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Running head: COMPREHENSIVE CASE STUDY
Comprehensive Clinical Case Study
Erin Vitale RN, BSN
Wright State University-Miami Valley College of Nursing and Health
NUR 7201
Dr. Kristine Scordo
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History and Physical
Identifying Data
The patient is a 47 year old African American male. The patient is alert, oriented, and
reliable and is providing the information. The patient’s primary language is English, secondary
language Spanish.
Chief Complaint
“I’m having ripping chest pain. It feels like it’s going through my chest to my back.”
History of Present Illness
The patient presents to the emergency room via EMS after watching a football game with
some friends. The patient experienced acute onset “ripping chest pain” that migrated to his back.
The pain was unrelenting so he decided to call 911. A 12 lead ECG was obtained and was
normal revealing sinus rhythm. CXR showed a widened mediastinum. The patient’s initial blood
pressure (BP) in the ER was 176/74, heart rate (HR) 74 beats per minute and the decision was
made to admit to the ICU. A complete blood count, renal function panel, and coagulation studies
were ordered by the emergency room (ER) physician and are pending.
Medications: The patient is currently prescribed hydrochlorothiazide 12.5 PO daily. The patient
denies use of complementary or alternative medicine.
Allergy: No known allergies.
Smoking, alcohol, drugs: The patient denies current use of smoking, alcohol, or drugs. The
patient does endorse “I used to party a lot in my day, but not anymore.” Additionally, endorses
smoking socially but stopped all together five years ago.
Past Medical History
Major childhood illnesses: Chickenpox at the age of 5. No other childhood illnesses known.
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Adult illnesses: Recently diagnosed with idiopathic HTN within past year. The patient denies
any recent illnesses or sick contacts.
Surgeries: Wisdom teeth extraction at the age of 18. No additional surgeries.
OB/Gynecology: Not applicable
Psychiatric: No known psychiatric illnesses.
Immunizations: Patient is unsure of childhood immunizations. Received annual influenza
vaccination for the past five years.
Personal and Social History
The patient was born in Cincinnati, Ohio and moved to Dayton, OH five years ago. The
patient is divorced and does not have any children that he is aware of. The patient graduated high
school and never attended college. The patient lives independently in a one bedroom apartment
without any pets. The patient was recently released from prison after serving one year for theft.
The patient works full time at a body shop and states he is able to pay his bills. The patient has
an aunt that lives locally that he sees about once a month. Other than the aunt, the patient does
not have any close relationship with additional family members. The patient feels he has a good
support system with a group of friends and has been experiencing some anxiety regarding
keeping his job due to recent layoffs.
Exercise and diet: The patient eats fast food almost daily and buys ready to eat meals otherwise.
The patient doesn’t drink juice or pop and drinks milk often. The patient doesn’t exercise but
states his job is very physically strenuous which helps keep him in shape. Occasionally, the
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patient plays basketball or football with his friends for exercise. He is thinking about attending
some church services in the future.
Leisure and hobbies: The patient enjoys watching sports on television and playing sports with
friends. The patient states “I used to have a lot more hobbies, but I’m trying not to get into
trouble anymore.”
Family History
The patient never knew his father and is unsure of his current health status. His mother
died when he was 10 years old and was raised by his grandparents, now deceased. His mother
was an alcoholic and died of complications from liver cirrhosis. The patient has two living sisters
and an aunt that have no significant health history. The patient is unsure of any additional family
health history.
Review of symptoms
General: Endorses being is good health overall. Denies night sweats, malaise, weight loss or
gain, changes in appetite, respiratory illnesses, or elevated temperature.
Skin: No rash, itching, changes in skin color, or alterations in skin integrity.
Neurological: Denies any dizziness, confusion, memory fluctuations, sensory, vision changes,
headache, weakness or mood swings.
HEENT: Head: denies any head injury, facial pain, swelling, headaches, or syncope. Eyes:
denies eye injury, pain, dryness, overproduction of tears, history of glaucoma or cataracts; uses
reading glasses, non-prescription. Does not see an ophthalmologist. Ears: no hearing changes,
infection, pain, swelling, occlusion, or ringing in the ears. Nose- no nose bleeds, nasal drainage,
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sneezing, or nasal stuffiness. Throat: no pain, swelling, difficulty in swallowing, or difficulty in
speaking. Mouth: denies mouth sores, pain, dysphagia, hoarseness, dry mouth, or bleeding.
