Clin Med Cardio Flashcards
91 year old female presents with dyspnea, syncope and angina. A mid-systolic crescendo-decrescendo murmur is heard at the RSB and 2nd ICS. There is a diminished S2 and a palpable LV heave/thrill. The murmur increases with squatting and decreases with standing. What is your diagnosis, what is the preferred imaging and what is your treatment? What is the most common cause of this disease?
Dx: Aortic Stenosis; Imaging: Echocardiogram; Tx: Valvotomy or valve replacement with a bioprosthetic valve unless the patient is already on anticoagulation therapy. This is caused by progressive calcification of the valves with age.
30 year old male presents with dyspnea, dizziness, and angina with exertion. There is a mid-systolic ejection murmur with an ejection click. There is a diminished S2, and the murmur is harsh and crescendo-decrescendo. There is a palpable LV heave or thirll. The murmur increases with squatting and decreases with standing. What is your diagnosis, preferred imaging and treatment?
Dx: congenital bicusp (this is the most common abnormalitiy although any number of cusps besides 3 is a problem) AS; imaging: echocardiogram; tx: valvotomy or valve replacement with a mechanical valve and lifetime anticoagulatnts if the patient does not have any anticoag contraindications.
9 year old male presents with dyspnea, dizziness, and angina with exertion. There is a mid-systolic ejection murmur with an ejection click. There is a diminished S2, and the murmur is harsh and crescendo-decrescendo. There is a palpable LV heave or thirll. You also see that the patient has a higher blood pressure in his upper extremities than his lower extremities. The murmur increases with squatting and decreases with standing. What is your diagnosis, preferred imaging and treatment?
Dx: congential bicusp with aortic coarctation; imaging - echocardiogram; tx: baloon valvuloplasty and limitations on physical activity. This patient has a severe murmur so they need an echo yearly and should not compete in high intensity athletics.
Patient presents for an annual exam and has an asymptomatic crescendo-decrescendo murmur heard at the apex and RSB. What is your diagnosis, imaging and treatment?
Dx: Mild AS; imaging: echocardiogram every 3-5 years if it remains asymptomatic; tx: monitor and complete exercise testing to indicate whether or not the patient can compete in competitive sports.
What are the types of valves used in valve replacement? What are the pros and cons?
Mechanical: St. Jude (ball and cage no longer being put in but will be seen in patients who have already had a valve replacement) last longer but require life long anticoagulation and can lead to anemia from the RBCs being damaged in the valve; Bioprosthetic: bovine or porcine, do not require anticoagulation but only last about 10 years and have a greater risk of infection in the first 18 months.
Patient presents because he/she is experiencing a new onset of fagitue, sweating, and weakness. Quinke’s pulses, watson’s hammer pulse, corrigan’s pulse, austin flint murmur, DeMusset sign and pulses bisferiens are noted. There is an early diastolic murmur heard at the 3rd ICS and LSB that is continuous and a decrescendo. The murmur increases with standing and valsalva. The Patient is diaphoretic, pallor, hypotensive, some cyanosis and weak but rapid pulse. What is your diagnosis, preferred imaging and treatment? What are the common causes of this disease?
Dx: Aortic Regurgitation/Insufficiency acute in onset; imaging: Echocaridogram; Tx: valve replacement/repair but no insertion of an intra-aortic baloon pump because it will worsen the problem. Common causes are damage to the AoV leaflets by calcification, high afterload, aortic dissection, infective endocarditis, traumatic rupture from blunt trauma, or failed balloon vavlotomy or surgical repair.
Patient presents for annual exam and is found that the there is a non-displaced PMI, but it is hyperdynamic and there is an early diastolic decrescendo murmur heard at the 3rd ICS and LSB. What is your diagnosis, preferred imaging and treatment?
Dx: Chronic AR; imaging: echocardiogram; treatment: if asymptomatic give vasodilators to reduce afterload and if LV impairment occurs then perform valve replacement surgery.
Patient presents with dyspnea, orthopnea, fatigue, palpitations, hemoptysis and hoarseness. On the exam you find that there is a palpable S1/opening snap, RV lift, a loud S1 and a diastolic rumble most prominent at the apex. The murmur increases with squatting and decreases with standing. The patient’s face has pink/purple patches on the cheeks. There is A. fib seen on the ECG and you suspect that there may be systemic embolism. The CXR shows that there is ‘double density’ on the R.Atrium. On Echo a ‘hockey stick appearance’ is present on the mitral valve. What is your diagnosis, preferred imaging and treatment? What are the common causes of this disease?
