Internal Medicine Flashcards
45 yoM with brief periods of chest pain when climbing up the four flights of stairs to his ailing mother’s apartment. Pain starts gradually and feels like a squeezing feeling “under my breastbone” and seems to go away with rest. It doesn’t change with breathing or with different positioning. What is going on?
Stable angina, due to increased myocardial O2 demand with narrowed coronary arteries leading to an imbalance between blood supply and O2 demand.
45 yoM with history of occasional substernal chest pressure and a normal resting ECG. Otherwise healthy except for T2DM, and says he can walk around his neighborhood without difficulty. What test should you use to make the diagnosis of CAD?
Exercise stress test - could do stress ECG or stress echo. He is able to exercise so he can do the exercise stress test on a treadmill. This information could be enhanced by doing perfusion imaging with a radioisotope during exercise. Perfusion imaging can help determine if there are areas of reversible ischemia.
62 yoF has a positive cardiac stress test. What are your recommendations?
Do cardiac catheterization! This should also be done in a patient with nondiagnostic noninvasive tests in angina, angina soon after MI, severely symptomatic angina, or any other situation with a need for revascularization, valvular disease, or a potential need for surgical intervention, or to revascularize with PCI.
70 yoM presents with unstable angina. Due to severe arthritis and COPD, he does not tolerate exercise well. What medications can you use to perform a cardiac stress test, and how do they work?
Adenosine or dipyridamole: coronary vasodilation. Diseased arteries are maximally dilated at rest, so they will receive less flow when the rest of the system is vasodilated.
Dobutamine: increases HR, BP, contractility, and therefore increases myocardial O2 demand
What lifestyle modifications might you recommend to your patients to reduce their risk of CAD?
Smoking cessation; management of HTN; reduce serum cholesterol; glycemic control in T2DM; weight loss; exercise; reduced saturated fat and cholesterol in diet
Mr. Jones is about to be discharged from the hospital after an MI. He does not have CHF. His diabetes is already optimally controlled. His acute MI was due to an occluded LAD, and so he underwent PCI and stenting. What new medications will he go home on, and why?
ASA - indicated in all CAD patients, reduces risk of MI, decreases morbidity.
Beta-blocker (metoprolol, atenolol) - reduces HR, BP, contractility, so decreases cardiac work, and decreases frequency of coronary events
Nitrates (nitroglycerin) - vasodilatory, so can relieve angina, reduce preload, reduce myocardial O2 demand
Clopidogrel - initiated in all patients who receive stenting via PCI. Dual antiplatelets (ASA+plavix) needs to continue for 30 days if a bare metal stent, and 12 months if a drug-eluting stent.
Statin: reduces risk of further coronary events
ACE inhibitor: reduces mortality and should be a part of long-term maintenance therapy.
Mrs. Stone has a history of MI, and coronary angiogram shows that she has three-vessel disease with 70%, 75%, and 90% stenosis, respectively. What intervention is indicated?
CABG: indicated for three-vessel disease with >70% stenosis in each vessel, or for left main coronary disease with >50% stenosis and LV dysfunction, or for high-risk patients.
A patient with a long history of right heart failure and pulmonary HTN presents to the ED with worsening symptoms, complaining of severe swelling in her legs. On exam you note ascites, hepatomegaly, JVD, and severe pitting edema. You also hear a blowing holosystolic murmur at the lower left sternal border that is more intense with inspiration. The patient is in Afib. What does this murmur signify? What treatment is most likely going to help?
This is a tricuspid regurgitation murmur in the setting of RHF/pulmonary HTN. It should be treated by treating the underlying cause, in this case his pulmonary HTN and RHF, as well as by treating his volume overload.
69yoF has chest pressure at rest, and presents to the ED for a workup. Troponin is normal. ECG does not show ST elevation or Q waves. What is going on, and how should she be initially managed?
Unstable angina - reduced resting coronary flow leads to decreased supply of O2 to myocardium. Medical management is required before stress testing.
Admission with cardiac monitoring, give O2, IV access.
Medical management - ASA, plavix, beta-blockers (first-line therapy), LMWH to prevent progression or development of clot, nitrates, oxygen if hypoxic, electrolyte repletion.
Patient with stable angina gets a lipid panel drawn, and has hyperlipidemia. What should their goal LDL be for reducing CAD morbidity/mortality?
