Cardiac Board Review-Part I

Cardiac Board Review
Part 1
A 20-year-old female college student is evaluated at the student health center to
establish care. She had no major medical problems prior to college, and there is
no family history of cardiovascular disease.
BP: 110/60 mm Hg and pulse is 70/min. S1 and S2 are normal and there is an S4
present. There is a harsh grade 2/6 midsystolic murmur heard best at the lower
left sternal border. The murmur does not radiate to the carotid arteries. A
Valsalva maneuver increases the intensity of the murmur; moving from a
standing position to a squatting position, performing a passive leg lift while
recumbent, and performing isometric handgrip exercises decrease the intensity.
Rapid upstrokes of the carotid pulses are present. Blood pressures in the upper
and lower extremities are equal.
Which of the following is the most likely diagnosis?
Aortic Coarctation
Bicuspid Aortic Valve
Hypertrophic Cardiomyopathy
Mitral Valve Prolapse
Ventricular Septal Defect
Hypertrophic Cardiomyopathy
Abnormal diastolic function with preserved systolic function
Murmur: midsystolic harsh murmur caused by turbulent flow and obstruction of
the LV outflow track
– Murmur increased with Valsalva or standing
– Murmur decreased with hand grip, squatting
– EKG: LV hypertrophy and strain and Q waves that mimic an MI
– Echo
– Cardiac MR: ventricular hypertrophy and areas of scarring
– Echo screening for first degree relatives
– Avoid strenuous exercise, intense isometric exercise
– Symptomatic patients or pts with high risk of cardiac death (prior arrest, sustained VT, FHx of
sudden death): B-blockers first line. Verapamil and disopyramide are second line.
– ICD for pt with increased risk of sudden death
– Myomectomy/alcohol ablation for refractory symptoms
A 76-year-old woman residing in an independent living facility is evaluated during a
routine examination. She ambulates well, using a cane because of hip pain, but does
not exercise regularly and takes public transportation to complete her daily shopping.
She does not have exertional chest discomfort, dizziness, palpitations, dyspnea, or
fatigue. She has hypertension. There is no known history of coronary artery disease.
She does not smoke. Medications are hydrochlorothiazide and low-dose aspirin.
On physical examination, temperature is normal and blood pressure is 150/80 mm Hg.
BMI is 22. Cardiac examination reveals a sustained apical impulse; normal S1; and a
single, soft S2. An S4 is present. There is a grade 3/6 early-onset systolic, late-peaking
murmur that is heard best at the right upper sternal border and radiates to the left
carotid artery. Carotid pulses are delayed. There is trace pedal edema.
Transthoracic echocardiography demonstrates severe aortic stenosis. No other
valvular abnormalities are seen. Biventricular function is normal. There is
left ventricular hypertrophy. Pulmonary pressures are at the upper limits of normal.
Which of the following is the most appropriate test to perform next?
Cardiac CT angiography
Coronary angiography
Exercise Treadmill Stress Test
Transesophageal echocardiography
No diagnostic testing at this time
Valvular Heart Disease
• Midsystolic murmurs grade 1-2/6 are usually benign
• Diagnosis:
– TTE for symptomatic pts, systolic mumur 3-6/6, continuous
murmur, diastolic murmur
– TEE for severe mitral regurgitation, prosthetic valves,
endocarditis and evaluation of LA appendage
– When symptoms or physical exam findings are discrepant
from echo findings, do BNP and exercise testing with echo.
• Asymptomic pts with severe disease having other
cardiac surgery should undergo surgical valve
Valvular Heart Disease
• Right sided murmurs and heart sounds are louder during
– The ejection click heard with Pulmonic Stenosis disappears with
• Stand-to-squat maneuver and passive leg lift transiently increase
venous return (preload)  increases left ventricular chamber size
and volume.
– Increases most murmurs, but decreased HCM and MVP
• The Valsalva maneuver and the squat-to-stand maneuver 
decrease venous return
– Decreases most murmurs, but increases HCM and MVP
• Handgrip exercise increases afterload and decreases the relative
pressure gradient across the left ventricular outflow tract
– Decreases HCM and AS, but increases MVP
Valvular Heart Disease
S2: results from aortic and pulmonic valve closure
at end of ventricular systole
 Physiologic split= P2 closes after A2 during inspiration,
but they close at the same time during expiration.
