N66337 Week 4 Cardiovascular Disorders: High-Yield
Pathophysiology, Risk Stratification, Clinical Presentation, Diagnostics,
and Management of Abdominal Aortic Aneurysm (AAA), Angina (Stable,
Microvascular, Variant, Silent), Acute Coronary Syndrome (UA/NSTEMI,
STEMI), Myocardial Infarction, Atrial and Ventricular Arrhythmias,
Palpitations, Syncope, Venous Thromboembolism (DVT, PE), Infective
Endocarditis, EKG Interpretation, Stress Testing, Echocardiography,
Pharmacologic and Surgical Interventions, Anticoagulation Therapy, and
Preventive Strategies Exam Questions Verified and Provided with
Complete A+ Graded Rationales Latest Updated 2026
AAA
Defined as a progressive local dilation of abdominal aorta (50% increase in diameter)
Disease of medial wall layer of the aorta
Risk for rupture and death significantly increases when size exceeds 5cm
Risk factors AAA
Male
Advanced age
Caucasian
HTN
Atherosclerotic vascualr disease (cardiac, carotid, PVD)
Smoking, COPD
Family history
PMH of hernias and other aneurysms
AAA clinical presentation
75% are asymptomatic
,Usually detected during incidental radiologic or surgical procedures for other conditions
In thin patients, pulsatile abdominal mass may be detected on routine supine abdominal exam
Complaints accompanying rupture: abdominal pain, flank pain, back with radiation down bilateral legs
(similar to claudication complaints)
AAA triad
Hypotension 42%
Pulsatile abdominal mass 91%
Pain - abdominal 58%, back 70%
AAA physical exam
Vitals: BP in both arms; watch for widening pulse pressure (this may be new for patient esp. if
expanding)
CV assessment: remember carotids, auscultate for (aortic) murmur and all pulses
Completed abdominal assessment: assess/palpate epigastric area down to the iliacs, ausculatate for
bruit
AAA diagnostics
Ultrasound for diagnosis - also used for follow-up for watchful waiting; SAAAVE
Abdominal CT with contrast: pre-op, detects leakage, expansion or rupture, used for emergent
situations
AAA differential diagnosis
Back strain
Arthritis
Bowel obstruction
,Pancreatitis
Renal calculi
Perorated gastric ulcer
AAA plan/management
Goal - prevent rupture and minimize surgical risk
Size is best predictor of rupture
Monitor annually
Expect > 10% size/year
Refer to surgeon at 4cm to begin yearly monitoring
Elective repair at 5-6cm
AAA management once referred
Preoperative assessment including cardiac risk stratification (ACC/AHA guidelines) determines surgical
treatment approach
Two surgical approaches - open surgical repair, endograft or endovascular repair
Patient education known AAA
Quit smoking
Lower BP
Healthy lifestyle
Stress importance of serial ultrasounds
Educate regarding signs and symptoms of impending rupture
Angina
, Most important thing with chest pain is determining cardiac versus noncardiac
You must rule out: musculoskeletal, GI, pulmonary, dermatologic, and mental health causes
Angina modifiable risk factors
Smoking, LDL, diet HTN, thrombogenic factors
Diabetes, physical inactivity, HDL, obesity, postmenopausal status
Stress, depression, triglycerides, homocysteine, oxidative stress
non-modifiable - age, gender, family history
Chronic stable angina pathophysiology
Precipitated by exertion and relieved with rest
Myocardial O2 demand - mismatch of O2 supply and demand
Goals for patient with stable angina - eliminate ischemia, abolish or reduce the frequency and severity of
angina attacks, prevent myocardial infarction, potentially improve the patent's long term survival
Chronic stable angina
Will likely be under the direction of cardiology
Patients will be on one or more of the following to help with symptoms: asa, nitrates, beta blockers,
calcium channel blockers, ace inhibitors (good choice depending on EF and possible DM hx), Ranexa
(costly)
Microvascuar angina (syndrome X)
History of angina with or without evidence of ECG changes
Angiogram fails to demonstrate obstruction or spasm