Brushes teeth after meals, flosses daily. Last dental visit was five years ago, does not see
regularly.
Neck: Denies tenderness, stiffness, pain, or swelling of lymph node areas. Endorses full range of
motion with neck.
Chest: No pain, swelling, or lumps. The patient states he has been working out to get better chest
muscular definition.
Respiratory: Denies shortness of breath, dyspnea upon exertion, wheezing, coughing, or any
productive sputum. Does not currently smoke, smoked cigarettes social in the past (greater than 5
years ago).
Cardiovascular: Denies palpitations, chest pain, edema, or dizziness. Recently diagnosed with
HTN and is prescribed HCTZ 12.5 mg PO daily. Patient admits he does not take it daily, usually
every other day or when he remembers.
Gastrointestinal: Denies nausea, vomiting, diarrhea, bowel irregularities, bloody stool,
hemorrhoids, heartburn, reflux, swallowing problems, or abdominal distention. Has a good
appetite, three big meals a day. Patient has daily bowel movements without straining.
Gastrourinary: Denies difficulty urinating, burning during urinating, infrequency of urinating,
incontinence, prostate abnormalities, or hematuria. Denies pain or swelling around groin.
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Genitalia: Denies discharge or lesions. Denies testicular swelling, itching, or lumps. Does not do
testicular self-exam. Denies sexual dysfunction and endorses regular, protected sex several times
a week with a girlfriend.
Musculoskeletal: Complains of moderate low back pain from bending over at his job multiple
times and lifting heavy objects, non-radiating pain. Pain is relieved by rest and hot showers.
Denies joint pain, recent falls, fractures, or muscular changes.
Psychosocial: Patient feels very anxious about what is causing this pain. Patient also feels
anxious about how long he is going to be off work. Patient denies depression, mood swings,
delusions, hallucinations, irritability, or thoughts of harming self or others. Patient has not had
problems sleeping or concentration.
Hematologic: Denies frequent bleeding, bruising, sickle cell anemia, or any hematologic
disorders.
Endocrine: Denies history of diabetes, thyroid problems, feelings of fatigue, over hyperactivity.
No increase or decrease in frequency of urination, thirst, or appetite. Denies temperature
irregularities or weight changes.
Physical Examination
General appearance: Patient is well groomed, tall, muscular, casually dressed, and appears
anxious. He answers questions appropriately and is leaning forward in the hospital bed.
Measurements/Vital signs: The patient is 6 feet 2 inches tall and weighs 180 pounds. Vital signs
include temperature of 97.4 o F, heart rate of 105 beats per minute, respirations 18 breaths per
minute, blood pressure 184/77 mmHg, and oxygen saturation of 96% on room air.
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Neurological: The patient is alert and oriented to self, date, location, and situation. Speech is
clear and appropriate, no swallowing difficulties. Memory and recall are intact. Pupils are equal,
round, and reactive to light. Extraocular movements are intact, no nystagmus noted. Face is
symmetrical. Strength in all four extremities is 5/5, denies sensory changes. No ataxia noted.
Gait is balanced, independent, and steady. Assessment of cranial nerves II through XII is normal.
Reflexes are 2 + and intact.
HEENT: Head is normocephalic and non-tender on palpation. Scalp without lesions, head
shaved. Tribal tattoo noted on back of head. Eyes: Conjunctiva pink, sclera clear. Ear: without
discharge, inflammation, or occlusions noted. Tympanic membranes visualized and are pearly
gray. No hearing loss noted. Nose: Clear drainage noted through nasal passages, no septal
deviation. Lips are pink, mucous membranes pink and moist. No mouth lesions or ulcers, silver
caps noted on back four teeth.
Neck: No lumps, goiter, swelling, thyromegaly, or lymphadenopathy. Trachea is midline, no
jugular venous distention noted. Neck is soft, supple, with full range of motion. Lymph nodes
unable to be palpated and are non-tender. No carotid bruits auscultated, carotid pulses 2+.
Respiratory: Thorax equal with good expansion and excursion. Lung fields are resonant upon
percussion. Breath sounds are vesicular with no extra sounds such as rales, wheezing, or rhonchi.