This is NORMAL.
 Persistently split (widened S2)= Pulmonic stenosis,
Mitral regurgitation
 Fixed split= splitting does not vary with inspiration.
 Paradoxically split S2= LBBB, HCM
Aortic Stenosis
• Calcification of tricuspid valve or bicuspid valve
– Pts with bicuspid valve should be evaluated for aortic
arch dilation with echo
• Sx: angina, syncope, heart failure
• Murmur: mid to late peaking systolic murmur to
the carotids, S4, single S2, pulsus parvus et
– Murmur louder with squatting
– Standing and valsalva decrease the murmur
AS Management
– Monitor with serial echos
• Severe AS (area <1.0 cm2): yearly echos
• Moderate AS: echos every 2 years
• Mild AS: echos every 5 years
– Valve replacement if
• undergoing other cardiac surgeries
• severe AS and EF <50%
• hypotension develops during exercise testing
• SYMPTOMATIC patients
– Valve replacement
Carotid Pulse
Valsalva or
Stand Squat
Carotid radiation
Pulsus Bisferiens
Aortic Stenosis
Pulsus Parvus et tardus
Acute Aortic Regurgitation
Most common causes are dissection and valve
destruction from endocarditis.
• Murmur: short diastolic
• Dx: TTE; do TEE/CT/MRI if dissection
suspected as cause
• Tx: IMMEDIATE surgery; avoid IABP
Chronic Aortic Regurgitation
Results from annular dilation or primary leaflet
• Murmur: decrescendo diastolic high pitched blowing,
soft S1, enhanced when leaning forward
• Wide pulse pressure and bounding pulse
• Tx:
• monitor with echos (6-12 months if LV dilation or 2-3 yrs with
normal LV)
• AV replacement if EF <50% or abnormal hemodynamic response to
exercise, undergoing other cardiac surgery
• AV replacement
Mitral Stenosis
• Caused by rheumatic valve disease.
• Murmur: diastolic low rumbling murmur with a
diastolic opening snap; loud S1
• CXR and EKG demonstrate LAE and normal LV
• Tx:
• monitor with echo
• Valvotomy
• Valve replacement if pt with severe mitral regurgitation
Mitral Regurgitation
• Acute: from chordae tendineae rupture from
endocarditis or papillary mm rupture from MI
– HF, shock, pulm edema
– Murmur: holosystolic radiates to axilla
– Tx: Urgent Surgery
• Chronic: from MVP and endocarditis
– Murmur: holosystolic murmur, radiates laterally and
posteriorly, widely split S2, S3 and increased P2
– Tx: diuretics, BB, ARB/ACEi
• ASYMPTOMATIC: monitor with echos; MV repair if EF <60%
• SYMPTOMATIC: MV repair (annuloplasty)
• Systolic buckling of MV leaflets into the LA;
MR occurs if faulty leaflet coaptation
• Murmur: high pitched midsystolic click with
late systolic murmur
– The click moves earlier in systole with standing
and valsalva (unlike click with PS which is fixed)
– Squatting delays the click and murmur
Aortic Stenosis
Midsystolic ejection
Hypertrophic Cardiomyopathy
Mid to late systolic
Mitral Valve Prolapse
Late Systolic
Mitral Regurge
Midsystolic click
Aortic Regurge
Early, high pitched
Mitral Stenosis
Low pitched rumble
Opening snap, Diastolic click
• Prophylaxis: Amoxicillin (clinda or azithro if pcn
allergic) indicated for dental procedures (no
longer indicated for GU/GI procedures), invasive
procedure of the respiratory tract and surgery on
infected soft tissues:
– Prosthetic valves
– Previous episode of endocarditis
– Congenital Heart Disease: unrepaired, repaired with
residual defects or within 6 months of procedure
– Cardiac Transplant pts with valve lesions
– NO prophylaxis for bicuspid aortic valve, MVP
A 54-year-old man is evaluated for right-sided chest pain that is described as sharp, begins
following large meals, lasts for several minutes, and usually resolves spontaneously. The episodes
are not clearly related to activity, nor are they relieved by rest. He has been experiencing the pain
for about 4 months. Several of the episodes have resolved with antacids. The most recent
episode, which occurred yesterday while walking, lasted 20 minutes and resolved.
