COMPREHENSIVE

CASE STUDY ON
PULMONARY
EMBOLISM

Prepared by:
Frances Leih C. Francisco Mariefer Rose D. Guevarra
Marry Lizeanne M. Gacutan Marc Daniel M. Ibarra
Janne Eira B. Garcia Kristopher John M. Jimenez
Juan Paulo Garcia Ela Rica M. Kabigting
Daren Joyce M. Genese

Prepared for:
Ma’am Jullie Ann D. Esconde, RN, MAN

Rotation Schedule:
November 27 and December 2-18, 2021

Date Submitted:
January 3, 2021

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I. INTRODUCTION

Pulmonary embolism is a blockage in one of the pulmonary arteries in the lungs

caused by a thrombus that formed and embolized from another vein from the body. A
common form of venous thrombosis is deep vein thrombosis (DVT) that forms in the deep
veins such as in the leg or pelvis including the popliteal vein, femoral vein, and iliac veins
of the pelvis. Occasionally, blockages in the blood vessels are also caused by substances
other than blood clots, such as fat from the marrow of a broken long bone, part of a tumor
and air bubbles. PE is a potentially life-threatening disease with significant morbidity and
potentially fatal outcomes. However, prompt treatment greatly reduces the risk of death.

According to a systematic review by Belohlavek, et. al while no exact

epidemiological data are available, the incidence of PE is estimated to be approximately
60 to 70 per 100,000, and that of venous thrombosis approximately 124 per 100,000 of
the general population. The European guidelines for the diagnosis and management of
PE report annual incidence rates of venous thrombosis and PE of approximately 0.5 to
1.0 per 1000 inhabitants. However, the actual figures are likely to be substantially higher
because silent PE can develop in up to 40% to 50% of patients with deep vein thrombosis
(DVT). In addition, autopsy studies have shown that PE had been diagnosed before death
in 30% to 45% of patients. After coronary artery disease and stroke, acute PE ranks third
among the most common types of cardiovascular diseases. It is believed to result from a
patient’s risk factors include obesity, cigarette use, age- wherein it disproportionately
affects the older population and incidence rates of VTE in those older than 70 years are
three times higher than those aged 45 to 69 years, which again are three times higher
than those aged 20 to 44 years but the reported incidence of VTE is inconsistent with
regard to gender, though several studies suggest higher incidence in males. Moreover, a
study of the University of California revealed race as a factor – African-Americans with
the highest risk and followed by Caucasians. Personal history of VTE, active malignancy
or another disabling conditions such as heart or respiratory failure, congenital or acquired
coagulation disorders, hormone replacement therapy and oral contraception.

The overwhelming majority of patients with PE tend to complain primarily of

sudden-onset or worsened resting dyspnea. PE, however, can also present as
progressive exercise-induced dyspnea. In addition, more than one-half of patients
experience chest pain that is sometimes difficult to distinguish from an angina of ischemic
origin. Other presentations of PE can include cough, hemoptysis and syncope. The often-
reported triad of dyspnea, chest pain and hemoptysis does not actually occur frequently.
Regardless, more than 90% of PE patients present with dyspnea, tachypnea or chest
pain. Surprisingly, a large number of patients, including those with massive PE, had mild
or nonspecific symptoms or even were asymptomatic. And the overall presentation also
could be easily confused with systemic disorders or other cardio-pulmonary diseases. In
addition, in the most serious cases, PE can ultimately result in cardiac arrest, shock or
hypotension.

Diagnosis is difficult in the presence of comorbidities such as bronchopneumonia,

chronic obstructive pulmonary disease (COPD), asthma or chronic fibrotizing pulmonary
processes. In contrast, PE is readily diagnosed in patients presenting with DVT. In the
process of diagnosis, clinical symptoms were recommended to be firstly assessed ideally

2
by a validated prediction model, although final diagnosis should be mainly based on
clinical findings, laboratory tests, and imaging data. Therefore, some of the initial
laboratory studies and diagnostic procedures that may be done includes ABG analysis,
d-dimer test, electrocardiogram (ECG), computed tomography (CT) scan, lung scan,
pulmonary angiogram, ultrasound of the leg that helps to identify blood clots in patients
who cannot have an X-ray due to dye allergies or who are too sick to leave their hospital
room and magnetic resonance imaging (MRI) of the legs or lungs.