LDL <100
55yoM presents with chief complaint of nocturnal chest pain. He is admitted and ECG on admission, when he is asymptomatic, is normal. In the middle of the night on his first night in the hospital, he complains of chest pain again, and ECG shows ST segment elevation that resolves on repeat ECG. What is likely to be going on, and how can you definitively show that?
Prinzmetal’s angina - transient coronary vasospasm, usually with angina at rest and occasionally with ventricular dysrhythmias. Usually occurs at night. Transient ST elevation on ECG during the pain, representing transmural ischemia.
Definitive test is angiography, with vasospasm when the patient is given IV ergonovine.
A patient presents to the ED with dizziness, fatigue, and syncope. She has a history of CHF. On ECG there is a sinus bradycardia. What could this be called?
Sick sinus syndrome - may require pacemaker implantation.
A patient has hypotension, elevated JVP, hepatomegaly. Her lungs are clear to auscultation bilaterally. You see ST segment changes in II, III, and aVF. Where is the pathology?
Likely a right ventricular infarct.
61 yoF, presenting to the ED with chest pain. He has had one prior MI 4 years ago. What ECG finding will you expect to find that reflects his PMH?
Q waves, which indicate prior MI. If there are new ST or T abnormalities, that suggests unstable angina or new MI may also be going on. Compare to a previous ECG to tease out what are actually new findings.
You see ST depression on an ECG. What does that suggest, compared to ST elevation?
ST depression suggests subendocardial injury whereas ST elevation suggests transmural infarct.
You are treating a patient for acute MI. What agents have been shown to reduce mortality in MI?
ASA, beta blockers, ACE inhibitors - should be used in long-term maintenance therapy
A 75yoM presents to the emergency department for dizziness following three days of nausea and vomiting. You place him on telemetry and vitals monitoring, noting that he is hemodynamically stable. You notice a few brief, self-limited runs of V-tach while he is in the emergency department. His dizziness resolves with IV fluids, Zofran, and PO fluids over the course of a few hours, and you determine that it was most likely due to volume depletion. What should you do about his findings on telemetry?
Nonsustained V-tach is usually asymptomatic but could be due to CAD and LV dysfunction, which are independent risk factors for sudden death. This patient needs to be evaluated for cardiac disease, as his nonsustained V-tach suggests that an underlying disease process might be present.
A patient who has had an anterior MI develops third-degree heart block. How should this be managed emergently?
This patient requires placement of a temporary pacemaker because new second-degree type II and third degree heart block in a patient with anterior MI have very poor prognosis. If the MI were inferior, then IV atropine can be used initially.
A patient has been admitted for GI bleeding and is found to have non-sustained V-tach on telemetry. The patient has a history of CHF. You determine that the V-tach is not likely related to the GI bleeding, which is mild bleeding from diverticulosis. What is the most effective treatment for this patient’s nonsustained V-tach?
ICD has been shown to be the most effective treatment for non-sustained V-tach in a patient with underlying heart disease.
A patient with a history of poor healthcare utilization presents to the ED with a multiple-year history of dyspnea on exertion and orthopnea, with palpitations that are worse when lying down, because the symptoms are finally bad enough that the patient thinks he needs care. On exam you note that the blood pressure is 180/65, and you hear a diastolic decrescendo murmur at the left eternal border. The murmur increases in intensity with sustained handgrip. What is your diagnosis? What treatments should you consider? What other evaluation might you want, and what would it show? What are possible causes?
Aortic regurgitation.
Further evaluation with CXR (shows LVH, aortic dilation), ECG (shows LVH), echocardiogram (dilated aortic root, LVH, reversal of blood flow in the aorta), and possibly cardiac catheterization.
Treat with conservative management if stable and asymptomatic (salt restriction, diuretics, vasodilators, digoxin, afterload reduction with ACEis or arterial dilators, and restrictions on strenuous activity). Treat with surgery for valve replacement if symptomatic or having significant LV dysfunction.
Possible causes: primary valvular (Rheumatic fever, bicuspid valve, Marfan, EDS, ankylosing spondylitis, SLE) and aortic root disease (syphilitic aortitis, osteogenesis imperfecta, aortic dissection, Behcet’s disease, Reiter’s syndrome, systemic HTN)
4 days after an acute MI, a patient experiences chest pain. On exam, the patient is hypotensive and has distended neck veins. Heart tones are muffled. An emergent bedside ultrasound shows free fluid within the pericardium. What event most likely occurred, and what treatment is needed?
