Kingdom of Bahrain

Ministry of Health
College of Health Sciences
Nursing Division
WHO Collaborating Center for Nursing Development
Generic BSc Nursing Program
Nursing 315 !"ult Healt# $
3
r"
%ear
Case study on
(COPD)
Prepared by: Juma Khalid Tarrar
St No. 0!0"#
Super$ised by: %rs. %out&a 'hali(a
1

NO Content Pa)e NO
* Content +
+ ,ntrodu-tion #
# Patient history !.
Ob/e-ti$es 0
. De(inition o( COPD 1!"
0 ,n-iden-e o( COPD "
1 Causes o( COPD "!2
" 3is' (a-tor (or COPD 2
2 Pathophysiolo)y o( COPD *0
*0 Clini-al mani(estation o( COPD **
** Compli-ation o( COPD *+
*+ Dia)nosti- e$aluation *#!*!*.!
*0
* %edi-al mana)ement *1!*"!*2
*. Sur)i-al mana)ement +0
*0 Nursin) mana)ement +*!++!+#!
+
*1
*"
Summary
3e(eren-es
+.
+0
2
&ntro"uction
, am a third year )eneri- 4S-.Nursin) student5 , 6as ha$in) a
-lini-al trainin) in 6ard *+ in 7l! Salmania medi-al -omple8 and
, ha$e been assi)ned to ta'e -are o( patients 6ith di((erent
-lini-al presentations5 , 6as interested in patient 6ith COPD5 so
, de-ided 6ith the a)reement o( my tea-her to do a -ase study
about him.
3
Patient &nformation's
• ,.7., is "0 years old5 4ahraini male.
• 9e is married5 li$es in 7:!4,:7D $illa)e and he is the (ather
o( + dau)hters and sons.
• Kno6n -ase o( COPD (or the last " years and not on re)ular
treatment.
o Chie( -omplain: Come to 7;< department 6ith history
o( shortness o( breath (or * day duration asso-iated
6ith dry -ou)h. Shortness o( breath a))ra$ated by
sleepin)5 not reli$ed by medi-ation. 7lso history o(
hyponatremia.
No history o(:
• =e$er
• >pper respiratory tra-t in(e-tions
• Chest pain
Current health status:
a)ed male 6ith normal bo6el mo$ements5 normal urine output
and -olor5 )ood air entry and bi mild 6hee&in). 9eart sounds
(S* and S+) is normal 6ith no murrmer. 7bdomen is so(t and
la8 6ith no or)anme)ally. ,.7., has mild s6ellin) at ri)ht le)
(pittin) oedema).
• Present illness: COPD e8a-erbation
=amily history: Patient (amily history is not si)ni(i-ant and didn?t
ha$e any -hroni- diseases.
4
5
HTN
+
Chol
ester
ol
SCD
Ob(ectives
• De(ine COPD a--urately.
• ,denti(y the in-iden-e o( COPD around the 6orld and in
4ahrain.
• Dis-uss the -auses and predisposin) (a-tors o( COPD
and relate it to my patient.
• <8plain the pathophysiolo)y o( COPD)
• Dis-uss the -lini-al mani(estations o( COPD and relate it
to my patient.
• Dis-uss the -ompli-ation o( COPD and relate it to my
patient.
• ,nterpret and dis-uss the dia)nosti- tests in COPD and
relate it to my patient.
• Dis-uss the medi-al mana)ement o( patient 6ith COPD
and relate it to my patient.
• Dis-uss the sur)i-al mana)ement o( patient 6ith COPD
and relate it to my patient.
• Dis-uss the nursin) mana)ement o( patient 6ith COPD
and relate it to my patient.
• Summary in-ludes the days o( -are )i$en to my patient.
6
• Definition of COPD*
Chroni- obstru-ti$e pulmonary disease (COPD) is a term re(errin) to t6o
lun) diseases5 -hroni- bron-hitis and emphysema5 that are -hara-teri&ed
by obstru-tion to air(lo6 that inter(eres 6ith normal breathin). 4oth o(
these -onditions (re@uently -o!e8ist5 hen-e physi-ians pre(er the term
COPD. ,t does not in-lude other obstru-ti$e diseases su-h as asthma.