Immediate medical treatment is necessary and the goal of treatment is to break up

clots and help keep other clots from forming. Treatment options include medicines and
procedures such as anticoagulants, or blood thinners that keep blood clots from getting
larger and stop new clots from forming and thrombolytics which are medicines to dissolve
blood clots. Procedures include catheter-assisted thrombus removal that uses a flexible
tube to reach a blood clot in the lung to break up the clot or to deliver medicine through
the tube; and a vena cava filter which may be used in some people who cannot take blood
thinners, the filter catches blood clots before they travel to the lungs, which prevents
pulmonary embolism but the filter does not stop new blood clots from forming.
Additionally, healthy lifestyle changes such as heart-healthy eating, exercise, and, quitting
smoking would also helpful in prevention as well as using compression stockings to
prevent deep vein thrombosis (DVT), moving the legs when sitting for long periods of time
such as on long trips and moving around as soon as possible after surgery or being
confined to a bed. It is also important to get regular checkups with the provider, to make
sure that the dosage of medicines is working to prevent blood clots but not causing
bleeding.
References:

Bĕlohlávek, J., Dytrych, V., Linhart, A.(2013). Pulmonary embolism, part I: Epidemiology, risk factors and
risk stratification, pathophysiology, clinical presentation, diagnosis and non-thrombotic pulmonary
embolism. U.S. National Library of Medicine.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3718593/

Ji, Qy., Wang, Mf., Su, Cm. et al. (2017). Clinical symptoms and related risk factors in pulmonary embolism
patients and cluster analysis based on these symptoms. https://doi.org/10.1038/s41598-017-
14888-7

Morrone, D., Morrone V. (2018, April 11). Acute Pulmonary Embolism: Focus on the Clinical Picture.
Korean Circulation Journal https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5940642/pdf/kcj-48-
365.pdf

Pulmonary Embolism. Mayo Clinic https://www.mayoclinic.org/diseases-conditions/pulmonary-

embolism/symptoms-causes/syc-20354647

Pulmonary Embolism- What are the treatments for a pulmonary embolism (PE)? National Library of
Medicine. MedlinePlus. https://medlineplus.gov/pulmonaryembolism.html

Roland, J. (2019, November 14). Does Alcohol Consumption Affect Your Risk for DVT, and Is It Safe If
You’ve Had a DVT? Healthline. https://www.healthline.com/health/dvt-and-alcohol

Suszynski, M., & Bass, P. F., III MD. (2014, August 20). Ethnicity and DVT Risk - DVT Center. Retrieved
December 16, 2021, from https://www.everydayhealth.com/heart-disease/dvt/ethnicity-and-dvt-
risk.aspx

3
II. PERSONAL DATA

Name: Mr. X

Age: 26 years old

Race: Caucasian

Chief Complaint: Sudden syncopal episode that lasted for 5 minutes

Admitting Diagnosis: Pulmonary embolism secondary to deep vein thrombosis

III. NURSING HISTORY

i. History of Present Illness

The patient brought himself to the Emergency Department reporting he

collapsed while standing and lost consciousness for 5 minutes all of a sudden. He
claimed to have recovered immediately but was extremely weak and dyspneic. He
was also diaphoretic and tachypneic, but denied any associated chest pain or
palpitations. No tonic-clonic activity was witnessed, and he experienced no
incontinence.

ii. Past Medical History

The patient reported to have no history of past diseases.

iii. Personal and Social History

The patient was a computer programmer and he had been working 18 hours a
day without rest periods for a month.

IV. THEORETICAL FRAMEWORK

DOROTHEA OREM’S THEORY OF SELF CARE

“Individuals, families, groups and communities need to be taught self-care.”

