Copd With Chf2

7/17/2019 Copd With Chf2

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CASE REPORT

Acute COPD Exacerbation with Congestive Heart Failure

Riski Dohartua, Amira Permatasari T Division of COPD

Departent of Pulonolog! an" Respirator! #e"icineSchool of #e"icine $niversitas Suatera $tara% A"a #ali& 'eneral

Hospital#e"an

Abstract

It has been reported in male patients aged 53 years, came to the hospital

with complaints of shortness of breath and early diagnosis of patients with

COPD exacerbations with CPC. Patients in the hospital joint with the cardiology.

rom the chest x!ray shows a pict"re emfisemat"s, diaphragm lies low, and

hiperl"sen pict"re, heart pict"re of the pend"l"m. #C$ showed a pict"re of the

CPC. %he res"lts showed abnormal spirometry obstr"ction and restriction. %he

res"lts showed #chocardiography C&. Patients were gi'en treatment therapy

(.)* +aCl with minophilin - mg -( drips/min"te, lixotide and 0entoline 1

ho"rly 'ia a neb"ls, Ceftriaxon injection of 2 g / 1 ho"rs, dexamethason injection

5gr amp/1 ho"rs, f"rosemide injection amp / 1 ho"r, salb"tamol tablets mg 3

times daily, digoxintablets (,-5 mg 3 times daily, spironolactone tablets -5 mg

daily, simarc tablets - mg daily, with stable COPD treatment res"lts and patient

was taen to the cardiac care.

Key Words : COPD, CHF.

()TROD$CT(O)

C& and COPD are two commonly enco"ntered conditions in clinical

practice. C& acco"nts for their fre4"ent coexistence. %he pre'alence of COPD

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ranges from -(* to 3-* in patients with. #02 is as good a predictor of

cardio'asc"lar mortality as ser"m cholesterol Ischemic heart disease, and not

respiratory fail"re, is the leading ca"se of death in COPD patients, with only a

small fraction dying of respiratory fail"re. %he relationship between COPD and

cardio'asc"lar e'ents remains "nclear. Patients with COPD are not at

increased ris for hypertension or left 'entric"lar hypertrophy howe'er, they

consistently show e'idence of low!grade systemic inflammation that plays an

increasingly recogni6ed role in the pathogenesis of atherosclerosis. Patients

with se'ere COPD are -.217-.8 times more liely to ha'e ele'ated or highly

ele'ated circ"lating C9P le'els than control s"bjects. woring hypothesisto

acco"nt for the high pre'alence of systolic dysf"nction in patients with COPD is

that low!grade systemic inflammation accelerates the progression of coronary

atherosclerosis, which "ltimately res"lts in ischemic cardiomyopathy. :"ch a

hypothesis fits the clinical obser'ation of a high incidence of left 'entric"lar wall

motion abnormalities noted in patients with COPD and left 'entric"lar

dysf"nction.2

CASE REPORT

Patients admitted to dam ;ali &ospita with main complain of

shortness of breath since < / ! = years ago, and become worse in 3 day. Chest

pain happened since 3 years ago and become worse if patient ha'e co"gh, lie

a p"nct"red!pric pain. Co"gh has occ"red since 2 months with yellowish.

:wellingon the both of legs happened since 2 wee ago.

0ital signs showed alert, >P ? 2-(/)( mm&g, P"lse ? 12 times/min"te,

9espiratory rate ? 3= times/min"te, %emperat"re ? 3=.3(C.

Physical examination showed inspection simetrical chest inspection,

tactil fremit"s was decreased on both of the l"ng. Perc"ssion was hypersonor

on both of the l"ng. 0esic"lar decreased breath so"nd on both of the l"ng. irst

and second heart so"nd irreg"lar, mid!diastolic m"rm"r grade - / = at the apex,

gallops not fo"nd.

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@aboratory findings ? &b ? 25,3 g/dl, A>C ? 22,1 x 2() /@, platelet ?21=

2(3/mm-, rterial blood gases ? p& ? 8.), PaO- ? 2( mm&g, PaCO- ? 32

mm&g, ># ? 2,(, &Co3 ? -5, mmol/@, :aO- ? ))*, interpretation ? respiratory

alcalosis.

Chest x 7 ray showed emphysemato"s on both of the l"ng, diapraghm

was flattein, tracheal in the midle position. C%9 53 *,Bfig.2. rom the #C$

showed 909 < 9D < 90&. #chocardiography showed :tenosis ;itral ec

P"lmonary &ypertension Big. -. :pirometry showed obstr"cti'e and restricti'e

abnormalities.

ig"re 2. %horax P, 2th :eptember -(22 dam ;ali &ospital

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ig"re -. #chocardiography, -th :eptember -(22 dam ;ali &ospital

#arly diagnosis of this patient COPD with CPC, was -th :eptember -(22

the woring diagnosis was COPD with C& c I!II ec :tenosis ;itral moderate.

