ClinicalArticle Massive Pulmonary Embolismccn.aacnjournals.org/content/27/1/39.full.pdf · pulmonary embolism. ... Discuss goals of treatment in the care of patients with pulmonary

http://ccn.aacnjournals.org CRITICALCARENURSE Vol 27, No. 1, FEBRUARY 2007 39

Kathleen Shaughnessy is the clinical director of cardiothoracic surgery at Abington Memorial Hospital, Abington, Pa.

Corresponding author: Kathleen Shaughnessy, Abington Memorial Hospital, 1200 Old York Road, Abington, PA 19001 (e-mail: [email protected]).

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The patient’s hemodynamic sta-

bility provided the multidisciplinary

team with an opportunity to perform

diagnostic tests to look for a possible

cause for the cardiac arrest. A 2-

dimensional echocardiogram showed

dilatation of the right ventricle and

moderate tricuspid regurgitation

with pulmonary artery systolic pres-

sures of 60 to 65 mm Hg, all abnor-

mal findings in a healthy heart. This

result, coupled with the postpartum

arrest, led to a tentative diagnosis of

pulmonary embolism. A ventilation/

perfusion scan indicated a high

probability of pulmonary embolism,

and a computed tomography scan of

the thorax showed a saddle embolism,

which confirmed the diagnosis.

The definitive diagnosis of pul-

monary embolism proved a great

threat to the patient’s survival, and

an urgent interdisciplinary team

meeting ensued. Physician represen-

tatives from obstetrics, cardiology,

pulmonary medicine, and cardio-

thoracic surgery, as well as a variety

of nursing representatives who

directly provided care for the patient,

played a crucial part in the decision-

making process. The critical care

nurses reported decerebrate postur-

ing of the patient after the cardiac

arrest, which may be indicative of

Kathleen Shaughnessy, MSN, CRNP, CCRN

Whenever a “Code Blue

Maternity” is announced over the

hospital’s loudspeaker, a collective

sigh and silent prayer go up among

the staff. Such an event is especially

traumatic to hospital personnel dur-

ing the holiday season. Our surgical

intensive care and maternity units

are worlds apart, but these worlds

collided one December afternoon

when a 35-year-old patient, whom

we will refer to as Shelby, had a car-

diac arrest shortly after an unevent-

ful cesarean-section delivery at 35

weeks’ gestation. The delivery had

produced a healthy, beautiful baby

girl. Reports of the patient becoming

acutely dyspneic, hypotensive, syn-

copal, and suffering cardiac arrest

quickly filtered through the hallways.

Only moments after the code blue

maternity was called, a group of

emergency personnel responded to

the scene. In conjunction with the

medical professionals already pres-

ent, they acted without hesitation to

save this patient.

Pulseless electrical activity was

quickly identified at the beginning of

the code, and cardiopulmonary resus-

citation was initiated. The patient was

immediately intubated and ventilated

with 100% oxygen. Boluses of intra-

venous epinephrine and atropine were

then given, followed by an infusion of

isotonic sodium chloride solution. The

patient responded to treatment, as evi-

denced by reestablishment of a pulse

and adequate blood pressure.

ClinicalArticle

Author

Massive PulmonaryEmbolism

* This article has been designated for CE credit. A closed-book, multiple-choice examination follows this article, which tests your knowledge of the following objectives:

1. Identify patients at risk for a massive

pulmonary embolus

2. Describe current assessment and diagnostic

strategies for pulmonary embolus

3. Summarize possible medical and surgical

interventions for pulmonary embolus

4. Discuss goals of treatment in the care of

patients with pulmonary embolus

by AACN on May 10, 2018http://ccn.aacnjournals.org/Downloaded from

http://ccn.aacnjournals.org/

poor neurological functioning.

Because time was of the essence, a

plan was quickly formulated and put

into action. Surgical embolectomy

was proposed because thrombolytic

therapy was contraindicated in this

patient’s immediate postoperative

state. Measures were quickly taken

by the nurses to ready the patient for

surgery. They also provided support

to the patient’s shocked, desperate

husband and family, who were agree-

able to any treatment that would

offer Shelby a chance for survival.

As the cardiothoracic surgical

nurses worked quickly to prepare

Shelby for surgery, they were acutely

aware that small fragments of throm-

bus could dislodge and travel farther

into the pulmonary arterial tree,

causing pulmonary infarction and

irreversible hypoxia. An intraopera-

tive transesophageal echocardiogram

obtained on the patient’s arrival in

the operating room confirmed a

massive pulmonary embolism. The

procedure was started by placing the

patient on cardiopulmonary bypass

(heart-lung machine) via femoral

cannulation to shunt blood away

from the main pulmonary artery and

provide a bloodless operating field.

The pulmonary artery was incised,

and the incision was extended into

the left and right pulmonary arteries.

A 10-cm-long thrombus was then

manually removed with forceps.

Transesophageal esophagography

after the procedure showed resolu-

tion of the tricuspid regurgitation,

good left ventricular function, and

unobstructed blood flow in the pul-

monary arteries. The patient was

successfully weaned from cardiopul-

monary bypass and transported to

the cardiac surgery intensive care

unit in stable condition. A Gunther

Tulip (Cook, Bloomington, Ind) fil-

ter was placed in the inferior vena

cava to decrease the likelihood of

further embolization. Surgery had

eliminated the primary problem, but

the patient’s full recovery was yet to

be realized.

The cardiothoracic nurses in the

cardiac surgical care unit applied

their skills and expertise to provide

care for this new mother, whose story

had touched them deeply. Many of

the nurses who took care of Shelby

were parents themselves and felt a

personal connection to her, her new

baby, and her family. Although Shelby

was not alert, by postoperative day 2,

her condition had begun to improve.

She demonstrated normal reflexes

and appropriate withdrawal from

painful stimuli, which reassured the

physicians and nurses who were

caring for her.

The nurses relayed the encour-

aging news to her vigilant husband

and family. A room close to the

intensive care unit was obtained for

the family, serving as a place for

them to retreat, shower, and sleep

without having to leave the hospi-

tal. They were encouraged to talk to

Shelby when at the bedside, to touch

her hand, and to participate in her

care whenever possible.

Although the demands of

Shelby’s care were great, the nurses

were acutely aware of how large a

part Shelby’s family played in her

recovery. The staff often inquired

about the whole family, including

Shelby’s newborn and 2 young

daughters, when speaking with her

husband. The family brought in pic-

tures of Shelby’s children to post at

the bedside. These photos warmed

the hearts of all who saw them. While

providing care for Shelby, the nurses

frequently mentioned her children

and their well-being in an effort to

reorient her. Her neurological status

continued to progress, but whether

she would be the Shelby her family

remembered was still uncertain.

