Cor Pulmonale

By : Ika Lukita Sari

Mentor : dr. Sumarni Sp.PJ
Definition
• Pulmonary disease with right ventricular hypertrophy
and / or dilatation due to impaired pulmonary function
and / or structure (after removing congenital heart
disease or other primary heart disease in the left
heart)
Clasification

Acute Cor pulmonale

• the most common acute cause is massive pulmonary embolism
and right ventricular dilatation usually occurs.

Chronic Cor pulmonale

• Chronic causes are chronic obstructive disase (COPD) and

right ventricular hypertrophy usually occurs.
Epidemiology
• According to research about 80-90% of cor pulmonale patients
have COPD and 25% of patients with COPD will develop cor
pulmonale.

• Men > woman

• Usually regarding middle to old age ( >45 years old)

• Smoking
Aetiology
Cor pulmonale is a state of cardiopulmonary dysfunction that may
result from several different aetiologies and pathophysiologic
mechanism :

Pulmonary vasoconstriction (secondary to alveolar hypoxia or

blood acidosis)

Anatomic reduction of the pulmonary vascular bed (emphysema,

pulmonary emboli, etc)

Increased blood viscosity 9polycythaemia,sicle-cell disease,etc0

Increased pulmonary blood flow

Major causes of cor
pulmonale
• The causes of cor pulmonale disease include:

1) Lung disease

o COPD

o Cystic fibrosis

o Interstitial lung disease

2) Disorders of the pulmonary circulation

o Pulmonary thromboembolism

o Primary pulmonary hypertension

o Tumor emboli

o Sickle cell anemia

o Schistosomiasis

o Pulmonary veno-occlusive disease

3) Neuromuscular disease

o Amytrophopic lateral sclerosis

o Myasthenia gravis

o Poliomyelitis

o Guillain-Barre syndrome

o Spinal cord lesions

o Bilateral diaphragmatic paralysis

4) Thoracic cage deformities
 Kyphoscoliosis

5) Disordersof ventilatory control

 Primary central hypoventilation

 Sleep apnoe syndromes

Pathomechanism
• Two basic mechanisms that lead to increased pulmonary
vascular resistance are :

(1) hypoxic vasoconstriction of the pulmonary arteries

(2) obstruction and / or obliteration of lung vascular woven.

Clinical Features
 Symptoms
There are, however, symptoms directly attributable to pulmonary
hypertension, including dyspnoe on exertion,fatigue, lethargy,
chest pain, and syncope with exertion.

 Physical findings
 The initial physical finding of pulmonary artery hypertension is
increased intensity of the pulmonic component of the scond
heart sound, may even become palpable. Second heart sound
may also be narrowly split, a change that will not be present if
right ventricular depolarisation is delayed because of concurrent
right bundle branch block.
 Auscultation of the heart may reveal a systolic ejection murmur,
in more severe disease, a diastolic pulmonary regurgitation
murmur.

 Right ventricular hypertrophy is characterised by a prominnt A

wave in the jugular venous pulse, associated with a right-sided
fourth heart sound and either a left parasternal heave or a
downward sub-xiphoid thrust.
 Right ventricular failure leads to systemic venous hypertension.
This can produce a variety findings, such as elevated jugular
venous pressure with a prominent V wave, a right ventricular
third heart sound, and a high-pitched tricuspid regurgitant
murmur.

 Oedema
Supporting investigation
 EKG
 Right axis deviation and R/S ratio greater than 1 in lead V1

 Increased P wave amplitudo in lead II (P pulmonale) due to right

atrial enlargement

 Incomplete or complete right bundle branch block

 In acute cor pulmonale, such as occur with acute pulmonary

embolism, a classic pattern of an S wave in lead I with a Q and
T wave in lead III may be seen
 Thoracic X-ray
 There are abnormalities with enlarged right ventricles, dilated
pulmonary arteries and prominent right atria

 Low and flat diaphragm and larger retrosternal airspace.

 Echocardiography
 The dimensions of the right ventricular space are enlarged,
but the structure and dimensions of the left ventricle are
normal.
  Pulmonary valve, the "a" wave disappears, indicating
pulmonary hypertension.

 Pulmonary valve is difficult to see because of the narrow

"acoustic window" due to lung disease.

 Cardiac catheterization
 There is an increase in right heart pressure and pulmonary
vessel resistance.
Management
• Low concentration oxygen.

• Diuretics

• Digoxin

• Vasodilators (hydralazine, nitrates, nifedipine, verapamil, and

ACE inhibitors)

• Theophylline and sympathomimetic amines (terbutaline)

• Almitrine

• Phlebotomy
• Preventive
 Stopping smoking !

 Gradual and regular exercise and breathing exercises are very

useful even though long-term.
Prognosis
• It varies greatly, depending on the natural course of the
underlying lung disease and the patient's adherence to
treatment. Systemic pulmonary bronchitis is a 5-year average
mortality rate of around 40-50%. Also chronic pulmonary
vascular obstruction with right ventricular hypertrophy has a
poor prognosis. Usually patients with pulmonary hypertension
chronic vascular obstruction only live 2-3 years after the onset of
symptoms.
Thank you