University of Santo Tomas

THE GRADUATE SCHOOL

ADVANCED MEDICAL-SURGICAL NURSING I
CASE SCENARIO
NURSING CARE OF CLIENTS ITH RES!IRATOR" !RO#LEMS
Prepared by: John Henry O. Valencia, RN, RM
Master of Arts in Nursing tudent
M.C. a 65-year-old man is admitted to your medical unit for exacerbation of his emphysema
(COPD). e has a history of atopic asthma durin! his childhood and hypertension "hich has been "ell
controlled by #nalopril for the last six years. e presents as a poorly nourished man "ho is
experiencin! difficulty breathin!. e complains of cou!hin! spells producti$e of thic% yello" sputum.
M.C. seems irritable and anxious "hen he tells you that he has been a t"o-pac%-a-day smo%er for &'
years. e tells you he has been sleepin! poorly and lately feels $ery tired most of the time e$en "hen
he has not done any physical acti$ity. is () are *6+,'-. *+-. &6. */+ 0. )aO+ ''1. is admittin!
dia!nosis is chronic emphysema "ith an acute exacerbation.
is admittin! orders are as follo"s2
Diet as tolerated
Out of bed "ith assistance
O+ at +3,nc
4( Plain 5))) *3 at 5/ ml,hr
)putum C 6 )
789s in 7M
C8C "ith :8C differential
C;< follo"ed by Pulmonary 0unction test in 7M
#C9
!. "hat are the significant data that you ha#e gathered$ "hat other rele#ant %uestions do you
need to as& M.'.$
(. "hat physical assess)ent findings do you e*pect to find$ :hat specific chan!es in the
respiratory system do you expect to find indicati$e of emphysema=
+. "hat is the )ost co))on cause of e)physe)a$ ,ased on this infor)ation, -hat %uestion -ill
you as& about his health beha#iors$ "hat do you belie#e are the )a.or cause/s of M.'0s
e)physe)a$
1. Are M.'.0s V and aO( appropriate$ 2f not, e*plain -hy.
3. 2s your patient -ith chronic hypo*ia$ 2s he co)pensating for his chronic hypo*ia$
4. "hy is the O( inhalation at (5PM inspite of the aO( at 667$ Ho- do -e e*plain the 8hypo*ic
dri#e9 in a pt. -ith e)physe)a$ "hat i)portant considerations do you ha#e to re)e)ber
regarding O( ad)inistration in a pt. -ith 'OP: li&e M.'.$
;. Ma&e an integrated pathophysiologic flowchart of M'0s disease condition.
6. <i#en M.'.0s history and your &no-ledge of pathophysiologic processes, e*plain the
pathophysiologic basis of the assess)ent findings in M.'$
Pa!e $ of %&
=. "hat are the possible co)plications of >)physe)a and their )anifestations$
!?. Ma&e a tabular co)parison of the pathogenesis and pathophysiologic changes of
>)physe)a, ,ronchitis and asth)a.
!!. ,ased on the assess)ent findings, identify fi#e priority proble)s that M.'. )ay be
e*periencing.
>he laboratory sends the ff. report se$eral hours after admission2 <8C ? &.'thou,cmm. :8C-
*&./// thou,cmm. !b *+!,d3. 789s2 p- @.+'. pO+ ? '/ mm!. pCO+ ? 65 mm!. CO& ? ++.
!(. 2nterpret the abo#e results. Ho- do the results relate to the pathophysiologic changes of
e)physe)a$
!+. "ith the A,< result, can you say that M.'. is in respiratory failure or respiratory insufficiency$
>*plain the scientific basis of your ans-er.
!1. "hat are the )a.or hall)ar&s of respiratory failure$ "hat do you belie#e are the principal
causes of this proble) in M.'.$>*plain your ans-er.
0i$e days after admission. M.C.As condition has remar%ably impro$ed. >he MD "ants all
medications continued and has shifted the antibiotics to oral preparations.
!3. "hat )ade the M: say M'0s condition has i)pro#ed$ <i#e the assess)ent findings that
supports the M:0s obser#ation.
!4. )ummary of Bournal readin!s (&) related to the case. Cse the table belo".
Dire'tions(
$) T*is s'enario is to +e a''om,-is*e. in.ivi./a--y an. to +e s/+mitte. on T/es.ay0Se,t $10
%&$2

T*is m/st +e ty,e3ritten in A2 +on. ,a,er /sin4 Aria- Narro3 font $$)
Late s/+mission 3i-- *ave .emerit ratin4) !-ease 'om,-y5
%) Dis'/ssion of t*e 'ase 3i-- +e .one on T/es.ay) !-ease 'ome ,re,are. for t*e .is'/ssion
6) Gra.in4 r/+ri' is atta'*e.) 7in.-y atta'* a 'o,y of t*is on t*e ,a,er yo/ 3i-- s/+mit
4)>4O5DO,C)>9),+/*-
7ns"ers2
$) *at are t*e si4nifi'ant .ata t*at yo/ *ave 4at*ere.8 *at ot*er re-evant 9/estions .o
yo/ nee. to as: M)C)8
!atient has a si!nificant istory of Chronic smo%in! (t"o-pac%-a-day smo%er for &' years).
Patient also has a history of atopic asthma and hypertension but "ell controlled by #nalopril.
Patient "as poorly nourished and experiencin! DO8. Cou!h producin! yello"-thic% sputum.
Re-evant ;/estions t*at 3e may as:e.(
)hortness of breath2
:hen "ere you first short of breath (at exercise or at rest)=
o" often are you short of breath=
o" lon! ha$e you been short of breath= 4s it !ettin! "orse=
o" far can you "al%. and ho" many steps can you climb before ha$in! to stop
because of shortness of breath=
Cou!hin!2
o" often and "hen do you cou!h=
o" lon! ha$e you been cou!hin!= 4s it !ettin! "orse=
Do you cou!h up mucus (sputum)= :hat color is it=
a$e you e$er cou!hed up blood=
)ocial istory2
Childhood respiratory illnesses.