Although the responses were

minimal at first, the mention of her

children’s names seemed to reassure

Shelby, quieting her moaning and

thrashing in the bed. This response

provided hope and encouragement

to her family and all who were car-

ing for her. Nursing staff continued

to monitor Shelby’s responses and

overall neurological status, while

caring for her many physical needs.

Shelby was successfully weaned

off of mechanical ventilation on

postoperative day 5; however, she

remained encephalopathic, moaning

and thrashing in the bed. Shelby’s

inability to respond appropriately

greatly disturbed her family, and they

feared a complete neurological recov-

ery would never occur. The nurses

encouraged the family to take it 1 day

at a time, reassuring them that hope

remained for a full recovery.

The nurses reevaluated Shelby’s

overall care at different intervals

throughout her course, and at this

point in her recovery they surmised

that the last thing Shelby remem-

bered was the delivery of her daugh-

ter. It was thought that she might

feel a longing for her baby. In an

attempt to reorient Shelby, the car-

diac surgery and maternity staff

nurses coordinated efforts to bring

mother and baby together at regular

intervals. Shelby became noticeably

calmer as the baby lay next to her.

The nurses observed a dramatic

reduction in Shelby’s heart rate, blood

pressure, and respiratory rate when-

ever she and the baby were united.

40 CRITICALCARENURSE Vol 27, No. 1, FEBRUARY 2007 http://ccn.aacnjournals.org




The union of mother and baby proved

to have a profound effect on Shelby

and to be of considerable therapeu-

tic value, reassuring the family and

staff of a possible full neurological

recovery. Visiting by Shelby’s family

had always been permitted and was

now strongly encouraged.

Shelby regained complete neuro-

logical functioning by postoperative

day 7, much to the relief of her fam-

ily. The dedicated team of medical

professionals, who had worked hard

to see that this family was preserved,

was also relieved. Their efforts dra-

matically improved Shelby’s chance

for a complete recovery. The love of

family and friends and the group of

once-strangers who walked into

Shelby’s life to “just do a good job”

made a difference. Shelby was cared

for and survived this traumatic expe-

rience to be reunited with her new-

born and family.

Shelby was discharged home to

her family on postoperative day 9,

neurologically intact, just 12 days

before Christmas. This patient’s

remarkable recovery was a Christmas

miracle, an answer to the many silent

prayers that helped bring about a

successful outcome.

Description of Pulmonary Embolism

Pulmonary embolism is the lead-

ing cause of maternal death after a live

birth, occurring in 2 out of 100000

live births.1 Pulmonary embolism has

an annual incidence of 60 to 70 per

100000 persons within the general

population.2 Seven world cases of

successful survival after postcesarean

pulmonary embolectomy have been

reported worldwide, and only 2 of

those patients survived without per-

manent neurological damage.1 Vir-

chow’s triad of venous stasis, hyper-

coagulability, and vessel wall damage

triggers a venous thrombus (clot) to

develop in susceptible patients.3 Pul-

monary embolism results when frag-

ments detach from a thrombus, travel

through the venous system, pass

through the right side of the heart,

and lodge in the main branches of

the pulmonary artery. A pulmonary

embolism can also occur as a result

of other fluids or material entering

the vasculature. Deep vein thrombo-

sis, amniotic fluid, air, and iatrogenic

causes are all sources of pulmonary

embolism. A venous thrombus most

commonly originates in the lower

extremities, the pelvis, or the kidneys.

The main symptom of pulmonary

embolism is often a vague complaint

of dyspnea or chest pain, and death

commonly occurs within 1 hour of the

onset of signs and symptoms4 if the

correct diagnosis is not established.

Pulmonary embolism may be

classified as massive, submassive, or

minor, depending on the amount of

pulmonary vasculature affected.

Massive pulmonary embolism is

defined as thrombus occluding more

than 50% of the pulmonary vascula-

ture. Thrombus that occludes the

bifurcation of the pulmonary artery

is termed a saddle embolus.5 When

the embolus lodges in the pulmonary

vasculature, blood flow to the alveoli

beyond the blockage is eliminated.6

The obstruction causes a section of

lung to be ventilated but not perfused,

thus creating intrapulmonary “dead

space.” The blockage acts like a dam,

causing blood pressure to increase in

the vessels upstream. The right ven-

tricle must then generate tremendous

pressure to overcome this obstacle

and maintain forward blood flow

and perfusion to distal organs.

If the right ventricle is unable to

maintain adequate forward blood

flow, right-sided heart failure devel-

ops and leads to hypoxemia, dyspnea,

hypotension, and syncope. In a mas-

sive pulmonary embolism, cardiac

arrest occurs because the left ventri-

cle is unable to maintain adequate

cardiac output.7 Pulseless electrical

activity is the most common rhythm

seen in cardiac arrest. Only 25% of

patients with cardiac arrest survive

the ordeal, and a preoperative cardiac

arrest is the strongest predictor of

postoperative mortality.

Massive pulmonary embolism

with cardiovascular collapse indi-

cates a significant accumulation of

thrombus within the pulmonary

arteries and carries a grim prognosis

if not diagnosed and treated quickly.

Although most patients with massive

pulmonary embolism do not present

in shock, mortality reaches 30% for

those who do.8

Risk FactorsRisk factors for the development

of venous thromboembolism center

on Virchow’s triad of venous stasis,

hypercoagulability, and vessel wall

damage. Advanced age, surgery, and

prolonged immobility from bed rest

or extended confined travel9 are

commonly identified risk factors in

critically ill patients. Anderson et al10

showed that 88% of patients treated

for acute deep venous thrombosis

and/or pulmonary embolism were

more than 40 years of age. Surgical

procedures cause direct damage of

vessel walls and often lead to a period

of postoperative immobilization. Any

abdominal or thoracic surgery lasting

more than 30 minutes increases the

risk of development of venous

thromboembolism.11 The sex of the



patient is not an independent risk

factor, but many women take oral

contraceptives or other forms of

hormone therapy that contribute to

a hypercoagulable state.3 Pulmonary

embolism is 10 times more likely to

develop in pregnant and postpartum

women than in nonpregnant women.