Dx: Mitral valve stenosis; imaging: echocardiogram to assess the severity, the size of the RV and it’s function as well as assess the valve morphology.; Tx: diuretics to prevent heart failure, control the A. fib with rate control (Beta or calcium channel blockers) and rhythm control if possible (cardiovert if HR is tachy), anticoagulation because of clot risk, do a PCI baloon valvuloplasty, mitral commissurotomy or valve replacement. Commonly caused by rheumatic heart disease causing thickening at the tips or congential diseases (papillary muscle displacement or a fused papillary muscle).
Patient presents with new onset dyspnea on exertion, fatigue, peripheral edema, orthopnea, PND, and hemoptysis. On exam the pulse is brisk and low volume, the apex is laterally displaced, hyperdynamic has a thrill and late parasternal lift. S2 is widely split and there is a pansystolic (fixed) or midsystolic (dynamic) murmur from the apex to the axilla that increases with standing. There may be a mid systolic click. The ECG shows LA enlargement and A. fib, LVH and RVH. The CXR shows increased size of LF and LA, pulm vascular markings, kerly B lines and calcium deposits on the mitral valve. What is your diagnosis, preferred imaging and treatment? What are the common causes of this disease?
Dx: Mitral Regurgitation; Imaging: echocardiogram - transthoracic or TEE; tx: emergent surgery if acute in onset to repair/replace the valve, if chronic complete serial exams and reduce the afterload with ACE-I while controling SVTs with B-blockers. Common causes are calcification, infective endocarditis, damage to the papillary muscles (CAD, hypertrophic cardiomyopathy, infiltrative disorders, dilation or trauma).
Patient presents with peripheral edema. On exam there is a diastolic rumble on the LSB and 4th ICS that increases with inspiration (Carvallo Sign), passive leg raising, and squatting. There is an opening snap. The lungs are clear despite JVD, hepatomegaly, hepatic pulsations, ascites and peripheral edema. ECG has no specific findings. What is your diagnosis, preferred imaging and treatment? What is the most common cause?
Dx: tricuspid stenosis; imaging: echocardiogram reveals limited mobility of the tricuspid valve and turbulent diastolic flow; tx: diuretics for volume control initially and eventual surgical replacement (usually with bioprosthetic). The most common cause is rheumatic but may be seen in conjunction with carcinoid syndrome and TV repair.
Patient presents with JVD, hepatomegaly, ascites and peripheral edema. During the history the patient admits to being a long term IV drug abuser. The physical exam shows a right sided S3 and S4 with a RV heave and holosystolic murmur that increases with squatting, passive leg raising and inspiration. The ECG reveals signs of RA or RV enlargement. What is your diagnosis, preferred imaging and treatment? What are some common causes of this disease?
Dx: Tricuspid Regurgitation; imaging: Echocardiogram but MRI is becoming the gold standard despite being expensive and not bedside because it can accurately detect RV function; Tx: treat the underlying cause (ie. Pulm HTN, infiltrative disease) and it will resolve, or tricuspid annuloplasy is preferred. TR is generally caused by tricuspid prolapse, collagen disease, endocarditis and RV pacemaker injury.
Patient presents with the sx of tricuspid regurgitation. Echo reveals that there is displacement of one or more of the TV leaflets into the RV. What is the diagnosis?
Ebstein’s anomoly
A 30 year old male presents with progressive dyspnea on exertion and impaired exercise capacity, orthopnea, PND, syncope, fatigue and peripheral edema. During the physical you find that there is an S3 sound. What is your diagnosis? What are ways to treat? What are some common causes and what test can distinguish them from one another?
Dilated Cardiomyopathy. Tx: beta blockers, ACE-I, aldosterone inhibitors, diuretics, anticoagulation and pacemaker/defibrillator if needed. Etiologies include stress, viral (Parvovirus, influenza), infectious (HIV, Chagas disease, Lyme Disease), genetic (autosomal dominant is the most common), L. ventricular non-compaction in utero, toxin exposure (alcohol, cocaine, medications and chemo - may return to normal if the toxin is discontinued), peripartum.
A 50 year old recent widow presents with sx of fatigue, dyspnea, snycope, peripheral edema, and subseternal chest pain. On the physical exam. You order an ECG and see an anterior ST elevation, and there are elevated biomarkers. On imaging there is noted apical ballooning. What do you order to diagnose? What is your diagnosis and treatment? What likely caused this?
Test: Echo to diagnose dilated cardiomyopathy and then an endomyocardial biopsy to distinguish which one. Dx: stress induced dilated cardiomyopathy; Tx: give beta blocker, ACE-I, aldosterone inhibitor, diuretic therapy and anticoagulation. Also educate the patient about reduction of stress level, offer grief counseling. This was likely caused by an increased release of catecholamines from the stress of losing her spouse.