0amily history of respiratory disease.
Other medical conditions you may ha$e and their treatment.
o" your condition is affectin! your Euality of life2 missed "or%. disrupted routines.
and depression. for example.
>he name and dose of all of the medicines you ta%e. includin! any inhalers you use.
:hat type of family and social support you ha$e.
o" lon! ha$e you had cou!h. shortness of breath. or "heeFe=
a$e you seen many doctors for it= :hat are you no" doin! to treat it=
o" many days did you miss from "or% last year because of the lun! problem=
:ere you in the hospital for it= o" lon! and ho" many times last year=
Describe your usual !ood day.
Do you ha$e more !ood days than bad days in a "ee%= :hat are you able to do "hen
you are feelin! youAre $ery best=
:ho do you li$e "ith=
:hat recreation do you prefer=
:hat ha$e you learned to do that helps you to li$e "ith it=
Does it e$er embarrass you to ha$e lun! trouble=
ealth history2
Does the patient ha$e a family history of COPD or other chronic respiratory diseases=
o" lon! has the patient had respiratory difficulty=
:hat is the pattern of symptom de$elopment=
Does exertion increase dyspnea= :hat type of exertion=
:hat are the limits of the patientAs tolerance for exercise=
7t "hat times durin! the day does the patient complain most of fati!ue and shortness of
breath=
:hich eatin! and sleepin! habits ha$e been affected=
:hat is the impact of respiratory disease on Euality of life=
:hat does the patient %no" about his disease=
Does patient has exacerbations or pre$ious hospitaliFations for respiratory problems=
7re comorbidities present=
o" appropriate are current medical treatment=
%) *at ,*ysi'a- assessment fin.in4s .o yo/ e<,e't to fin.8 *at s,e'ifi' '*an4es in t*e
res,iratory system .o yo/ e<,e't to fin. in.i'ative of em,*ysema8
Assessment fin.in4s in'-/.e(
INS!ECTION
increased anterior-posterior diameter. or Gbarrel chestG
use of accessory muscles to assist breathin!
tripod position
shortness of breath common. especially on exertion
tachypnea
!AL!ATION
tactile fremitus decreased
Chest expansion decreased.
!ERCUSSION hyperresonant
AUSCULTATION
decreased $esicular breath sounds
may ha$e prolon!ed expiration
muffled heart sounds from o$er distention of lun!s
usually no ad$entitious soundsH occasional "heeFe
6) *at is t*e most 'ommon 'a/se of em,*ysema8 #ase. on t*is information0 3*at
9/estion 3i-- yo/ as: a+o/t *is *ea-t* +e*aviors8 *at .o yo/ +e-ieve are t*e ma=or
'a/se>s of M)C?s em,*ysema8
SMO7ING IS A MA@OR CAUSE OF EM!H"SEMA
4n the $ast maBority of people. smo%in! is the cause of emphysema.#xactly ho" smo%i
n! destroys the air sac linin!s in the lun!s isnIt%no"n. o"e$er. population studies sho" that s
mo%ers are about sixtimes more li%ely to de$elop emphysema than nonsmo%ers.
#stimates $ary. but more than +- million people in the C.). li%ely ha$e emphysema or
another form of COPD. and probably many of them donIt %no" it. #mphysema and chronic
bronchitis are the third-leadin! cause of death in the C.).
4nterestin!ly. most hea$y smo%ers do not de$elop emphysema. :hy some smo%ers
!et emphysema and others do not is un%no"n. 7ll hea$y smo%ers experience other ne!ati$e
health effects of smo%in!. thou!h.
AL!HA-$ ANTITR"!SIN DEFICIENC"
8esides smo%in!. the other maBor %no"n cause of emphysema is alpha-* antitrypsin
deficiency. o"e$er. this is a minor cause compared to smo%in!.
7lpha-* antitrypsin (77>) is a natural protein circulatin! in human blood. 4ts main
function is to %eep "hite blood cells from dama!in! normal tissues. :hite blood cells contain
destructi$e substances they use to fi!ht infections.
)ome people -- perhaps *//./// in the C.). -- ha$e a !enetic condition that ma%es
them deficient in alpha-* antitrypsin. Deficient le$els of the 77> protein in the blood allo"
normal "hite blood cells to continuously dama!e lun! tissue. 4f people "ith 77> deficiency
smo%e. the dama!e is e$en "orse.
O$er years. most people "ith se$ere 77> deficiency de$elop emphysema. 4tIs not
%no"n ho" many people ha$e emphysema caused by 77> deficiency. #xperts estimate that
about +1 to &1 of people "ith emphysema ha$e 77> deficiency.
#mphysema in 77>-deficient patients has the same symptoms as emphysema
caused by smo%in!. o"e$er. people "ith 77> deficiency often de$elop emphysema at a
youn!er a!e. 3i$er problems may also occur in people "ith emphysema from 77> deficiency.
SECONDHAND SMO7E AND OTHER !OTENTIAL CAUSES
)econdhand smo%e may contribute to emphysema. #xposure to en$ironmental
ci!arette smo%e is %no"n to dama!e the lun!s. )e$eral studies su!!est that people exposed
to hi!h amounts of secondhand smo%e are probably at hi!her ris% for emphysema.
7ir pollution is also belie$ed to contribute to emphysema. althou!h ho" much is
un%no"n. Most people are exposed to pollution. and emphysema ta%es years to de$elop.
ma%in! this effect hard to study.
4n the 78O(# scenario. MCAs condition "as caused by his lon! exposure to ci!arette.
