Pericardial type shi

PAS  |  CAM II  |  Spring 2026

Myo-Pericardial Syndromes & Infective Endocarditis

50-Question High-Yield Clinical Application Practice Exam

Select the single best answer for each clinical scenario.

Answer Key with Clinical Explanations on Page 2

Section 1: Acute Pericarditis — Etiology, Diagnosis & Treatment (Questions 1–12)

1.  A 24-year-old male presents with sharp chest pain that began 2 days after a URI. The pain is worse when he lies flat and improves when he sits up and leans forward. Temperature is 38.2°C and heart rate is 102 bpm.

What is the MOST likely diagnosis?

A.  Acute STEMI — ST elevation in a young patient post-viral illness

B.  ACUTE PERICARDITIS — sharp pleuritic positional chest pain, low fever, tachycardia, and preceding viral illness; pain worsens supine and improves leaning forward

C.  Pulmonary embolism — pleuritic pain after viral illness

D.  Myocarditis only — fever and tachycardia without pleuritic pain

2.  A 28-year-old woman with chest pain sits forward during your exam. You auscultate a scratchy, high-pitched sound at the left sternal border that seems to have 2-3 components and changes character with repositioning.

What is this sound and what is the diagnostic significance?

A.  S3 gallop — indicates heart failure with volume overload

B.  PERICARDIAL FRICTION RUB — pathognomonic finding in acute pericarditis; scratchy/leathery triphasic sound (atrial systole, ventricular systole, ventricular diastole components); transient and comes and goes; best heard sitting up and leaning forward

C.  Mitral stenosis opening snap — fixed in timing and location

D.  Pleuritis friction rub — disappears with breath-holding; cardiac friction rub persists with breath holding

3.  A 30-year-old presents with acute pericarditis. His ECG is shown. The tracing shows diffuse ST-segment elevation in leads I, II, aVF, V3-V6 with PR-segment depression in the same leads. There is also a down-sloping appearance to the TP-segment baseline.

What is the ECG finding that specifically refers to the down-sloping TP-segment, and what makes this ECG pattern different from an acute STEMI?

A.  Wellens pattern — indicates critical LAD disease; distinguishes ischemia from pericarditis

B.  SPODICK SIGN (down-sloping TP segment) — The ECG shows diffuse ST elevation (not just one territory) + PR segment depression in the SAME leads + Spodick sign; in STEMI, ST elevation is in a coronary distribution (not diffuse), there is reciprocal ST depression in opposite leads (NOT PR depression), and PR depression is absent

C.  Delta wave — Wolff-Parkinson-White; short PR with slurred upstroke

D.  Brugada pattern — right bundle branch morphology in V1-V2 with ST elevation

4.  A 32-year-old with acute pericarditis has the following: WBC 14,000, CRP 58, ESR 72. His troponin returns at 0.8 ng/mL (elevated). Heart rate is 110 bpm and persistent.

What do the elevated troponin and persistent tachycardia suggest, and how does this change management?

A.  These are normal findings in pericarditis — no change in management needed

B.  MYOCARDITIS/MYOPERICARDITIS — elevated troponin indicates myocardial involvement; persistent tachycardia is another red flag; both are criteria for HOSPITAL ADMISSION; treatment shifts to heart failure management, supportive care, and close monitoring

C.  Troponin elevation rules out pericarditis and confirms STEMI requiring cath lab activation

D.  The WBC elevation is more clinically significant than the troponin in guiding admission

5.  A 29-year-old is diagnosed with acute pericarditis and has no contraindications. His physician discusses the first-line treatment.

What is the standard first-line treatment for acute pericarditis and why is one agent specifically included?

A.  Prednisone taper alone — steroids are first-line for all inflammatory conditions

B.  DUAL ANTI-INFLAMMATORY THERAPY: Colchicine + High-dose NSAIDs (Indomethacin) OR Aspirin (if concomitant ischemic heart disease/Dressler's syndrome) — colchicine is added because 15-20% of patients NOT treated with colchicine will experience recurrence

C.  Colchicine alone for 3 months — NSAIDs are not needed

D.  IV methylprednisolone + oral ibuprofen — corticosteroids plus an NSAID is first-line

6.  A 45-year-old male had an anterior MI 3 weeks ago. He now presents with chest pain, low-grade fever, and a pericardial friction rub. WBC is mildly elevated.

What is this condition and which anti-inflammatory agent is preferred over NSAIDs in this setting?

A.  Reinfarction — repeat coronary angiography is indicated

B.  DRESSLER'S SYNDROME (Post-MI pericarditis) — autoimmune pericarditis occurring weeks after MI; ASPIRIN is preferred over other NSAIDs because the patient has underlying ischemic heart disease; aspirin is cardioprotective, while indomethacin and ibuprofen may impair coronary vasodilation and infarct healing

C.  Uremic pericarditis — requires emergent dialysis

D.  Malignant pericarditis — CT scan for occult malignancy is the immediate priority

7.  A 35-year-old has recurrent pericarditis — this is her third episode in 14 months. She has been treated with colchicine + NSAIDs twice. Her CRP remains elevated. She asks about further management.