Medical history includes hypertension and hyperlipidemia. Family history is notable for a brother
who had coronary stent placement at the age of 43 years. Current medications are aspirin,
atenolol, and atorvastatin.
Physical examination is notable for estimated central venous pressure of 6 cm H2O; normal
carotid upstroke; and no cardiac murmurs, rubs, or S3. Lung fields are clear. Extremities show no
edema, and peripheral pulses are normal bilaterally.
Hematocrit, 44%; troponin I at presentation is 0.0 ng/mL; troponin I at 4 hours is 0.0 ng/mL ;
creatine kinase, 50 U/L.
EKG: shows normal sinus rhythm and no ST- or T-wave changes. CXR: shows a normal cardiac
silhouette, no infiltrates, and no pleural effusions.
Which of the following is the best diagnostic option?
Coronary angiography
Exercise stress test
Empiric treatment with a proton pump inhibitor
A 68-year-old woman is evaluated for atypical chest pain of 3 months’ duration. She describes the
pain as a left-sided burning that occurs both at rest and when she exercises. It lasts for about 10
minutes, and is relieved by rest and eating. The patient has no history of cardiac disease. She has
hypertension, for which she currently takes hydrochlorothiazide. She is a smoker and she has
asthma, for which she takes inhaled corticosteroids and frequently uses inhaled bronchodilators.
If she pretreats herself with the inhaled bronchodilator, she can walk long distances at a brisk
She is afebrile, her blood pressure is 158/84 mm Hg, her pulse is 64/min, and her respiration rate
is 18/min. Estimated central venous pressure is 5 cm H2O. On cardiac examination, no murmurs,
rubs, or extra heart sounds are noted. The lungs are clear to auscultation. There is trace
peripheral edema.
Total cholesterol, 200 mg/dL LDL 140; and HDL 50 mg/dL EKG: normal
Which of the following is the most appropriate diagnostic test for this patient?
Adenosine nuclear perfusion stress test
Coronary angiography
Coronary artery calcium score
Dobutamine stress echocardiography
Exercise stress test
Diagnostic test for CAD
Exercise Treadmill Testing:
EKG: Good for testing functional capacity, ischemia and prognosis; it will
NOT localize ischemia
Echo: indicates wall motion abnormalities that indicate ischemia
Nuclear myocardial perfusion: determine the area of ischemia and if its
Pharmacologic Stress Testing:
Dobutamine echo
Dobutamine nuclear perfusion
Adenosine nuclear perfusion
Coronary angiography
Coronary artery calcium testing: risk stratify asymptomatic pts at
intermediate risk with strong family history
Coronary CT imaging
CMR imaging
Diagnosing CAD
1. Pretest probability of having CAD
a) Categorize the nature of the chest pain
b) Estimate the pretest probability of CAD based on
sex, age, and character
2. Determine if patient can have an exercise test
based on their abilities and comorbidities
3. If doing an exercise study, look at the findings
on resting EKG
1. Pretest probability of having CAD
a) Categorize the nature of the chest pain:
1. Typical Chest Pain: 3 of 3
1. Substernal chest pain or discomfort
2. Provoked by exertion or emotional stress
3. Relieved by rest and/or nitroglycerin
2. Atypical Chest Pain: 2 of the 3
3. Non-anginal Chest Pain: none of the components
1. Pretest probability of having CAD
b) Estimate the pretest probability of CAD based
on sex, age, and character
Low Probability
Intermediate Probability
High Probability
Asymptomatic M and W of
all ages
Men of all ages with
atypical CP
Men > 40 with typical CP
Women <50 with atypical
Women >50 with atypical
Women >60 with typical
Women < 60 with typical
•Low risk: no further testing
•Intermediate risk: Noninvasive stress test
•High risk: begin medical therapy for CAD
2. Can they have an exercise test?
• If patient can exercise exercise stress
• If patient cannot exercise because of arthritis, severe pulmonary disease
or physical deconditioning or with a pacemaker pharmacologic stress
– Adenosine/Dipyridamole: Contraindicated with: bronchospastic airway
disease, theophylline use, baseline 2nd degree Heart Block
– Dobutamine: Contraindicated with: severe hypertension or arrhythmias. Must
hold BB before test.