SELF-CARE THEORY

• Self- Care. Practice of activities that individuals initiates and perform on their own
behalf in maintaining life, health and well-being.
• Self-care Agency. Individual’s ability to perform the self-care activities.
• Self-Care Requisites. Action directed towards provision of self-care
• Therapeutic Self-Care Demand. Totality of self-care actions to be performed for
some duration in order to meet self-care requisite by using valid methods and
related sets of operations and actions.

In this case, the theory shall be utilized to focus on the performance or practice of
activities that Mr. X can and will perform on his own behalf. As aforementioned, Mr. X is
a computer programmer that works for 18 hours day without rest. Knowing his occupation,
we expect that the time spent for it is time that he has prolonged sitting position, which
disrupts the proper blood circulation to his lower extremities. On a positive note, Mr. X
reports to have no other lifestyle habits that exacerbated the development of DVT.

4
 Furthermore, this theory can be used as a ground to patient education – that Mr.
X shall need to practice physical activity more often despite his job, and to continue
avoiding vices that can induce the recurrence of his DVT and PE. As stated in the case,
interventions were successful for Mr. X reported to not have experienced another episode
of syncope or PE.

V. PHYSICAL ASSESSMENT

VITAL SIGNS TECHNIQUE ASSESSMENT INTERPRETATION

Respiratory Rate Inspection 32 breaths/min Tachypneic
Palpation 128 bpm Regular but
Pulse Rate
tachycardic
Use of Aneroid
Blood Pressure 126/72 mmHg Normal
Sphygmomanometer
Oxygen Use of Pulse
90% Hypoxemia
Saturation Oximeter

HEAD TO TOE EXAMINATION

BODY PART TECHNIQUE ASSESSMENT INTERPRETATION
General Interview and No abnormality detected,
Normal
Appearance Inspection conversant
HEENT

Head Inspection No lesions, trauma or presence Normal, Atraumatic

and Palpation of parasites

Eyes Inspection, Anicteric Sclerae, moist Normal appearance

PERRLA conjunctivae; no lid-lag and vision

Throat and Inspection Normal hard and soft palate Normal

Mouth

Neck Inspection Trachea midline, FROM is Normal position

and Palpation supple and range of
motion, no
presence of
thyromegaly or
lymphadenopathy

Chest and Reduced breath sounds Air or fluid in or

Auscultation
Lungs bilaterally at the lung bases around the lungs
Cardio-
Auscultation Regular rate and rhythm Normal
vascular
Inspection,
Soft, non-tender; no masses or
Abdomen Percussion Normal
hepatosplenomegaly
and Palpation
DVT in left leg, (+) Homans' sign
in the left leg, and the left calf
Extremities Inspection DVT, edema
measured 3 cm more than the
right one
Normal temperature, turgor and
Inspection
Skin texture; no rash, ulcers or Normal
and Palpation
subcutaneous nodules

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 HEAD TO TOE EXAMINATION
BODY PART TECHNIQUE ASSESSMENT INTERPRETATION
Appropriate affect, alert and
Mental Interview and
oriented to person, place and Normal
Status Observation
time

