Cor Pulmonale - doc meg`s hideout

Cor Pulmonale
Dr. Meg-angela Christi Amores
• Cor Pulmonale
– pulmonary heart disease
– dilation and hypertrophy of the right ventricle (RV)
in response to diseases of the pulmonary
vasculature and/or lung parenchyma.
– excluded congenital heart disease and those
diseases in which the right heart fails secondary to
dysfunction of the left side of the heart
Etiology and Epidemiology
• develops in response to acute or chronic
changes in the pulmonary vasculature
• Changes that are sufficient to cause
pulmonary hypertension
• Once patients with chronic pulmonary or
pulmonary vascular disease develop cor
pulmonale, their prognosis worsens
• pulmonary hypertension that is sufficient to
lead to RV dilation, with or without the
development of concomitant RV hypertrophy
• Right ventricle: thin walled, compliant
– Better suited for high volumes than high pressure
• Sustained pressure overload (pulm HPN) and
increased vascular resistance causes RV to fail
• Acute Cor Pulmonale
– occurs after a sudden and severe stimulus with RV
dilatation and failure but no RV hypertrophy
• e.g massive pulmonary embolus
• Chronic Cor pulmonale
– more slowly evolving and slowly progressive
pulmonary hypertension that leads to RV dilation
and hypertrophy
Factors that determine severity
• hypoxia secondary to alterations in gas
• Hypercapnia
• Acidosis
• alterations in RV volume overload that are
affected by:
• exercise, heart rate, polycythemia, or increased salt and
retention because of a fall in cardiac output
Clinical presentation
• Symptoms:
– Dyspnea, the most common symptom
– usually the result of the increased work of breathing
secondary to changes in elastic recoil of the lung (fibrosing
lung diseases) or altered respiratory mechanics
– Orthopnea and paroxysmal nocturnal dyspnea are
rarely symptoms of isolated right HF
– reflect the increased work of breathing in the supine position
that results from compromised excursion of the diaphragm
Clinical presentation
• Symptoms:
– Tussive or effort-related syncope
– because of the inability of the RV to deliver blood adequately
to the left side of the heart
– Abdominal pain and ascites
– Due to right heart failure
– Lower extremity edema
– secondary to neurohormonal activation, elevated RV filling
pressures, or increased levels of carbon dioxide and hypoxia,
Clinical presentation
• Signs
– tachypnea
– elevated jugular venous pressures
– hepatomegaly
– lower-extremity edema
– Cyanosis is a late finding
– P pulmonale, right axis deviation, and RV
• Chest X Ray
– enlargement of the main pulmonary artery, hilar
vessels, and the descending right pulmonary
• Spiral CT
– acute thromboembolic disease
• 2D echo
– measuring RV thickness and chamber dimensions
• Doppler echocardiography
– assess pulmonary artery pressures
– assessing RV structure and function, particularly in
patients who are difficult to image with 2-D
echocardiography because of severe lung disease
• Primary goal: target the underlying pulmonary
• decrease in pulmonary vascular resistance and relieve the
pressure overload on the RV
• General principles:
• decreasing the work of breathing using noninvasive
mechanical ventilation, bronchodilation, and steroids
• treating any underlying infection
– Adequate oxygenation (oxygen saturation 90–92%)
will also decrease pulmonary vascular resistance and
reduce the demands on the RV
– Diuretics
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