Smoking, pre-eclampsia, and delivery

by cesarean section are reported to

increase pregnancy-related risk of

venous thromboembolism.12 The

expanding uterus obstructs venous

blood return, posing increased risk

for thrombus formation in the

venous system of the pelvis or lower

extremities. Polycythemia, sickle cell

anemia, and inherited or acquired

thrombophilia, including antithrom-

bin III deficiency, protein C defi-

ciency, protein S deficiency, and

factor V Leiden, also increase the

risk for thromboemboli.13 Obesity,

trauma, burns, cancer, and cardiac

disease are also conditions con-

tributing to the abnormalities that

define Virchow’s triad. Our patient’s

only risk factor for deep venous

thrombosis or pulmonary embolism

was her pregnancy (Table 1).

Signs and Symptoms of Massive Pulmonary Embolism

The “classic” signs and symptoms

of pulmonary embolism, namely

dyspnea, hemoptysis, and chest pain,

occur in fewer than 20% of patients.14

Acute-onset dyspnea and tachypnea

are the most common initial signs

and symptoms, and patients often

report a feeling of apprehension. In

massive pulmonary embolism, 10%

to 15% of patients present with syn-

cope,7 which results from obstruction

of the pulmonary outflow tract by

embolic material. Pressure increases

within the right ventricle, causing

dilatation and dysfunction.15 Dilata-

tion of the right ventricle causes the

tricuspid leaflets to separate, result-

ing in tricuspid regurgitation and

symptoms of right-sided heart failure.

The physical findings include disten-

tion of the jugular vein, increased

central venous pressure, tachycardia,

tachypnea, hypotension, a new mur-

mur due to tricuspid regurgitation,

and decreased oxygen saturation

shown by pulse oximetry (Table 2).

Hypoxemia results from a mismatch

between regional alveolar ventila-

tion and pulmonary blood flow.

Therefore, early recognition and

diagnostic investigation of signs and

symptoms are paramount for avoid-

ance of a catastrophe.

Differential Diagnosis of Chest Pain and Dyspnea

Chest pain and dyspnea are

vague symptoms associated with

many disease processes. Acute

coronary syndrome, aortic dissec-

tion, pneumothorax, acute asthma

or exacerbation of chronic obstruc-

tive pulmonary disease, pneumo-

nia, pericarditis, rib fracture, and

musculoskeletal pain must be

quickly excluded from the list of

possible diagnoses.

Diagnostic FindingsWhen a patient complains of

chest discomfort, an electrocardio-

gram is usually the first test ordered.

This test may eliminate other causes

of chest pain such as myocardial

infarction or aortic dissection.

Anterior T-wave inversion is evi-

dent in 85% of cases of pulmonary

embolism.16 This abnormality reflects

inferoposterior ischemia that results

from pressure overload.17(p1902) A pat-

tern of acute right ventricular strain

is highly suggestive of pulmonary

embolism but is present in only 20%

of the cases. This pattern is evidenced

by an S wave in lead I, a Q wave in

lead III, and a T-wave inversion in

lead III (Figure 1). Tall peaked P waves,

tachycardia, new incomplete right

bundle branch block, and right-axis

deviation are the most common

abnormalities noted in patients with

pulmonary embolism. This test was

not performed on Shelby because she

never complained of chest pain. Her

rapid deterioration from acute dysp-

nea to cardiac arrest with pulseless

electrical activity precluded the oppor-

tunity to obtain an electrocardiogram.

Chest radiographs are not diag-

nostic for pulmonary embolism but


Table 1 Risk factors for pulmonaryembolism

AgeRecent surgeryProlonged immobilityCancerFemale sexPregnancyPolycythemiaSickle cell anemiaGenetic or acquired thrombophiliaObesityTraumaBurnsCardiac disease/congestive heart

failurePrevious deep venous thrombosis or

pulmonary embolism

Table 2 Signs and symptoms ofmassive pulmonary embolism

Acute onset of dyspneaTachypneaTachycardiaHypotensionSyncopeNew murmur due to tricuspid

regurgitationIncrease in central venous pressureDistention of jugular veinDecrease in oxygen saturation shown

by pulse oximetry




can exclude other diseases that may

mimic pulmonary embolism. Pleural

effusions are noted in 48% of patients

with pulmonary embolism. The

Hampton hump, a triangular wedge-

shaped pleural infiltrate, is a rare

finding of an embolus resulting in

pulmonary infarction (Figure 2).

The Westermark sign is dilata-

tion of the pulmonary vasculature

near the embolus in contrast to

decreased vascular markings in the

affected regions14 (Figure 3). This

finding, if present, may point clini-

cians toward the possibility of pul-

monary embolism. Shelby’s chest

radiograph did not include any of

these findings.

Arterial blood gas analysis is

not diagnostic for pulmonary

embolism but typically shows PaO2less than 80 mm Hg and PaCO2 less

than 36 mm Hg on room air.

Hypoxia is an indicator of meta-

bolic derangement and should

prompt critical care nurses to con-

sider probable causes and pursue

further diagnostic workup. Respira-

tory alkalosis and hypoxemia with

a widened alveolar-arterial differ-

ence in PaO2 develop.18(p463) Increased

physiological dead space and muscle

fatigue then lead to respiratory aci-

dosis. Finally, metabolic acidosis

results from tissue hypoxemia and

shock. It is vital to remember that a

normal PO2 does not exclude pul-

monary embolism.

The D-dimer assay is a sensitive

but nonspecific test to detect the

presence of venous thromboem-

bolism. D-dimers are produced dur-

ing the degradation of fibrin clot by

plasmin. The D-dimer level may be

elevated in other conditions, such as

infection, cancer, pregnancy, sur-

gery, renal fail-

ure, or heart

failure.2 The D-

dimer assay has

a negative pre-

dictive value of

90% when

results are less

than 500

mg/L.3 In

essence, the

nurse is virtu-

ally assured

that pulmonary

embolism is

excluded from

the list of possi-

ble diagnoses

when the D-

dimer level is

less than 500

mg/L. This test

was not per-

formed because

Shelby’s recent

pregnancy

would have ele-

vated her D-

dimer levels.

Duplex

ultrasonogra-

phy of the lower

Figure 1 Electrocardiogram shows pattern of right ventricular strain (S wave in leadI, Q wave in lead III, and T-wave inversion in lead III).

I

II

III

II

aVF

aVL

aVR V1

V2

V3 V6

V5

V4

Figure 3 Chest radiograph shows the Westermark sign.

