Cor pulmonale is the term used to describe the alterations in the structure or function of the right ventricle which may be induced by pulmonary hypertension secondary to primary lung disease.
Pathophystology of cor pulmonale
Cor pulmonale may be acute or chronic. Alveolar hypoxia and hypoxaemia, respiratory acidosis and hypercapnoea combine to increase pulmonary vascular resistance. Pulmonary hypertension results in acute or chronic right ventricular pressure overload, right ventricular hypertrophy and eventually signs of right-sided failure.
Acute cor pulmonale caused by pulmonary thromboembolism or heartworm disease is of ten fatal and in most cases may not be diagnosed. Pulmonary thromboembolism can occur as a complication of chronic renal disease (especially glomerulo-nephropathy), hyperadrenocorticism, immune-mediated haemolytic anaemia and pancreatitis.
Chronic cor pulmonale may occur as a sequel to chronic obstructive pulmonary disease. It has been associated with chronic bronchitis, bronchiectasis, pulmonary fibrosis, infiltrative lung disease (for example neoplasia), chronic partial upper airway obstruction due to collapsing trachea, laryngeal paralysis or elongation of the soft palate, and heartworm disease.
Clinical signs of cor pulmonale
Animals with acute cor pulmonale due to pulmonary thrombosis present with severe dyspnoea and are often cyanotic. The mortality rate is high. The clinical signs of chronic cor pulmonale depend on the nature and severity of the underlying respiratory disorder. A chronic cough and / or wheezing is common in dogs with chronic bronchitis, bronchiectasis and collapsing trachea; dogs with chronic partial upper airway obstruction due to an elongated soft palate or laryngeal dysfunction may become progressively dyspnoeic with signs of inspiratory stridor / stertor. Failure to treat the underlying problem may lead to signs of right-sided congestive heart failure.
Pulmonary hypertension and resultant right ventricular hypertrophy may result in tall P waves (right atrial enlargement) and deep Q or S waves in leads I. II. III and aVF (right ventricular enlargement). The mean electrical axis may shift to the right and myocardial hypoxia may result in ST segment depression.
Acute pulmonary thromboembolism results in pulmonary hypoperfusion and lobar hyperlucency. Pulmonary vessels may appear truncated especially towards the periphery. A minimal amount of pleural fluid may be present. Right ventricular enlargement is a feature of chronic cor pulmonale and many animals will show concurrent radiographic changes consistent with chronic lung disease, for example a diffuse bronchial and / or interstitial pattern or bronchiectasis.
Blood gas analysis
Hypoxia (PaO2 <80 mm Hg), hypercapnoea (PaCO2 >40 mm Hg) and acidosis (pH <7.4) reflect the severity of the underlying pulmonary pathology. Chronic hypoxia occasionally results in secondary polycythaemia. Animals with acute pulmonary thromboembolism may become thrombocytopenic and show other laboratory evidence of disseminated intravascular coagulation. Pulmonary hypertension and right ventricular pressure overload result in an increase in central venous pressure.
In addition to the above, diagnostic investigations such as bronchoscopy and tracheal or bronchoalveolar lavage should be performed where appropriate to establish the nature of the underlying respiratory disorder responsible for the cardiac changes.
Cor pulmonale: Treatment
Treatment of the underlying pulmonary condition should be instituted as quickly as possible. Acute pulmonary thromboembolism should be treated with cage rest, oxygen and antithrombotic drugs such as heparin and aspirin. The prognosis is generally poor if signs of right-sided heart failure are present.