2) Are M)C)?s VS an. SaO% a,,ro,riate8 If not0 e<,-ain 3*y)
Patients (ital si!ns are2 *6+,'-mm!. *+-bpm. &6pm. */+ 0. )aO+ ''1.
Patients () are all abnormal indicatin! that the patient "as in exacerbation of his condition.
"hile his )aO+ is some"hat hi!h this is due to bodyAs compensatory mechanism.
A) Is yo/r ,atient 3it* '*roni' *y,o<ia8 Is *e 'om,ensatin4 for *is '*roni' *y,o<ia8
Patient is e$idently experiencin! chronic hypoxia. Jes. patient is compensatin! as e$idenced
by increased < and increased <<.
TO#ACCO SMO7E
4nflammation of the air"ay epithelium
4nfiltration of inflammatory cells and cyto%ines
@neutrophils, )acrophages, ly)phocytes, leu&otrienes and interleu&insA
4ncreased protease acti$ity "ith brea%do"n of elastin in connecti$e tissues of the lun!s
@>lastases, 'athepsins, etc.A
Destruction of al$eolar septa and loss of elastic recoil of bronchial "alls
BEM!H"SEMAC
7ir >rappin! 3oss of surface area for !as exchan!e
O$er Distended 3un!s
>otal 3un! Capacity and
<esidual (olume
4nsufficient al$eolar $entilation
ypercapnia and
ypoxemia
7l$eolocapillary distribution
abnormality
yperexpansion of chest
8arrel Chest
C<O54C JPO;47
Central Chemoreceptors
((entrolateral Medullary )urface)
4ncreased <ate and
Depth of 8reathin!
Peripheral Chemoreceptor
(Carotid and 7ortic 8odies)
Chemoreceptor <elflexes
Cse of 7ccessory muscles
yperpnea
<elease of #pinephrine and
5orepinephrine
)plenic Contraction
<elease of stored <8C
in blood from the
spleen
#rythrocytosis
Cardiac )tro%e (olume (asoconstriction
Physical 7cti$ity
#rythropoiesis
Heart Rate
D$%2 +,mE
#-oo. !ress/re
D$1% > F2 mmH4E
8asal Metabolic <ate
Tem,erat/re
D6F)G
o
C > $&%
o
FE
Res,iratory Rate
D61 +,mE
8A55 OB CH>> changes in the Vital igns are result of bodies
COMPENSATORY MECHANISM to hypo*ia9
1) *y is t*e O% in*a-ation at %L!M in s,ite of t*e SaO% at FFH8 Ho3 .o 3e e<,-ain t*e
B*y,o<i' .riveC in a ,t) 3it* em,*ysema8 *at im,ortant 'onsi.erations .o yo/ *ave to
remem+er re4ar.in4 O% a.ministration in a ,t) 3it* CO!D -i:e M)C)8
0irst thin!s first. 4t is important to understand that ypoxic Dri$e does exist. it is not a myth.
but the ypoxic Dri$e >heory is a myth. )o let me differentiate the t"o2
o Hypoic !ri"e( >his is "hen a personAs body relies on lo" le$els of O+ to si!nal them
to breathe faster. 7 person "ithout COPD normally relies on hi!h le$els of CO+ to
si!nal them to increase their breathin! rate.
o Hypoic !ri"e Theory( :hen you !i$e a person "ith COPD hi!h concentrations of
O+. say *//1 O+. it "ill cause their hypoxic dri$e (their need to breathe) to shut off
and they may stop breathin!. !o into respiratory failure. and die because of too much
oxy!en.
7ccordin! to Dr. Kohn oyt in his article :ebun&ing Myths of 'hronic Obstructi#e 5ung
:isease2
82t is true that ad)inistration of o*ygen to a patient -ith an e*acerbated chronic obstructi#e lung
disease and acute respiratory failure )ay lead to an increased 'O(. 2t is true that
the hypercarbia )ay beco)e se#ere and be associated -ith cardiorespiratory arrest. Che
proble) is -ith interpreting the cause of the e#entsD9
8oth emphysema and chronic bronchitis patients may de$elop a hypoxic dri$e to breathe.
ealthy people !et their dri$e to breathe from the amount of carbon dioxide in the blood.
Patients "ho ha$e emphysema or chronic bronchitis build up consistently hi!h le$els of carbon
dioxide. 8ecause of this. the body loo%s to the le$els of oxy!en. rather than carbon dioxide. to
determine the need to breathe. 4f oxy!en le$els are lo". they breathe faster to !et more oxy!en.
9i$in! oxy!en to a patient "ith hypoxic dri$e can be a problem. 7fter oxy!en is administered.
its le$el in the blood increases. 4n the patient "ith a true hypoxic dri$e. increased le$els of
oxy!en may si!nal the body to slo" do"n or e$en stop breathin!.
:hen you !i$e a COPD patient O+. there are se$eral "ays in "hich it can increase CO+
accordin! to @eff *itna':?s The !eath of Hypoic !ri"e Theory(
Ha-.ane Effe't2 Describes the property of b!. >he idea to this is that if b! is carryin! a lot
of O+ (oxy!enated blood) then it has a lo"er capacity to carry CO+. 4t "or%s in re$erse too2 if
b! is carryin! $ery fe" O+ (deoxy!enated blood) then it can ta%e on more CO+.
Hy,o<i' !/-monary Vaso'onstri'tion DH!VE2 >his occurs "hen the al$eoli in the lun!s are
poorly $entilated and causes the pulmonary arteries to constrict in order to di$ert more blood to
the oxy!en star$ed al$eoli to better $entilate it. o"e$er. if "e !i$e *//1 O+ to the pt. it fools
our body. and this constriction does not happen. and CO+ "ill continue to build and be trapped
in the al$eoli. >his causes a (,L mismatch and increase physiolo!ical dead space in some
patients (5e". +//6).