Figure 2 Chest radiograph shows the Hampton hump.



extremity is a noninvasive imaging

study used to detect deep venous

thrombosis. Although its sensitivity

and specificity for deep venous

thrombosis above the knee exceeds

95%, duplex ultrasonography is not

accurate in detecting deep venous

thrombosis in pelvic vessels or small

vessels in the calf. About 50% of

patients with a documented pul-

monary embolism have no evidence

of deep venous thrombosis. Critical

care nurses must carefully assess

patients’ extremities for unilateral

increase in size, warmth, redness, or

pain that may be present in patients

with deep venous thrombosis.

Because of Shelby’s urgent situation,

investigation for a source of the

emboli was suspended.

If clinical suspicion for pulmonary

embolism remains high, a noninva-

sive scintigraphic lung scan (ventila-

tion/perfusion scan) is done to

calculate pulmonary air flow and

blood flow. Pulmonary embolism is

suspected when areas of adequate

lung ventilation exhibit decreased

perfusion (getting the air but not the

blood flow). A normal ventilation/

perfusion ratio is reported as 0.8:1.

A high-probability result is defined

as 2 or more segmental perfusion

defects in the presence of normal

ventilation and is associated with an

85% to 90% likelihood of pulmonary

embolism. A low- or intermediate-

probability result does not exclude a

diagnosis of pulmonary embolism

and is not an acceptable end point if

clinical suspicion of pulmonary

embolism is high. In the Prospective

Investigation of Pulmonary Embolism

Diagnosis (PIOPED) study of 1990,

investigators concluded that a scan

with a high-probability result usually

indicates pulmonary embolism, but

that only a small percentage of

patients with pulmonary embolism

have a scan with a high-probability

result19(p1084); therefore, further testing

is mandatory. Patients with previous

pneumonia,

atelectasis, or pul-

monary embolism

may show a per-

sistent mismatch

between ventila-

tion and perfu-

sion for several

months following

the event (Figure

4).

Helical (spi-

ral) computed

tomography (Fig-

ure 5) is highly

accurate for direct

visualization of

large emboli in

the main or lobar

pulmonary arter-

ies, but it requires

a 20- to 30-second

breath-hold,

which may not be

feasible in

patients who are

in unstable condi-

tion.20(pp78-79) This

diagnostic imag-

ing technique is

replacing the ven-

tilation/perfusion scan in some

institutions.

Echocardiography is performed

to identify structural causes of chest

discomfort (Figure 6). This imaging

technique is not diagnostic for pul-

monary embolism, but evidence of

right ventricular hypocontractility

and dysfunction is seen in 95% of

patients who are in unstable condi-

tion. This test is useful in differenti-

ating between massive pulmonary

embolism and other causes of hemo-

dynamic compromise. Transthoracic

echocardiography can visualize intra-

cardiac thrombi, and transesophageal


Figure 4 Ventilation/perfusion scan(scintigraphic lung scan) shows mis-match in right lung.

Figure 5 Helical (spiral) computed tomography scan showsembolus in main pulmonary artery.

Figure 6 Transthoracic echocardiogram shows dilated rightventricle often seen in massive pulmonary embolism.




echocardiography can show thrombi

within the central pulmonary

artery.21

Moderate to severe tricuspid

regurgitation due to right ventricular

pressure overload leads clinicians to

suspect pulmonary embolism. The

finding of severe tricuspid regurgita-

tion on Shelby’s transthoracic echocar-

diogram provided the first clue to the

diagnosis of pulmonary embolism.

Nurses should inform nonintubated

patients that a transthoracic echocar-

diogram is a surface ultrasound image

obtained by placing a probe over the

chest to identify cardiac chambers,

valves, and the pulmonary artery.

The patient will feel pressure as the

technician glides the probe over the

chest wall. If a nonintubated patient

is scheduled for transesophageal

echocardiography, the nurse should

explain that the patient will be lightly

sedated and a probe will be passed

into the esophagus to assess the heart

and pulmonary artery more accu-

rately. Reassure the patient that he

or she will not recall the procedure.

Pulmonary angiography or aor-

tography is the reference standard

test for diagnosing pulmonary

embolism. Catheterization of the

right side of the heart with injec-

tion of contrast dye allows direct

visualization of the pulmonary vas-

culature and identification of areas

of obstruction. This test must be

performed when pulmonary

embolism cannot be reliably diag-

nosed or excluded by means of non-

invasive testing22 (Table 3). The

nurse explains that a catheter is

inserted into the femoral or brachial

artery and dye is injected thorough

the catheter in order to visualize the

pulmonary arteries and identify

areas of obstructed blood flow.

Goals of TreatmentThe goals of medical and/or sur-

gical interventions (Table 4) are to

relieve pulmonary obstruction, stop

clot propagation, regain or main-

tain hemodynamic stability, pre-

vent clot recurrence, and prevent

pulmonary hypertension.

Management of Pulmonary EmbolismMedical Management

Circulatory

Support. Medical

interventions for

treating massive

pulmonary

embolism are

aimed at preserv-

ing circulatory

support by maintaining blood pres-

sure, managing the airway, and pre-

venting new thrombus formation.

Airway management and oxygen

administration are paramount in the

treatment of pulmonary embolism.

Mechanical ventilation is often

required to maximize oxygen delivery

to the patient with circulatory col-

lapse. Cautious use of sedatives dur-

ing induction is warranted as these

drugs can blunt the catecholamine

Table 3 Diagnostic tests for pulmonary embolism

Diagnostic test

Electrocardiography

Chest radiography

Arterial blood gas analysis

D-dimer assay

Duplex ultrasonography

Ventilation/perfusionscintigraphy

Helical (spiral) computedtomography

Echocardiography

Aortography

Highlights

Rule out myocardial infarction, aortic dissectionAnterior T-wave inversion common in pulmonary embolismStrain pattern in right side of heart (S wave in lead I, Q

wave in lead III, T-wave inversion in lead III), new rightbundle branch block, and right-axis deviation seen inpulmonary embolism

The Westermark sign, the Hampton hump, and pleural effusion in pulmonary embolism

Rule out other causes of dyspnea

PaO2 < 80 mm Hg and respiratory alkalosisNormal PaO2 does not exclude pulmonary embolism

90% negative predictive value if <500 mg/L

95% sensitivity and specificity for detecting deep venousthrombosis above knee

A low or indeterminate result does not eliminate diagnosisof pulmonary embolism

High accuracy for detection of emboli in main or lobarpulmonary arteries

New severe tricuspid regurgitation and pressure overloadin right ventricle in pulmonary embolism

Transthoracic echocardiography for detection of intra-cardiac thrombi

Transesophageal echocardiography for detection ofthrombi in central pulmonary artery

Reference standard testAllows direct visualization of pulmonary vasculature to

identify areas of obstruction

Table 4 Treatment of pulmonary embolism

Medical options

Volume resuscitation

Administration of vasopressors

Anticoagulation

Administration of thrombolytics

Surgical options

Catheter embolectomy

Placement of filter in inferiorvena cava

Surgical embolectomy



response that the patient depends on

to maintain blood pressure through

peripheral vasoconstriction. Hypoten-

sion is initially treated with judicious

volume resuscitation of 1 to 2 L of

crystalloid infused over 1 hour. If

hypotension persists, the addition

of a vasopressor such as norepineph-

rine, epinephrine, dopamine, or

phenylephrine is warranted.