VI. LABORATORY RESULTS AND DIAGNOSTIC PROCEDURES

COMPLETE BLOOD COUNT

TEST RESULT NORMAL VALUES INTERPRETATION
Normal based on
WBC Not provided 4.0-10 × 109/L
case
Neutrophils 2500 – 8000 per mm3
Lymphocytes 1000 – 4000 per mm3
Normal based on
Monocytes Not provided 100 – 700 per mm3
case
Eosinophils 50 – 500 per mm3
Basophils 25 – 100 per mm3
M: 4.5-6.3 million Normal based on
RBC Not provided
F: 4.2-5.4 million case
M: 39-52% Normal based on
Hct Not provided
F: 36-45% case
M: 14-18 g/dL Normal based on
Hgb Not provided
F: 12-16 g/dL case
Normal based on
MCV Not provided 77 – 97 × 10-15/L
case
Normal based on
MCH Not provided 26 – 32 g/dL
case
M: 11.8 – 14. 5% Normal based on
RDW Not provided
F: 12.2 – 16. 1% case
Platelet Normal based on
Not provided 140 – 440 × 109/L
count case
7 – 12 fL (150,000 – 450,000 Normal based on
MPV Not provided
platelets/mL of blood) case
THROMBOPHILIA PANEL
TEST RESULT NORMAL VALUES INTERPRETATION
Prothrombin
gene Normal based on
Not provided Negative
mutation case
(G20210A)
Protein C Normal based on
Not provided 68-170 IU dL-1
Deficiency case
Protein S Normal based on
Not provided 64-147 IU dL-1
Deficiency case
Antithrombin Normal based on
Not provided 83-123 IU dL-1
Deficiency case
ARTERIAL BLOOD GAS
TEST RESULT NORMAL VALUES INTERPRETATION
Low;
With an elevated
Oxygen alveolar-arterial
90% 94% - 100%
Saturation oxygen gradient
(result not provided
on case)
Normal based on
pH Not provided 7.35 – 7.45
case
Carbon
Carbon dioxide is not
Dioxide 58 mmHg 35-45 mmHg
emitted adequately
(PaCO2)
Oxygen Normal based on
Not provided 75 – 100 mmHg
(PaO2) case

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 ARTERIAL BLOOD GAS
TEST RESULT NORMAL VALUES INTERPRETATION
Bicarbonate Normal based on
22 – 26 mEq/L Not provided
9 (HCO3) case
LIVER AND KIDNEY FUNCTION TEST
TEST RESULT NORMAL VALUES INTERPRETATION
Blood Uric Normal based on
Not provided 202.30-416.50 umol/L
Acid case
Normal based on
BUN Not provided 2.14-7.14 mmol/L 4.20
case
Normal based on
SGPT (ALT) Not provided 0-33 U/L
case
Normal based on
SGOT (AST) Not provided 0-32 U/L
case
Normal based on
Creatinine Not provided 45-84 umol/L
case
Normal based on
Potassium Not provided 3.50-5.10 mmol/L
case
Normal based on
Sodium Not provided 136-145 mmol/L
case
BLOOD GLUCOSE LEVEL
TEST RESULT NORMAL VALUES INTERPRETATION
Normal based on
FBS Not provided <100 mg/dL
case
DIAGNOSTIC PROCEDURES
EXAM RESULT INTERPRETATION
Negative for bleeding, Aneurysm or and
CT scan of Head Normal
embolic event
CXR Clear Normal
Regular rhythm consistent with sinus
ECG Tachycardia
tachycardia
Normal left ventricle function without a
Transthoracic patent foramen ovale; an atrial septal defect Mild pulmonary
Echocardiogram or a ventricular septal defect with mild hypertension
pulmonary hypertension (42 mmHg)
VENTILATION-PERFUSION SCAN
RESULT FINDING INTERPRETATION

Decreased
perfusion is
seen to the right
lung Unmatched
(particularly segmental
evident in the perfusion defect
right lower lobe
on the RPO
image)

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 VENTILATION-PERFUSION SCAN
RESULT FINDING INTERPRETATION

There is no
significant
ventilation
defect.

VII. ANATOMY AND PHYSIOLOGY

CIRCULATORY SYSTEM

The circulatory system consists of the heart and the arteries and veins that convey
blood throughout the body. Blood must always circulate to sustain life as it carries oxygen
to cells throughout the body. The pumping of the heart drives this blood flow through the
arteries, capillaries, and veins.

• TWO TYPES OF CIRCULATION

The circulatory and respiratory systems work together to sustain the body with
oxygen and to remove carbon dioxide. Pulmonary circulation moves blood between
the heart and the lungs and facilitates the process of external respiration –
deoxygenated blood flows into the lungs. It absorbs oxygen from the alveoli and
releases carbon dioxide to be exhaled.