C#ronic bronc#itis: Chroni- bron-hitis is the in(lammation and e$entual
s-arrin) o( the linin) o( the bron-hial tubes. Ahen the bron-hi are in(lamed
and;or in(e-ted5 less air is able to (lo6 to and (rom the lun)s and a hea$y
mu-us or phle)m is -ou)hed up.
+mp#,sema* ,s a -hroni- obstru-ti$e lun) disease that destroys al$eoli
6alls. The al$eoli -an be -ompared to a balloon that has been blo6n up and
the air has been let out. ,t no lon)er snaps ba-' into pla-e 6hen stret-hed
but lies (loppy. Ahen (resh air enters a lun) 6ith emphysema5 it enters the
al$eoli be-ause o( -han)es in pressure. The (resh air no6 in the al$eoli
should )i$e o(( o8y)en and ta'e on -arbon dio8ide to e8hale and rid it (rom
the body. 9o6e$er5 instead o( bein) e8haled5 the air be-omes trapped and
unable to be pushed out be-ause o( the la-' o( elasti-ity o( the al$eoli.
&nci"ence of COPD aroun" t#e -orl"*
Aorld6ide data are sparse5 but the rates li'ely are hi)her be-ause more than
*.+ billion humans are e8posed to the ra$a)es o( smo'in). 7 population!
based epidemiolo)i- study (rom Spain determined the pre$alen-e o( COPD in
indi$iduals a)ed 0!02 years at 2.*B (1"B 6ere men).
&nci"ence of COPD in !merica*
7
.ortalit,/.orbi"it,* COPD is the (ourth leadin) -ause o( death in the >nited
States5 a((e-tin) #+ million adults.
Se0* %en are more li'ely to ha$e COPD than 6omen.
!ge* COPD o--urs predominantly in indi$iduals older than 0 years.
&nci"ence of COPD in Ba#rain*
D,SC9
:ess than " hrs %ore than " hrs
Total
4ahraini Non 4ahraini 4ahraini Non 4ahraini
%ale ! ! . ! .
=emale * ! 0 ! 1
Causes an" pre"isposing factors of COPD*
Causes*
• Smo1ing
Smo'in) is responsible (or 20B o( COPD in the >nited States. 7lthou)h not
all -i)arette smo'ers 6ill de$elop COPD5 it is estimated that *.B 6ill.
Smo'ers 6ith COPD ha$e hi)her death rates than nonsmo'ers 6ith COPD.
They also ha$e more (re@uent respiratory symptoms su-h as -ou)hin) and
shortness o( breath. and more deterioration in lun) (un-tion than non!
smo'ers.
Ci)arette smo'in) dama)es the lun)s in many 6ays. =or e8ample5 the
irritatin) e((e-t o( -i)arette smo'e attra-ts -ells to the lun)s that promote
in(lammation. Ci)arette smo'e also stimulates these in(lammatory -ells to
release elastase5 an en&yme that brea's do6n the elasti- (ibers in lun) tissue.
• Deficienc, of alp#a1 antitr,psin 2!!34
8
7nother 6ell!established -ause o( COPD is a de(i-ien-y o( alpha!* antitrypsin
(77T). 77T de(i-ien-y is a rare )eneti- (inherited) disorder that a--ounts (or
less than *B o( the COPD in the >nited States.
Normal (un-tion o( the lun) is dependent on elasti- (ibers surroundin) the
air6ays and in the al$eolar 6alls. <lasti- (ibers are -omposed o( a protein
-alled elastin. 7n en&yme -alled elastase that is (ound e$en in normal lun)s
-an brea' do6n the elastin and dama)e the air6ays and al$eoli. Protein
alpha!* antitrypsin (77T) 6hi-h is produ-ed by the li$er and released into the
blood is present in normal lun)s and -an blo-' the dama)in) e((e-ts o(
elastase on elastin.
,ndi$iduals 6ho inherit t6o de(e-ti$e 77T )enes (one (rom ea-h parent) ha$e
either lo6 amounts o( 77T in the blood or 77T that does not (un-tion properly.
The redu-ed a-tion o( 77T in these indi$iduals allo6s the destru-tion o( tissue
in the lun)s by elastase to -ontinue unopposed.