Thrombolytic Therapy. Patients in

stable condition are treated with anti-

coagulation alone, but thrombolytics

are the treatment of choice in hemo-

dynamically unstable patients.

Thrombolytics convert plasminogen

to plasmin and directly lyse the clot.

Plasminogen activation interferes

with coagulation by inactivating

fibrinogen and factors II, V, and VII.

Clot lysis results in faster improvement

in pulmonary perfusion, hemody-

namic alterations, and gas exchange,

which rapidly reduces right ventric-

ular afterload and dysfunction. The

thrombolysis process is nonselective

and can cause a major bleeding event.

Bleeding complications occur in 20%

of patients, and intracranial hemor-

rhage occurs in 3% of patients.

Contraindications to use of

thrombolytics include pregnancy

and obstetric delivery, recent major

or minor trauma including cardiopul-

monary resuscitation, recent surgery

(within past 10 days), acute internal

bleeding (within past 6 months),

hemorrhagic retinopathy, uncon-

trolled hypertension (systolic blood

pressure >200 mm Hg or diastolic

blood pressure >100 mm Hg), recent

stroke (within past 2 months), active

intracranial disease (aneurysm, arte-

riovenous malformation, neoplasm),

puncture of a noncompressible vessel,

organ biopsy, infective endocarditis,

pericarditis, and aneurysm.23

In the United States, 3 thrombolyt-

ics have been approved for treatment

of pulmonary embolism. Streptoki-

nase, a bacterial protein derivative,

is produced from streptococcal bac-

teria and often causes febrile reactions.

Streptokinase is administered as an

intravenous infusion of 250000 IU

over 30 minutes, followed by 100000

IU/h intravenously for 24 to 72 hours.

This product is highly antigenic and

may be administered only once dur-

ing a 6-month period. Febrile reac-

tions respond to treatment with

acetaminophen (Tylenol).24

Urokinase is produced from cul-

tures of human source materials and

thus has a small potential to transmit

infectious agents. Urokinase is admin-

istered as an intravenous bolus of

4400 U/kg over 10 minutes, followed

by 4400 U/kg per hour intravenously

for 12 hours.24

The third choice, alteplase,

uses recombinant DNA technology

and is synthesized by a human

melanoma cell line. This enzyme

binds to fibrin in a thrombus, caus-

ing conversion of plasminogen to

plasmin. Alteplase is administered

as a 100-mg intravenous infusion

over 2 hours27 (Table 5).

Anticoagulation. Anticoagulation

with unfractionated heparin and war-

farin is the standard treatment for pul-

monary embolism in stable patients.

Heparin. Heparin acts as a cata-

lyst to activate prothrombin, which

inhibits factor Xa and thrombin.

Heparin is unable to dissolve existing

thrombus because of the inability to

inhibit thrombin bound to fibrin.

The activated partial thromboplas-

tin time (aPTT) is maintained at 60

to 100 seconds or according to insti-

tutional policy. The nonspecific bind-

ing of unfractionated heparin to other

plasma proteins contributes to a vari-

able dose response among patients.

Low-Molecular-Weight Heparin.

Low-molecular-weight heparin is a

heparin-based product used in

patients with submassive pulmonary

embolism and deep venous throm-

bosis, but it remains an unproven

treatment option for patients with

massive pulmonary embolism. Low-

molecular- weight heparin is also

contraindicated in patients with

heparin-induced thrombocytopenia

(HIT).

Warfarin. Warfarin (Coumadin)

therapy should overlap with heparin

therapy for 4 days to avoid transient

hypercoagulability that may occur

with isolated administration of war-

farin. The warfarin-induced decline

in levels of coagulation factors is a

function of the half-life of each factor,

which varies from 5 hours for factor

VII to 72 hours for factor II. The half-

life of warfarin is 36 to 42 hours;

therefore, an increase in the interna-

tional normalized ratio (INR) is not

seen until 2 days after the first dose

is administered. The goal for the INR

is 2 to 2.5 for 3 to 6 months.8 War-

farin may be initiated after 48 hours


Table 5 Thrombolytic therapy

Drug

Streptokinase (Kabikinase)

Urokinase (Abbokinase)

Alteplase (Activase)

Loading dose

250∞000 IU in 30 min

4400 IU/kg in 10 min

100 mg in 2 h

Maintenance

100∞000 IU/h for 24-72 h

4400 IU/kg/h for 12 h

None




of direct thrombin inhibitor therapy

as long as the platelet count is

greater than 100 × 109/L.25 Warfarin

is contraindicated in pregnancy

because it crosses the placenta. War-

farin is safely used in lactating

patients because it is not excreted in

breast milk.

Heparin-Induced Thrombocytopenia

HIT or “heparin allergy” is an

important complication of heparin

therapy and can result in severe

venous and arterial thrombosis.26

This autoimmune disorder occurs in

1% to 3% of patients who receive

heparin-based products. HIT results

from the development of heparin-

associated antibodies. These anti-

bodies induce platelet aggregation in

the presence of heparin. Thrombosis

may occur in both arterial and venous

circulation. All patients who receive

heparin are at risk for HIT, because

no known characteristics of patients

can be used to predict the develop-

ment of HIT.

HIT occurs in 2 forms: HIT-1, also

known as heparin-associated throm-

bocytopenia, is a nonimmune disor-

der that occurs 2 to 3 days after

initiation of heparin therapy. This

disorder may occur in up to 15% of

patients exposed to heparin. The

thrombocytopenia is transient, and

platelet counts rarely decrease to less

than 100 × 109/L. Patients are not at

risk for development of significant

thrombosis. HIT-2 is an immune-

mediated disorder that occurs in 1%

to 3% of patients who receive heparin

and is frequently associated with life-

or limb-threatening thromboembolic

complications (deep venous throm-

bosis, pulmonary embolism, cere-

brovascular accident, myocardial

infarction, extremity ischemia, gan-

grene, and death). This disorder

causes a significant decrease in platelet

count. Thrombocytopenia manifests

5 to 10 days after the start of heparin

therapy, and platelet count decreases

30% to 50%, to less than 100 × 109/L.27

HIT is a clinical diagnosis sup-

ported by confirmatory laboratory

work. The C-serotonin release assay

combines serum from patients with

suspected HIT with serum from

healthy donors and adds this to ther-

apeutic concentrations of heparin. A

positive result detects the C-serotonin

released from the serum of the patient

with suspected HIT.

