Cor pulmonale
Amalkumar Bhattacharya
Abstract
Cor pulmonale is defined as enlargement of the right ventricle secondary to abnormality of the lung, thorax, pulmonary vasculature,
or circulation. This leads to right ventricular failure, with elevation of transmural right ventriclular end-diastolic pressure. It may
be acute, e.g., in pulmonary thromboembolism; or chronic, as in stable severe chronic obstructive pulmonary disease (COPD); or
acute-on-chronic as in COPD with superimposed infection and intensification of hypoxia.
20% of hospital admissions of heart failure are due to right heart failure associated with cor pulmonale. This is high where COPD
incidence is high.
Key words : COPD, Cor pulmonale, Right heart failure.
Aetiology
Cor pulmonale is a state of cardiopulmonary dysfunction
that may result from several different aetiologies and
pathophysiologic mechanisms (table I):
* Associate Professor, Department of Medicine, Government Medical College, Surat - 395 001, Gujarat.
Prognosis
Development of cor pulmonale associated with
pulmonary hypertension often has important prognostic
implications. In COPD, for example, the development of
pulmonary hypertension and peripheral oedema heralds
a poor prognosis. Patients who develop peripheral
oedema have a five year survival of only approximately
30 percent, and those whose pulmonary vascular
resistance exceeds 550 dynes-sec/cm5 rarely survive for
more than 3 years1,2.
However, rather than having a substantial direct effect on
mortality, the development of cor pulmonale in COPD may
just reflect the severity of the underlying obstructive
disease and its effect on mortality. Even in severe COPD,
for example, it is uncommon to observe mean pulmonary
artery pressures above 40 mmHg; such levels are far below
those found in many patients with primary pulmonary
hypertension or chronic unresolved pulmonary emboli.
Clinical characteristics
Clinical detection and assessment of cor pulmonale are
difficult due to the subtle and often non-specific signs and
symptoms. The development of peripheral oedema in
COPD is not necessarily a reliable marker of pulmonary
hypertension.
Symptoms : There are, however, symptoms directly
attributable to pulmonary hypertension, including
dyspnoea on exertion, fatigue, lethargy, chest pain, and
syncope with exertion.
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Evaluation
Because of the non-specificity of symptoms and signs,
ancillary evaluation may be useful, including the following
techniques4:
Chest radiography
Electrocardiography
Radionuclide ventriculography
Lung biopsy
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Fig. 2 : Right ventricular hypertrophy : Right ventricular hypertrophy due, in this case, to primary pulmonary hypertension. The characteristic
features include marked right axis deviation (+210 which is equal to 150), tall R wave in V1 (as part of a qR complex), delayed precordial
transition zone with prominent S waves in leads V5 and V6, inverted T waves and ST depression in V1 to V3 consistent with right ventricular
strain, and peaked P waves in lead II consistent with concomitant right atrial enlargement.
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Doppler echocardiography: It is the most reliable noninvasive estimation of the pulmonary artery pressure. This
technique takes advantage of the functional tricuspid
insufficiency usually present in PAH. The maximum
tricuspid regurgitant jet velocity is recorded, and the
pulmonary artery pressure (PAP) is then calculated by the
modified Bernoulli equation :
PAP systolic = (4 x tricuspid jet velocity squared) + RAP
where RAP is the right atrial pressure estimated from the
size and respiratory variation of flow in the inferior vena
cava. Other findings associated with pulmonary
hypertension are pulmonic insufficiency and mid-systolic
closure of the pulmonic valve.
The efficacy of Doppler echocardiography may be limited
by the ability to identify an adequate tricuspid regurgitant
jet. It may also be less sensitive because of alterations
induced by the underlying disease. For example, acoustic
windows in patients with COPD may be limited by the
increased antero-posterior diameter of the chest.
Despite these potential problems, Doppler estimation
using tricuspid regurgitation is far more sensitive than the
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Fig. 4 : Atrial enlargement : P wave morphology with atrial enlargement in leads I, II, and VI. The P waves in left atrial enlargement
(left panel) are wide (> 0.12 sec) and notched in leads I and II and the terminal segment has a negative deflection that is deep and
delayed in VI. In right atrial enlargement (middle panel), the P wave amplitude is increased (0.28 mV) in lead II. Bi-atrial enlargement
(right panel) has characteristics of both atrial abnormalities: the P wave amplitude (0.22 mV) and duration (0.12 sec) are increased
in lead II and there is deep terminal negativity in VI.
Treatment
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Fig. 5 (Echocardiography 4) : Tricuspid regurgitation : Subcostal view from a 2D echocardiograms with colour flow
doppler shows retrograde flow into dilated hepatic veins as a
result of severe tricuspid regurgitation.
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References
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