CASE REPORT

Acute COPD Exacerbation with Congestive Heart Failure

Riski Dohartua, Amira Permatasari T
Division of COPD
Department of Pulmonology and Respiratory Medicine
School of Medicine Universitas Sumatera Utara, Adam Malik General
Hospital
Medan

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.
From the chest x-ray shows a picture emfisematus, diaphragm lies low, and
hiperlusen picture, heart picture of the pendulum. ECG showed a picture of the
CPC. The results showed abnormal spirometry obstruction and restriction. The
results showed Echocardiography CHF. Patients were given treatment therapy
0.9% NaCl with Aminophilin 24 mg 20 drips/minute, Flixotide and Ventoline 8
hourly via a nebuls, Ceftriaxon injection of 1 g / 8 hours, dexamethason injection
5gr amp/8 hours, furosemide injection amp / 8 hour, salbutamol tablets 4 mg 3
times daily, digoxintablets 0,25 mg 3 times daily, spironolactone tablets 25 mg
daily, simarc tablets 2 mg daily, with stable COPD treatment results and patient
was taken to the cardiac care.
Key Words : COPD, CHF.

INTRODUCTION
CHF and COPD are two commonly encountered conditions in clinical
practice. CHF accounts for their frequent coexistence. The prevalence of COPD

ranges from 20% to 32% in patients with. FEV1 is as good a predictor of

cardiovascular mortality as serum cholesterol Ischemic heart disease, and not
respiratory failure, is the leading cause of death in COPD patients, with only a
small fraction dying of respiratory failure. The relationship between COPD and
cardiovascular events remains unclear. Patients with COPD are not at
increased risk for hypertension or left ventricular hypertrophy; however, they
consistently show evidence of low-grade systemic inflammation that plays an
increasingly recognized role in the pathogenesis of atherosclerosis. Patients
with severe COPD are 2.182.74 times more likely to have elevated or highly
elevated circulating CRP levels than control subjects. A working hypothesisto
account for the high prevalence of systolic dysfunction in patients with COPD is
that low-grade systemic inflammation accelerates the progression of coronary
atherosclerosis, which ultimately results in ischemic cardiomyopathy. Such a
hypothesis fits the clinical observation of a high incidence of left ventricular wall
motion abnormalities noted in patients with COPD and left ventricular
dysfunction.1
CASE REPORT
Patients admitted to Adam Malik Hospita with main complain of
shortness of breath since + / - 6 years ago, and become worse in 3 day. Chest
pain happened since 3 years ago and become worse if patient have cough, like
a punctured-prick pain. Cough has occured since 1 months with yellowish.
Swellingon the both of legs happened since 1 week ago.
Vital signs showed alert, BP : 120/90 mmHg, Pulse : 81 times/minute,
Respiratory rate : 36 times/minute, Temperature : 36.3 0C.
Physical examination showed inspection simetrical chest inspection,
tactil fremitus was decreased on both of the lung. Percussion was hypersonor
on both of the lung. Vesicular decreased breath sound on both of the lung. First
and second heart sound irregular, mid-diastolic murmur grade 2 / 6 at the apex,
gallops not found.

Laboratory findings : Hb : 15,3 g/dl, WBC : 11,8 x 10 9 /L, platelet :186

103/mm2, Arterial blood gases : pH : 7.49, PaO2 : 140 mmHg, PaCO2 : 31
mmHg, BE : 1,0, HCo3 : 25,4 mmol/L, SaO2 : 99%, interpretation : respiratory
alcalosis.

Chest x ray showed emphysematous on both of the lung, diapraghm

was flattein, tracheal in the midle position. CTR 53 %,(fig.1). From the ECG
showed AF RVR + RAD + RVH. Echocardiography showed Stenosis Mitral ec
Pulmonary Hypertension (Fig. 2). Spirometry showed obstructive and restrictive
abnormalities.

Figure 1. Thorax PA, 14th September 2011 Adam Malik Hospital

Figure 2. Echocardiography, 24th September 2011 Adam Malik Hospital

Early diagnosis of this patient COPD with CPC, was 24 th September 2011
the working diagnosis was COPD with CHF Fc I-II ec Stenosis Mitral moderate.
Patients were given treatment therapy 0.9% NaCl with Aminophilin 24
mg 20 drips/minute, Flixotide and Ventoline 8 hourly via a nebuls, Ceftriaxon
injection of 1 g / 8 hours, dexamethason injection 5gr amp/8 hours, furosemide
injection amp / 8 hour, salbutamol tablets 4 mg 3 times daily, digoxintablets 0,25
mg 3 times daily, spironolactone tablets 25 mg daily, simarc tablets 2 mg daily.
DISCUSSION

COPD is characterized by progressive blood gas abnormalities. Mild

hypoxaemia may be present in the early stages of COPD, and it usually
progresses as the disease worsens. Hypercapnia may accompany more severe
disease. Untreated hypoxaemia and hypercapnia can cause pulmonary
hypertension and cor pulmonale, which contribute to the morbidity and mortality
associated with this disease. The structural derangements and specific
mechanisms responsible for gas exchange abnormalities in COPD are
exceedingly complex and imperfectly understood.