The treatment for HIT is imme-

diate cessation of use of all heparin-

based products, including

heparin-coated catheters and heparin

flushes. Patients with HIT who require

anticoagulation for deep venous

thrombosis or pulmonary embolism

are treated with a direct thrombin

inhibitor, such as lipirudin or arga-

troban. The direct thrombin inhibitor

is administered until the platelet

count has increased to 100 × 109/L.

Lipirudin is administered as an

intravenous bolus of 0.4 mg/kg fol-

lowed by infusion of 0.15 mg/kg

per hour for an aPTT 1.5 to 2.5

times the time at baseline. Lipirudin

is renally excreted and requires

decreased dosing in patients with

renal insufficiency. Argatroban is

administered as a 2 mg/kg per

minute intravenous infusion, with-

out bolus for an aPTT 1.5 to 3 times

the aPTT at baseline. Argatroban is

metabolized by the liver and may be

useful for a patient with renal

impairment.28(pp2044-2045) Concomitant

warfarin therapy is started once the

platelet count reaches 100 × 109/L.

Argatroban should be continued

until the INR is 4 or greater. This

direct thrombin inhibitor is then dis-

continued and the INR is rechecked

in 4 to 6 hours. If the INR remains at

a therapeutic level (>2), argatroban

does not need to be restarted.

Bivalrudin (Angiomax) is another

direct thrombin inhibitor that is cur-

rently approved by the Food and Drug

Administration for use in patients

undergoing coronary angioplasty

with unstable angina and concomi-

tant aspirin therapy. This drug is used

off-label in some institutions as an

alternative to heparin in patients

with HIT. At this time, however,

there is not enough evidence to sup-

port this indication.

Surgical Management

Catheter Embolectomy. Surgical

interventions are usually reserved for

patients in unstable condition with

contraindications to thrombolytic

therapy. Percutaneous catheter

embolectomy is performed during

pulmonary angiography in an effort to

remove the obstructive embolus. This

procedure may be performed by one

of 2 techniques. The first method is

aspiration embolectomy, in which suc-

tion is applied to remove the embolic

material. The second technique is

mechanical embolectomy, which

involves maceration or fragmentation

of the embolus.2 Mechanical embolec-

tomy has a success rate of 80%, but

there is danger of distal migration of

the pulmonary embolism.

Vena Caval Filters. Percutaneous

filters are placed in the inferior vena

cava to prevent recurrent pulmonary

embolism by preventing clot migra-

tion. These filters are often used for

patients with contraindications to

anticoagulation, those with recur-

rent pulmonary embolism, or those



who have underlying cardiac or pul-

monary disease in whom a pulmonary

embolism would be fatal. Several fil-

ters are available for use in the United

States, including Greenfield (Boston

Scientific, Natick, Mass), Vena-Tech

LGN or LP (Braun, Bethleham, Pa),

Simon-Nitinol (Bard, Murray Hill,

NJ), Recovery (Bard) bird’s nest, and

Gunther-Tulip (Cook). Complications

of filter placement include thrombo-

sis at the insertion site, filter migra-

tion, erosion through the wall of the

inferior vena cava, or obstruction of

the inferior vena cava during deploy-

ment of the filter.29

Surgical Embolectomy. Surgical

embolectomy involves manual

removal of the thrombus from the

pulmonary artery. This procedure is

usually reserved for patients in unsta-

ble condition who have contraindi-

cations to thrombolytic therapy.29

Extracorporeal membrane oxygena-

tion is a temporary cardiopulmonary

support system used sparingly in the

treatment of patients with circulatory

collapse due to pulmonary embolism.

Extracorporeal membrane oxygena-

tion is used to maintain oxygenation

and tissue perfusion until the throm-

bus can be dissolved or removed.

Nursing CarePreventative measures for deep

venous thrombosis must be used

routinely for any hospitalized patient.

Compression stockings should be

placed on the lower extremities

before the patient gets out of bed.

External pneumatic compression

boots, which intermittently compress

the calf and accelerate deep venous

flow, may be used in bed-bound

patients. Adequate hydration and

early ambulation are encouraged to

prevent deep venous thrombosis.

Daily assessment of extremities for

pain, erythema, and size discrepancy

is vitally important. The Homan sign

(pain on dorsiflexion) is apparent in

only 30% of the cases. The nurse must

recognize risk factors for pulmonary

embolism and vigilantly monitor

patients who are immobilized or

have had their activity restricted for

unexplained tachypnea, tachycardia,

and restlessness. These signs must

not be attributed to anxiety unless a

physical cause has been sought first.

Critically ill or postoperative

patients are at high risk for venous

thromboembolism and should be

assessed for use of prophylactic

heparin or low-molecular-weight

heparin subcutaneously or intra-

venously. If pulmonary embolism is

discovered and the patient is hemo-

dynamically unstable, the nurse will

institute appropriate fluid adminis-

tration and inotropic support to

maintain a systolic blood pressure of

90 mm Hg. If pulmonary hyperten-

sion and right-sided heart failure are

present, the nurse may consider cau-

tious use of a vasodilator such as

nitric oxide. The nurse can provide

short explanations of the diagnostic

tests and invasive procedures to

reassure the patient that this life-

threatening condition is treatable.

Neurological and vascular assess-

ments should be performed hourly

to evaluate organ perfusion. Confu-

sion or agitation may indicate respi-

ratory acidosis (increased PaCO2 and

decreased pH). Weakened pulses

and cool, mottled extremities are

late physical findings that indicate

impending circulatory collapse.

The nurse should suspect pul-

monary embolism as an underlying

cause of syncope and cardiac arrest

with pulseless electrical activity.

Vigilance during anticoagulation or

administration of thrombolytic agents

is warranted to prevent significant

bleeding complications. A decrease

in hemoglobin level and hematocrit

may alert the nurse to occult bleed-

ing in the retroperitoneum or gas-

trointestinal tract. If the nurse

encounters a change in mental sta-

tus or new focal neurological deficits

in a patient receiving thrombolytics,

intracranial hemorrhage must be

eliminated as a possible cause. An

emergent neurosurgical consultation

and an unenhanced computed tomog-

raphy scan of the brain is warranted

in this situation.

