Pulmonary

Embolism

Pulmonary embolism facts

What is a pulmonary embolism?

What are the causes and risk factors for pulmonary embolism?

What are the signs and symptoms of pulmonary embolism?

How is pulmonary embolism diagnosed?

History and physical examination

Basic testing (CBC, electrolytes, BUN, creatinine blood test, chest x-ray, EKG)

Pulmonary angiogram

d-Dimer blood test

CT Scan

Ventilation-perfusion scans

Venous Doppler study

Echocardiography (EKG, ECG)

What is the treatment for pulmonary embolism?

Anticoagulation

Thrombolytic therapy

What is the prognosis for pulmonary embolism?

Can pulmonary embolism be prevented?

Pulmonary embolism facts

Pulmonary embolism is a diagnosis that should

be considered in patients with chest

pain and/orshortness of breath, and is one of the

causes of sudden death.

The diagnosis of pulmonary embolism may be

difficult to make, and is often missed. Diagnostic

strategies need to be individualized to each

patient and situation.

Anticoagulation is the treatment of choice for

pulmonary embolism and the patient may be

required to continue treatment for months.

Prevention is the best treatment for pulmonary

embolism, which can be accomplished by minimizing

the risk factors for deep vein thrombosis (DVT).

What is a pulmonary

embolism?

The lungs are primarily responsible for the

exchange of oxygen and carbon dioxide between

the air we breathe and blood.

If a blood clot (thrombus) forms in the one of the body's

veins (deep vein thrombosis or DVT), it has the

potential to break off and enter the circulatory system

and travel (or embolize) through the heart and

become lodged in the one of the branches of the

pulmonary artery of the lung.

A pulmonary embolus clogs the artery that provides

blood supply to part of the lung. The embolus not

only prevents the exchange of oxygen and carbon

dioxide, but it also decreases blood supply to the

lung tissue itself, potentially causing lung tissue to

die (infarct).

A pulmonary embolus is one of the life-threatening

causes of chest pain and should always be

considered when a patient presents to a healthcare

provider with complaints of chest pain and shortness

of breath.

There are special types of pulmonary embolus that

are not due to blood clots, but instead are due to

other body materials.

These are rare occurrences and include:

fat emboli from a broken femur,

an amniotic fluid embolus in pregnancy, and

in some cases, tumor tissue from cancer.

The signs and symptoms are the same as that of a

blood clot, and is caused by blockage of part of the

arterial tree of the lung, and prevents the bloods

ability to reach all parts of the lung tissue.

Picture of a blood clot is formed

What are the causes and risk

factors for pulmonary embolism?

Pulmonary embolus is the end result of a deep vein

thrombosis or blood clot elsewhere in the body.

Most commonly, the DVT begins in the leg, but they

also can occur in veins within the abdominal

cavity or in the arms.

The risk factors for a pulmonary embolism are the

same as the risk factors for deep vein thrombosis.

These are referred to as Virchow's triad and include:

prolonged immobilization or alterations in normal

blood flow (stasis)

increased clotting potential of the blood

(hypercoagulability)

any damage to the walls of the veins.

Examples of these include the

following:

Prolonged immobilization

Extended travel (sitting in a car, airplane, train,

etc.)

Hospitalization or prolonged bed rest

Increased blood clotting

potential

Medications: birth control pills, estrogen

Smoking

Genetic predisposition most commonly, Factor V

Leiden deficiency, Protein C or Protein S

deficiencies or anitithrobin III deficiency

Polycythemia

Cancer

Pregnancy, including 6-8 weeks after delivery

Surgery

Damage to vessel wall

Prior deep venous thrombosis

Trauma to the lower leg with or without surgery or

casting

Major acquired risk factors for venous thromboembolism:

1- advancing age.

2- arterial disease including carotid & coronary disease.

3- obesity.

4- cigarette smoking.

5- C. O. P. D.

6- personal or family H.O. VTE

7- recent surgery, trauma, or immobility including stroke.