A 5 week post-partum mother presents with extreme fatigue, increasing dyspnea, syoncope and orthopnea. You order an echo and see that the heart is dilated. What do you do?
Diuretics, pacemaker and transplant if it does not show signs of improvement. Monitor closely because there is a high mortality rate although some may return to baseline in 6 months.
You diagnose your patient with a hereditary cardiomyopathy, what do you do to screen family?
All first degree relatives should be screened every 3-5 years by ECG and echocardiogram. If disease is found then evaluate every 1-3 years depending on severity.
A variety of mutations that cause hypertrophy of the L. Ventricle and occasionally the R. Ventricle but is not associated with HTN, rather is associated with myocyte-myofibril disarray. Hypertrophy generally occurs on the septum and there is a small internal diameter of the L. ventricle that can cause SAM. There is normal systolic function but there is impaired diastolic function. What is the disease and what are the 4 types?
Hypertrophic Cardiomyopathy. Type I is “classic” anteroseptal hypertrophy. Type II is anterior and posteroseptal hypertrophy sparing the lateral, posterior and inferior walls. Type III is extensive thickening with the only normal segment being the basal segment of the posterior wall. Type IV is isolated apical hypertrophy that is more commonly seen in the Asian population.
A 43 year old male presents with dyspnea on exertion, severe exertion related chest discomfort and syncope. He noticed that his exercise tolerance is not getting better as he continually tries to get into shape, he has been pretty sedentary his whole life until now. On physical exam you find that they are hypertensive and you hear a midsystolic crescendo-decrescendo murmur at the RSB and 2nd ICS that increases with standing and valsalva but decreases wtih rapid squatting. Additionally you hear a holosystolic murmur at the apex that increases with squatting and decreases with standing and valsalva. What is your diagnosis, and what do you expect to see on the imaging studies? What is your treatment?
Dx: HOCM. Imaging: the echo would show that there is anterior mitral leaflet movement during systole that obstructs the aortic valve, additionall there is LV hypertrophy and L. Atrial enlargement. Tx: keep him hydrated!!!!!! Beta blockers to decrease chronotropy and inotropy along with calcium channel blockers to improve diastolic filling and anti-arrhythmic drugs to prevent him going into atril arrhythmia. An implantable cardioverter defibrillator may be inserted to prevent sudden cardiac death. Surgery can be done to ablate some of the septum or a myectomy can be performed to decrease obstruction or a heart transplant. Screen all first degree relatives!
A patient presents with decreased exercise tolerance, pulm HTN, dyspnea, PND, orthopnea, ascites, fatigue and weakness, arrhythimia and PERIPHERAL EDEMA. They have non-dilated ventricles with impaired ventricular filling but normal systolic function and bi-atrial enlargement. Caused by secondary restrictive pathology, non-infiltrative diseases, infiltrative diseases, storage diseases, endomyocardial disease and radiation/toxic exposures. What is this? What testing do your run? What are the possible forms of treatment?
Restrictive Cardiomyopathy. A Sed rate and CBC should be done to see if it’s infiltrative. A CXR shows RV enlargement and ECG has non-specific findings of low voltage, poor R wave progression, RV hypertrophy changes and atrial arrhythmias. An echo shows severe bilateral enlargement, thickened ventricular walls with unusual myocardial texture. Cardiac cath (gold standard!) measures pressures during inspiration and an endomyocardial biopsy can be done. Can be treated with diuretics, drugs to slow the HR (Beta blockers and antiarrhythmics) and drugs to improve diastolic function (Ca channel blockers, beta blockers and ACE-I), blood pressure control (avoiding digitalis) and anticoagulation if A. fib presents. Transplant may be necessary if persistent and severe.
Patient presents with sx of restrictive cardiomyopathy and you are told that there is ground glass appearance of the myocardium on the echo. What is your diagnosis, what type of RCM is this?
Amyloidosis is the most common infiltrative RCM
A 73 year old man presents to your office 2 months after an MI and has acute illness. He has a sudden onset of sharp chest pain over the anterior chest that is improved by sitting up and leaning forward. On physical exam you hear a superficial scratchy/squaking sound best heard with the diaphragm over the LSB. There are increases in troponin, elevated WBCs, ESR, and C-reactive protein. What is your suspected diagnosis, what do further tests show and how do you treat?
Pericarditis. ECG shows widespread ST elevation and PR depression, with a normal CXR and a normal echo. Tx: if viral it resolves in 3-4 weeks with bed rest and NSAIDs, bacterial reqiures decompression of the pericardial sac immediately and IV abx for 4 weeks with supportive care (S.aureus is the most common pathogen), Hemorrhagic requires draininage. May respond to corticosteroids if autoimmune, and dialysis if uremic.