T*e Most Im,ortant Me'*anism
)o "e no" %no" that aldane #ffect and P(. "hich leads to (,L mismatch and increase
in physiolo!ical dead space. plays a role in increasin! CO+ "ithin a COPD pt. 8ut ho" bi! of
a role does it play= :ell. a''or.in4 to Irven H "o/n4(
8D-orsening #entilationEperfusion )is)atching and an acco)panying increase in dead space
#entilation contribute about 3?7 of the increase in carbon dio*ide le#els.9
Cnderstandin! these effects are important because it shifts our focus of the possible
exacerbation of respiratory failure in COPD patients from gi#ing o*ygen to CO+ bein! trapped.
:e all %no" that if "e donAt !et O+. "e become hypoxic and "e die. o"e$er. hypercapnia
de$elops at a slo"er rate than hypo*ae)ia (5e". +//6). 7s !r# $%s&o wonderf%lly
s%''ari(es)
8Hypo*ia &ills, hypercapnia happens9.
)o "hat does this all mean= 4t means "e should !i$e COPD pts hi!h concentrations of O+
because they need it. but "e should do somethin! about the CO+ build up. :e need to help
them blo" off the CO+. :e can do this by )echanical #entilation (8us%o).
TO#ACCO SMO7E
4nflammation of the air"ay epithelium
4nfiltration of inflammatory cells and cyto%ines
@neutrophils, )acrophages, ly)phocytes, leu&otrienes and interleu&insA
4ncreased protease acti$ity "ith brea%do"n of elastin in connecti$e tissues of the lun!s
@>lastases, 'athepsins, etc.A
Destruction of al$eolar septa and loss of elastic recoil of bronchial "alls
#MPJ)#M7
3oss of surface area for !as exchan!e
7l$eolocapillary distribution abnormality
Co+ in the blood
Chemoreceptor <eflex
(Central and Peripheral)
7cti$ation of
ypoxic Dri$e
ypoxia , ypercapnia
HALDANE
EFFECT
H"!OIIC !ULMONAR"
VASOCONSTRICTION

Genera- ,oints a+o/t oygen therapy in '*roni' o+str/'tive ,/-monary .isease(

>he respiratory dri$e is normally lar!ely initiated by PaCO
+
but in chronic obstructi$e
pulmonary disease (COPD) hypoxia can be a stron! dri$in! force and so if the hypoxia is
corrected then the respiratory dri$e "ill be reduced. >here "ill also be a loss of physiolo!ical
hypoxic $asoconstriction "hich is partly protectin! the patient from the effects of areas of !ross
al$eolar hypo$entilation.
>herefore. oxy!en therapy in COPD must be used "ith care in the acute settin! but it can
ha$e distinct benefits in the lon!-term.
Chronic hypoxaemia causes slo"ly pro!ressi$e pulmonary "ith the de$elopment of ri!ht
$entricular hypertrophy and possible cor pulmonale "ith secondary polycythaemia.
)econdary polycythaemia increases blood $iscosity and hence resistance to flo". >here is also
slud!in! and a tendency to thrombosis.

CO
+
Diffuses to
<8C
Carbonic acid
Carbonic
7nhydrase
Carbinohaemo!lobin
Diffusion rate of CO
+
from
the tissue
Deoxyhaemo!lobin
Cpta%e of CO
+
by the
<8C
7cidity
<elease of
M

M
binds to CO&
M
Creatin! Carbonic :ater
<espiratory center
tri!ered
CONTINOUS #REATHING
)ympathetic 5er$ous
system stimulation
<elease of #pinephrine and
5orepinephrine
Pulmonary 7rtery $asoconstriction
8lood !oes to the O
+
rich al$eoli
4mpro$ed (,L <atio
ARTERIAL OI"GENATION
DSaO
%
of FF HE
8Patient should be on a lo- le#el of O( support to
continuously trigger this HYPO*IC !RI+ES to
)aintain o*ygenation9
8Haldane >ffect and Hypo*ic Pul)onary
Vasoconstriction are both part of the Hypo*ic
:ri#e9
J) Ma:e an inte4rate. ,at*o,*ysio-o4i' f-o3'*art of MC?s .isease 'on.ition)
F) Given M)C)?s *istory an. yo/r :no3-e.4e of ,at*o,*ysio-o4i' ,ro'esses0 e<,-ain t*e ,at*o,*ysio-o4i' +asis of t*e assessment fin.in4s in M)C8
Note(
Nu)bers se#en and eight -ill be discussed together by the belo- sche)atic diagra) of the pathophysiologic basis of >)physe)a and its )anifestations.
TO#ACCO SMO7ING
Oxidati$e >oxins
4nitiates immune and inflammatory response
<elease of inflammatory Mediators from ALVEOLAR Macropha!es
@25E4, 25E!, 25E6 and CNBEFG MetaloproteasesA
Pa!e $& of %&
4nterleu%ins and >50-N
<ecruit 5eutrophils to the site
DCHEMOTAIISE
)ecretes P<O>#7)#)
(#lastases and Cathepsins)
Metaloprotease
Dama!e to the surroundin! tissue
Dama!e to the elastic fibres surroundin! the al$eoli and
terminal bronchioles
<ecruits >-3ymphocytes
>-Cell Mediated 7poptosis
Cells "ill ha$e an unpro!rammed
cell death
Colla!en deposition
0ibrosis formation
4rre$ersible enlar!ement of the air spaces
distal to the terminal bronchiole
:estruction of al#eolar -alls and septa and
loss of elastic recoil of bronchial -alls
DEM!H"SEMAE
5egend:
#OLD 3or.s( Present signs and sy)pto)s
#LUE 3or.s( 3aboratory and dia!nostic tests
Green or.s( >reatment
Re. or.s( Potential complications
Pa!e $$ of %&
3oss of fibrous and muscle tissue
8rea%do"n of 7l$eolar #lasticity
3ar!e spaces "ithin lun!