,ndi$iduals 6ith one normal and one de(e-ti$e 77T )ene ha$e 77T le$els that
are lo6er than normal but hi)her than indi$iduals 6ith t6o de(e-ti$e )enes.
These indi$iduals %7C ha$e an in-reased ris' o( de$elopin) COPD i( they do
not smo'e -i)arettes. ho6e$er5 their ris' o( COPD probably is hi)her than
normal i( they smo'e.
Predisposin) (a-tors:
Occupational pollutants
Some o--upational pollutants su-h as -admium and sili-a do in-rease the ris'
o( COPD. Persons at ris' (or this type o( o--upational pollution in-lude -oal
miners5 -onstru-tion 6or'ers5 and metal 6or'ers. These o--upations are
more o(ten asso-iated 6ith interstitial lun) diseases5 espe-ially the
pneumo-oniosis. Ne$ertheless5 the ad$erse e((e-ts o( smo'in) -i)arettes on
lun) (un-tion are (ar )reater than o--upational e8posure.
Secon"#an" smo1e
<((e-ts o( passi$e smo'in) or Dse-ond!hand smo'eD on the lun)s are not 6ell!
'no6nE ho6e$er5 e$iden-e su))ests that COPD in-idents are more -ommon
in people 6ho li$e in households 6here other smo'e.
!ir pollution
7ir pollution -an -ause problems (or persons 6ith lun) disease5 but it is
un-lear 6hether outdoor air pollution -ontributes to the de$elopment o(
COPD. 9o6e$er5 in the non!industriali&ed 6orld5 the most -ommon in-idents
o( COPD o--ur 6here there is indoor air pollution. This is usually due to
indoor sto$es used (or -oo'in).
9
My patient is non smoer! ho"e#er! he is li#in$ in a resi%ent "here there
are smoers& 'lso he (se% to )oo *oo% (sin$ )oal "hi)h may )ontri+(te
to his )on%ition& 'lso! he "as "orin$ as )leaner in ministry o*
e%()ation *or 2, years &
1,
Pat#op#,siolog,*
COPD is a mi8ture o( + separate disease pro-esses that to)ether (orm the
-omplete -lini-al and pathophysiolo)i-al pi-ture. These pro-esses are -hroni-
bron-hitis5 emphysema.
C#ronic bronc#itis
,n this type5 -hroni- bron-hitis plays the ma/or role. Chroni- bron-hitis is
de(ined by e8-essi$e mu-us produ-tion 6ith air6ay obstru-tion and notable
hyperplasia o( mu-us!produ-in) )lands.
Dama)e to the endothelium impairs the mu-o-iliary response that -lears
ba-teria and mu-us. ,n(lammation and se-retions pro$ide the obstru-ti$e
-omponent o( -hroni- bron-hitis. ,n -ontrast to emphysema5 -hroni- bron-hitis
is asso-iated 6ith a relati$ely undama)ed pulmonary -apillary bed.
<mphysema is present to a $ariable de)ree but usually is -entrilobular rather
than panlobular. The body responds by de-reasin) $entilation and in-reasin)
-ardia- output. This results in rapid -ir-ulation in a poorly $entilated lun)5
leadin) to hypo8emia and poly-ythemia.
<$entually5 hyper-apnia and respiratory a-idosis de$elop5 leadin) to
pulmonary artery $aso-onstri-tion and -or pulmonale. Aith the ensuin)
hypo8emia5 poly-ythemia5 and in-reased CO
+
retention5 COPD patients ha$e
si)ns o( ri)ht heart (ailure and are 'no6n as Dblue bloaters.D
+mp#,sema
The se-ond ma/or type is that in 6hi-h emphysema is the primary underlyin)
pro-ess. <mphysema is de(ined by destru-tion o( air6ays distal to the
terminal bron-hiole.