Patients were gi'en treatment therapy (.)* +aCl with minophilin -

mg -( drips/min"te, lixotide and 0entoline 1 ho"rly 'ia a neb"ls, Ceftriaxon

injection of 2 g / 1 ho"rs, dexamethason injection 5gr amp/1 ho"rs, f"rosemide

injection amp / 1 ho"r, salb"tamol tablets mg 3 times daily, digoxintablets (,-5

mg 3 times daily, spironolactone tablets -5 mg daily, simarc tablets - mg daily.

D(SC$SS(O)

COPD is characteri6ed by progressi'e blood gas abnormalities. ;ild

hypoxaemia may be present in the early stages of COPD, and it "s"ally

progresses as the disease worsens. &ypercapnia may accompany more se'ere

disease. ntreated hypoxaemia and hypercapnia can ca"se p"lmonary

hypertension and cor p"lmonale, which contrib"te to the morbidity and mortality

associated with this disease. %he str"ct"ral derangements and specific

mechanisms responsible for gas exchange abnormalities in COPD are

exceedingly complex and imperfectly "nderstood. -

COPD is a disease state characteri6ed by airflow limitation that is not

f"lly re'ersible. %he airflow limitation is "s"ally both progressi'e and associated

with an abnormal inflammatory response of the l"ngs to noxio"s particles or

gases.3

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Patients with COPD characteristically complain of the symptoms of

breathlessness on exertion, sometimes accompanied by whee6e and co"gh.

%he co"gh is often, b"t not in'ariably, prod"cti'e. >reathlessness is the

symptom that commonly ca"ses the patient to see medical attention and is

"s"ally the most disabling problem. Patients often date the onset of their illness

to an ac"te exacerbation of co"gh with sp"t"m prod"ction, which lea'es them

with a degree of chronic breathlessness. Close 4"estioning, howe'er, "s"ally

re'eals many years of a Esmoers co"ghF with the prod"ction of small amo"nts

of m"coid sp"t"m B"s"ally G=( m@/day often in the morning for many years.

prod"cti'e co"gh occ"rs in "p to 5(* of cigarette smoers and may precede

the onset of breathlessness. ;any patients may dismiss this as simply being

related to their smoing. %he fre4"ency of noct"rnal co"gh does not seem to be

increased in stable COPD. Paroxysms of co"ghing in the presence of se'ere

airway obstr"ction generate high intrathoracic press"res, which can prod"ce

syncope and Eco"gh fract"resF of the ribs.

P"lmonary f"nction is often dist"rbed d"ring left 'entric"lar fail"re.

d'anced left 'entric"lar fail"re prod"ces mared impairment in p"lmonary

f"nction, whereas early left 'entric"lar fail"re, with its attendant mild p"lmonary

hypertension Be.g., p"lmonary artery wedge press"re HPAP of 25 to -( mm

&g, act"ally impro'es gas exchange thro"gh an increased p"lmonary blood

'ol"me and impro'ed 'entilation!perf"sion B0./J.matching. s left 'entric"lar

f"nction deteriorates and increasing p"lmonary congestion occ"rs, l"ng water

increases. %his ca"ses decreases in l"ng 'ol"me and diff"sion capacity and

increases in airway resistance and 0./J. mismatching. :e'ere fail"re and franal'eolar flooding are often accompanied by a dramatic deterioration in forced

'ital capacity B0C, forced expiratory 'ol"me in 2 second B#02, l"ng

compliance, and gas exchange, as well as a mixed respiratory and metabolic

acidosis. %hese changes can ca"se f"rther heart fail"re, which ca"ses f"rther

p"lmonary dysf"nction, and th"s a 'icio"s circle of fail"re begins. 5

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&eart fail"re is a clinical syndrome in which patients ha'e the following

feat"res?=

2. :ymptoms typical of heart fail"re

Bbreathlessness at rest or on exercise, fatig"e, tiredness, anle swelling-. :igns typical of heart fail"re

Btachycardia, tachypnoea, p"lmonary rales, ple"ral eff"sion, raised j"g"lar

'eno"s press"re, peripheral oedema, hepatomegaly3. Objecti'e e'idence of a str"ct"ral or f"nctional abnormality of the heart at

risBcardiomegaly, third heart so"nd, cardiac m"rm"rs, abnormality on the

echocardiogram, raised natri"retic peptide concentration

ig"re 3. Key feat"res of the clinical history in patients with heart fail"re.

$i'en this differential diagnosis, foc"sed laboratory testing is of 'al"e in

the assessment of a patient with a s"spected c"te #xacerbation COPD.

