Clinical Science Of Cor-Pulmonale

Definition

Cor- pulmonale, often referred to as pulmonary heart disease , is defined as dilation and hypertrophy
of the right ventricle in response to diseases of the pulmonary vasculature and/or lung parenchyma.

Cor pulmonale adalah pembesaran ventrikel kanan sekunder terhadap penyakit paru, toraks atau
sirkulasi paru. Kadang-kadang disertai dengan gagal ventrikel kanan. Tipe cor pulmonale disebut akut
jika dilatasi belahan jantung kanan setelah embolisasi akut paru, tipe kronis ditentukan lamanya
gangguan pulmoner yang membawa ke pembesaran jantung. Berapa lama dan sampai tahap apa
jantung tetap membesar akan bergantung pada fluktuasi-fluktuasi pada ketinggian tekanan arterial
pulmoner.

Etiology
Cor pulmonale develops in response to acute or chronic changes in the pulmonary vasculature and/or
the lung parenchyma that are sufficient to cause pulmonary hypertension.

Pathophysiology :
Although many conditions can lead to cor pulmonale, the common pathophysiologic mechanism in
each case is pulmonary hypertension that is sufficient to lead to RV dilation, with or without the
development of concomitant RV hypertrophy. The systemic consequences of cor pulmonale relate
to alterations in cardiac output as well as salt and water homeostasis.
Anatomically, the RV is a thin-walled, compliant chamber that is better suited to handle volume
overload than pressure overload. Thus, the sustained pressure overload imposed by pulmonary
hypertension and increased pulmonary vascular resistance eventually causes the RV to fail.
The response of the RV to pulmonary hypertension depends on the acuteness and severity of the
pressure overload. Acute cor-pulmonale occurs after a sudden and severe stimulus (e.g., massive
pulmonary embolus), with RV dilatation and failure but no RV hypertrophy. Chronic cor
pulmonale, however, is associated with a more slowly evolving and progressive pulmonary
hypertension that leads to initial modest RV hypertrophy and subsequent RV dilation.
Decompensation of chronic cor pulmonale can be aggravated by intermittent events that induce
pulmonary vasoconstriction and RV afterload, such as hypoxemia and especially
hypercarbiainduced respiratory acidosis as well as sustained events, including COPD
exacerbations, acute pulmonary emboli, and positive-pressure (mechanical) ventilation. RV failure
also can
be precipitated by alterations in RV volume that occur in various settings, including increased salt and
fluid retention, atrial arrhythmias, polycythemia, sepsis, and a large left-to-right (extracardiac)
shunt.

Clinical manifestation
Dyspnea, the most common symptom, is usually the result of the increased work of breathing
secondary to changes in elastic recoil of the lung (fibrosinglung diseases), altered respiratory
mechanics (e.g., overinflation with COPD), or inefficient ventilation (e.g., primary pulmonary
vascular disease). Orthopnea and paroxysmal nocturnal dyspnea are rarely symptoms of isolated
right HF and usually point toward concurrent left heart dysfunction. Rarely, these symptoms reflect
increased work of breathing in the supine position resulting from compromised diaphragmatic
excursion. Tussive or effort-related syncope may occur because of the inability of the RV to deliver
blood adequately to the left side of the heart. Abdominal pain and ascites that occur with cor
pulmonale are similar to the right-heart failure that ensues in chronic HF. Lower-extremity edema
may occur secondary to neurohormonal activation, elevated RV filling pressures, or increased
levels of carbon dioxide and hypoxemia, which can lead to peripheral vasodilation and edema
formation.

Many of the signs encountered in cor pulmonale are also present in HF patients with a depressed EF,
including tachypnea, elevated jugular venous pressures, hepatomegaly, and lower-extremity
edema.
Patients may have prominent v waves in the jugular venous pulse as a result of tricuspid regurgitation.
Other cardiovascular signs include an RV heave palpable along the left sternal border or in the
epigastrium. The increase in intensity of the holosystolic murmur of tricuspid regurgitation with
inspiration (“Carvallo᾽s sign”) may be lost eventually as RV failure worsens. Cyanosis is a late
finding in cor pulmonale and is secondary to a low cardiac output with systemic vasoconstriction and
ventilation-perfusion mismatches in the lung.

Diagnosis.

Testing will also include :

 CT scans, which take images of parts of the body

 an echocardiogram, which uses sound waves to produce images of your heart
 chest X-rays, which takes images of various parts of your body
 a lung scan, which is used to detect blood clots
 lung function tests, which determine how well your lungs work
 right heart catheterization

Treatment

The primary treatment goal of cor pulmonale is to target the underlying pulmonary disease, since this
will decrease pulmonary vascular resistance and lessen RV afterload. Most pulmonary diseases that
lead to chronic cor pulmonale are advanced and therefore are less amenable to treatment. General
principles of treatment include decreasing work of breathing by using noninvasive mechanical
ventilation and bronchodilation, as well as treating any underlying infection. Adequate oxygenation
(oxygen saturation ≥90–92%) and correcting respiratory acidosis are vital for decreasing pulmonary
vascular resistance and reducing demands on the RV. Patients should be transfused if they are
anemic, and phlebotomy may be considered in extreme cases of polycythemia.

Diuretics are effective in RV failure, and indications are similar to those for chronic HF. One caveat
of chronic diuretic use is to avoid inducing contraction alkalosis and worsening hypercapnia.
Digoxin is of uncertain benefit in the treatment of cor pulmonale and may lead to arrhythmias
in the setting of tissue hypoxemia and acidosis. Therefore, if digoxin is administered, it should be
given at low doses and monitored carefully. Pulmonary vasodilators can effectively improve
symptoms through modest reduction of pulmonary pressures and RV afterload when isolated
pulmonary arterial hypertension is present.Vasodilators are unproven in cases of pulmonary
hypertension and cor pulmonale due to parenchymal lung diseases or hypoventilation syndromes.