• If patient cannot exercise because of the following comorbidities 
pharmacologic stress:
Recent MI or UA
Uncontrolled arrhythmias
Symptomatic severe aortic stenosis
Decompensated heart failure
Acute PE
Aortic dissection
3. If doing an exercise study, look at
the findings on resting EKG
If resting EKG ST changes or with any of the
• Greater than 1mm ST depression
• Paced rhythm
Must do echo or nuclear myocardial perfusion as
the diagnostic test.
A 65-year-old man is evaluated during a routine follow-up examination for coronary artery
disease. He was diagnosed with a myocardial infarction 5 years previously, and was started on
medical therapy with aspirin, metoprolol, atorvastatin, lisinopril, and sublingual nitroglycerin. He
was asymptomatic until 3 months ago, when he noted progressive exertional angina after walking
two blocks. He now uses sublingual nitroglycerin on a daily basis. He has not had any episodes of
pain at rest or prolonged chest pain that were not relieved by sublingual nitroglycerin. He has
hyperlipidemia and hypertension.
PE: a well-developed man who appears comfortable. BP 140/60 mm Hg HR 85/min. Carotid
upstrokes are normal with no bruits. Cardiac examination reveals no murmurs. The lungs are
clear. Peripheral pulses are equal throughout and there is no peripheral edema.
His electrocardiogram is unchanged since the last visit, with no evidence of acute changes.
In addition to adding a long-acting nitrate, which of the following is the most appropriate
management for this patient?
Add ranolazine
Increase metoprolol
Coronary angiography
Exercise treadmill stress testing
Contraindications for BB: bradycardia,
severe depression, decompensated
HF, severe restrictive airway disease
Contraindications for long acting
nitrate: severe AS, HCM, PDEi
Contraindications for ranolazine:
hepatic impairment, QT prolongation
or if pt on dilt, verapamil
PCI does NOT decrease future
cardiovascular events or increase
survival, it does decrease frequency
and severity of anginal symptoms
CABG for:
- Severe L main disease
- 3 vessel disease
- 2 vessel disease (prox LAD) with
reduced LV function
- DM with multivessel disease
A 66-year-old man is evaluated in the emergency department for left-sided chest pain that began
at rest, lasted for 15 minutes, and has since resolved. A similar episode occurred at rest
yesterday, and multiple similar episodes that were associated with exertion have occurred over
the past 2 weeks. Pertinent medical history includes hypertension and type 2 diabetes mellitus.
Family history is notable for his father undergoing coronary artery bypass graft surgery at age 69
years and his brother undergoing coronary artery bypass graft surgery at age 54 years. Current
medications are amlodipine, glyburide, and aspirin.
BP 125/65 mm Hg, HR 70/min, RR 12/min. Estimated central venous pressure is 6 cm H2O, carotid
upstroke is normal, there are no cardiac murmurs, and the lung fields are clear. Extremities show
no edema, and peripheral pulses are normal bilaterally.
Troponin I level of 1.2 ng/mL and a creatinine 1.4 mg/ dL
EKG: 1-mm ST-segment depression in leads aVL, V5, and V6. CXR: normal cardiac silhouette, with
no infiltrates and no pleural effusions.
The patient is treated with aspirin, intravenous nitroglycerin, unfractionated heparin, metoprolol,
and pravastatin.
Which of the following should be the next step in this patient’s management?