8- acute infection.

9- long-haul air travel.

10- cancer & cancer chemo therapy.

11- pregnancy, oral contraceptive pills, or H.R.T.

12- pace maker, implantable cardiac defibril. leads or indwelling central venous catheters .

Major thrombophilias associated with

VTE:

i. Inherited:

- Factor V-leiden resulting in activated protein C

resistance.

- Prothrombin gene mutation 20210.

- Anti thrombin III deficiency.

- Protein C deficiency.

- Protein S deficiency.

ii. Acquired:

- Anti phospholipid anti-body syndrome.

- Hyperhomocysteinemia.

What are the signs and symptoms

of pulmonary embolism?

A pulmonary embolus may present with the sudden

onset of chest pain and shortness of breath.

The pain is classically sharp and worsens when

taking a deep breath, often called pleuritic pain

or pleurisy.

There may be cough that produces bloody sputum.

The patient may have stable vital signs (blood

pressure, heart rate, respiratory rate, and oxygen

saturation) but frequently presents with an elevated

heart rate.

If the blood clot is large enough, it can block blood

from leaving the right side of the heart thus

preventing blood from entering the lungs.

There is then no blood entering the left side of the

heart to pump to the rest of the body.

This can result in circulatory collapse (shock) and

death.

Often referred to as saddle embolus (named such as it

sits in the division between the left and right

pulmonary artery like a saddle).

Depending on the amount of blood clot (clot burden or

clot load), oxygen saturation can be variably affected

as can the blood pressure and heart rate.

Classic signs are such that the heart rate and

respiratory rate are elevated as the body tries to

compensate for less oxygen transfer capabilities in

the lung.

Oxygen saturation may be decreased.

Oxygen saturation in a healthy individual approaches

100% at sea level.

The patient may be cyanotic , lightheaded, and weak.

In some cases, pulmonary embolus will present with

sudden death.

Most common symptoms or signs of

P.E. :

Symptoms:

- Un explained dyspnea.

- Chest pain, either pleuritic or atypical.

Signs:

- Tachypnea.

- TachyCardia.

- Low-grade fever.

- Tri cuspid reg. murmur.

-Accentuated P2.

How is pulmonary embolism

diagnosed?

History and physical examination

There always needs to be a high a level of

suspicion that a pulmonary embolus may be the

cause of chest pain or shortness of breath.

The health care professional will take a history of

the chest pain, including its characteristics, its

onset, and any associated symptoms that may

direct the diagnosis to pulmonary embolism.

It may include asking about risk factors for deep

vein thrombosis.

Coughing up blood sputum may be a sign of

pulmonary embolism.

Physical examination will concentrate initially on the

heart and lungs, since chest pain and shortness of

breath may also be the presenting complaints

for heart attack,

pneumonia, pneumothorax (collapsed lung),

dissection of an aortic aneurysm, among others.

With pulmonary embolism, the chest examination is

often normal, but if there is some associated

inflammation on the surface of the lung , a rub may

be heard.

The surfaces of the lung and the inside of the chest

wall are covered by a membrane (the pleura) that is

full of nerve endings.

When the pleura becomes inflamed, as can occur in

pulmonary embolus, a sharp pain can result that is

worsened by breathing, so-called pleurisy or pleuritic

chest pain.

The physical examination may include examining an extremity, looking for signs of a DVT, including warmth, redness, tenderness, and swelling.

It is important to note, however, that the signs associated with deep vein thrombosis may be completely absent even in the presence of a clot. Again, risk factors for clotting must be taken into consideration when making an assessment.

Clinical decision rule:> 4 score points = high probability

=/< 4 score points = non high probability

3DVT symptoms or signs

3An alternative diagnosis is

less likely P.E.

1.5HR > 100/min

1.5Immobilization or surgery

within 4 weeks

1Hemoptysis

1Cancer treated within 6/12 or

metastatic

D. D. of P.E.

1- anxiety, pleurisy, costochondritis.