parenchyma (8ullae)
7ir space adBacent to pleurae
(8lebs)
<educed pulmonary elastic recoil
#nd-expiratory (<esidual) lun! $olume
Dynamic yperinflation
O$er 4nflated 3un!s
<econfi!uration of the
<ib ca!e
Dys,nea on
E<ertion
8arrel Chest
@AP / Crans#erse ratio: H!:(A
oriFontal
<ibca!e
:idened retrospinal clear
space
3o" 0lat Diaphra!m
@I; anteriorly and I!?
posteriorlyA
Pulmonary
0unction >est
(entilation Perfusion Mismatch
@V/J Ratio of I ?.6 or I1/3A
7ir >rappin!
yperexpansion of
chest
:or% of breathin!
Cse of accessory
muscles
La+ore.
#reat*in4
Chest ;-<ay
Persistent inflammatory
response
yperacti$ity of
bronchi
yperacti$ity of
epithelial cells
8ronchoconstriction >hic% yello"
sputum
production
Cou!h <eflex
tri!!ered
Co/4*in4 S,e--s
8ronchodilators
7irflo" 3imitation
3oss of <espiratory
Membrane
<atio of 7ir to 3un!
>issue
Diffusion Defects
5umber of Pulmonary
capillaries
Pulmonary resistance
4nability of the al$eoli to recoil normally
after expandin!
Ta'ti-e fremet/s on
!a-,ation
7l$eolar collapse on
expiration
Cra':-es
*eeKin4
Pulmonary
hypertension
Right +entric%lar Hypertrophy
,Cor P%l'onale-
Chest ;-<ay
#lectrocardio!raphy
#xpectorants
Hy,er resonan'e on C*est
!er'/ssion
ypercapnia , ypoxemia
<uptured 8ullae
Spontaneo%s Pne%'othora
ypoxia
!/rse. -i,
#reat*in4
4mpaired 9lucose deli$ery
and use
<elease of cathecolamines
and cortisol
9lyco!enesis 9luconeo!enesis
#ner!y )tores
Fati4/e
M/s'-e astin4
Diaphra!matic
function
yperinflation of
al$eoli
Res,iratory
A'i.osis
789
7nalysis
7ppetite
ei4*t Loss
C>>
Chemoreceptor reflexes
4ncreased rate and
depth of breathin!
yperpnea
In'rease. res,iratory
Rate
)putum C6)
G) *at are t*e ,ossi+-e 'om,-i'ations of Em,*ysema an. t*eir manifestations8
I) ACUTE EIACER#ATIONS
7cute exacerbations are episodes that occur "hen air"ays suddenly become
obstructed and symptoms "orsen. )uch e$ents are associated "ith inflammation in the
air"ays and are !enerally tri!!ered by an infection in the air"ay or throu!hout the body.
Other factors that can tri!!er serious lun! e$ents2
Certain medications
#xposure to irritants in the air
)easonal chan!es
7cute exacerbations include the follo"in! symptoms2
4ncreased $olume of sputum
)putum that is thic%er and dar%er
:orsened shortness of breath that causes the patient to breathe faster and
harder. >his is the most common and distressin! acute symptom.
7cute exacerbations occur. on a$era!e. bet"een t"o and three times a year in
patients "ith moderate-to-se$ere #mphysema. 4n about '/1 of the cases. they are tri!!ered
by infections. )mo%ers ha$e more episodes than nonsmo%ers.
II) REDUCED ;UALIT" OF LIFE AND MOOD
5early half of patients "ith #mphysema report a limitation in daily acti$ities. >hey
ha$e trouble "al%in! up stairs or carryin! e$en small pac%a!es. 8reathin! becomes hard "or%.
More than half of patients "ith #mphysema ha$e insomnia. )uch impairment in Euality of life
can ne!ati$ely affect mood.
7lmost half of patients "ith #mphysema ha$e anxiety. depression. or another
psychiatric disorder. compared "ith &*1 of people in the !eneral population. :omen "ith
COPD are more susceptible to psycholo!ical problems than men. 4f patients "ith #mphysema
become anxious or depressed. they may ha$e a poorer outloo% than those "ithout these
emotional problems. COPD patients "ith moderate-to-se$ere depression face a !reater &-year
mortality rate than those "ho experience less depression. 3o" oxy!en le$els also can impair
mental function and short-term memory. Psycholo!ical inter$entions may be particularly helpful
for people "ith COPD.
Pa!e $% of %&
)plenic Contraction
<elease of #pinephrine and
5orepinephrine
<elease of <8C from spleen into the
bloodstream
#rythropoeisis
Eryt*ro'ytosis C8C
Cardiac )tro%e (olume
Heart Rate
(asoconstriction
#-oo. !ress/re
8asal Metabolic <ate
Tem,erat/re
III) MALNOURISHMENT
People "ith #mphysema often lac% !ood nutrition. Patients "ith chronic bronchitis
tend to be obese. Patients "ith emphysema tend to be under"ei!ht. 3oss of "ei!ht and
muscle mass is associated "ith a poor outcome in #mphysema. 9ood nutrition impro$es the
ability to exercise. "hich in turn builds muscle stren!th and lun! function. Obese patients "ith
#mphysema "ho lose "ei!ht sleep better.
IV) HEART DISEASE
O$er time. #mphysema causes lo" le$els of oxy!en (hypo*ia) and hi!h le$els of
carbon dioxide (hypercapnia) in the body. 4n order to boost oxy!en deli$ery. the body
compensates in a number of "ays2
8lood $essels in the lun! constrict to force blood and oxy!en throu!h the
circulatory system. >his leads to hi!h blood pressure in the lun!s (pul)onary
hypertension).