Avoidance of unnecessary phle-

botomy, arterial puncture, and other

invasive procedures may reduce the

risk of hemorrhage during throm-

bolytic administration. Significant

hemorrhage requires discontinua-

tion of the thrombolytic agent and

administration of cryoprecipitate or

fresh frozen plasma to reverse the

coagulopathy. Decreasing platelet

counts during heparin administra-

tion may suggest a diagnosis of HIT.

Education of PatientsDuring recovery, the nurses were

instrumental in preparing the patient

for discharge. The nurses instructed

Shelby and her family on the impor-

tance of continued warfarin admin-

istration for 3 to 6 months to prevent

further thrombus development.

Foods high in vitamin K, such as dark

green vegetables and apricots, must

be limited during this time period to

prevent decreased warfarin action.

The nurses informed Shelby that a

therapeutic INR value is between 2

and 3 and that adjustments in the

dosage of warfarin may be needed to

maintain her INR in this range.





Shelby was advised not to use war-

farin with acetaminophen, nons-

teroidal anti-inflammatory drugs,

amiodarone, or fluoroquinolone

antibiotics because such combina-

tions can quickly elevate the INR.

The nurses reminded Shelby to

stretch every hour during confined

travel and to remain well hydrated

because patients with history of deep

venous thrombosis or pulmonary

embolism are at a greater risk for

subsequent development of venous

thrombosis.15 The nurses encouraged

Shelby to recount her history of deep

venous thrombosis and pulmonary

embolism to future healthcare

providers and to wear a Medic-Alert

bracelet indicating her history of

pulmonary embolism.

SummaryMassive pulmonary embolism in

the setting of syncope and cardiac

arrest is often fatal if not diagnosed

rapidly and correctly. The patient’s

cardiopulmonary status before the

embolic event is a predictor of mor-

bidity and mortality. This postpartum

patient posed unique challenges to

the usual management of pulmonary

embolism. Spiral computed tomog-

raphy could not be used for diagno-

sis because of the patient’s unstable

hemodynamics. Thrombolytic agents

were contraindicated because of the

recent obstetrical delivery and car-

diopulmonary resuscitation. There-

fore, surgical embolectomy and

placement of a filter in the inferior

vena cava were the treatments of

choice. Shelby also received standard

medical treatment, including external

pneumatic compression, heparin,

and warfarin postoperatively.

Two factors were paramount in

the successful outcome of this case.

The first was the rapid diagnosis and

intervention that made survival a

possibility. The second, but perhaps

the most important, factor was the

nursing care of this patient’s entire

family, including her husband, par-

ents, newborn baby, and 2 young

children. The bedside staff facilitated

visits between mother and newborn

in the surgical intensive care unit

and provided expert care, unyielding

support, and encouragement during

this life-threatening event. The

orchestrated interdisciplinary efforts

of many nurses and physicians paved

the way for a modern-day Christmas

miracle for Shelby and her family.

References1. Marty AT, Hilton FL, Spear RK, Greyson B.

Postcesarean pulmonary embolism, sus-tained cardiopulmonary resuscitation,embolectomy, and near death experience.Obstet Gynecol. 2005;106:1153-1155.

2. Owen AR, Gibson MR. Pulmonaryembolism: advances in diagnosis and treat-ment. Care Crit Ill. 2004;20:79-84.

3. Feied C, Handler JA. Pulmonary Embolism.2006. Available at: http://www.emedicine.com/EMERG/topic490.htm. AccessedNovember 15, 2006.

4. Smeltzer SC, Bare BG. Management ofpatients with chest and lower respiratorytract disorders. In: Brunner and Suddarth’sTextbook of Medical-Surgical Nursing.Philadelphia, Pa: Lippincott Williams andWilkins; 2000:471-475.

5. Seifert PC. Cardiac trauma and emergencysurgery. In: Cardiac Surgery PerioperativePatient Care. Philadelphia, Pa: Mosby;2002:559-561.

6. Sole ML, Lamborn ML, Hartshorn JC.Acute respiratory failure. In: Introduction toCritical Care Nursing. 3rd ed. Philadelphia,Pa: WB Saunders; 2001:365-368.

7. Gawlinski A, Hamwi D. Pulmonary disor-ders. In: Acute Care Nurse Practitioner: ClinicalCurriculum and Certification Review. Philadel-phia, Pa: WB Saunders; 1999:90-101.

8. Wan S, Quinlan DJ, Agnelli G, EikelboomJW. Thrombolysis compared with heparinfor the initial treatment of pulmonaryembolism. Circulation. 2004;110:744-749.

9. Scurr JH, Machin SJ, Bailey-King S, MackieIJ, McDonald S, Smith PD. Frequency andprevention of symptom less deep veinthrombosis in long-haul flight: a random-ized trial. Lancet. 2001;357:1485-1489.

10. Anderson FA, Wheeler HB, Goldberg RJ, etal. A population-based perspective of thehospital incidence and case-fatality rates ofdeep vein thrombosis and pulmonaryembolism: the Worcester DVT study. ArchIntern Med. 1991;51:933-935.

11. Anderson FA, Spencer FA. Risk factors forvenous thromboembolism. Circulation.2003;107(suppl):I9-I16.

12. Ros HS, Lichtenstein P, Bellocco R, Peters-son G, Cnattingius S. Pulmonary embolismand stroke in relation to pregnancy: howcan high-risk women be identified? Am JObstet Gynecol. 2002;186:198-203.

13. Fedullo PF, Tapson VF. The evaluation ofsuspected pulmonary embolism. N Engl JMed. 2003;349:1247-1255.

14. Koschel MJ. Pulmonary embolism. Am JNurs. 2004;104:46-50.

15. Cardin T, Martinelli A. Pulmonaryembolism. Crit Care Nurs Q. 2004;27:310-322.

16. Ferrari E, Imbert A, Chevalier T, Mihoubi A,Morand P, Baudouy M. The ECG in pul-monary embolism: predictive value of nega-tive T-waves in precordial leads, 80 casereports. Chest. 1997;111:537-543.

17. Kouchoukos NT, Blacstone EH, Doty DB,Hanley FL, Karp RB, eds. Kirklin/Barratt-Boyes Cardiac Surgery. 3rd ed. Philadelphia,Pa: Churchill-Livingstone; 2003.

18. Fishman AP, Elias JA, Fishman JA, GrippiMA, Kaiser LR, Senior RM. Fishman’s Man-ual of Pulmonary Diseases and Disorders. 3rded. New York, NY: McGraw-Hill; 2002.