Cardiovascular: Jugular venous pressure 1.5 cm above sternum, with head of examining table
raised to 30 degrees. Carotid upstroke brisk and without bruits. Crisp S1, S2; no S3 or S4 heart
sounds, murmurs, clicks, or rubs. Lower extremity pulses 1+, right upper extremity
radial/brachial pulse 2+, left upper extremity radial/brachial pulse 1+. Edema not present. Blood
pressure re-checked manually on left upper extremity, 144/74 mmHg; right upper extremity
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176/76 mmHg. The patient endorses severe, stabbing, unrelenting 10/10 pain that starts in his
chest and feel like it is reaching through to his back. Onset was within the past hour without any
relieving or aggravating factors, constant in nature.
Chest: Symmetric pectoral muscles, without masses. No discharge noted from nipples. Pain as
described above.
Gastrointestinal: Active bowel sounds auscultated in all four quadrants. Abdomen flat, nontender, and soft. No pulsations noted. Tympany heard upon percussion. Spleen, kidneys, and
liver unable to be palpated. Denies tenderness at the costovertebral angle.
Genitourinary/Rectal: No lesions or discharge noted on genitalia. Urine appearance is clear
yellow. No hemorrhoids, fissures, lesions, or bleeding noted from rectum. Full rectal exam
deferred.
Extremities: Warm and without edema. Capillary refills sluggish in lower extremities. Pulses are
1+ in bilateral lower extremities. Right upper extremity 2+, left upper extremity 1+.
Musculoskeletal: All extremities 5/5 strength. No limitations on joints or range of motion. No
warmth or swelling of joints. Gait is steady. Musculature is well defined.
Skin: Warm and slightly diaphoretic. No rashes, abnormal nevi, lesions, or ulcers. Multiple
tattoos on extremities. No rashes, lesions, or bruises.
Differential Diagnosis
Acute Aortic Dissection (AAD)
AAD results from a spontaneous tear in the intimal linings of the aorta. The tear results
in blood dissecting into the media of the aorta. The tear likely occurs as a result from the
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repeated force applied during the cardiac cycle to the ascending and proximal descending aorta.
There are two types of AAD; type A dissection and type B dissection. Type A dissection
involves the aorta proximal to the left subclavian artery and type B dissections involves the
proximal descending aorta traditionally right past the left subclavian artery. The intimal tear of
the aorta may extend the dissection to the abdominal aorta, lower extremities, subclavian arteries,
or carotid arteries. Type A and type B dissection both carry a high mortality rate making
recognition and treatment crucial. Risk factors for AAD include HTN, pregnancy, coarctation,
bicuspid aortic valve, and/or irregularities of elastic tissue, collagen, or smooth muscle.
Indicators of AAD include acute onset of intense chest pain that may radiate to the back, neck, or
abdomen, hypertension, widened mediastinum on a chest X-ray (CXR), and evidence of a pulse
deficit or discrepancy. ECG findings may be normal in patients, demonstrate left ventricular
hypertrophy from prolonged hypertension, or show inferior wall abnormalities since dissection
usually compromises the right versus the left coronary artery. Examination features that alert the
clinician the patient is high risk for AAD include any evidence of perfusion deficit (pulse deficit,
blood pressure limb differential, new aortic regurgitation, and neurologic changes) (Rapp,
Owens, & Johnson, 2013).
AAD is included in the differential diagnosis list due to the patient’s history of HTN,
severe chest pain, and evidence of perfusion deficit. The patient has unequal radial pulse strength
in the upper extremities, and blood pressure limb differential >20 mmHg. Additionally, the CXR
obtained in the ETC revealed a widened mediastinum, supportive of AAD. The patient is
considered high risk and high probability for AAD given the patient’s presenting symptoms,
physical examination, and CXR results. Since AAD is suspected, immediate control of blood
pressure between 100-120 mm Hg systolic to limit the extent of tearing even before diagnosis is
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confirmed. Due to the high mortality rates associated with AAD, timely diagnostic imaging to
confirm or rule out suspected AAD may be life-saving (Rapp, Owens, & Johnson, 2013).
Additional diagnostic tests ordered to confirm or rule out AAD include a multiplanar
computed tomography (CT) scan, magnetic resonance imaging (MRI), aortography, and
transesophageal echocardiogram (TEE). Further diagnostic testing can be used to support the
diagnosis of AAD in conjunction with the 12 lead ECG and CXR already obtained in the ETC.
Once an AAD is suspected, a cardiothoracic surgeon should be consulted in the event the patient
requires immediate surgery (Elefteriades, Olin, & Halperin, & 2011).
Diagnostic tests ordered. Diagnostic tests ordered for AAD include multiplanar CT
scan, magnetic resonance imaging, echocardiogram, and aortography.
