Cor Pulmonale and Pulmonary hypertension

The four primary mechanisms which result in cor pulmonale are related to an increase in pulmonary vascular resistance and right ventricular workload:

Hypoventilation (V/Q mismatch leading to hypercapnia, decreased PAO2 and hypoxemia). Destruction of alveolar-capillary units. Hypoxemia. Polycythemia (increased hematocrit).

treatment of Cor pulmonale

Oxygen therapy. Diuretics. Xanthenes. Phlebotomy. - Oxygen therapy - either with nocturnal use via cannula or CPAP, or continuous O2 therapy significantly reduces the pulmonary vascular resistance. The goal is to maintain a PaO2 greater than approximately 60 mmHg, above which hypoxic vasoconstriction is largely eliminated. - Diuretics - reduce the total blood volume (by means of reducing water volume in the blood). - Xanthenes - improve cardiac output, mostly by increasing HR. - Phlebotomy - reduces total blood volume and viscosity

Pulmonary hypertension may be caused by a myriad of underlying factors including

Pulmonary arteriole constriction - aka hypoxic pulmonary vasoconstriction (alveolar hypoxia, enhanced by acidosis). Thickening of the arterial walls (inflammation). Loss of pulmonary capillary bed (destruction of alveolar walls ~ emphysema). Compression of pulmonary capillary bed by hyperinflated alveoli. Occlusion of the pulmonary artery by a thrombus or other obstruction. Unknown ("idiopathic") / genetic ("familial") cause. Pulmonary hypertension merely refers to the elevation of pulmonary vascular pressure. This elevation may be acute or chronic, depending on the underlying cause. Regardless of the cause, right ventricular hypertrophy will result. Cor pulmonale is a potential complication associated with Chronic Obstructive Pulmonary Disease as a result of pulmonary arterial hypertension.

right ventricular hypertrophy

The right ventricular hypertrophy is a normal muscle response to work. Recall the Frank-Starling Law related to ventricular function. As the ventricle is filled more (stretched) it will pump harder (contract). But when the ventricle (pump) is overfilled (over-stretched) it cannot contract well (failure). As a result, the right atrial pressures and central venous pressures increase as blood "backs up" into the venous circulation. This chain of retrograde pressure changes is revealed in the clinical signs and symptoms.

pathway to cor pulmonale

alveolar hypoxia. Hypoxic pulmonary vasoconstriction. (hypoxemia, acidemia). Increased pulmonary vascular resistance. (capillary destruction; emphysema). Pulmonary hypertension. (polycythemia). Increased RV after load. Right ventricular hypertrophy. (Cor pulmonale) Right ventricular failure. (cor pulmonale)

Pulmonary arterial hypertension

an increased pulmonary artery pressure (mean pulmonary arterial pressure > 25 mmHg) which results in an increased pulmonary vascular resistance and right ventricular afterload.

clinical signs of cor pulmonale

cyanosis. loud second heart sounds. right axis shift on EKG. JVD, Peripheral edema and hepatomegaly. - Cyanosis is a common presentation, since the patient has reduced pulmonary blood flow and polycythemia. - The closing of the pulmonic valve against the increased pressure causes a loud second heart sound (P2) <boom-BOOM> and may actually be palpated as a left parasternal lift (ventricular heave) as the chest wall moves with this action. - Right ventricular hypertrophy will cause a right axis shift on EKG. - Because of the retrograde pressure changes in venous circulation, jugular venous distension, peripheral edema and hepatomegaly (venous congestion) are often observed.

Cor pulmonale

defined as hypertrophy of the right ventricle secondary to abnormal lung structure and/or function, which results in right ventricular dilation and failure.