19. Cunningham FG, Leveno KJ, Bloom SL,Hauth JC, Gilstrap LC, Wenstrom KD.Williams Obstetrics. 22nd ed. New York, NY:McGraw-Hill; 2005.

20. Todd BA. Acute Care Nurse PractitionerSecrets. St. Louis, Mo: Elsevier Mosby; 2005.

21. Kearon C. Diagnosis of pulmonary embolism.Can Med Assoc J. 2003;168:183-194.

22. Goldhaber SZ. Acute pulmonary embolism:I, epidemiology, pathophysiology, and diag-nosis. Circulation. 2003;108:2726-2729.

23. Goldhaber SZ. Acute pulmonary embolism:II, risk stratification, treatment, and preven-tion. Circulation. 2003;108: 2834-2838.

24. Spratto GR, Woods AL. 2003 Nurse’s DrugHandbook. Clifton Park, NY: Thomson Del-mar Learning; 2003.

25. Sadosty AT. Pulmonary embolism. EmergMed Clin North Am. 2003;21:917-920.

26. Yang JC. Prevention and treatment of deepvein thrombosis and pulmonary embolismin critically ill patients. Crit Care Nurs Q.2005;28:72-79.

27. Barcelona R. Type II heparin-induced throm-bocytopenia: new treatment options. Avail-able at: http://www.clevelandclinicmeded.com/medical_info/pharmacy/septoct2001/thrombocytopenia.htm. Accessed Novem-ber 15, 2006.

28. Lichtman MA, Beutler E, Kipps TJ, Selig-sohn U, Kaushansky K, Prchal J, eds.Williams Hematology. 7th ed. New York, NY:McGraw-Hill; 2006.

29. Dalen JE. Pulmonary embolism: what havewe learned since Virchow? Treatment andprevention. Chest. 2002;122:1801-1817.



CE Test Test ID C0713: Massive Pulmonary EmbolismLearning objectives: 1. Identify patients at risk for a massive pulmonary embolus 2. Describe current assessment and diagnostic strategies for pulmonary embolus3. Summarize possible medical and surgical interventions for pulmonary embolus 4. Discuss goals of treatment in the care of patients with pulmonary embolus

Program evaluationYes No

Objective 1 was met � �Objective 2 was met � �Objective 3 was met � �Objective 4 was met � �Content was relevant to my

nursing practice � �My expectations were met � �This method of CE is effective

for this content � �The level of difficulty of this test was: � easy � medium � difficult

To complete this program, it took me hours/minutes.

Test answers: Mark only one box for your answer to each question. You may photocopy this form.

1. What is the annual incidence of pulmonary embolus resulting in maternaldeaths per 100 000 live births versus the pulmonary embolus death rate in thegeneral population per 100 000?a. 65 versus 2b. 70 versus 60c. 2 versus 65d. 7 versus 65

2. Which of the following is a risk factor for a pulmonary embolus?a. Recent surgery b. Recent emotional stressor c. Recent blood transfusion d. Recent placement of a central catheter

3. Which is of the following is a preventative nursing measure that can beimplemented in the hospital to reduce the risk of deep vein thrombosis?a. Compression stockings or pneumatic bootsb. Bed rest or limited mobilityc. Assessment of arms for pain, erythema, or size differencesd. Frequent D-dimers or leg ultrasounds

4. A massive pulmonary embolus occurs when a thrombus occludes more than what percentage of the pulmonary vasculature?a. 75%b. 50%c. 90%d. 40%

5. What do the main sources of thrombi in massive pulmonary embolus include?a. Carotid, upper extremities, and cardiac vasculatureb. Lower extremities, pelvis, and kidney vasculaturec. Lower extremities, upper extremities, and pelvis vasculatured. Upper extremities, pelvis and carotid vasculature

6. What is a single common characteristic shared by patients at risk forheparin-induced thrombocytopenia?a. Development of venous and arterial thrombosisb. Previous exposure to heparinc. Life- and limb-threatening complicationsd. Need for lifelong heparin treatment

7. What is the most common rhythm seen after a cardiac arrest related to a pulmonary rhythm?a. Pulseless electrical activityb. Ventricular fibrillationc. Asystoled. Tachycardia

8. What do the 3 classic signs and symptoms of a pulmonary embolusinclude?a. Gradual onset tachycardia, apnea, and feeling of apprehensionb. Acute onset dyspnea, hemoptysis, and chest painc. Acute onset tachycardia, tachypnea, and chest paind. Gradual onset dyspnea, tachypnea, and chest pain

9. How is the D-dimer test used to detect the presence of pulmonary embolus?a. If less than 500 mg/L it has a negative predictive value of 90% b. If greater than 500 mg/L it has a negative predictive value of 90% c. If less than 500 mg/L it has a positive predictive value of 90% d. If greater than 500 mg/L it has a positive predictive value of 90%

10. If clinical suspicion remains high after initial noninvasive test(s) butpulmonary emboli cannot be def initely diagnosed (possible false negativeresults), what is the standard reference test?a. Chest spiral computed tomographyb. Ventilation/perfusion scintigraphyc. Aortography d. Cardiac catherization

11. What is the standard treatment for pulmonary embolus in a stablepatient?a. Low-molecular-weight heparin injections followed by an unfractionated

heparin infusionb. Low-molecular-weight heparin injectionsc. Coumadin therapyd. Unfractionated heparin infusion with overlapping warfarin therapy

12. What is a surgical intervention aimed at primary prevention of newpulmonary emboli?a. Direct thrombolytic therapyb. Insertion of inferior vena cava filter c. Surgical embolectomyd. Catheter embolectomy

13. What are the 2 main goals of circulatory support in patients with massive pulmonary embolus?a. Maintaining blood pressure with fluids and vasopressors along with providing

adequate oxygenationb. Avoiding hypertension with vasodilators and providing adequate oxygenationc. Provide support to the family while keeping the patient sedatedd. Early detection of embolus along with administering coumadi

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Test ID: C0713 Form expires: February 1, 2009 Contact hours: 1.5 Fee: $11 Passing score: 10 correct (77%) Category: A Test writer: Patti McCluskey-Andre, RN, MSN, ACNP-C/CCNS

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Kathleen ShaughnessyMassive Pulmonary Embolism

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ClinicalArticle Massive Pulmonary Embolismccn.aacnjournals.org/content/27/1/39.full.pdf · pulmonary embolism. ... Discuss goals of treatment in the care of patients with pulmonary