Multiplanar CT scan. Multiplanar CT scanning is fast and gives the clinician immediate
diagnostic imaging which is crucial when the patient is determined to have a high likelihood of
AAD. The chest and abdomen should be included in the CT imaging to allow the clinician to
visualize the extent of dissection. Additionally, CT imaging shows the location of the intimal tear
and flap, presence of intramural hematoma, size of the false and true lumen, branch involvement,
and the presence of pericardial or pleural fluid (Mamkin & Heitner, 2011). Intravenous contrast
agent will be given during the scan putting the patient at risk for contrast induced nephropathy
(CIN). Administration of intravenous fluids and evaluating the patient’s creatinine level are
important to minimize the risk for CIN. IF a CT scan was performed, a renal function panel
would be ordered and reviewed. Multiplanar CT scan is typically the diagnostic test of choice to
determine the presence of AAD when the patient demonstrates high risk features and is
hypertensive (Rapp, Owens, & Johnson, 2013).
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Magnetic resonance imaging (MRI). MRI is a diagnostic test that provides excellent
imaging and visualization of dissections. MRI is more appropriate for evaluation of chronic
dissections, not to be used in the acute dissection cases. MRI is not appropriate for the patient
potentially having an acute dissection because the lengthy imaging time (30-45 minutes),
difficulty to monitor vitals, and challenges to medication administration. Blood pressure control
is important for the patient suspected with AAD and the MRI test would have to be stopped
every time the clinical staff would have to administer anti-hypertension medications further
delaying testing results (Rapp, Owens, & Johnson, 2013).
Transesophageal echocardiogram (TEE). TEE is another diagnostic test used to
evaluate the presence of AAD. The anatomic closeness of the esophagus to the aorta makes
visualization better with TEE compared to transthoracic echocardiogram (TTE). However, even
with the proximity of the esophagus to the aorta the proximal aortic arch is still challenging to
visualize due to the trachea and main stem bronchus. TEE is a highly sensitive and specific, 98
and 95%, and allows the clinician to visualize differential flow between the false and true
lumens. A benefit of TEE is not requiring intravenous contrast or radiation and can be performed
at the bedside for hemodynamically unstable patients. Additionally, TEE can evaluate or confirm
regurgitations or valvular abnormalities. However, TEE may cause bradycardia, hypertension,
hypotension, aspiration, and less frequently esophageal perforation. Additionally, TEE may be
frequently available in more rural healthcare settings (Mamkin & Heitner, 2011).
Aortography. Aortography was once considered the gold standard of testing for AAD by
allowing visualization of the intimal flap, true lumen, and false lumen. Aortography assesses the
presence and severity of aortic regurgitation and the involvement of the coronary arteries through
contrast injection and XR of the aorta. However, the availability of less invasive and highly
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effective testing lessens the amount aortography is used. Risks associated with aortography
include CIN, risk of perforation of the false lumen, and time delay because the patient has to be
transferred to the procedure room and prepped (Mamkin & Heitner, 2011). Although the patients
presenting signs and symptoms match closely with AAD, ruling out other causes that can
produce similar signs and symptoms prior to endorsing the final diagnosis is imperative.
Myocardial Infarction (MI)
A second differential diagnosis for the patient’s presenting signs and symptoms includes
MI. MI occurs from occlusion of a coronary artery that consequently results in tissue damage and
death in the area supplied by that coronary artery. MI can produce a variety of clinical
manifestations from asymptomatic to unrelenting chest pain. Risk factors for development of a
MI include male gender, smoking, advanced age, high cholesterol, diabetes, hypertension, poor
diet, and alcohol abuse. In addition to chest pain, patients with a MI may experience shortness of
breath, nausea, palpitations, and anxiety or a feeling of doom. A thorough assessment and
physical exam is crucial and patients should be evaluated for jugular venous distention,
diaphoresis, abnormal heart sounds, and arrhythmias. Essentials of diagnosis of a MI include
chest pain (typical and atypical presentations), ECG changes, and cardiac enzyme abnormalities
(Jaffe & Boyle, 2009).
The patient’s presentation of severe chest pain in conjunction with MI risk factors makes
MI an appropriate differential diagnosis. Although the patient presents with several features
indicative of MI, the pulse and BP inequality is not typically seen with MI making aortic
dissection a more probable diagnosis. Additional diagnostic tests should be ordered in a timely
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manner to confirm or rule out MI and include cardiac enzyme biomarkers, follow up 12 lead
ECG, and TTE or TEE (Jaffe & Boyle, 2009).