Coronary angiography
Obtain B-type natriuretic peptide level
Pharmacologic stress testing
Thrombolytic therapy
A 65-year-old woman is evaluated in the hospital 36 hours after presenting in the emergency department with
midsternal chest pain. Electrocardiogram on presentation demonstrated no ST-segment shifts, but T-wave
inversion was present in leads V3 and V4. She was given nitroglycerin, unfractionated heparin, and a
glycoprotein IIb/IIIa inhibitor and was admitted to the hospital. She has a history of hypertension and
hyperlipidemia and is a prior smoker. Her medications prior to admission were metoprolol, 25 mg twice daily;
atorvastatin, 80 mg/d; and aspirin, 325 mg/d.
The patient is afebrile. BP 132/82 mm Hg, HR 68/min and regular, RR 16/min. BMI is 25. There is no jugular
venous distention, and no crackles are auscultated. Heart sounds are normal. There is no rub, murmur, or
Her serum cardiac troponin I level rose to a peak of 4.2 ng/mL at 24 hours following the index event. Results of
a basic metabolic profile, including blood glucose levels, are normal.
Coronary angiography demonstrates diffuse, mild luminal irregularities in all coronary arteries, along with
diffuse severe disease in the distal left anterior descending coronary artery not amenable to percutaneous
coronary intervention. Left ventriculography demonstrates a left ventricular ejection fraction of 55% with a
small focal region of hypokinesis in the apex. The left ventricular end-diastolic pressure is 12 mm Hg.
The glycoprotein IIb/IIIa inhibitor is discontinued.
Which one of the following agents should be added to this patient’s medication regimen?
Acute Coronary Syndromes
• STEMI: ST segment elevation (or new LBBB)
with elevated enzymes
• NSTEMI: ST segment depression, T wave
inversion, or nonspecific EKG with elevated
• Unstable Angina: Nonspecific EKG findings
and normal enzymes
• Age >65yo
• > 3 CAD RF
• Coronary obs >50%
• ST segment deviation
• > 2 anginal episodes in
last 24 hours
• Aspirin use in last week
• Elevated biomarkers
High/Intermediate Risk (TIMI > 3)
• Aspirin
• B-blockers:
– Avoid in decompensated HF, sBP <90, bradycardia with HR <50, or
second degree AV block
– Can use CCB (except nifedipine) in those with CI to BB and in those
with continued angina despite optimum BB and nitrates
Glycoprotein IIb/IIIa inhibitors (tirofiban, eptifibatide, abciximab)
Unfractionated heparin, low molecular weight heparin, or direct
thrombin inhibitor (bivalirudin)
– Avoid low molecular weight heparin in renal failure
• High dose statin
• Coronary Angiography
Low Risk (TIMI 0-2)
Unfractionated heparin, low molecular weight
heparin, or direct thrombin inhibitor (bivalirudin)
• High dose statin
• Predischarge stress test
A 67-year-old woman is evaluated in the ED for substernal chest pressure that has lasted for just over 3 hours.
The pressure has not remitted despite administration of one dose of sublingual nitroglycerin on the way to the
hospital. The emergency department is in a community hospital that does not have percutaneous coronary
intervention (PCI) capability. The nearest hospital with PCI capability is 45 minutes away.
The patient has a history of hypertension and hyperlipidemia. There is no history of recent surgery or bleeding
diathesis. Current medications include lisinopril, hydrochlorothiazide, and simvastatin. She has no known drug
allergies. Aspirin and sublingual nitroglycerin are administered upon arrival.
Temperature is 37.2 °C (99.0 °F), BP 146/92 mm Hg, HR 104/min and regular, RR 18/min. The patient appears
uncomfortable. Crackles are heard at the bases of both lung fields. The S1 is normal; the S2 is paradoxically split.
No murmur or gallop is present.
Results of a complete blood count, basic metabolic profile, and clotting studies are normal. Initial serum
troponin I level is 0.5 ng/mL. A stool sample tests negative for occult blood.
EKG: normal sinus rhythm with a left bundle branch block. No prior tracing is available for comparison.
Intravenous heparin, β-blockers, and morphine are administered.
Which of the following is the most appropriate next step in the management of this patient?