Physiolo)y o( emphysema in$ol$es )radual destru-tion o( al$eolar septae and
o( the pulmonary -apillary bed5 leadin) to de-reased ability to o8y)enate
blood. The body -ompensates 6ith lo6ered -ardia- output and
hyper$entilation. This results in relati$ely limited blood (lo6 throu)h a (airly
6ell o8y)enated lun) 6ith normal blood )ases and pressures in the lun)5 in
-ontrast to the situation in blue bloaters. 4e-ause o( lo6 -ardia- output5
ho6e$er5 the rest o( the body su((ers (rom tissue hypo8ia and pulmonary
-a-he8ia. <$entually5 these patients de$elop mus-le 6astin) and 6ei)ht loss
and are identi(ied as Dpin' pu((ers.D
11
Clinical manifestations of COPD:
,n patients a((e-ted predominantly by emphysema5 shortness o( breath may
be the ma/or symptom. Dyspnea usually is most noti-eable durin) in-reased
physi-al a-ti$ity5 but as emphysema pro)resses5 dyspnea o--urs at rest.
Patient may be $ery thin 6ith barrel -hest. They typi-ally ha$e little or no
-ou)h or e8pe-toration. 4reathin) may be assisted by usin) a--essory
respiratory mus-les.
,n patients 6ith -hroni- bron-hitis as 6ell as bron-hie-tasis5 -hroni- -ou)h
and sputum produ-tion are the ma/or symptoms. The sputum is usually -lear
and thi-'. Periodi- -hest in(e-tions -an -ause (e$er5 dyspnea5 -ou)hin)5
produ-tion o( purulent sputum and 6hee&in). ,n(e-tions o--ur more (re@uently
as bron-hitis and bron-hie-tasis pro)ress. >se o( a--essory mus-les o(
respiration is -ommon.
,n ad$an-ed COPD5 patients may de$elop -yanosis due to a la-' o( o8y)en
in blood. They may ha$e 4arrarel -hest5 They also may de$elop mornin)
heada-hes due to an inability to remo$e -arbon dio8ide (rom the blood.
Aei)ht loss o--urs in some patients5 primarily (other possibility is redu-ed
inta'e o( (ood) be-ause o( the additional ener)y that is re@uired /ust to
breathe. ,n ad$an-ed COPD5 small blood $essels in the lun)s are destroyed5
and this blo-'s the (lo6 o( blood throu)h the lun)s. 7s a result5 the heart must
pump 6ith in-reased (or-e and pressure to )et blood to (lo6 throu)h the
lun)s. (The ele$ated pressure in the blood $essels o( the lun)s is -alled
pulmonary hypertension.) ,( the heart -annot mana)e the additional 6or'5
ri)ht heart (ailure also 'no6n as Cor pulmonale results and leads to s6ellin)
o( the (eet and an'les. Patients 6ith COPD may -ou)h up blood (hemoptysis).
>sually hemoptysis is due to dama)e to the inner linin) o( the air6ays and the
air6ays? blood $esselsE ho6e$er5 o--asionally5 hemoptysis may si)nal the
de$elopment o( lun) -an-er.
12
%y patient presents 6ith shortness o( breath asso-iated 6ith dry
-ou)h. Shortness o( breath a))ra$ated by sleepin). Ahee&in)5
6ei)ht loss5 hyponatremia5 mild s6ellin) at ri)ht le) (pittin)
oedema).9e 6as usin) a--essoary mus-le (or breathin) .

Complication of COPD:
5espirator, failure
Ahen respiratory (ailure o--urs5 there is a slo6 de-line in lun) (un-tion and risin) le$els o(
-arbon dio8ide in the blood. The in-reasin) -arbon dio8ide -reates a nar-oti- e((e-t in the
patient5 6ho slo6ly loses -ons-iousness and stops breathin).
Pneumonia
-aused by ba-terial in(e-tion -an lead to respiratory (ailure in these patients. Strepto-o--us
pneumoniae is the most -ommon -ause o( ba-terial pneumonia in patients 6ith COPD.
Pneumot#ora0
O--urs 6hen a hole de$elops in the lun)5 allo6in) air to es-ape into the spa-e bet6een the
lun) and the -hest 6all and -ollapsin) the lun). Patients 6ith COPD are at in-reased ris' (or
spontaneously de$elopin) these holes be-ause o( 6ea'ened lun) stru-ture. 7 pneumothora8
-an lead to se$ere respiratory distress and is treated by insertin) a tube into the spa-e
bet6een the lun) and the -hest 6all to allo6 the air to es-ape out o( the spa-e and
ree8pandin) the lun). The tube must remain in the spa-e until the hole is repaired.