In the pulmonary loop, deoxygenated blood exits the right ventricle of the heart
and passes through the pulmonary trunk. The pulmonary trunk splits into the right and
left pulmonary arteries. These arteries transport the deoxygenated blood to arterioles
and capillary beds in the lungs. There, carbon dioxide is released and oxygen is
absorbed. Oxygenated blood then passes from the capillary beds through venules into
the pulmonary veins. The pulmonary veins transport it to the left atrium of the heart.
The pulmonary arteries are the only arteries that carry deoxygenated blood, and the
pulmonary veins are the only veins that carry oxygenated blood.

On the other hand, systemic circulation moves blood between the heart and the
rest of the body and facilitates internal respiration –oxygenated blood flows into
capillaries through the rest of the body. The blood diffuses oxygen into cells and
absorbs carbon dioxide.

In the systemic loop, oxygenated blood is pumped from the left ventricle of the
heart through the aorta, the largest artery in the body. The blood moves from the aorta
through the systemic arteries, then to arterioles and capillary beds that supply body
tissues. Here, oxygen and nutrients are released and carbon dioxide and other waste
substances are absorbed. Deoxygenated blood then moves from the capillary beds
through venules into the systemic veins. The systemic veins feed into the inferior and

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 superior venae cava, the largest veins in the body. The venae cava flow deoxygenated
blood to the right atrium of the heart.

• HEART

The heart pumps oxygenated blood out of the left ventricle and into the aorta
to begin systemic circulation. After the blood has supplied cells throughout the body
with oxygen and nutrients, it returns deoxygenated blood to the right atrium of the
heart. The deoxygenated blood shoots down from the right atrium to the right ventricle.
The heart then pumps it out of the right ventricle and into the pulmonary arteries to
begin pulmonary circulation. The blood moves to the lungs, exchanges carbon dioxide
for oxygen, and returns to the left atrium. The oxygenated blood shoots from the left
atrium to the left ventricle below, to begin systemic circulation again.

B. PULMONARY ARTERY

The main pulmonary artery, also called the pulmonary trunk, is a vessel that
emerges from the heart. It divides into the left and right pulmonary arteries . They are
large, and like tubes with a lumen and sends blood to the left and right lungs,
respectively. They carry blood with relatively low oxygen content and high carbon
dioxide waste content into the pulmonary capillaries of the lungs, where this exchange
takes place. There, it is replenished with inhaled oxygen and excess carbon dioxide
is dropped off to be released from the body via exhalation.

When the blood is enriched with oxygen and cleared of carbon dioxide waste, it
flows back through the pulmonary veins to the heart's right ventricle. From there, the
blood is pumped to the left ventricle and finally dispersed through the aorta to the
arteries that carry the oxygen-rich blood throughout the body.

C. DEEP VEINS OF THE LOWER LIMB

The deep veins play a significant role in propelling blood toward the heart. The
one-way valves in deep veins prevent blood from flowing backward, and the muscles
surrounding the deep veins compress them, helping force the blood toward the heart.
The deep veins carry 90% or more of the blood from the legs toward the heart.

The deep veins of the lower limb can be separated into four main groups, according
to their location:

• VEINS OF THE THIGH

a. Femoral vein. This is a continuation of the popliteal vein and accompanies the
femoral artery. It begins at the opening of the adductor magnus muscle and ends posterior
to the inguinal ligament as the external iliac vein.

Its relationship to the femoral artery is variable. Within the distal adductor canal, it
is located posterolateral to the artery, whilst in the proximal canal and in the apex of the
femoral triangle, it lies posterior to the artery. Within the base of the femoral triangle, it is
found medial to the femoral artery. It is contained within the middle compartment of
the femoral sheath and usually has four or five valves.