Administer thrombolytics
Administer glycoprotein IIb/IIIa
Obtain serial cardiac enzyme measurements
Transfer to nearest hospital with PCI capability
A 62-year-old woman is brought to the emergency department by paramedics for chest pain that
has been present for 5 hours. Medical history is notable for type 2 diabetes mellitus,
hypertension, and a stroke 1 year ago. Medications include glyburide, lisinopril, atorvastatin, and
On physical examination, she appears comfortable. She is afebrile, blood pressure is 190/90 mm
Hg, pulse rate is 88/min and respiration rate is 16/min. Cardiac examination shows no murmurs,
extra sounds, or rubs. The lungs are clear and pulses are equal bilaterally. Neurologic examination
is normal.
The electrocardiogram shows 2-mm ST-segment elevation in leads II, III, and aVF.
A coronary catheterization laboratory is not available, and the nearest hospital with
percutaneous intervention capability is 1 hour away.
Which of the following is the best management option for this patient?
1. Aggressive medical therapy
without reperfusion attempt
2. Immediate thrombolytic therapy
3. Transfer for coronary artery
bypass graft surgery
4. Transfer for percutaneous
coronary intervention
STEMI management
• Initiate medical therapy: aspirin, clopidogrel, BB, nitrates,
heparin, statins
– ACEi with reduced EF
• Decide on reperfusion therapy. Evaluate:
– Contraindications to thrombolytics: PCI preferred
– If > 3 hours from symptom onset: PCI preferred
– High risk features (shock or HF or h/o CABG): PCI preferred
• If facility without onsite PCI: give thrombolytics, place IABP and
transfer to PCI facility
– Time to achieve balloon inflation
• Door to balloon time: < 90 minutes
• Door to needle time: < 30 minutes
– If facility without onsite PCI, transfer to facility with PCI capability only if they
can undergo PCI within 90 minutes of first medical contact (medical contact to
balloon time)
Contraindications to Thrombolytics
• Absolute:
previous hemorrhagic stroke any time or any CVA within 3 months
Intracranial neoplasm or cerebrovascular lesion
Active internal bleeding
Suspected aortic dissection
Closed head or facial trauma within last 3 months
• Relative:
BP >180/110
INR >2-3
Recent major trauma (2-4 wks)
Active peptic ulcer
Non-compressible vascular puncture
Any stroke history
• Continued CP, lack of ST elevation improvement,
hemodynamic instability, and ventricular arrhythmias
indicate failure of thrombolytics  rescue PCI
• Improvement in ST elevation >50% on EKG obtained 60
min after therapy indicates successful reperfusion.
– Reperfusion arrhythmias (accelerated idioventricular
arrhythmia) indicate successful thrombolysis
• Must risk stratify prior to discharge:
– Echo or nuclear imaging to assess LV function
• EF <40%  angiography
– Pharmacologic stress test
• Significant ischemia angiography
An 85-year-old woman is admitted to the coronary care unit following successful thrombolytic therapy
for an acute anterior wall STEMI. Prior to the myocardial infarction she had been active without any
medical problems and was taking no medications.
BP 120/70 mm Hg and heart rate is 90/ min. There is no jugular venous distention and no cardiac
murmurs. The lung fields are clear and there is no peripheral edema. Medications started in the hospital
are aspirin, low-molecular-weight heparin, intravenous nitroglycerin, and oral metoprolol.
EKG shows Q waves in the anterior leads with upsloping ST segments.
On hospital day 3, the patient experiences acute onset of respiratory distress, and her systolic blood
pressure falls to 80 mm Hg. Her oxygen saturation remains at 80% despite the administration of 100%
oxygen by face mask. She is given dopamine and intravenous furosemide. On physical examination,
blood pressure is 96/40 mm Hg, pulse rate is 100/min, and respiration rate is 28/min. Findings include
jugular venous distention, crackles throughout both lung fields, and a grade 4/6 systolic murmur
associated with a thrill. A pulmonary artery catheter is placed via the right internal jugular vein. The
pulmonary capillary wedge pressure tracing shows prominent v waves
Which of the following is the best immediate treatment option?