2- Pneumonia, bronchitis.

3- MI.

4- Pericarditis.

5- Congestive Heart failure.

6- Idiopathic pulm. HTN.

Basic testingBasic testing may include:

CBC (complete blood count)

Electrolytes,

BUN (blood urea nitrogen),

Creatinine blood test,

Chest X-ray, and

Electrocardiogram (EKG or ECG).

* Normal values of the alveolar-arterial Oxygen

grdient did not rule out the diagnosis of acute P.E.

So A.B.G. determination shouldn’t be part of the

routine diagnostic strategy.

The chest X-ray is often normal in

pulmonary embolism.

A Hampton hump in a person with a right lower

lobe pulmonary embolism

* A near-normal CXR in the setting of severe

respiratory compromise

is highly suggestive of massive P.E.

* CXR may show:-

focal oligmia (wester mark sign)

A peripheral wedge shaped density above the

diaphragm (Hampton hump) -> indicate pulm.

infarction

If there is significant

blockage in a

pulmonary artery, it

acts like a dam and

it is harder for the

right side of the

heart to push blood

past the

obstructing clot or

clots.

The EKG may be usually normal, but may demonstrate a

rapid heart rate, a sinus tachycardia (heart rate > 100

bpm).

The EKG can demonstrate a right heart strain.

Since the cost of missing the diagnosis of

pulmonary embolus can be death, the

health care professional has to consider the

diagnosis when caring for a patient

complaining of chest pain or shortness of

breath.

Pulmonary angiogram

In the past, the gold

standard for the

diagnosis of pulmonary

embolus is a

pulmonary angiogram.

Dye is injected and a clot

or clots can be

identified on imaging

studies.

This is considered an

invasive test and is

rarely performed.

Pulm. Angio is required when:-

1- intervention are planned such as suction catheter

embolectomy.

2- mechanical clot fragmentation.

3- catheter directed thrombolysis.

d-Dimer blood test

If the healthcare provider's suspicion for pulmonary

embolism is low, a d-Dimer blood test can be used.

The d-Dimer blood test measures one of the

breakdown products of a blood clot.

If this test is normal, then the likelihood of a pulmonary

embolism is very low. Unfortunately, this test is not

specific for blood clots in the lung.

It can be positive for a variety of reasons including

pregnancy, injury, recent surgery, or infection. D-

dimer is not helpful if the potential risk for a blood

clot is high.

CT scanIf there is greater suspicion,

then computerized

tomography (CT scan) of

the chest with

angiography can be

done.

Contrast dye is injected into

an intravenous line in the

arm while the CT is being

taken, and the pulmonary

arteries can be

visualized.

There are some limitations of the test, especially if a

pulmonary embolism involves the smaller arteries in

the lung. However similar problems are seen with

the more invasive pulmonary angiogram.

As CT scan has become more and more sophisticated,

not identifying significant emboli is unusual.

There are risks with this test since some patients are

allergic to the dye, and the contrast dye can be

harsh on kidney function.

It may be wise to limit the patient's exposure to

radiation, especially in pregnant patients.

However, since pulmonary embolus can be fatal,

even in pregnancy this test can be performed,

preferably after the first trimester.

* CT scan can be used as a “one-stop shop” for

diagnosis or detection of source of thrombus &

prognosis.

Ventilation-perfusion scans

Ventilation-perfusion scans (VQ scans) use labeled

chemicals to identify inhaled air into the lungs and

match it with blood flow in the arteries.

If a mismatch occurs, meaning that there is lung tissue

that has good air entry but no blood flow, it may be

indicative of a pulmonary embolus.

These tests are read by a radiologist as having a low,

moderate, or high probability of having a pulmonary

embolism.

There are limitations to the test, since there may be a

5%-10% risk that a pulmonary embolism exists even

with a low probability V/Q result.

Venous Doppler study

Ultrasound of the legs, also known as venous Doppler studies, may be used to look for blood clots in the legs of a patient suspected of having a pulmonary embolus.