Diagnostic tests ordered. Diagnostic tests appropriate for the differential diagnosis of
MI include cardiac biomarkers, 12 lead ECG, and an echocardiogram.
Cardiac enzyme biomarkers. Serum markers include creatinine kinase-myoglobin (CKMB), MB, and Troponin T and I. CK-MB lacks specificity for cardiac muscle and can become
elevated from skeletal muscle trauma or kidney dysfunction. CK-MB changes can be seen within
the first six hours of infarction with peak levels occurring around 18-24 hours. CK-MB levels
typically return to normal within 48 hours of infarction or skeletal tissue injury. MB is not
specific to cardiac injury and elevations can be seen in patients with kidney dysfunction or
skeletal muscle injury as well. MB is present within two hours of injury and is rapidly excreted
by the renal system. Troponin T and I are more sensitive to myocardial infarction or damage than
CK-MB or MB. Troponin levels increase around four to six hours after injury, then decreases,
but remains higher than normal for approximately a week. Troponin’s sensitivity to cardiac
infarction makes Troponin the favored biomarker for diagnosing an acute MI tool (Jaffe &
Boyle, 2009).
12 lead ECG. A rapid and essential test in evaluating patients with possible MI is a 12
lead ECG. The changes on a 12 lead ECG represent different kind of myocardial infarctions,
including NSTEMI and STEMI. The patient has one ECG already performed that was normal.
However, when MI is suspected, serial ECGs every 15-30 minutes should be obtained to
evaluate for acute changes or until diagnosis is made. Management and treatment strategies are
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different depending on the location of the MI and ST elevation making a 12 lead ECG an
important tool (Jaffe & Boyle, 2009).
Echocardiogram. In the acute setting for diagnosing MI, diagnosis is made based on
history, physical exam, cardiac biomarkers, and 12 lead ECG. However, when the history or
physical exam is atypical and the 12 lead ECG is undiagnostic, a TEE or TTE may be necessary.
An echocardiogram (either version) can be done at the bedside and allows the clinician to assess
if there are wall motion abnormalities with preserved thickness, indicative of an acute MI.
Additionally, since the patient is high risk for AAD, TTE or TEE is an appropriate diagnostic test
that would help narrow the differential diagnosis list down without delaying care (Jaffe & Boyle,
2009).
Acute Pericarditis
Acute inflammation or irritation of pericardium can result in pericarditis. Inflammation
can originate from infection, renal failure, systemic diseases, neoplasms, radiation, post-cardiac
surgery, drug toxicity, or hemopericardium. Often, the pathologic process that causes pericardial
inflammation involves the myocardium. Diagnosis basics include an anterior pleuritic chest pain
that is constant in nature, pericardial rub, and 12 lead ECG changes with ST segment elevations
throughout with associated PR segment depression. Additional manifestations included are fever,
elevated erythrocyte sedimentation rate (ESR) and white blood cell count, and dyspnea. The
chest pain may be sharp, dull, aching, unrelenting, and worsened by lying flat, movement,
coughing, or deep breathing (Bashore, Granger, Hranitzky, & Patel, 2013).
The patient’s presentation of severe, unrelenting chest pain that is constant warrants
pericarditis to be included in the differential diagnosis list. However, the patient has not
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demonstrated any 12 lead ECG changes consistent with pericarditis and the patient does not have
the typical pericarditis clinical manifestation of the pericardial friction rub making acute
pericarditis a less likely diagnosis. Additionally, the patient’s CXR showed mediastinum
widening, representative of AAD and not pericarditis. Laboratory studies, echocardiogram, and
additional 12 lead ECGs can assist the practitioner in determining if the patient has acute
pericarditis (Bashore, Granger, Hranitzky, & Patel, 2013).
Diagnostic tests ordered. Laboratory studies, echocardiogram, and a 12 lead ECG are
appropriate diagnostic tests to order when pericarditis is suspected (Braunwald, 2012).
Laboratory studies. Evaluating a complete blood count (CBC) with differential and ESR
allows the practitioner to evaluate underlying infection or inflammation. Cardiac enzymes (CKMB, Troponin, and MB) are helpful to evaluate for any cardiac tissue injury or infarct. Testing
for HIV, tuberculosis, thyroid abnormalities, rheumatoid factors, anti-nuclear antibody, and
lactate dehydrogenase are helpful to determine any additional underlying cause(s) for acute
pericarditis (Braunwald, 2012).