Mitral valve repair
Pulmonary artery thrombectomy
Ventricular septal defect repair
Complications after MI
• RV infarction: hypotension, clear lungs and elevated JVD in setting
of inferior wall MI
– DX: R sided EKG and echo
– Tx: IVF, dobutamine and PCI. Avoid nitrates and preload reducing
• Arrhythmias and blocks
• Mechanical complications:
– Rupture of papillary muscle with mitral regurge: 3-7days after inferior
MI. Pt develops shock. Short early systolic murmur.
– VSD: 3-7days after anteroseptal MI. Shock. Loud, holosystolic mumur
with a thrill
– LV free wall rupture: 3-7 days after anterior MI. Syncope and
– LV thrombus: most common with anterior MI. Anticoagulate for 3-6
mo to treat.
A 67-year-old business man is evaluated during a routine health examination. He has a 30 packyear history of smoking, but quit 5 years ago. He consumes two or more alcoholic beverages on
most days. He is asymptomatic, but performs no regular physical exercise. He takes no
On physical examination, his blood pressure is 148/92 mm Hg and heart rate is 78/min and
regular. His pulses are full, he has no bruits, and results of his lung, heart, abdominal, and rectal
examinations are unremarkable.
Total serum cholesterol is 240 mg/dL (6.2 mmol/L), HDL cholesterol is 40 mg/dL (1.0 mmol/L),
and triglyceride level is 100 mg/dL (1.1 mmol/L). Results of other serum laboratory studies are
An abdominal ultrasound for screening purposes demonstrates an infrarenal abdominal aortic
aneurysm measuring 4 cm in diameter.
In addition to treatment of this patient’s hyperlipidemia and hypertension and discussion about
his at-risk drinking, which of the following is the best management option?
Abdominal CT with IV contrast
Antithrombotic therapy
Follow up US in 6-12 months
Placement of endovascular stent graft
Thoracic Aortic Aneurysm
• Serial CT or MRI for surveillance
• Tx: B-blockers or ARBs
– Surgical Repair if:
symptoms (hoarseness, dysphagia, back pain)
rapid growth (>1 cm/yr)
Severe dilation (>5 cm ascending or >6 cm descending)
Abdominal Aortic Aneurysm
• Screen with US in men 65-75 yo who have ever
• US q6-12 months for AAA >4cm
• Tx:
– Surgical Repair:
• AAA >5.5 cm
• Progression of > 0.5cm per year
• Ruptured AAA signs: abdominal/back/flank pain,
hypotension, syncope or shock.
– Dx: CT or MRI (US is not accurate for diagnosis)
A 48-year-old man is evaluated in the emergency department for sudden onset of
severe discomfort in the chest and between the shoulder blades. The pain was
maximal in intensity at its onset 90 minutes ago and is unaffected by position or
breathing. He has a history of hypertension, for which he takes hydrochlorothiazide,
25 mg/d; and lisinopril, 40 mg/d.
BP is 200/120 mm Hg, pulse is 100/min, and respiration rate is 20/min. An S4 gallop is
present. No cardiac murmur or pericardial rub is present. The lungs are clear to
auscultation. Distal pulses are equal and symmetric. Results of a neurologic
examination are normal.
UDS: positive for cocaine. Serum creatinine is 2.2 mg/dL. His creatinine 0.8 mg/dL at
the time of his last office evaluation. Serum cardiac troponin and myoglobin levels are
normal. An electrocardiogram reveals left ventricular hypertrophy with a secondary
repolarization abnormality and sinus tachycardia. Chest radiograph is normal.
In addition to emergently lowering the blood pressure and heart rate, which of the
following diagnostic tests should be performed next?
CT scan of chest with intravenous contrast
Nuclear myocardial perfusion scan
Transesophageal echocardiogram
Ventilation-perfusion lung scan
Aortic Dissection
• Dx:
– CT
– Trasesophageal echo
• Type A: ascending aortic arch
– Surgical emergency
• Type B: distal to L subclavian artery.
– Tx medically with IV B-blockers with goal HR 60-80.
– Monitor at 1,3,6 months then q6-12 months if
aneurysmal dilation present

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