This is likely to be a free wall rupture, producing cardiac tamponade. Pericarditis can also lead to tamponade after an MI, but the free fluid on US is concerning for hemopericardium. This is most often fatal. Tx with hemodynamic stabilization and resuscitation, pericardiocentesis, and then emergent surgical repair.
Your patient has an ECG with early P waves that differ in morphology. The patient has been experiencing palpitations. What is this arrhythmia called, and is any treatment indicated?
Premature atrial complexes. Often asymptomatic and do not require treatment. If symptomatic (palpitations), beta blockers may help.
You are assessing a patient who complains of orthopnea, paroxysmal nocturnal dyspnea, and overall shortness of breath. What physical exam findings might you find, and what does that indicate?
These are symptoms of left-sided heart failure. Exam may show displaced PMI due to cardiomegaly, pathologic S3 heard best at the apex with the bell (rapid filling into a non-compliant LV), S4 gallop heard best at the left sternal border with the bell (atrial systole, with blood ejected into a stiff/non-compliant LV), and crackles/rales at lung bases due to pulmonary edema (rales suggests at least moderate severity of LV heart failure). Increased intensity of the pulmonic component of the second heart sound suggests pulmonary HTN.
You’re reading an ECG and see a large R wave and ST depression in V1 and V2, as well as prominent upright T waves in V1 and V2. What does that indicate?
Posterior MI
A 69 yoM presents to the emergency department with shortness of breath. On history he endorses orthopnea. He has a history of HTN and previous MI. On exam he has an S3 and some crackles at the bases of his lungs, as well as pedal edema. What tests will you order on this patient, and what would you be looking for to support the diagnosis at the top of your differential?
This is a picture consistent with CHF.
CXR: look for cardiomegaly, Kerley B lines (short horizontal lines near the periphery of the lung and near the costophrenic angles indicating pulmonary congestion and dilation of pulmonary lymphatics), pleural effusion
TTE (initial test of choice): evaluate for systolic vs diastolic dysfunction and see if a pericardial, myocardial, or valvular process is involved. Also estimates EF.
ECG: rule out MI, may help detect chamber enlargement
Labs - cardiac enzymes and CBC to rule out MI and see if there is anemia, BNP to evaluate atrial stretch
You are reviewing an ECG and see that the P wave progressively gets longer and longer until you see a dropped beat, with a P wave but no QRS. What is this and what treatment is needed?
2nd degree AV block, Mobitz type I (Wenckebach). P wave progressively prolongs. AV nodal block. Usually does not require treatment.
You have a patient with HFrEF, with an ejection fraction of 35%. Her BMI is 40, and she smokes 1 pack/day and drinks alcohol about 5 times a week. Her current medication list includes a baby aspirin daily and a statin. She is also on metoprolol following an MI that she had three years ago. What lifestyle modifications will you recommend, and what medications will you add for management of her heart failure?
Lifestyle mods: sodium restriction, weight loss, smoking cessation, restricting alcohol use, exercise, monitoring weight to detect fluid accumulation.
Medications: Add a diuretic (symptom control) like furosemide (loop) or hydrochlorothiazide (thiazide, modest potency), and an ACE inhibitor (reduces mortality). She is already on a beta blocker.
Other meds can be added as needed - spironolactone or eplerenone (doesn’t cause gynecomastia), digitalis, hydralazine and isosorbide dinitrate. The aldosterone antags prolong survival in classes III and IV, but you need to monitor K and renal function. Digitalis/digoxin is an inotrope, which can provide symptomatic relief in patients who are symptomatic despite being on all other medication options. Hydralazine/isosorbide is used in patients who don’t tolerate ACEis/ARBs.
A patient presents with a CHF exacerbation. You place the patient on telemetry and notice a heart rate around 150, with an atrial rate around 300. What finding do you expect to see on ECG?
Sawtooth flutter waves, best seen in the inferior leads (II, III, aVF) - atrial flutter.
A patient presents with HFpEF. She is in volume overload. What medications are indicated?
Beta blockers are indicated for reducing HTN, and they have a clear benefit. Diuretics are used for volume overload. DO NOT use digoxin and spironolactone.