Pol,c,t#emia
in COPD is the body?s attempt to ad/ust to de-reased amounts o( blood o8y)en by in-reasin)
the produ-tion o( o8y)en!-arryin) red blood -ells. Ahile this may be help(ul in the short term5
o$erprodu-tion e$entually -lo)s small blood $essels.
13
%y patient presents didn?t de$elope any -ompli-ation5 instead5 his
-ondition impro$ed a(ter his admission in 6ard *+ .
Diagnostic evaluation*
6ab Stu"ies*
• 7rterial blood )as
o 7rterial blood )as (74F) analysis pro$ides the best -lues as to
a-uteness and se$erity.
o ,n )eneral5 renal -ompensation o--urs e$en in -hroni- CO
+

retainers thus5 p9 usually is near normal.
o Fenerally5 -onsider any p9 belo6 1.# a si)n o( a-ute respiratory
-ompromise.
• Serum -hemistry
o These patients tend to retain sodium.
o Diureti-s5 beta!adrener)i- a)onists5 and theophylline a-t to
lo6er potassium le$elsE thus5 serum potassium should be
monitored -are(ully.
o 4eta!adrener)i- a)onists also in-rease renal e8-retion o( serum
-al-ium and ma)nesium5 6hi-h may be important in the
presen-e o( hypo'alemia.
• C4C to dete-t Poly-ythemia
&maging Stu"ies*
• Chest 8!ray
o Chroni- bron-hitis is asso-iated 6ith in-reased bron-ho$as-ular
mar'in)s and -ardiome)aly.
o <mphysema is asso-iated 6ith a small heart5 hyperin(lation5 (lat
hemidiaphra)ms5 and possible bullous -han)es.
Ot#er 3ests*
• Pulse o8imetry
o Pulse o8imetry does not o((er as mu-h in(ormation as 74F.
o Ahen -ombined 6ith -lini-al obser$ation5 this test -an be a
po6er(ul tool (or instant (eedba-' on the patient?s status.
14
• <le-tro-ardio)ram
o The presen-e o( underlyin) -ardia- disease is hi)hly li'ely.
o <stablish that hypo8ia is not resultin) in is-hemia.
o <stablish that the underlyin) -ause o( respiratory di((i-ulty is not
-ardia- in nature.
• Pulmonary (un-tion tests (spirometry)
o De-reased (or-ed e8piratory $olume in * se-ond (=<G
*
) 6ith
-on-omitant redu-tion in =<G
*
;(or-ed $ital -apa-ity (=GC) ratio
o Poor;absent re$ersibility 6ith bron-hodilators
o =GC normal or redu-ed
o Normal or in-reased total lun) -apa-ity (T:C)
o ,n-reased residual $olume (3G)
o Normal or redu-ed di((usin) -apa-ity

3ests
results
Pulmonary (un-tion tests (spirometry) =<G
*
B predi-ted : .#B
Chest 8 ray
!Sho6s no si)ni(i-ant
per(usion de(e-t
!:o6 probability (or
pulmonary embolism
7rterial blood )as

• *
st
result : *";1;+001
o P9  1.+1 (lo6)
o PCO+  00.0mmh)
(hi)h)
o PO+  2.#mmh)
15
($ery lo6)
o 9CO#  +1.. mmolH:
o SaO+  "#B (lo6)
• :ast result: ++;1;+001
o P9  1.#2 (normal)
o PCO+  0mmh)
(6ithin normal)
o PO+  " mmh)
(normal)
o 9CO#  +1 mmolH:
o SaO+  2"B (normal)
6ab result * (abnormalities)
4lood test *
st
result *";1;+001 :ast result ++;1;+001
KI #.+ mmol;: lo6 #.1 mmol;: normal
A4C +0.* J 2K*0 L *0." J 2K*0 L
9b "." )Md: N ".+ )Md: N
Creatnine 00 mmol;: lo6 0 normal
>rea +.1 mmol;: lo6 #.. mmol;: normal
sodium *+2 mmol;: lo6 *+ mmol;: lo6
-hloride 2 mmol;: lo6 2" mmol;: lo6
16
.e"ical .anagement
Smo1ing Cessation 2if applicable4
,t is -riti-ally important that COPD patients @uit smo'in). On-e a patient has
@uit5 the rate o( de-line o( lun) (un-tion slo6s -onsiderably.