Echocardiogram. Echocardiogram (TTE or TEE) is an appropriate diagnostic test to
order for this patient to help differentiate the diagnosis between AAD, MI, and acute pericarditis.
Echocardiograph can be performed at the bedside and evaluates the quantity and presence of
pericardial fluid, valvular abnormalities, and restrictive filling patterns. The heart may be
visualized swinging within the pericardia sac and be associated with electrical alternans in severe
cases. Additional radiographic testing will become necessary if the acute pericarditis progresses
to constrictive pericarditis (Bashore, Granger, Hranitzky, & Patel, 2013).
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12 lead ECG. The 12 lead ECG for acute pericarditis evolves through four stages. There
is a sequence of changes showing generalized ST and T wave changes that may begin with
diffuse ST elevation, return to baseline, and then progressing to T wave inversion. Injury to the
atria may be present and is demonstrated as PR depression in all leads except aVR and V1. The
patient’s initial 12 lead ECG was normal but serial ECGs should be performed to evaluate for
any changes associated with acute pericarditis (Braunwald, 2012).
Pulmonary Embolism (PE)
Patient’s coagulation status is affected by stasis, vascular wall injury, and
hypercoagulability. Typically, a PE originates from deep veins in the lower extremities although
PE can originate from any venous bed. Risk factors for PE include advanced age, history of deep
vein thrombosis (DVT) or PE, varicose veins, heart failure, MI, obesity, immobility, varicosities,
pregnancy, cerebrovascular accident, cancer, and bleeding disorders. Clinical manifestations
include dyspnea, pleuritic chest pain, hemoptysis, cough, anxiety, syncope, tachycardia, and
tachypnea. A large PE may cause right ventricular dysfunction, accentuated pulmonary heart
sounds, S3 gallop, pleural rub, tricuspid regurgitation, hypotension, and/or jugular venous
distention. A 12 lead EKG supportive of PE has a S1Q3T3 pattern with T-wave inversion in leads
V1-V6, and may have a right bundle branch block (RBBB) (Fedullo, 2011).
The patient’s chest pain and anxiety triggered the clinician to include PE in the
differential diagnosis list. The patient’s chest pain is described as severe, unrelenting, starting
anteriorly and going to his back which is varied from the pleuritic chest pain typically described
by patients with a PE. The patient does not have any risk factors for DVT or PE, is not
experiencing dyspnea, and oxygen saturations are normal making PE a less probable diagnosis.
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Additional testing should be performed to completely exclude this diagnosis from the differential
list. However, due to the high probability of the patient experiencing an AAD, delay of
diagnostic tests to determine the presence of AAD should not be delayed for other differential
diagnosis testing (Fedullo, 2011; Marino, 2009).
Diagnostic tests ordered. Arterial blood gas, ventilation-perfusion scan, CT
angiography, venous ultrasound studies, and laboratory studies assist the practitioner in
determining the likelihood of the patient having a PE (Marino, 2009).
Arterial blood gas. Although the patient’s monitored oxygen saturations have been
appropriate and the patient is not appearing or endorsing dyspnea, an ABG better evaluates the
patient’s oxygenation and assesses arterial pH, C02, HC03, and P02 levels. If the ABG is normal
and the patient does not develop hypoxemia, additional testing may be unnecessary (Marino,
2009).
Ventilation-perfusion scan (V/Q). An additional diagnostic test for PE is a V/Q scan.
V/Q scan should be reserved for patients without lung or cardiac dysfunction because a V/Q scan
will have abnormal results 90% of the time due to a baseline of ventilation and/or perfusion
dysfunction. A normal V/Q scan excludes the diagnosis, a high probability V/Q supports the
diagnosis, and a low-probability V/Q scan does not support or rule out a diagnosis of PE.
Intermediate or indeterminate V/Q results require additional testing to support or exclude PE as a
diagnosis (Marino, 2009).
Spiral computed tomography (CT) angiography. When a V/Q scan is undiagnostic or
the patient has baseline cardiac/pulmonary dysfunction, spiral CT angiography is an appropriate
diagnostic test to order. Patients must be able to follow commands to be able to complete the test
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unless the facility has a more rapid version available. Spiral CT angiography tests for PE by
analyzing filling defects in the pulmonary arteries. The dye used in the procedure can be
nephrotoxic and close monitoring of the patient’s hydration status and creatinine level is
important to prevent renal complications (Fedullo, 2011).