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 Tributaries of the femoral vein include:

• medial circumflex vein

• lateral circumflex vein
• long saphenous vein
• profunda femoris vein, which drains 4-12 cm distal to the inguinal ligament

The profunda femoris vein, also referred to as the deep vein of the thigh, is located
superficial to the profunda femoris artery. Veins accompanying the perforating branches
of the profunda femoris artery drain the thigh muscles and empty into the profunda femoris
vein. The medial and lateral circumflex veins are sometimes tributaries of the profunda
femoris vein.

• VEINS OF THE KNEE

a. Popliteal vein. This is located within the popliteal fossa and pierces
the adductor magnus muscle, where it becomes the femoral vein. Distally it is medial to
the popliteal artery. Between the two heads of the gastrocnemius muscle, it is superficial
to it and proximally it is posterolateral to it.

The popliteal vein usually has 4 or 5 valves and many tributaries. All of the three
main veins of the leg drain into it, as well as the short saphenous vein and two muscular
veins from each head of the gastrocnemius muscle.

• VEINS OF THE LEG

a. Anterior tibial veins. These are formed by the vena comitantes or companion
veins, of the dorsalis pedis artery.

b. Posterior tibial veins. These are formed by the medial and lateral plantar veins
and accompany the posterior tibial artery. Veins from the calf muscles drain into
posterior tibial veins. They also receive connections from the superficial veins and the
fibular veins.

c. Fibular veins. These also formed by the medial and lateral plantar veins and
run with the fibular artery. They receive tributaries from superficial veins and veins
draining the soleus muscle.

• VEINS OF THE FOOT

The foot consists of two main types of deep veins:

a. Plantar veins, which drain the plantar surface or underside of the foot. Venous
plexuses within the plantar regions of the toes join to form plantar digital veins. These
veins connect with their dorsal counterparts, the dorsal digital veins, to form four
plantar metatarsal veins. These veins run proximally within the intermetatarsal spaces
and then continue on to form the deep plantar venous arch. Medial and lateral plantar
veins arise from this arch.

b. Dorsal veins, which drain the dorsal or upper surface of the foot. A dorsal venous
arch is also present and is formed by the dorsal metatarsal veins, which are also
formed by the dorsal and plantar digital veins.

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VIII. PATHOPHYSIOLOGY OF THE DISEASE

Male
Venous stasis Lack of physical
(Virchow’s triad) activity
Caucasian

Deep vein thrombosis

dislodgement of thrombus and travel to other blood vessels as embolus
Edema (3cm
difference of left to
right leg) Pulmonary embolism

Positive
Homan’s sign Mechanical occlusion

Tachycardia V/Q Hypoxemia Dyspnea;

(128 bpm) mismatch (90%) tachypnea

Syncope

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IX. DRUG STUDY
DOSAGE/ MECHANISM OF
DRUGS TIME/ ROUTE
CLASSIFICATION INDICATIONS CONTRAINDICATIONS ADVERSE EFFECT NURSING RESPONSIBILITIES
ACTION
Unfractionated 5000 units Anticoagulant The mechanism of • Prophylaxis and • Known sensitivity • Rashes • Monitor symptoms of deep
heparin SC q8-12hrs action of heparin is treatment of • Past or present • Drug-induced vein thrombosis to
(Calciparine) ATIII-dependent. It venous thrombosis heparin-induced hepatitis determine if drug therapy
or acts mainly by and its extension thrombocytopenia • Urticaria is effective in preventing or
accelerating the rate • Active bleeding • Anemia reducing venous
7500 units of the neutralization of • Prevention of post- • Thrombocytopenia thrombosis.
SC q12hrs certain activated operative deep • Pain and irritation
maintenance coagulation factors by venous thrombosis at injection site • Assess for signs of
dose antithrombin, but and pulmonary bleeding and hemorrhage,
other mechanisms embolism including bleeding gums,
may also be involved. nosebleeds, unusual
The antithrombotic • Prevention of bruising, black/tarry stools,
effect of heparin is clotting in arterial hematuria, and fall in
well correlated to the and cardiac hematocrit or blood
inhibition of factor Xa. surgery. pressure.
Heparin is not a
thrombolytic or • Prevent • Monitor signs of allergic
fibrinolytic. It prevents embolisms in reactions and anaphylaxis
progression of patients with atrial including pulmonary and
existing clots by fibrillation skin reactions.
inhibiting further
clotting. The lysis of • Adjunct • Be alert for acute arterial
existing clots relies on antithrombin or venous thrombosis
endogenous therapy in patients caused by heparin-induced
thrombolytics. with unstable thrombocytopenia.
angina
• Watch for unusual fatigue
and weakness that might
be due to anemia.