There are numerous ni-otine repla-ement systems that help smo'ers
6ithdra6 (rom ni-otine5 in-ludin) ni-otine )um5 pat-hes5 inhalers5 and nasal
sprays. Ni-otine )um 6as the (irst ni-otine repla-ement therapy a$ailable.
<a-h pie-e o( )um -ontains + m) o( ni-otine. ,t is -he6ed slo6ly 6hen
symptoms o( 6ithdra6al are e8perien-ed. The )um de-reases5 but does not
eliminate5 physi-al 6ithdra6al symptoms.
P#armac#oligical t#erap,
Beta$ agonists
,t rela8 the smooth mus-le thereby de-reasin) bron-ho-onstri-tion and air(lo6
obstru-tion. They also impro$e the ability to -lear mu-us and the enduran-e
o( (ati)ued respiratory mus-les.
!ntic#olinergic
7nti-holiner)i-s su-h as ,pratropium bromide has a )reater bron-hodilatory
e((e-t than beta+ a)onists and has (e6er side e((e-ts. ,pratropium bromide is
)enerally re-ommended (or COPD patients 6ho e8perien-e symptoms daily.
Corticosteroi"s
7re o(ten used to treat in(lamed air6ays5 but their lon) term bene(it is not
-lear. Steroids ha$e not been sho6n to slo6 lun) de-line in COPD. They may
redu-e the number o( e8a-erbations and impro$e symptoms in some patients5
but there is no -on$in-in) e$iden-e to support this.
,t is di((i-ult to 6ean patients o(( steroids and many patients are le(t on inhaled
steroids be-ause they do 6ell on them. Corti-osteroids are no6 )i$en5
6hene$er possible5 in an inhaled (orm rather than orally or intra$enously.
There are many ad$erse side e((e-ts asso-iated 6ith lon) term use.
.ucol,tics
%u-us retention narro6s the air6ays and in-reases symptoms o( COPD. 7 lot
o( e((ort has been put into de$elopin) medi-ations that brea' up and allo6
mu-us to be -leared more e((e-ti$ely (rom the air6ays. >n(ortunately5 this has
met 6ith only $ery modest su--ess.
!ntibiotics
7ntibioti-s are )enerally used only (or a-ute e8a-erbations. Patients 6ho
e8perien-e (re@uent e8a-erbations 6ith purulent sputum (a si)n o( in(e-tion)
17
durin) the year may be pla-ed on a s-hedule o( prophyla-ti- (pre$entati$e)
treatment 6ith antibioti-s the (irst *0 days o( ea-h month. This is done (or
spe-ial -ases only.
O0,gen
O8y)en is the only treatment that has been sho6n to impro$e sur$i$al. Nasal
-annula is the most -ommonly used o8y)en deli$ery system.
,ndi-ations (or o8y)en therapy in-lude: arterial PaO+ O .. mm 9)5 or an O+
saturation o( ""B 6ith arterial PaO+ o( ..!.2 mm 9)5 or an O+ saturation o(
"2B a--ompanied by -or pulmonale (ri)ht!sided heart (ailure)5 or
poly-ythemia (proportion o( red blood -ells abo$e .0B o( blood sample).
7 patient 6ho does not @uali(y (or o8y)en as des-ribed may need o8y)en
6hile sleepin) or e8er-isin). O8y)en may be used at ni)ht only i( the PaO+ at
ni)ht is less than .. mm 9) or the O+ saturation is less than ""B. ,( the
PaO+ is less than .. mm 9) or the O+ saturation is less than ""B durin)
e8er-ise5 o8y)en may be pres-ribed.
Nutritional Support
Nutrition is -riti-ally important (or patients 6ho lose a lot o( 6ei)ht. 9i)h (at5
lo6 -arbohydrate diets are re-ommended. ,( a patient is si)ni(i-antly
o$er6ei)ht5 losin) 6ei)ht may be appropriate.
Patient Drugs*
Dru) Purpose
Gentolin * ml P 0 hrs Neb 4ron-hodilator 6or' by rela8in)
the mus-les around air6ays.
This type o( medi-ine helps to
open the air6ays @ui-'ly and
ma'e breathin) easier.
