A full 3^rd of PE deaths will occur in the first hour & 66% of these patients will not be suspected of PE at the time of death. Because survival from PE is dependent on rapid recognition & treatment, we must learn to identify this cardiovascular disorder quickly. 

A pulmonary emboli occurs when a thrombus in the venous system breaks loose and moves into the Right Atrium then to the Right Ventricle and finally into the pulmonary arteries. The emboli will lodge in the pulmonary arterial system once it hits a vessel that is too small to allow it past.  

Usually the PE lodges in the lower lobes and more often in the right than the left due to the increased blood flow in these parts of the lung. Most PE are harmless because of the collateral blood flow between the pulmonary and bronchial circulations. Only 10% of the emboli cause problems. In a way the pulmonary capillary bed acts as a filtration system for the systemic blood flow.

RISK FACTORS  

Persons at increased risk of a PE include immobile patients. Elderly persons who get placed into traction for pelvic fractures are at extremely high risk of a PE due to stasis of blood.  The severe neuromuscular patient who is bedridden is also at risk because there is no skeletal muscle activity in the lower limbs to keep venous blood moving along.  

The presence of deep vein thrombosis [DVT] displayed by pain and swelling in the lower legs unfortunately only shows up in 30% of the cases. 

Someone who has been in atrial fibrillation for a prolonged period of time can have clots forming in the right atrium that can break loose & move into the pulmonary artery system if the atrial fibrillation was to be halted by cardioversion. 

Persons who smoke cigarettes or take cocaine suffer widespread vasoconstriction which puts them at increased risk of thrombus formation as well as hypertension. Women who both smoke and take birth control are at increased risk for clotting.

Pulmonary embolism is a rare complication of pregnancy.  

Pregnant women have increased coagulation of the blood to get ready for safe delivery. Pregnant women are subject to thrombus formation because the enlarged uterus impedes blood flow from the lower extremities. Both of these can increase incidence of PE during pregnancy and labor.  

Persons with polycythemia can have slow blood flow that clots more easily—especially if these people get dehydrated 

Trauma patients can get fat emboli.

An air emboli can complicate sudden decompression [scuba diving or HBO] sickness.

PATHOPHYSIOLOGY 

The damage from a PE is size-dependent.  All of the lung tissue downstream from the PE will have decreased perfusion, so that infarction and tissue death results. The larger the clot, obviously, the more infarction and tissue damage will result. If the PE is large enough to block a massive amount of the lung, the patient dies from circulatory collapse rather than hypoxemia. 

Multiple clots can break loose and move into multiple smaller vessels in the lung. 

The portion of the lung that suffers decreased perfusion will suffer necrotic infarction if the blood flow is not reestablished quickly. 

There is an increased V/Q as the alveoli in the affected area fail to get the perfusion they needed. These alveoli are now Vd [ventilation without perfusion], so there is increased Vd ventilation. 

There is a release of inflammatory chemicals [serotonin and histamine] which causes bronchospasm; there are increased RBC's in the alveolar spaces and destruction of the alveolar wall. In areas blocked by the PE, the affected area loses surfactant. 

Once there is 50% blockage of the pulmonary bed, we see increased blood pressure upstream from the obstruction which puts additional work on the right side of the heart. RV and RA pressures can rise. Once the mean pulmonary bed pressure exceeds 40 mmHg, there is RV failure.

As the pulmonary pressure rises, the J-receptors trigger several effects such as a feeling of dyspnea and rapid, shallow breathing. At the same time the patient’s glottis closes a bit during exhalation—an effort to create PEEP? 

If there is enough blockage through the pulmonary bed, the downstream blood flow decreases, so that there is less blood returning to the left side of the heart, the stroke volume of the LV decreases -- CO decreases.

S/S

·          On interview, the patient will c/o sudden onset of dyspnea, and a feeling of anxiety. He may c/o pleuritic pain and even faint.

·          On inspection, you will note rapid, shallow breathing

·          On palpation, there might be a fever

·          On auscultation of the chest you might hear crackles, rarely wheezing. On auscultation of the heart you may hear a loud second heart sound [P2] 

·          He may have a dry cough, but 13% will have bloody sputum. 

X-ray:

·          The chest film may show an opacity that is wedge-shaped with the narrow part of the wedge facing the central airways. The opacity will move all the way to the pleura.

·          There could be a small pleural effusion, and sometimes cardiomegaly. Sometimes the right descending pulmonary artery might be enlarged.

·          Sometimes we see nothing on the chest film 

The V/Q scan: high V/Q

 Nuclear Medicine VQ Scan 

In the normal patient when we administer a radioactive xenon gas by inhalation, then via an IV we add another contrast into the bloodstream [tagged albumin], in the normal lung we see areas of ventilation paired with perfusion.  

In the patient with COPD, we see low ventilation followed by lower perfusion to the same area, but in the patient with a PE we will see good ventilation everywhere, but in the same area we will see decreased perfusion.  

Angiogram  

Pulmonary Embolus 

3D MR Angiogram showing the form of the aorta, pulmonary vessels and left atrium.

The V/Q scan might miss a few PE, but sending a contrast into the pulmonary arterial system will show the PE missed by V/Q scan. 

The EKG: 

·          Tachycardia

·          Sometimes, a depressed ST segment.

·          On a 12-lead EKG, we might see T-wave inversion in the right pre-cordial lead or T-wave inversion in leads V1 & V2. 

The ABG 

·          Oddly enough, the ABG may not be helpful in diagnosis of the PE patient without a pulmonary background, because in 15%-25% of the cases, there is a Pa0₂ over 80 torr.

·          In the COPD patient who is intubated, however, a sudden decrease in Pa0₂ and increase in PaC0₂ might hint at a PE. 

Treatment: 

Prevention of PE is important:

·          Persons with long-term A-Fibrillation need to be given anti-coagulants to prevent clot formation in the RA

·          immobile patients can be given high pressure hose [TET hose] to keep blood flow going in the lower extremities to prevent DVT [deep vein thrombus] 

Once there is a DVT or a PE, we need to give heparin by continuous infusion to inhibit further clotting. This needs to be maximized in the first 24-48 hours.  We want the PTT time to be 1.5 x the control. This needs to last 5-7 days and is followed by oral Coumadin.  

The AHI states that fibrinolytic agents may be used in a case-by-case basis in PE. Egan states that if clot-busters are used, we need to defer the heparin.

We need to give supplementary 0₂ for documented hypoxemia and analgesics for pain and anxiety. 

If the patient is hypotensive, he needs fluid resuscitation and vasopressors to get the systemic blood pressure back up.