9ecent data ha'e s"ggested a 'al"able role for the meas"rement of natri"retic

peptides in differentiating congesti'e heart fail"re from non!cardiac disorders in

patients with ac"te breathlessness, incl"ding patients with c"te #xacerbation

COPD. +"mero"s in'estigators ha'e confirmed that this ne"rohormone is

ele'ated in patients with left 'entric"lar dysf"nction and correlates with se'erity

as well as prognosis in C&.8,1

Chronic obstr"cti'e p"lmonary disease BCOPD and heart fail"re BC&

are common conditions. %he pre'alence of COPD ranges from -(* to 3(* in

patients with C&. %he diagnosis of C& can remain "ns"spected in patients

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with COPD, beca"se shortness of breath is attrib"ted to COPD. ;eas"rement

of plasma >!type natri"retic peptide B>+P le'els helps to "nco'er "ns"spected

C& in patients with COPD and clinical deterioration. +onin'asi'e assessment

of cardiac f"nction may be preferable to >+P to "nco'er "ns"spected left

'entric"lar B@0 systolic dysf"nction in patients with stable COPD. Patients with

COPD or C& de'elop seletal m"scle alterations that are striingly similar.

"nctional intolerance correlates with se'erity of seletal m"scle alterations b"t

not with se'erity of p"lmonary or cardiac impairment in COPD and C&,

respecti'ely. Impro'ement of p"lmonary or cardiac f"nction does not translate

into relief of f"nctional intolerance in patients with COPD or C& "nless seletal

m"scle alterations concomitantly regress. %he mechanisms responsible for

seletal m"scle alterations are incompletely "nderstood in COPD and in C&.

Dis"se and low!le'el systemic inflammation leading to protein

synthesis/degradation imbalance are liely to contrib"te. %he presence of

COPD impacts on the treatment of C&, as COPD is still 'iewed as a

contraindication to beta!blocade. %herefore, COPD often depri'es patients with

C& d"e to @0 systolic dysf"nction of the most beneficial pharmacologic

inter'ention. large body of data indicates that patients with COPD tolerate well

selecti'e beta!blocade that sho"ld not be denied to C& patients with

concomitant COPD.),2(

Conclusion

It has been reported in male patients aged 53 years, came to the hospital

with complaints of shortness of breath and early diagnosis of patients with

COPD exacerbations with CPC. Patients in the hospital joint with the cardiology.

rom the chest x!ray shows a pict"re emfisemat"s, diaphragm lies low, and

hiperl"sen pict"re, heart pict"re of the pend"l"m. #C$ showed a pict"re of the

CPC. %he res"lts showed abnormal spirometry obstr"ction and restriction. %he

res"lts showed #chocardiography C&. Patients were gi'en treatment therapy

(.)* +aCl with minophilin - mg -( drips/min"te, lixotide and 0entoline 1

ho"rly 'ia a neb"ls, Ceftriaxon injection of 2 g / 1 ho"rs, dexamethason injection

5gr amp/1 ho"rs, f"rosemide injection amp / 1 ho"r, salb"tamol tablets mg 3

times daily, digoxintablets (,-5 mg 3 times daily, spironolactone tablets -5 mg

7



daily, simarc tablets - mg daily, with stable COPD treatment res"lts and patient

was taen to the cardiac care.

REFERE)CES

2. abbri @eonardo ;, @"ppi abri6io, >eghe >ianca. %he ;"ltiple Components of

COPD. In? L +icola . &anania, mir :harafhaneh, #d. COPD $"de to

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Diagnosis and Clinical ;anagement. &o"ston? >aylor College of ;edicine,

-(22. p. 2(-. +iewoehner Dennis #. :tr"ct"re!f"nction relationships? the pathophysiology of

airflow obstr"ction. In? Chronic Obstr"cti'e P"lmonary Disease. 2st #D p. 5,

12.3. ;acnee Ailliam. Chronic Obstr"cti'e P"lmonary Disease ? #pedemiology,

Physiology, and Clinical #'al"ation. In? Clinical 9espiratory ;edicine. 3rd #d.

Philadelpia? ;osby -((1. p. 5(1.. &ics $eorge &, ;arsha rth"r >. &eart ail"re. In? 9epiratory Disease

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#'al"ation and ;anagement of Chronic &eart ail"re in the d"lt? #xec"ti'e

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Chronic Obstr"cti'e P"lmonary Disease. L of the +ew #ngland Lo"rnal of

;edicine +o'ember -8, -((1. p. -355.). Lelic :anja, & %hierry, Lemtel @e. Diagnostic and %herape"tic Challenges in

Patients Aith coexistent Chronic Obstr"cti'e P"lmonary Disease and Chronic

&eart ail"re. L of the merican College of Cardiology.-((8. p. 28-.

10. :tromberg , ;artensson L, ridl"nd >, @e'in @, Karlsson L#, Dahlstrom

.+"rse!led heart fail"re clinics impro'e s"r'i'al and self!care beha'io"r

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&eart L -((3-?2(272(-3.

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