Patient presents for an annual exam. The heart sounds are muffled on ascultation (quiet precoridum) and there is dullness with decreased breath sounds over the posterior L lung. Arterial and jugular pulses are normal with a normal BP. The 12-lead ECG shows electrical alternans. What is your diagnosis, what do tests show and what is your treatment?
Dx: Pericardial Effusion; CXR shows cardiomegaly.; Tx: pericardiocentesis and leave a pericardial window in case future centesis needs to be performed. The procedure should be guided with echo to avoid hitting the heart with the needle as it enters the pericardial cavity.
Your patient with a pericardial effusion has not been treated yet, and you notice a huge variance in his blood pressures. JVD develops, helpatomegaly, edema and dyspnea. He begins to cough, become agitated and restless, he is tired and has episodes of syncope and goes into shock. You find pulsus paradoxus and electrical alternans on the ECG. What is happening, why and how do you treat it?
The patient is going into cardiac tamponade because there is an increased accumulation of pericardial fluid and the increased pressure is inhibiting diastolic filling of the RV therefore limiting the CO. Echo can show how much and where the fluid is located so that it can be treated with urgent pericardiocentesis.
What are the three signs of Beck’s triad and what are they associated with?
- elevated venous pressure; 2. Hypotension; 3. Quiet heart; these are associated with cardiac tamponade.
Exaggerated cyclic decrease in systolic BP during normal inspiration of >10mmHg that causes the interventricular septum to shift left because of decreased LV volume and therefore decreased stroke volume.
Pulsus paradoxus
A 30 year old body builder comes to your office with dyspnea, ascites and edema. On physical exam you find that he has Kussmaul’s sign (inspriation rise in venous pressure) and a pericardial knock that is best heard during inspriation. On CXR the pericardium appears calcified and is thickened. What is your diagnosis, diagnostic testing and treatment?
Dx: Constrictive pericarditis; Testing: cath to measure diastolic pressures and filling pattern of the RV as well as a pericardial biopsy; Tx: viral usually resolves in 3-4 weeks with rest and NSAIDs, bacterial can be life threatening and requires immediate decompression of the pericardial space with IV abx therapy for 4+ weeks and supportive care (S.aureus is the most common). A pericardectomy can be done (pericardial stripping)
A 25 year old male who is a known IV drug user comes to your office complaining of fatigue/weakness, weight loss, petechiae, painful red spots on his hands and feet with some being painful and some not. On physical examination you note clubbing, splenomegaly, splinter hemorrhages, osler nodes, and Janeway’s lesions. There are noted roth spots on the fundascopic exam and you hear a murmur on the tricuspid valve. The CBC reveals elevated WBCs, anemia, and the presence of S. aureus or S. viridans. What is your suspected diagnosis, what further testing do you do to confirm and what is your treatment?
Dx: infective endocarditis; Testing: ESR is elevated, abnormal UA (hematuria, proteinuria and pyuria), ECG usually normal, CXR may show septic pulmonary emboli and Echo is the gold standard but requires a vegetations to be larger than 3mm. Tx: empiric abx (Vanco) until cultures come back and then targeted therapy for generally 2-6 weeks. Repeat blood cultures 48-72 hours post abx initiation to check for response. Surgery if CHF, fungal IE, aggressive abx strain is present, embolic events in the first week, persistent infection after 1 week of abx, and valve perforation/rupture/fistula or abscess.
What are fatty streaks? When do they begin formation?
Focal thickening of the intima with accumulation of intracellular lipid deposits or extracellular lipids or both. This begins as early as the teens.
What are the methods of primary prevention of CAD?
Risk factor assessment including blood pressure, lipid levels, presence of DM, tobacco abuse and presence of family hx (Framingham risk assessment) to give a 10 year risk score.
A 65 year old male presents with chest pain in the left chest with raidation to the jaw and left arm. The pain is made worse on exertion and is not reproducable by pushing on chest or moving. He also reports some dyspnea, nausea, dizziness and he is diaphoretic. What tests do you order, and with your differential diagnosis, what do you expect to see?
ECG may show ST elevation if there is transmural infarction or ST depression if there is endocardial ischemia. Cardiac enzymes - myoglobin will rise within 2-4 hours, CK-MB will rise within 4-8 hours and Troponin will rise within 6-12 hours, you expect them all to elevate with ischemia or infarction. Lipid panel will likely show elevated LDL and low HDL. Screen for diabetes.
