Tuesday, August 5, 2014

Pulmonary Circulation

Pulmonary Circulation-

-Cor Pulmonale-


-Cor Pulmonale is the impaired function of the right side ventricle that comes from pulmonary hypertension and is associated with lung disease, vascular problems such as pulmonary artery hypertension, upper airway problems (obstructive sleep apnea), or chest wall impingement (kyphoscoliosis)

-Cor Pulmonale is mostly a complication of pulmonary hypertension

-Cor Pulmonale usually presents as  a slow insidious process.  It can also be acute though. 

-Common presenting symptoms of Cor Pulmonale include:  dyspnea on exertion, lethargy, exertional syncope, or exertional chest pain

-Anorexia can also come from RUQ pain secondary to passive congestion of the liver and bowel due to right ventricular dysfunction

-Common physical findings include:  increased intensity of the second heart sound, a narrowly split S2, a holosystolic murmur, and a diastolic pulmonary regurgitation murmur

-Right ventricle will become hypertrophied.  Will see elevated central venous pressure and elevated and may see jugular venous distention on both sides

-Patients with end stage cor pulmonale may develop signs of cardiogenic shock, hypotension, tachycardia, oliguria, and cool extremities.  Pulmonary edema is also a late stage finding

-Chest x ray usually demonstrates enlargement of central pulmonary arteries and may show loss of retrosternal space due to right ventricular hypertrophy

-EKG usually shows a right bundle branch block and right axis deviation.  

-ECHO usually shows an enlarged right ventricle 

-Right heart catheterization is the gold standard for diagnosis or cor pulmonale.  Findings will show right ventricular dysfunction, evidence of pulmonary artery hypertension, and no evidence of left heart disease

-Treatment of Cor Pulmonale is targeted at reduction of right ventricle afterload (reduction of pulmonary artery pressure), decrease of right ventricular pressure, and improvement of right ventricular contractility

-Right ventricular afterload can be helped by administering oxygen.  Treatment of pulmonary hypertension itself dose help right ventricular afterload

-Right ventricular pressure may be reduced by diuretic therapy

-Improvement of right ventricular contractility may be helped by dobutamine and milrinone.  Inhaled nitrous oxide may help also.  Oral digoxin should be avoided and can make worse


-Pulmonary Embolism-


-Pulmonary embolism refers to an obstruction of the pulmonary artery or one of its branches by material.

-The material causing the obstruction may be a thrombus, air, or fat that came from somewhere else in the body

-Pulmonary emboli can be classified by massive or submassive.

-Massive pulmonary emboli cause hypotension (SBP less than 90 mm Hg or a drop in SBP by 40 mm Hg in 15 minutes).  This is classified as a catastrophic entity that can result in right ventricular failure and then death

-All other pulmonary emboli that do not meet this definition are classified as submassive

-Saddle pulmonary emboli occur at the bifurcation of the main pulmonary artery into the right and left pulmonary arteries

-Most of the  pulmonary emboli arise from the deep venous system of the lower extremities (approximately 80 percent)

-The remainder of pulmonary emboli arise from the upper extremities and pelvic veins (about 1 percent arise from the pelvic veins)

-Virchow's Triad describes the pathogenesis of thromboembolism
1.  Alterations of blood flow
2.  Vascular Endothelial Injury
3.  Alterations in the constituents of blood (inherited or acquired hypercoagulable states)

-Risk factors include:  more than 48 hours of immobilization in the last month, hospital admission in the last 3 months, surgery in the last 3 months, malignancy in the last 3 months, infection in the last 3 months, current hospitalization, trauma, recent major surgery, central venous catheter, immobilization, pregnancy, use of oral contraception, anti-phospholipid syndrome

-Other medical conditions predisposing to venous thromboembolism include:  Factor V Leiden, Prothrombin Mutation gene, Protein C and S deficiency, Anti-Thrombin III deficiency, and Dysfibrinogenemia

-Additional risk factors include obesity, HTN, and heavy cigarette smoking

-Signs and symptoms of pulmonary emboli include:  dyspnea at rest or with exertion, pleuritic pain, cough, orthopnea, tachypnea, jugular venous distention, S3 gallop, and tachycardia

-Diagnosis is made by CTA of Chest or Ventilation Perfusion (V/Q) scan of the lungs

-Anti-coagulation is the mainstay of treatment with pulmonary emboli.  Can also be treated with embolectomy.  Insertion of inferior vena cava filter can help from recurrent DVT migrating to the lungs but not 100 percent.

-If patient is hemodynamically unstable, thrombolytic therapy should be instituted

-Compared to IV unfractionated heparin, low molecular weight heparin has lower mortality and fewer recurrent thromboembolic events, and less bleeding

-Subcutaneous unfractionated heparin and low molecular weight heparin have similar effects on mortality and morbidity

-IV unfractionated heparin is the only anticoagulant that has been compared in clinical trials to no treatment.  The majority of the data show either equivalent or slightly superior efficacy of low molecular weight heparin

-IV heparin is still the preferred agent when there is persistent hypotension, increased risk of bleeding, and thrombolysis is being considered.

-The antidote for heparin is protamine sulfate

-Once the PTT is greater than 55 seconds, oral anticoagulation such as warfarin can be introduced.  The goal INR is 2-3.

-Pregnant patients will need to be on lovenox as opposed to warfarin because of warfarin crossing the placental barrier

-Treatment for 3-6 months is recommended for the first episode of PE when there is a reversible risk factor

-The second pulmonary embolus should have lifelong anticoagulation


-Pulmonary Hypertension-


-Pulmonary hypertension is defined as a mean arterial pulmonary pressure over 25 mm Hg.

-Normal pulmonary artery systolic pressure is 15-30 mm Hg, and normal pulmonary artery diastolic pressure is 4-12 mm Hg.

-The pathogenesis of pulmonary hypertension is multifactorial.  Largely a proliferative vasculopathy of the small muscular pulmonary arterioles

-Pulmonary hypertension can present with exertional dyspnea, atypical chest pain, and unexplained syncope.  Non specific symptoms such as exertional dyspnea and fatigue can manifest itself.  Peripheral edema may be present.

-If a patient is suspected of pulmonary hypertension, right heart catheterization which is the gold standard for diagnosis should be performed

-ECHO often times will provide evidence suggestive of pulmonary hypertension.  If left heart disease is present, it may be sufficient enough to explain pulmonary hypertension.

-Patient should also have pulmonary function tests, overnight pulse oximetry, VQ scan, ANA, HIV serology, and LFT's to exclude other pathology of symptoms

-For patients with idiopathic pulmonary hypertension additional genetic and catheterization criteria need to be performed to exclude other causes of heart failure such as left heart disease, lung disease, or thromboembolic disease

-Patients should undergo an invasive hemodynamic assessment prior to the initiation of advanced therapy.  Vasoreactivity test should be performed as part of their work up.

-Patients with a positive vasoreactivity test should be given a trial of oral calcium channel blocker therapy.

-If negative vasoactive response, means patient has class II-IV pulmonary hypertension.  Need to institute prostanoids such s prostacyclin, treprostinil.  Endothelial receptor antagonists are another option.

-If refractory to above or there is deterioration need to consider combination therapy.

-If that fails, need to consider atrial septostomy or lung transplant



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