7tro$ent * ml P 0 hrs Neb To treat the narro6in) o( lun)
air6ays.
Ta&o-in .. m) P " hrs ,G 4a-terial in(e-tions are a
-ommon -ompli-ation o( a-ute
e8a-erbations
o( COPD5 and antibioti-s are
used to pre$ent this in(e-tion.
18
Surgical management
=or some people 6ith se$ere COPD5 sur)ery may be re-ommended. Sur)ery
is usually done (or people 6ho ha$e:
• Se$ere symptoms
• Not had impro$ement (rom ta'in) medi-ines
• 7 $ery hard time breathin) most o( the time
sur)eries -onsidered in the treatment o( se$ere COPD are:
• 4ulle-tomy. ,n this pro-edure5 do-tors remo$e one or more $ery lar)e
bullae (rom the lun)s o( people 6ho ha$e emphysema. 4ullae are air
spa-es that are (ormed 6hen the 6alls o( the air sa-s brea'. The air
spa-es -an be-ome so lar)e that they inter(ere 6ith breathin).
• :un) $olume redu-tion sur)ery (:G3S). ,n this pro-edure5 sur)eons
remo$e se-tions o( dama)ed tissue (rom the lun)s o( patients 6ith
emphysema.
• 7 lun) transplant may be done (or some people 6ith $ery se$ere
COPD. 7 transplant in$ol$es remo$in) the lun) o( a person 6ith COPD
and repla-in) it 6ith a healthy lun) (rom a donor.
19
My patient )on%ition %i%n-t re.(ire any s(r$i)al inter#ention &
Nursing management
,mplementation o( appropriate nursin) inter$entions5 in-ludin) medi-ations5
-ontrolled o8y)en therapy5 $entilation modalities5 and strate)ies (or se-retion
-learan-e5 ener)y -onser$in)5 rela8ation5 nutrition5 and breathin) retrainin).
• Tea-hin) smo'in) -essation strate)ies.
• 7dministration o( the (ollo6in) pharma-olo)i-al a)ents as pres-ribed:
bron-hodilators5 o8y)en5 -orti-osteroids5 antibioti-s5 psy-hotropi-s5 opioids
• 7dministration o( o8y)en therapy as pres-ribed.
• 7ssessment o( inhaler te-hni@ue and tea-hin) proper te-hni@ue.
• Dis-uss 6ith -lient medi-ation?s side e((e-ts and pre-autions.
• 3e-ommendation o( annual in(luen&a $a--ination and pneumo-o--al
$a--ine.
• 7-ti$ity pa-in) is important as -lient 6ith COPD has de-reased e8er-ise
toleran-e durin) spe-i(i- periods o( days espe-ially in the mornin).
• Promotion o( e8er-ise trainin) and pulmonary rehabilitation as appropriate
a4 3eac#ing "iap#ragmatic breat#ing -#ic#*
/ 3edu-e the respiratory rate
/ ,n-rease al$eolar $entilation
/ 9elps e8pel as mu-h as air as possible durin) e8piration
b 43eac#ing Purse" lip breat#ing -#ic#*
/ Slo6 e8piration
/ Pre$ents -ollapse o( small air6ays
/ 9elp the -lient to -ontrol the rate Q depth o( respiration
/ Promotes rela8ation
/ <nablin) the pt to )ain -ontrol o( dyspnea Q redu-e (eelin)s o( pani-
c4 &nspiration muscle training
2,
/ This pro)ram re@uires that the -lient breathe a)ainst resistant (or *0 to
*. min e$ery day.
/ 7s the resistant is )radually in-reases the mus-le be-ome better.
• Patient edu-ation:
o <du-ate patients to the dan)ers o( smo'in) and the
impro$ement in @uality o( li(e attainable 6ith smo'in) -essation.
o ,nstru-t patients 6ith COPD to present early durin) an
e8a-erbation and not 6ait until they are in distress.
o Tea-h -lient about ho6 to use his %edi-ations Q home o8y)en
therapy.
o Tea-h -lient the important o( (ollo6in) diet re)ime ordered by
dietitian.