• Monitor and report signs of

drug-induced hepatitis.

• Assess injection site for

pain, swelling, and
irritation.

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 DOSAGE/ MECHANISM OF
DRUGS TIME/ ROUTE
CLASSIFICATION INDICATIONS CONTRAINDICATIONS ADVERSE EFFECT NURSING RESPONSIBILITIES
ACTION
Warfarin 2-5mg PO Anticoagulant Interferes with clotting • Prophylaxis and • Pregnant woman • Fever • Assess for signs of
(Coumadin) QD for 2-4 factors II, VII, IX, and X treatment of • Patient with allergy • Nausea bleeding and hemorrhage,
days as they are formed by venous thrombosis or severe reactions • Stomach cramps including bleeding gums,
vitamin K in the liver. and it’s extension, to warfarin • Death of skin nosebleeds, unusual
or This drug will not pulmonary tissue bruising, black/tarry stools,
interfere with clotting embolism • Kidney injury hematuria, and fall in
2-10mg PO factors already formed • Purple toes hematocrit or blood
QD for and in circulation in the • Prophylaxis and syndrome pressure.
maintenance body. treatment of
dose thromboembolic • Monitor skin reactions,
complications and report any severe or
associated with untoward reactions such
atrial fibrillation as dermal necrosis.
and or cardiac
valve replacement • Instruct patient to
immediately report signs
• Recurrent of GI bleeding.
myocardial
infarction • Instruct patient to report
other troublesome side
• Thromboembolic effects such as fever,
events such as nausea, or stomach
stroke or systemic cramps.
embolization.

13
X. NURSING CARE PLAN

NURSING DIAGNOSIS DATA PLANNING INTERVENTIONS RATIONALE EVALUATUON

Impaired gas exchange • Dyspnea Client will maintain Assess the skin Cool, pale skin occurs as a Goal met.
related to pulmonary • Tachycardic adequate gas exchange, color, nail beds, and compensatory response to Client maintains
embolism as evidence as evidenced by ABGs mucous membranes for hypoxemia. When oxygen adequate gas exchange,
• Syncope due to low
by decreased lung within the normal range, color changes. and perfusion become as evidenced by ABGs
oxygen in the blood impaired, peripheral
perfusion oxygen saturation of within the normal range,
and brain tissues become cyanotic.
90% or greater, relaxed oxygen saturation of
• DVT noted in left leg breathing, and baseline 90% or greater, relaxed
• Positive Homan’s sign Monitor for any changes in In initial hypoxia and
PR for the client. vital signs hypercapnia, there is an breathing, and baseline
in left leg PR for the client.
increase in the respiratory
• Diaphoresis rate, heart rate, and blood
• Left calf measured 3 pressure. As the
cm more than the hypercapnia and hypoxia
right one. get worse, blood pressure
• VS: may drop, heart rate tends
• PR: 128bpm to continue to be rapid and
includes dysrhythmias, and
• RR: 32 cycles
respiratory failure ensues,
• BP: 126/72 mmHg with the client unable to
• O2 Sat: 90% maintain the rapid
respiratory rate.
Assess for the signs and Hypoxia results from
symptoms of hypoxia increased dead space
(such as confusion, (ventilation without
headache, diaphoresis, perfusion) that reduces
restlessness, tachycardia, effective gas exchange.
and pale skin).

Auscultate lung sounds, Crackles are common

noting areas of decreased clinical findings with
ventilation and the pulmonary embolism.
presence of adventitious
sounds.