Venous ultrasound studies. Due to the increased probability that a PE originated from a
DVT, venous ultrasound studies are helpful to support the likelihood of PE (Marino, 2009).
Laboratory testing. An ELISA Degradation-dimer (D-dimer) or non-elevated non latex
D-dimer laboratory test is greater than normal in the setting of PE and DVT. Additional
conditions besides PE or DVT can cause an elevated D-dimer including infection, cancer,
pregnancy, renal failure, and heart failure making an elevated D-dimer only appropriate for
exclusionary purposes (Marino, 2009). Further laboratory testing should be performed to
determine if the patient is in a hypercoagulable state, making them at increased risk for DVT or
PE development. Protein C and S and antithrombin deficiency increase the patient’s risk for
blood clots. Evaluating anti-phospholipid antibody, factor V mutation, and
hyperhomocysteinemia levels will also assist the practitioner in determining the risk probability
present in the patient. Before administration of any anticoagulants, these levels should be checks
to prevent any alteration of the results (Fedullo, 2011). Additionally, AAD must be ruled out
before administration of anticoagulants to prevent rapid decompensation in the patient (Austin,
2005).
Diagnosis
After careful review of the patient’s history, physical exam, chief complaint, CXR
results, differential diagnosis list, and vital signs, the diagnosis of AAD is made. The multiplanar
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CT scan revealed Type A aortic dissection. The patient’s prioritized plan will be based on the
diagnosis of AAD.
Prioritized Plan
Preventing death or complications is of highest importance in the patient with AAD.
Identifying appropriate consults, monitoring, pharmacological interventions, and health
promotion activities are important to ensure the patient has well-rounded care (Johnson & Prince,
2011).
Consultations
Immediate consultation of a cardiothoracic surgeon once AAD is suspected is crucial
because rapid emergency surgery may be necessitated. Type A dissection involves the aorta
proximal to the origin of the left subclavian artery and typically requires immediate surgical
intervention. Type B dissection is limited to the descending aorta and is treated with medical
intervention unless medical therapy fails or the aortic branch becomes compromised. Until
diagnostic testing confirms Type A or Type B AAD, the treating practitioner should assume
surgery will be warranted making a consult to a cardiothoracic surgeon of upmost importance.
The cardiothoracic surgeon will decide what kind of surgical procedure will be most appropriate
for the patient given their past medical history, patency of the coronary arteries, aortic branch
compromise, and overall quality of the aortic tissue (Johnson & Prince, 2011).
Monitoring
To optimize patient survival, inpatient critical care monitoring should be initiated with
close monitoring, with specific focus on heart rate, blood pressure, oxygen saturation, alertness,
and pain. Pharmacological management of blood pressure and pain should begin before the
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complete diagnosis is made, in addition to the consultation of a cardiothoracic surgeon.
Telemetry monitoring should be performed continuously with an intra-arterial line for constant
evaluation of blood pressure. The patient should have a central catheter with capability to
monitor central venous pressures to monitor volume status. A urinary catheter is prudent to
monitor hourly urinary output and promote bedrest. A complete blood count with differential and
renal function panel should be collected to monitor for electrolyte changes, kidney function, and
blood loss. Additionally, a type and screen should be ordered in case transfusions are needed for
possible surgery. In the occurrence of hypotension from AAD, intravenous fluid may be needed
for volume support. Sequential compression devices should be placed continuously for deep vein
thrombosis prophylaxis. Frequent assessments, telemetry monitoring, and laboratory evaluations
are necessary to evaluate for hemodynamic stability, neurologic function, or any indication of
organ ischemia (Austin, 2005; Johnson & Prince, 2011).
Pharmacological Interventions
Typically, patients with AAD are hypertensive and require rapid lowering of their blood
pressure to minimize further dissection. An antihypertensive with a negative inotropic effect is
the drug of choice because blood pressure can be lowered without causing greater shearing force
on the intimal flap of the aorta, making beta-blockers (BB) the appropriate pharmacologic
intervention. If the patient has a contraindication to BB (allergy, chronic obstructive lung
disease, bradycardia, cocaine abuse, or aortic regurgitation), nondihydropyridine calcium
channel blocks can be used instead. Intravenous verapamil (0.15 mg/kg/min for a maximum dose
of 30 mg) or diltiazem (10 mg bolus then 5-15 mg/hr) would be acceptable alternatives in the
case of BB contraindication (Johnson & Prince, 2011; Lexi-Comp Inc., 2012).