More red blood cells are produced to increase the bloodIs oxy!en-carryin!
capacity.
>he heart rate increases to pump more blood.
>he rate of breathin! increases.
#$entually these acti$ities can lead to $ery serious and e$en life-threatenin!
conditions2
7bnormally hi!h blood pressure in the lun!s can cause a complication called cor
pul)onale. in "hich the ri!ht $entricle of the heart enlar!es. e$entually leadin! to
heart failure.
Patients "ith prolon!ed and se$ere hypoxia and hypercapnia are at ris% for acute
respiratory failure, "hich can cause heart rhythm abnormalities or other life-
threatenin! conditions.
V) OTHER SERIOUS MEDICAL !RO#LEMS ASSOCIATED ITH CO!D
>he smo%in! that causes COPD is associated "ith hi!h ris%s of pneumonia. lun!
cancer. stro%e. and heart attac%. >obacco smo%e contains more than -// substances. many of
"hich are oxidants. metals (such as lead. cadmium. and aluminum). and carcino!ens. 5icotine
itself may not dama!e tissues. but it is the chemical that addicts the smo%er to tobacco.
Sleep !ist%r.ance# 7bout half of all people "ith se$ere COPD experience sleep disorders
such as sleep-related hypoxia or insomnia. 5octurnal hypoxia. a lac% of oxy!en durin! sleep.
occurs "hen breathin! is shallo"est durin! rapid-eye-mo$ement (<#M) sleep. 4t may be due
to suppression of the cou!h reflex and a build-up of mucus. 5octurnal hypoxia is treated "ith
o$erni!ht oxy!en therapy. 7s COPD "orsens. many patients ha$e trouble fallin! or stayin!
asleep. COPD patients should not use sleep medications. 5i!httime oxy!en or a chan!e in
COPD medications from beta-a!onists to anticholiner!ics can sometimes help restore restful
sleep.
Osteoporosis# Osteoporosis is a si!nificant problem in patients "ith COPD. Many conditions
associated "ith COPD. includin! smo%in!. $itamin D deficiency. sedentary lifestyle. and the
use of corticosteroid medications put people at ris% for bone density loss and osteoporosis.
/astroesophageal Refl% ,/ER!-) More than half of patients "ith se$ere COPD ha$e
9#<D. a condition in "hich stomach acids bac% up from the stomach into the esopha!us.
o"e$er. many COPD patients donIt report experiencin! 9#<D symptoms such as heartburn.
$&) Ma:e a ta+/-ar 'om,arison of t*e ,at*o4enesis an. ,at*o,*ysio-o4i' '*an4es of
Em,*ysema0 #ron'*itis an. ast*ma)
ASTHMA
CO!D
CHRONIC #RONCHITIS EM!H"SEMA
Age at onset
7t 7ny 7!e (usually O-/
years)
Csually P-/ Jears
)o&ing history Possible Csually P*/ pac%s per year
'ough at >*acerbation Csually bet"een + to 6am 9radual 4ncrease
putu) production 4nfreEuent Common Possible
Allergy Common 4nfreEuent
Air3ay Inf-ammation
Main portion 3ar!e 7ir"ays )mall 7ir"ays (8ronchi) )mall 7ir"ays (7l$eoli)
Pathophysiology
8asement membrane
>hic%enin!
0ibrosis of 8ronchi
Destruction of al$eolar
"all
,ronchial ,iopsies >h-+ dominant > Cells >h-* dominant > Cells
5eutrophils and
Proteases
Re#ersibility @Pea&
Blo- ResultsA
5ormaliFe "ith time
May impro$e but not
normaliFe
5on <e$ersible
Ba)ily History common Cncommon
Possible (7lpha*
7ntitrypsin deficiency)
C-ini'a- Manifestations
Cactile Bre)itus 5ormal 5ormal Decreased
Percussion
<esonant to hyper
resonant
<esonant yper <esonant
Auscultation :heeFes
5ormal to decreased
breath soundH "heeFes
Decreased intensity of
breath sounds. usually
"ith prolon!ed expiration
Producti#e 'ough 5one
Classic sign Late in course with
infection
:yspnea Common
Late in course
Common
"heeKing Continuous 4ntermittent Minimal
,arrel 'hest 5one Occasionally Classic
Prolonged >*piration 5ot Present 7l"ays present 7l"ays present
'yanosis Common Common Cncommon
'hronic Hypo#entilation yper$entilation Common 3ate in Course
Polycythe)ia Cncommon Common 3ate in Course
'or Pul)onale Cncommon Common 3ate in Course
$$) #ase. on t*e assessment fin.in4s0 i.entify five ,riority ,ro+-ems t*at M)C) may +e
e<,erien'in4)
!riorities are(
a. 7chie$in! 7ir"ay Clearance
b. 4mpro$in! 8reathin! Patterns
c. 4mpro$in! 7cti$ity >olerance
d. Monitorin! and Mana!in! potential complications
e. Continuous assessment of the patient
<elease of #pinephrine and
5orepinephrine
N/rsin4 Care !riorities(
f. 4mpaired 9as exchan!e and air"ay clearance due to chronic inhalation of toxins
GOAL( 2)pro#e)ent in gas e*change
!. 4mpaired !as #xchan!e related to $entilation-perfusion ineEuality
GOAL( 2)pro#e)ent in gas e*change
h. 4neffecti$e air"ay clearance related to bronchoconstriction. increased mucous
production ineffecti$e cou!h. bronchopulmonary infections and other complications
GOAL( Achie#e)ent of air-ay clearance
i. 4neffecti$e breathin! pattern related to shortness of breath. mucus. bronchoconstriction
and air"ay irritants
GOAL( 2)pro#e)ent in breathing pattern
B. 7cti$ity intolerance due to fati!ue. hypoxemia and ineffecti$e breathin! patterns
GOAL( 2)pro#e)ent in acti#ity tolerance
>he laboratory sends the ff. report se$eral hours after admission2 <8C ? &.'thou,cmm. :8C-
*&./// thou,cmm. !b *+!,d3. 789s2 p- @.+'. pO+ ? '/ mm!. pCO+ ? 65 mm!. CO& ? ++.
