacity is exceeded,

methemoglobin can rise above safe levels.

When fhese levels reach 15% fo 20%, fhe

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EMSWORLD.com I SEPTEMBER 2013 5 7

PATIENT MONITORING

patient is likely to present with cyonosis or

a brown colorotion,^

It is important to be clear on the

precise effects ot these rising levels of

methemoglobin. Recall that hemoglobin

is 0 tetramer that has tour iron molecules.

Some of these will be directly atfected by

the conversion to the terric (Fe *̂) state,

while others in the same hemoglobin

molecule will remoin in the ferrous (Fê + or

functional) form,The non-tunctional parts

of the hemoglobin will not be able to carry

oxygen, but this is only port of the problem

in methemogiobinemia. In addition to the

direct impairment of hemoglobin due to

the inability of the terric form fo fransport

oxygen, the othenwise functional terrous

heme groups'ability fo unlood oxygen also

becomes impaired.' High levels theretore

cause a left shitf ot the oxyhemogiobin

dissociation curve because of fhis impaired

unloading ot oxygen at the tissues.

Though rare, this could be caused by

a variety of agenfs such as lignocaine,

nifroglycerin, metoclopramlde or nitrites,'"

In adults, if is mosf commonly caused by

exposure fo volafile nifrites due fo inhalanf

abuse,'" In intonts, it can be caused by

topical benzocaine (sold under the trade

nome Orajel in the Unifed Sfafes).""'^

Infections are another cause in this age

group,'''''^ Intants are particularly vulner-

able fo methemogiobinemia since they

have relatively low cyfochrome b5 reduc-

fase levels."

Pafients with methemogiobinemia will

typically present with tachypneo, tachy-

cordia and cyanosis.'" Wifh traditional

pulse oximefry, there is often an unreliable

low reading in potients with mild methe-

mogiobinemia and an unreliable high

reading in patients with high-level mefhe-

moglobinemia,'" There is no prehospital

treatment for this condition available to

most prehospital providers so treafmenf is

generally supportive. Upon arrival at hospital.

the patient may receive charcoal if the

substance wos ingested. Méthylène blue

may also be administered depending on fhe

level of mefhemoglobin,'" Some specialist

prehospifal hazardous-materials teams may

also be able to inifiafe this treafmenf.

The preceding discussion has two

primary implicotions.The first implication,

specific fo fhe use ot oxygen saturation

monitoring. Is that it is very unlikely you will

ever come across a patient who presents

wifh cyanosis and a high oxygen safuratlon

wifh a good wavetorm on a funcfioning

monitor. New technology has also now

led to more sensitive probes that can

detect methemoglobin.'Hhis technology

is avouable on both monitors currently in

the marketplace.

The second and more important

implication is the importance ot consid-

ering the underlying pathophysioiogy as

If relafes to fhe assessments we perform,

Undersfanding the pathophysioiogy is the

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PATIENT M O N I T O R I N G

only way fo fruly undersfand fhe clinical

findings. Even when fechnology helps us to

assess pafienfs,wemusf undersfand whaf

fhese devices acfually assess or measure.

Though if will be uncommon fo see a

case of mefhemoglobinemia, fhis sfruc-

tured examination of the possibilities helps

prompt a review of fhe imporfanf physiology

as if reiafes fo oxygen safurafion moniforing.

Through fhis discussion, we have

reviewed a number of imporfanf consid-

erafions for using oxygen safurafion as a

part of overall pafient assessment, if is only

a single assessmenf, but when used with

fhe underlying physiology and limifations

in mind, if can offer crucial guidance for

pafienf c a r e . ( ^

ACKNOWLEDGEMENT We are grateful to Dr. Claytan Kazan. Cathryn MacKinnan and Or. Steven Parrillo for their assistanoe witti ttiis article. We olso appreciate the thorough review from an anonymous reviewer, which further helped ta strengthen the article.

REFERENCES 1, O'Connor RE. Brady W. Brooks SC. et al. Part 10: acute coronar/ syndromes: 2010 American Heart Association Guidelines for Cardiopulmonory Resuscitation and Emergency Cardiovascular Core, Ctrcutation, 2010; 122(18Suppl3):S787-817,

2, Fernandez-Frackelton M, Bocock J, "Cyanosis," In Morx JA, Hockberger RS.Walls RM, eds, Rasen's Emergency Uedtctne, 7th ed, Philadelphia. PA; Mosby; 2009,

3, Snider HL"Cyanosis," In Walker HK. Hall WD, Hurst JW. ed, Cttnicat Methods: The Htstory, Physicat, and Laboratory Examinations, 3rd ed, Boston: Buttetworlhs: 1990,

4, Pork JG, 'Pulmonary diseases," In Habermann TM. ed. Mayo CItntc tnternat Medicine Review, 7th ed. New York. NY: Informa Healthcore; 2006,

5, Jubran A, Pulse oximetry. Intensive Care Med, 2004; 30(11):2017-2020, 6, Ferri FF, Ferri's Clinical Advisor 2013. Philadelphia. PA:

7, Lee DC. Ferguson KL, fvlethemoglobinemia in emergency medicine, http;//emedicine,medscape,com/ article/815Ó13-overview,

8, Kruse JA, Sounders Manual ot Critical Care. Philadelphia. PA: Saunders: 2003,

9, Curry SC, Methemoglobinemia. Aim Emerg Med, 1982;

10, Witt S.'WIethemoglabinemio,' In Horris CR, The Toxicotogy Handbook for Clinicians, St, Louis. UO: Eisevier; 2006, 11, Bong CL. Hilliord J. Seefelder C, Severe methemoglobinemia from topical benzocaine 7,5% (baby orojel) use tor teething pain in a toddler, din Pediatr

(Phtta),2009;AB{2):209-U. 12, Chung NY. Botra R. Itzkevitch Wl. et al. Severe methemoglabinemia linked fo gel-type topical benzocaine use; 0 case report, J Emerg Med, 2010; 38(5);601-ó,

13, Skold A. Cosco DL. Klein R, Mefhemoglobinemia; patiiogenesis. diagnosis, and management, Sauth Med J, 2 0 1 1 ; 1 0 4 ( l l ) ; 7 5 7 - 6 1 , 14, Luk G. Riggs D. Luque M, Severe methemoglobinemia in d 3-week-old intont with a urinary tract infection. Crtt Core Meii.I991;19(10);1325-7,

15,Yano SS. Danish EH. HsioYE,Translent methemoglobinemio with acidosis in infants, J Pedtatr, 1982; 100(3);415-8,

16, Curry SC'Hematologic consequences ot poisoning," In Shonnon MW, Borrón SW. Burns M, Haddad and Wtnchester's Ctinicat Management ct Pciscning and Drug Overdase, 4th ed, Philadelphia: Saunders; 2007, 17, Eisenkraft JB, Pulse oximeter desaturation due to methemoglobinemia, /Ifies/hes/ö/og/. 1988; ó8;279-282 18, Feiner JR. Bicicler PE, Improved accuracy ot methemoglobin detection by pulse CO-oximetry during hypoxia, 4nesft/lno;g. 2010; 111(5);1160-11Ó7,

Christopher R. Foerster, PCP. is a primary care para-

medic Víith Lombton EMS in Ontario, Cañado and a

paramedic tutor for the University of Queensland,

He can be reached at foerster@alumni,utoronto,ca,

Anthony G, Mendoza. BA. EMT-P. is an EMT/paramedic

educator at UCLA's Center for Prehospital Care, He

fiofis fhe field in Los Angeles and Ventura counties.

He may be contacted at [email protected].

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