Sxs similar to classic angina
Pathophysiology, Risk Stratification, Clinical Presentation, Diagnostics,
and Management of Abdominal Aortic Aneurysm (AAA), Angina (Stable,
Microvascular, Variant, Silent), Acute Coronary Syndrome (UA/NSTEMI,
STEMI), Myocardial Infarction, Atrial and Ventricular Arrhythmias,
Palpitations, Syncope, Venous Thromboembolism (DVT, PE), Infective
Endocarditis, EKG Interpretation, Stress Testing, Echocardiography,
Pharmacologic and Surgical Interventions, Anticoagulation Therapy, and
Preventive Strategies Exam Questions Verified and Provided with
Complete A+ Graded Rationales Latest Updated 2026
AAA
Defined as a progressive local dilation of abdominal aorta (50% increase in diameter)
Disease of medial wall layer of the aorta
Risk for rupture and death significantly increases when size exceeds 5cm
Risk factors AAA
Male
Advanced age
Caucasian
HTN
Atherosclerotic vascualr disease (cardiac, carotid, PVD)
Smoking, COPD
Family history
PMH of hernias and other aneurysms
AAA clinical presentation
75% are asymptomatic
,Usually detected during incidental radiologic or surgical procedures for other conditions
In thin patients, pulsatile abdominal mass may be detected on routine supine abdominal exam
Complaints accompanying rupture: abdominal pain, flank pain, back with radiation down bilateral legs
(similar to claudication complaints)
AAA triad
Hypotension 42%
Pulsatile abdominal mass 91%
Pain - abdominal 58%, back 70%
AAA physical exam
Vitals: BP in both arms; watch for widening pulse pressure (this may be new for patient esp. if
expanding)
CV assessment: remember carotids, auscultate for (aortic) murmur and all pulses
Completed abdominal assessment: assess/palpate epigastric area down to the iliacs, ausculatate for
bruit
AAA diagnostics
Ultrasound for diagnosis - also used for follow-up for watchful waiting; SAAAVE
Abdominal CT with contrast: pre-op, detects leakage, expansion or rupture, used for emergent
situations
AAA differential diagnosis
Back strain
Arthritis
Bowel obstruction
,Pancreatitis
Renal calculi
Perorated gastric ulcer
AAA plan/management
Goal - prevent rupture and minimize surgical risk
Size is best predictor of rupture
Monitor annually
Expect > 10% size/year
Refer to surgeon at 4cm to begin yearly monitoring
Elective repair at 5-6cm
AAA management once referred
Preoperative assessment including cardiac risk stratification (ACC/AHA guidelines) determines surgical
treatment approach
Two surgical approaches - open surgical repair, endograft or endovascular repair
Patient education known AAA
Quit smoking
Lower BP
Healthy lifestyle
Stress importance of serial ultrasounds
Educate regarding signs and symptoms of impending rupture
Angina
, Most important thing with chest pain is determining cardiac versus noncardiac
You must rule out: musculoskeletal, GI, pulmonary, dermatologic, and mental health causes
Angina modifiable risk factors
Smoking, LDL, diet HTN, thrombogenic factors
Diabetes, physical inactivity, HDL, obesity, postmenopausal status
Stress, depression, triglycerides, homocysteine, oxidative stress
non-modifiable - age, gender, family history
Chronic stable angina pathophysiology
Precipitated by exertion and relieved with rest
Myocardial O2 demand - mismatch of O2 supply and demand
Goals for patient with stable angina - eliminate ischemia, abolish or reduce the frequency and severity of
angina attacks, prevent myocardial infarction, potentially improve the patent's long term survival
Chronic stable angina
Will likely be under the direction of cardiology
Patients will be on one or more of the following to help with symptoms: asa, nitrates, beta blockers,
calcium channel blockers, ace inhibitors (good choice depending on EF and possible DM hx), Ranexa
(costly)
Microvascuar angina (syndrome X)
History of angina with or without evidence of ECG changes
Angiogram fails to demonstrate obstruction or spasm
Sxs similar to classic angina