$%) Inter,ret t*e a+ove res/-ts) Ho3 .o t*e res/-ts re-ate to t*e ,at*o,*ysio-o4i' '*an4es of
em,*ysema8
R#C2 &. '//. /// cells,Q3 (5ormal (alue2 -.@ to 6.* million, Q3)
H4+2 *+ !,d3 (5ormal (alue2 *&.5 ? *@.5 !,d3)
7nemia of chronic illness is typically a normocytic anemia and is most commonly obser$ed
in patients "ith concurrent infectious. and inflammatory or neoplastic diseases. CO!D f/-fi--s
t*e 'riteria of a '*roni'0 inf-ammatory0 m/-tisystemi' .isease -ea.in4 to t*e e<,e'tation
of anemia)
7nemia in COPD is an immune disorder that has been reported in numerous diseases "ith
an inflammatory component. 4nflammatory cyto%ines ha$e $arious effects that play a %ey role in
the patho!enesis of this form of anemia and ultimately interfere "ith the normal mechanisms of
erythropoiesis. >he follo"in! possible mechanisms ha$e been proposed2
!# Dysre4/-ation of iron *omeostasis caused by the accumulation and retention of iron
"ithin cells of the reticuloendothelial system !i$in! rise to a conseEuent decrease in a$ailable
iron for use by pro!enitor cells. >he administration of 43-* and >50-N has been sho"n to lead
to the de$elopment of hypoferremia in experimental animals.
(. Im,aire. ,ro-iferation of eryt*roi. ,re'/rsors. >he most potent inhibitor is interferon-R .
althou!h the free radicals !enerated by oxidati$e stress also ha$e this effect. >his
phenomenon can result in an increase in the apoptosis of these cells or a decrease in the
expression of #PO in their receptors.
+. Im,aire. +one marro3 res,onse to E!O 'a/se. .ire't-y +y 'yto:ines) 43-* and >50-N
inhibit the expression of this hormone in $itro. 0inally. the acti$ation of these mediators may
stimulate the production of hepcidin. a recently disco$ered polypeptide synthesiFed in the li$er
that participates in the process of iron absorption and is thou!ht to play a %ey role in the
de$elopment of anemia of chronic disease.
A#Gs( p- @.+'. pO+ ? '/ mm!. pCO+ ? 65 mm!. CO& ? ++.
Patient is experiencin! Cncompensated <espiratory 7cidosis a classic si!n found in
patients "ith emphysema @see sche)atic diagra) of the clinical )anifestationsA.
CO!D INFLAMMATION
Cyto%ine release
7cute-Phase <eactants
(C<P.3D. 0ibrino!en)
>50-N. 43-6. 43-' epcidin
4nhibition of #rythroid
precursors
4nteference "ith the
action of #PO
Macropha!e 4ron
)eEuestration
4nhibition of 4ron
7bsorption
4nhibition of
#rythropoiesis
<8C production
@+, 6??, ??? cells/L5A
75#M47
,Hg.: !( g/d5A
<eference2
1. Agusti AG, Noguera A, Sauleda J, et al. Systemic effects of chronic obstructive pulmonary
disease. Eur Respir J !!"# 1$"%&'"(!
AUTHORL
SOURCE
TITLE !RO#LEM SUMMAR" OF FINDINGS
SIGNIFICANCE TO
NURSING
Matthias Kohn.
MD. PhD.
)oeren
oerni!. MD
Anemia
an.
Inf-amm
ation in
CO!D
7lthou!h chronic
obstructi$e
pulmonary disease
(COPD) is
traditionally
associated "ith
polycythemia. its
systemic
inflammatory
components can
interfere "ith
erythropoietin and
result in anemia of
chronic disease.
<esearchers
assessed the
freEuency of
anemia and its
relation to serum
erythropoietin
(#PO) le$els and
se$erity of the
disease in a !roup
of COPD patients.
>his study documents
that anemia occurs relati$ely
freEuently in COPD patients
and is related to the presence
of inflammation. 7nemia is an
understudied issue in COPD
but may be of !reat importance
in this disease. 4n our cohort.
anemia ("ith hemo!lobin
concentrations O *+./ !,d3 in
"omen and O *&.5 !,d3 in
men) "as present in as many
as *&1 of all COPD patients.
>his may be an
underestimation of the anemia
pre$alence. as "e ha$e
excluded patients "ith anemia
related to bleedin! and %no"n
folate or $itamin 8
*+
deficiency.
0urthermore. anemic COPD
patients sho"ed increased
le$els of erythropoietin
compared to nonanemic
patients and normal control
subBects.
7nemia of chronic illness is
typically a normocytic anemia
and is most commonly
obser$ed in patients "ith
concurrent infectious. and
inflammatory or neoplastic
diseases. COPD fulfills the
criteria of a chronic.
inflammatory. multisystemic
>he present study is
limited by a relati$e small
number of patients. 0or
future in$esti!ations.
lar!er study populations
are needed. >his "ould
allo" in$esti!atin!
"hether anemia is related
to the primary disease
process per se or to
secondary systemic
manifestations such as
"ei!ht loss. loss of lean
tissue mass. hypoxia. or
systemic inflammation.