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

fully reversible. The airflow limitation is usually both progressive and associated
with an abnormal inflammatory response of the lungs to noxious particles or
gases.3

Patients with COPD characteristically complain of the symptoms of

breathlessness on exertion, sometimes accompanied by wheeze and cough.
The cough is often, but not invariably, productive. Breathlessness is the
symptom that commonly causes the patient to seek medical attention and is
usually the most disabling problem. Patients often date the onset of their illness
to an acute exacerbation of cough with sputum production, which leaves them
with a degree of chronic breathlessness. Close questioning, however, usually
reveals many years of a smokers cough with the production of small amounts
of mucoid sputum (usually <60 mL/day) often in the morning for many years. A
productive cough occurs in up to 50% of cigarette smokers and may precede
the onset of breathlessness. Many patients may dismiss this as simply being
related to their smoking. The frequency of nocturnal cough does not seem to be
increased in stable COPD. Paroxysms of coughing in the presence of severe
airway obstruction generate high intrathoracic pressures, which can produce
syncope and cough fractures of the ribs. 4
Pulmonary function is often disturbed during left ventricular failure.
Advanced left ventricular failure produces marked impairment in pulmonary
function, whereas early left ventricular failure, with its attendant mild pulmonary
hypertension (e.g., pulmonary artery wedge pressure [PAWP] of 15 to 20 mm
Hg), actually improves gas exchange through an increased pulmonary blood
volume and improved ventilation-perfusion (V./Q.)matching. As left ventricular
function deteriorates and increasing pulmonary congestion occurs, lung water
increases. This causes decreases in lung volume and diffusion capacity and
increases in airway resistance and V./Q. mismatching. Severe failure and frank
alveolar flooding are often accompanied by a dramatic deterioration in forced
vital capacity (FVC), forced expiratory volume in 1 second (FEV1), lung
compliance, and gas exchange, as well as a mixed respiratory and metabolic
acidosis. These changes can cause further heart failure, which causes further
pulmonary dysfunction, and thus a vicious circle of failure begins.

Heart failure is a clinical syndrome in which patients have the following

features:6
1. Symptoms typical of heart failure
(breathlessness at rest or on exercise, fatigue, tiredness, ankle swelling)
2. Signs typical of heart failure
(tachycardia, tachypnoea, pulmonary rales, pleural effusion, raised jugular
venous pressure, peripheral oedema, hepatomegaly)
3. Objective evidence of a structural or functional abnormality of the heart at
risk
(cardiomegaly, third heart sound, cardiac

murmurs, abnormality on the

echocardiogram, raised natriuretic peptide concentration)

Figure 3. Key features of the clinical history in patients with heart failure.

Given this differential diagnosis, focused laboratory testing is of value in

the assessment of a patient with a suspected Acute Exacerbation COPD.
Recent data have suggested a valuable role for the measurement of natriuretic
peptides in differentiating congestive heart failure from non-cardiac disorders in
patients with acute breathlessness, including patients with Acute Exacerbation
COPD. Numerous investigators have confirmed that this neurohormone is
elevated in patients with left ventricular dysfunction and correlates with severity
as well as prognosis in CHF.7,8
Chronic obstructive pulmonary disease (COPD) and heart failure (CHF)
are common conditions. The prevalence of COPD ranges from 20% to 30% in
patients with CHF. The diagnosis of CHF can remain unsuspected in patients
6

with COPD, because shortness of breath is attributed to COPD. Measurement

of plasma B-type natriuretic peptide (BNP) levels helps to uncover unsuspected
CHF in patients with COPD and clinical deterioration. Noninvasive assessment
of cardiac function may be preferable to BNP to uncover unsuspected left
ventricular (LV) systolic dysfunction in patients with stable COPD. Patients with
COPD or CHF develop skeletal muscle alterations that are strikingly similar.
Functional intolerance correlates with severity of skeletal muscle alterations but
not with severity of pulmonary or cardiac impairment in COPD and CHF,
respectively. Improvement of pulmonary or cardiac function does not translate
into relief of functional intolerance in patients with COPD or CHF unless skeletal
muscle alterations concomitantly regress. The mechanisms responsible for
skeletal muscle alterations are incompletely understood in COPD and in CHF.
Disuse

and

low-level

systemic

inflammation

leading

to

protein

synthesis/degradation imbalance are likely to contribute. The presence of

COPD impacts on the treatment of CHF, as COPD is still viewed as a
contraindication to beta-blockade. Therefore, COPD often deprives patients with
CHF due to LV systolic dysfunction of the most beneficial pharmacologic
intervention. A large body of data indicates that patients with COPD tolerate well
selective beta-blockade that should not be denied to CHF patients with
concomitant COPD.9,10
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.
From the chest x-ray shows a picture emfisematus, diaphragm lies low, and
hiperlusen picture, heart picture of the pendulum. ECG showed a picture of the
CPC. The results showed abnormal spirometry obstruction and restriction. The
results showed Echocardiography CHF. Patients were given treatment therapy
0.9% NaCl with Aminophilin 24 mg 20 drips/minute, Flixotide and Ventoline 8
hourly via a nebuls, Ceftriaxon injection of 1 g / 8 hours, dexamethason injection
5gr amp/8 hours, furosemide injection amp / 8 hour, salbutamol tablets 4 mg 3
times daily, digoxintablets 0,25 mg 3 times daily, spironolactone tablets 25 mg
7

daily, simarc tablets 2 mg daily, with stable COPD treatment results and patient
was taken to the cardiac care.

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