If a deep vein thrombosis exists, it can be inferred that chest pain and shortness of breath may be due to a pulmonary embolism.

The treatment for deep vein thrombosis and pulmonary embolus is generally the same.

The primary diagnostic criterion for DVT is loss of vein compressibility.

Echocardiography (EKG, ECG)

Echocardiography or ultrasound of the heart may be

helpful if it shows that there is strain on the right side of

the heart.

RV enlargement or H.K. especially free wall H.K. must

sparing of the apex (the MC cannel sign)

If non-invasive tests are negative and the

healthcare provider still has significant concerns,

then the healthcare provider and the patient need

to discuss the benefits and risks of treatment

versus invasive testing like angiography.

Risk stratification: * Clinical prediction of increased mortality:

1- S.B.P. =/< 100 mmHg

2- Age > 70 years

3- H.R. > 100 beat/min

4- C.H.F.

5- Ch. Lung disease

6- Cancer

* Cardiac biomarkers & imaging prediction of increased mortality:

1- Elevated troponin I or T.

2- Elevated BNP or pre BNP.

3- R.V. - H.K. on Echo.

4- R.V. enlargement on chest C.T.

What is the treatment for

pulmonary embolism?

The best treatment for a pulmonary embolus is

prevention.

Minimizing the risk of deep vein thrombosis is key in

preventing a potentially fatal illness.

The initial decision is whether the patient requires

hospitalization.

Recent studies suggest that those patients with a small

pulmonary embolus, who are hemodynamically stable

(normal vital signs) may be treated at home with close

outpatient care.

AnticoagulationThe first step in stable patients with pulmonary embolism

is anticoagulation.

This is a two step process. Warfarin (Coumadin) is the

drug of choice for anti-coagulation.

It is taken by mouth beginning immediately upon the

diagnosis of pulmonary embolism, but may take up to

week for the blood to be appropriately thinned or

anticoagulated.

As an immediate solution and as a bridge until the

Coumadin becomes effective, low molecular weight

heparin (enoxaparin(Lovenox) or pentasaccharide

(Fondaparinux, Arixtra) is administered at the same

time.It thins the blood via a different mechanism.

Enoxaparin or Fondaparinux injections can be

administered as an outpatient.

For those patients who have contraindications to the

use of enoxaparin (Lovenox) (for example, kidney

failure does not allow the drug to be metabolized),

intravenous heparin can be used as the first step.

This requires admission to the hospital and careful

patient monitoring with blood tests.

Anticoagulation is usually suggested for a minimum of six months, but each patient will have their treatment regimen individualized.

The blood test utilized to monitor warfarin therapy is referred to as the INR or international normalized ratio.

This test can be performed by finger stick or venous stick depending on the laboratory procedures.

Essentially, this ratio is determined by measuring the patients prothrombin time.

This value is divided by the lab standard normal value.

For patients with a pulmonary embolism, the warfarindosing will be titrated so that the INR value will be 2.0 –3.0, basically the blood needs to be 2 to 3 times thinner than the normal value.

It is very helpful for the patient to participate in their health management by keeping a diary of their warfarin dose, the date of testing, and their INR values.

Intravenous unfractionated Heparin

“Raschke Nomogram”

ActionVariable

80 U/kg bolus, then 18 U/kg/hrInitial heparin polus

80 U/kg bolus, then increase by 4

U/kg/hr

aPTT < 35 second (<1.2 * control)

40 U/kg bolus, then increase by 2

U/kg/hr

aPTT 35 to 45 second (1.2 to 1.5 *

control)

No changeaPTT 46 to 70 second (1.5 to 2.3 *

control)

Decrease infusion rate by 2 U/kg/hraPTT 71 to 90 second (2.3 to 3 *

control)

Hold infusion 1 hr, then decrease

infusion rate by 3 U/kg/hr

aPTT > 90 second ( >3 * control)

Fondaparinux dosing for patients

with Acute P.E. or DVT

>100 kg50 – 100 kg< 50 kgPatient

weight

10 mg7.5 mg5 mgDaily dose

of

Fondaparinu

x

Thrombolytic therapy

Pulmonary embolism can be fatal, especially if

involves a large amount of clot.