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21
The goal for systolic blood pressure in the patient with AAD is 100-120 mmHg and heart
rate approximately 60 beats per minute, but can be modified to each patient’s situation taking
into consideration their baseline blood pressure and past medical history. Labetalol is a BB that
has half-life of five to eight hours with a bolus infusion of 0.25 mg/kg over two minutes that can
be repeated every ten minutes. Labetalol can also be administered via continuous infusion one to
two mg/min with a maximum dosage of 300 mg. Esmolol is appropriate as well with a half-life
of nine to ten minutes. The bolus infusion dose of esmolol is 0.5 mg/kg over one minute
followed by a continuous infusion of 0.05 mg/kg/min with appropriate rate increase every four
minutes. If blood pressure control is not within goal parameters after initiation of BB,
vasodilators may be added for better BP control. Nitroprusside has a half-life of three to four
minutes and may be started at a dose of 0.3 mcg/kg/min. The BB should be started first for BP
and HR control and then add on vasodilators if necessary. Rate control should be completed
before initiation of vasodilators to minimize the reflex tachycardia that occurs as a compensatory
cardiovascular mechanism when BP decreases. If vasodilators are started first, reflex tachycardia
can increase aortic stress and expand the dissection. Angiotensin converting enzyme (ACE)
inhibitors can be added on to the pharmacological treatments if the patient has continued
hypertension despite the use of BBs and nitroprusside. Intravenous opioids should be given for
pain relief to further help with BP and HR control with morphine, 4 mg intravenous every two
hours as needed, being the drug of choice (Johnson & Prince, 2011).
According to the Ohio Board of Nursing (OBN), an advanced practice nurse with a
certificate to prescribe can prescribe verapamil, diltiazem, labetalol, esmolol, nitroprusside, and
morphine (in the hospital setting) to medically manage the patient with AAD (2013).
COMPREHENSIVE CASE STUDY
22
Follow Up
Regardless of whether the patient has undergone surgical repair for an AAD, ongoing
control of the patient’s blood pressure is important. Post-dissection aneurysms can develop and
rupture leading to approximately 30% of late deaths. Post-operatively, the systolic BP is
sustained at the lowest level possible to maintain organ function per laboratory values, urinary
output, and mental status. Blood pressure control will be recommended life-long to decrease the
risk of redissection or aneurysmal development. The patient must follow up within two weeks of
discharge to evaluate blood pressure control, symptoms, or any concerns the patient needs to
address. The patient will be discharged home with a portable machine that he can check his BP
with twice a day. Additionally, the patient will follow up with their primary care provider for
ongoing blood pressure management (goal home systolic BP 100-120 mmHg) with follow up
appointments every three-six months to evaluate BP control. The patient will have an additional
CT scan three months after discharge, then every six months for the first two years post
dissection. After two years without complications, CT scans may be obtained annually. The
cardiothoracic surgeon will be evaluating for any additional dissections or aneurysms (Rapp,
Owens, & Johnson, 2013).
Health Promotion Activities
Addressing barriers to patient compliance include medication side effects, medication
dosing schedules, restrictions on diet, depression, frustration, lack of social support and those
acutely or chronically ill. Identifying any feelings of depression or continued anxiety the patient
is experiencing are important to encourage treatment compliance and ensure the patient has an
appropriate support system in place. Education regarding the appropriate follow up, medication
compliance, immunizations, and appropriate lifestyle choices are necessary and should be
COMPREHENSIVE CASE STUDY
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completed at every follow up appointment. Additionally, involving social services may be
necessary if patient has difficulty affording medications or follow up care. Continued smoking
cessation and initiating a healthy diet and regular exercise are important to improve the patient’s
overall health status and hypertension management (Williams, Haskard, & DiMatteo, 2008).
Exercise can still be performed post dissection and management, but heavy lifting, contact
sports, or strenuous activities should be avoided (Juang, Braverman, & Eagle, 2008). Arranging a
dietary specialist to see the patient while in the hospital to review healthy, affordable nutrition
choices would support the patient making healthier choices along with developing a weekly
fitness regimen. Despite education and patient compliance, aneurysmal development may occur.
Patient education regarding the signs and symptoms of AAD should be reviewed extensively to
encourage the patient to call 911 as soon as symptoms develop to prevent further complications
or death. Avoiding judgment and including the patient as an important collaborator in their care
can improve patient adherence and outcomes (Williams, Haskard, & DiMatteo, 2008).
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24
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