21
Nursing care plan
Patient problems*
0 De*i)it in o1y$enation at al#eoli )apillary mem+rane
0 ,nspiration and e8piration that doesn?t pro$ide ade@uate
$entilation
0 ,nsu((i-ient ener)ey to -omplete desired daily a-ti$ities
0 Disruption o( sleep pattern
0 Psy-holo)i-al disturban-e related to trans(er to ne6
en$ironment
Nursing "iagnosis*
2oss o* l(n$ elasti)ity
0 relo)ation stress syn%rome
0 3mpaire% $as e1)han$e 45T
22
<$aluation:
! 61y$en sat(ration has +e)ome 987
! 8ital sin$s are sta+le
! 6hee&in) +reath so(n% not hear%
Summar, inclu"es t#e "a,s of care given to t#e patient)
,.7., is "0 years old5 4ahraini male5 -ome to 7;< department
6ith history o( shortness o( breath (or * day duration asso-iated
6ith dry -ou)h. Shortness o( breath a))ra$ated by sleepin)5 not
reli$ed by medi-ation. 7lso history o( hyponatremia. 9e is
Subjective
data
Objective data Patient
problem
Nursing
diagnosis
Nursing
objectives
9atient )5o
shortness
o* +reath
8,yrs ol% 0
0 Hypo1ia
PO+R2.#
mmh)
0 61y$en
sat(ration
: 837
0 ;hee<in$
+reath so(n%
0 %e*i)it in
o1y$enation
at al#eoli
)apillary
mem+rane
0 3mpaire% $as
e1)han$e 45T
2oss o* l(n$
elasti)ity
0 9atient "ill
ha#e a%e.(ate
o1y$enation o*
tiss(es +y
'=>-s res(lts
a*ter my
inter#entions &
interventions rational
0 9ro#i%e o1y$en therapy 203 2 as %o)tor
or%er &
0 '%minister #entolin 1 ml . 8 hrs an%
atro#ent 1 ml . 8 hr as %o)tor or%er &
0 a%minister ta<o)in 4&5m$ . 8 hrs as
%o)tor or%er
0 ?le#ate hea% o* the +e% &
0 '(s)(ltate +reath so(n%s an% assess
#ital si$ns &
0 To in)rease o1y$en )on)entration
in the +o%y &
0 To "i%ene% small air"ays
0 To pre#ent +a)terial in*e)tion &
0 To maintain air"ay +y %e)reasin$
press(re on the %iaphra$m an%
enhan)in$ %raina$e to %i**erent l(n$
se$ements &
$0 To as)ertain respiratory stat(s
an% note pro$ress &
23
'no6n -ase o( COPD (or the last " years and not on re)ular
treatment.
Dr. 7hmed 7:!araidh ordered many tests to be done in-ludin):
C4C 5 >rea5 CaI5 %)I5 NaI5urine osmolarity5 urine routine
mi-ro 74F5 PT5PTT. 7lso ordered Normal Saline +:;+ hrs5
maintain ,;O -hart5 restri-t oral s6eat5 O8y)en +!#: and
medi-ation in-ludin): Gentolin5 7tro$ent5 Ta&o-in.
,n the three days that , 6as ta'in) -are o( my -lient and
assessin) and e$aluatin) his respiratory status5 , also pro$ided
o8y)en therapy as do-tor ordered and )i$en pres-ribed
medi-ation5 maintainin) ,;O -hart. , also 6as -he-'in) patient
homodynami- status by -he-'in) his $ital sin)s. =inally , tau)ht
patient deep breathin) e8er-ise and en-oura)ed him to rela8 to
)et better soon.
24
5eferences
• 4runner Q Suddarth?s te8t boo' o( medi-al sur)i-al nursin)5
p:.02
• http:;;666.)uideline.)o$;summary;summary.asp8S
ssR*.Qdo-TidR100"QnbrR+*1
• http:;;666.lt-pra-ti-e.-om;-ontent;node!0;-lini-ians;-op.htm
• http:;;en.6i'ipedia.or);6i'i;COPD
• http:;;(amilydo-tor.or);online;(amdo-en;home;arti-les;100.ht
ml
• http:;;666.medi-inenet.-om;-hroni-Tobstru-ti$eTpulmonary
TdiseaseT-opd
• http:;;666.nlm.nih.)o$;medlineplus;en-y;arti-le;00002*.htm
UDe(inition
25