7nemia in COPD is
understudied. >here are
no pre$ious reports on
anemia freEuency and
pathophysiolo!y in
COPD. More detailed
in$esti!ations on
hematolo!ic and clinical
parameters ( ie .
pre$alence of anemia in
COPD and its !ender
relatedness. exercise
capacity. 6-min "al% test)
and pro!nosis are
reEuired to pro$ide
indications "hether
anemia is merely a
mar%er or a mediator of
pathophysiolo!ic
disease leadin! to the
expectation of anemia. :hile
anemia in chronic heart failure
or renal insufficiency has been
freEuently in$esti!ated. it is
understudied in COPD.
>he mechanism of anemia
de$elopment in COPD mi!ht
be similar to that in other
chronic diseases. 4t has been
sho"n that mediators of the
immune and inflammatory
response. such as tumor
necrosis factor-N. 43-6. and
interferon-R are potentially
in$ol$ed in the de$elopment of
anemia in chronic illness. >he
increased le$els of
inflammatory cyto%ines lead to
a shortened <8C sur$i$al. "ith
a demand for a sli!ht increase
in <8C production. >he bone
marro" cannot adeEuately
respond to the increased
demand for <8Cs. >his is
caused by a relati$e
erythropoietin resistance due
to an impaired ability of <8C
pro!enitors to respond to
erythropoietin. 7n impaired
mobiliFation of
reticuloendothelial iron stores
is an additional
pathophysiolo!ic factor.
processes that may impair
physical functionin! in
COPD. 4nter$entions "ith
erythropoietin and iron
supplementation "ould
then seem $ery promisin!
in order to impro$e the
poor health status and
pro!nosis of patients "ith
COPD.
Monica K
0letcher. 8irthe
Dahl
#xpandin
! nurse
practice
in COPD2
is it %ey
>he pre$alence of
chronic obstructi$e
pulmonary disease
(COPD). a common
>he nursin! role in COPD ? and
essentially in all chronic diseases ?
is becomin! increasin!ly important
and is characterised by continuity
5urses represent an
appropriate resource to deli$er
care and support to indi$iduals
"ith COPD throu!hout the
to
pro$idin!
hi!h
Euality.
effecti$e
and safe
patient
care=
and pre$entable
chronic disease. is
on the increase.
and so are the
financial and social
burdens associated
"ith it. >he
mana!ement of
COPD is
particularly
challen!in!. as
patients ha$e
complex health and
social needs
reEuirin! life-lon!
monitorin! and
treatment. 4n order
to address these
issues and reduce
the burden
imposed by COPD.
the de$elopment of
inno$ati$e disease
mana!ement
models is $ital.
5urses are in a %ey
position to assume
a leadin! role in the
mana!ement of
COPD since they
freEuently
represent the first
point of contact for
patients and are
in$ol$ed in all
sta!es of care.
7lthou!h e$idence
is still limited. an
increasin! number
of studies ha$e
su!!ested that
nurse-led
consultations and
inter$entions for
the mana!ement of
COPD ha$e the
potential to impact
positi$ely on the
of care. 5urses are in$ol$ed in the
mana!ement of COPD at all
sta!es. from pre$ention to pro$ision
of end-of-life care "ithin a $ariety of
settin!s. both in the community
(includin! patientsA o"n homes and
family practice) and hospitals.
5urses often play a %ey role in ne"
care models based on different
types of telemedicine
support.
5.6
5urse-led consultations
and disease mana!ement
inter$entions are important
inter$entions "hich enable nurses
to pro$ide. complement. or extend
the care deli$ered by doctors.
5urse-led consultations carried out
by experienced nurses freEuently
include tas%s that traditionally
belon! to physicians. such as
physical examination of patients.
dia!nosis and. in countries such as
the CD. prescription of medicines.
5urse-led mana!ement
inter$entions are aimed at helpin!
patients cope "ith their condition
and impro$e their Euality of life.
>hey include patient education.
!uided self-mana!ement. smo%in!
cessation. and pulmonary
rehabilitation pro!rammes.
entire course of the disease.
#$en thou!h more research is
needed to establish the
effecti$eness of nurse-led
inter$entions and
consultations. there is some
!ro"in! e$idence to
demonstrate the benefits
pro$ided by these
inter$entions. particularly in
relation to the hospital-at-
home and early dischar!e
schemes. smo%in! cessation.
and pulmonary rehabilitation
pro!rammes as "ell as
inter$entions aimed at
impro$in! self-mana!ement
beha$iour. )tudies ha$e also
sho"n that nurses are able to
deli$er care that is as effecti$e
as that pro$ided by doctors.
o"e$er. a paucity of
standardised competencies
and specified trainin!
reEuirements ? coupled "ith a
lac% of clinical super$ision.
appropriate fundin!. and
"or%load pressures amon!
nurses deli$erin! COPD care
? hi!hli!ht specific areas for
impro$ement. 5urses need to
stren!then their role to plan
and deli$er more strate!ies to
impro$e the Euality of life of
patients "ith COPD and
reduce the burden of this
disease in the future. 4n doin!
so. nurses cannot assume an
increased responsibility in
isolation. More coordinated
efforts and better mentorship
and support from collea!ues.
alon! "ith a formal reco!nition
of their ne" role. is needed to
allo" nurses to pro$ide hi!h-
Euality. safe. and cost-effecti$e
care and. in that "ay. to
optimise the use of limited
health and Euality
of life of patients.
>he role of nurses
in the mana!ement
of COPD around
the "orld could be
si!nificantly
expanded and
stren!thened.
Pro$idin! adeEuate
educational
opportunities and
support to nurses.
as "ell as
addressin! fundin!
issues and system
barriers and
reco!nisin! the
importance of the
expandin! roles of
nurses. is $ital to
the "ell-bein! of
patients "ith lon!-
term medical
conditions such as
COPD and to
society as a "hole.
in order to reduce
the burden of this
disease.
healthcare resources
"orld"ide.