When the patient is unconscious, has low or no blood

pressure or are not breathing, clot busting or

thrombolytic therapy using medications like TPA

(tissue plasminogen activator) may be considered.

It is also often considered when signs of right heart

strain are present.

In certain centers, a special procedure can be

performed where is catherter is placed in the right

side of the heart and the clot is essentially vacuumed

out.

Inferior vena cava filter

Used inferior vena cava filter.

If anticoagulant therapy is contraindicated and/or

ineffective, or to prevent new emboli from

entering the pulmonary artery and combining with

an existing blockage, an inferior vena cava

filter may be implanted

Surgery

Surgical management of acute pulmonary

embolism (pulmonary thrombectomy) is

uncommon and has largely been abandoned

because of poor long-term outcomes. However,

recently, it came back again with the revision of

the surgical technique and is thought to benefit

certain people. Chronic pulmonary embolism

leading to pulmonary hypertension (known

as chronic thromboembolic hypertension) is

treated with a surgical procedure known as

a pulmonary thromboendarterectomy.

Optimal Duration of Anticoagulation

Recommendation Clinical setting

6 moFirst provoked PE/proximal

leg DVT

3 moFirst provoked upper

extremity DVT or isolated

calf DVT

12 mo or indefinite durationSecond provoked VTE

Indefinite durationThird VTE

6 mo or indefinite durationCancer

Consider indefinite durationUnprovoked VTE

What is the prognosis for

pulmonary embolism?

Patient survival depends upon:

the underlying health of the patient,

size of the pulmonary embolus,

the cause of the pulmonary embolus, and

the ability for a diagnosis to be made and treatment

initiated.

The diagnosis is often difficult, and it is estimated to

that there are up to 400,000 cases of pulmonary

embolus that are not diagnosed in the United States

each year.

In those patients where the diagnosis is made,

the mortality rate is less than 20% when

considering all patients.

Usually, however, the mortality risk is much

less in most patients.

The higher incidence of death occurs in

patients that are older, have other underlying

illnesses, or have a delay in diagnosis.

Racial differences may also exist, but probably

are due more to access to quality care than a

specific genetic difference.

How can pulmonary embolism be

prevented?

Minimizing the risk of deep vein thrombosis

minimizes the risk of pulmonary

embolism.

The embolism cannot occur without the

initial DVT.

In the hospital setting, the staff works hard to minimize the potential for clot formation in immobilized patients. Compression stockings are routinely used.

Surgery patients are out of bed walking (ambulatory) earlier and low dose heparin or enoxaparin is being used for deep vein thrombosis prophylaxis (measures taken to prevent deep vein thrombosis).

For those who travel, it is recommended that they get up and walk every couple of hours during a long trip.

Compression stockings may be helpful in preventing future deep vein thrombus formation in patients with a previous history of a clot.

Clinical syndrome of P.E.TherapyPresentationClassificati

on

Thrombosis or

embolictomy or IVC

filter plus:- anti co-

ag.

Systemic B.P. < 90 mmHg

Or poor tissue perfusion

or multisystem organ faliure

Plus :- right or left main pulm, artery

thrombosis or high clot burden

Massive P.E.

Addition of

thrombolysis

emboletomy or

filter remains

controversal

Hemodynamically stable but moderate

or sever R.V. dysfunction or

enlargement.

Submassive

P.E.

Anti co-ag.Normal hemodynamic of normal R.V.

size & function.

Pulm. infarction.

Small to

moderate

P.E.

Anti co-agA sudden stroke & concomitant V.T.E.

DVT --> thrombus --> arterial system

through P.F.O.

Paradoxical

embolism

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