14
NURSING DIAGNOSIS DATA PLANNING INTERVENTIONS RATIONALE EVALUATUON
Assess for calf tenderness, Pulmonary embolism often
redness, swelling, and arises from a deep vein
hardened areas. thrombosis and may have
been previously
overlooked.

Position the client properly Upright and sitting position

to facilitate ventilation- optimize diaphragmatic
perfusion matching. excursions and lung
perfusion. When the client
is positioned on one side,
the affected area should
not be dependent.

Anticipate the need to start Heparin or enoxaparin

anticoagulant therapy and, (Lovenox) is used to
if there is massive prevent the recurrence of
thromboembolism, the use emboli. These medications
of thrombolytic therapy. do not dissolve clots that
already exist. If a massive
thrombus is present or the
client is hemodynamically
unstable, thrombolytic
therapy is used to directly
lyse or dissolve the clot.
Ineffective tissue • Upon diagnostic Client will maintain Assess for contributing Most clients with DVT are Goal met.
perfusion related to examinations, Doppler optimal peripheral tissue factors: (1) Immobility, asymptomatic. Knowledge Client had maintained
increased coagulability perfusion in the affected (2) Smoking, and of high-risk situations helps the optimal peripheral
scan of the legs
of blood as evidenced extremity, shall be (3) Venous statis in early detection. tissue perfusion in the
revealed an acute
by swelling and pitting DVT in the patient's evidenced by strong affected extremity, as
Maintain adequate Hydration prevents an
edema on the affected left leg, in the popliteal palpable pulses, hydration. increased viscosity of evidenced by strong
site reduction in and/or blood, which contributes to palpable pulses,
vein.
absence of pain, warm, venous stasis and clotting. reduction in and/or
• Positive Homans' sign and dry extremities, and absence of pain, warm,
in the left leg adequate capillary refill. Encourage bedrest and Clients usually require bed and dry extremities, and
• Asymmetric leg/calf keep the affected leg rest until symptoms are adequate capillary refill.
swelling and pitting elevated (depending on relieved. The affected leg
should be elevated to a

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NURSING DIAGNOSIS DATA PLANNING INTERVENTIONS RATIONALE EVALUATUON
edema on the affected size and location of the position above the heart to
site. clot) as indicated. decrease swelling.

Provide warm, moist heat Heat promotes comfort

to the affected site. and reduces inflammation.

Apply below-knee Compression stockings

compression stockings as enhance circulation by
prescribed. Ensure that the providing a graduated
stockings are the correct pressure on the affected
size and are applied leg to help return the
correctly. venous blood to the heart.
Inaccurately applied
stockings can serve as a
tourniquet and can
promote clot formation.

Administer anticoagulants Treatment with

as prescribed. anticoagulant is used
primarily to prevent the
formation of new clots by
decreasing the normal
activity of the clotting
mechanism.
Readiness of enhanced • The patient was Client’s imaging results The patient must continue It will prevent blood clots Goal met.
independent heath discharged on oral from the Department of taking oral anticoagulation from recurring on his After 4 months from
management Pulmonary Disease, will as prescribe by his pulmonary arteries. hospitalization, the imaging
warfarin therapy.
show no significant physician. test of lungs from
• Patient was on long- Department of Pulmonary
term follow-up check ventilation defect and no
Patient must develop a Aerobic activity can help Disease showed no
embolus present. healthy lifestyle by the lungs work better after significant ventilation
up with the
Department of introducing physical a pulmonary embolism. It defect and no embolus
Pulmonary Disease. activity to daily life and can also promote better present.
maintaining avoidance to blood circulation.
vices, such as smoking
and drinking. Smoking changes the
surface of blood platelets,
making it easier for them to
clump together. Damage to

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NURSING DIAGNOSIS DATA PLANNING INTERVENTIONS RATIONALE EVALUATUON
the lining of blood vessel
walls is also associated
with smoking, which
increases the potential for
clots to form.

Alcohol consumption is
increases the risk of
developing pulmonary
embolism.

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