What is the recommended treatment for recurrent/incessant pericarditis refractory to first-line therapies?

A.  Indefinite oral prednisone at 1 mg/kg/day until symptoms resolve

B.  ANTI-INTERLEUKIN-1 AGENTS (anakinra or rilonacept) — recommended for recurrent/incessant pericarditis after failure of first-line therapies (colchicine + NSAIDs) and/or corticosteroids; interleukin-1 is a key inflammatory mediator in recurrent pericarditis

C.  Surgical pericardiectomy — indicated for any pericarditis with more than 2 recurrences

D.  Repeat echocardiogram to confirm diagnosis before changing treatment

8.  A patient is diagnosed with acute pericarditis in the ED. He wants to return to the gym the next day.

What is the appropriate activity restriction and duration?

A.  No activity restriction is necessary — pericarditis is not a cardiac condition that affects exercise tolerance

B.  EXERCISE RESTRICTION for AT LEAST 1 MONTH — physical exertion can exacerbate inflammation, provoke arrhythmias, and increase the risk of myocardial involvement; athletes require additional evaluation before return to sport

C.  Activity restriction only until fever resolves, typically 3-5 days

D.  Restriction until troponin normalizes, which typically takes 48 hours

9.  A patient with acute pericarditis has severe GI intolerance to NSAIDs. He has no history of peptic ulcer disease, but experiences significant nausea with any NSAID dose. He asks about alternatives.

What is the appropriate second-line therapy when NSAIDs are contraindicated or not tolerated?

A.  Increase colchicine dose and discontinue NSAIDs — colchicine alone is sufficient

B.  TAPERED CORTICOSTEROIDS (prednisone) — used as secondary therapy when NSAIDs/Aspirin are contraindicated or not tolerated; however, steroids are associated with a higher recurrence rate compared to NSAIDs, so they are NOT first-line

C.  IV ketorolac as an alternative NSAID with less GI side effects

D.  Hydroxychloroquine — used for SLE-related pericarditis but not for routine NSAID intolerance

10.  A chest X-ray of a patient with acute pericarditis is described as 'normal cardiac silhouette, no effusion, clear lung fields.'

What is the expected chest X-ray finding in isolated acute pericarditis and when does it change?

A.  Cardiomegaly is always present in acute pericarditis on chest X-ray

B.  NORMAL chest X-ray — isolated acute pericarditis without effusion produces a normal chest X-ray; the cardiac silhouette only enlarges when a PERICARDIAL EFFUSION is present (water bottle heart shape); the CXR itself is not the primary diagnostic tool

C.  Bilateral pleural effusions are the hallmark finding of acute pericarditis on CXR

D.  Hilar enlargement is the primary CXR finding in viral pericarditis

11.  A patient with acute pericarditis has a CRP of 85 mg/L at diagnosis. She asks how long to continue anti-inflammatory therapy.

When should NSAIDs be tapered and discontinued in acute pericarditis?

A.  After 7 days regardless of symptoms or labs

B.  After SYMPTOMS RESOLVE AND INFLAMMATORY MARKERS (CRP, ESR) NORMALIZE — typically several weeks; tapering based on symptoms alone (without lab normalization) increases recurrence risk; CRP is the most useful marker for guiding treatment duration

C.  After the pericardial friction rub is no longer audible

D.  Immediately after completing the 4-week course regardless of CRP

12.  A provider is explaining the causes of pericarditis to a student. They list viral, uremic, post-MI, drug-induced, and malignancy-related causes.

Which viral organisms are MOST commonly associated with infectious pericarditis, and which drugs are classically implicated in drug-induced pericarditis?

A.  HIV and CMV are most common; rifampin and isoniazid are implicated drugs

B.  ECHOVIRUS AND COXSACKIE VIRUS are the most common viral causes; PROCAINAMIDE and HYDRALAZINE are the classic drug-induced causes; lung and breast cancer are the most common malignancies causing pericarditis

C.  Influenza A and RSV are most common viral causes; methotrexate and cyclophosphamide are implicated drugs

D.  EBV and HSV are most common; aspirin and colchicine are implicated (paradoxically)

Section 2: Constrictive Pericarditis (Questions 13–17)

13.  A 58-year-old male with a history of thoracic radiation for esophageal cancer 8 years ago presents with progressive dyspnea on exertion, bilateral leg edema, hepatomegaly, and elevated JVP. Echocardiogram shows thickened pericardium and septal bounce.

What is the diagnosis and what is the mechanism causing his symptoms?

A.  Restrictive cardiomyopathy — radiation-induced infiltration of myocardium

B.  CONSTRICTIVE PERICARDITIS — thickened, fibrotic, adherent pericardium (from radiation in this case) restricts diastolic filling and produces elevated venous pressures; leads to right-sided heart failure symptoms: DOE, edema, hepatomegaly, elevated JVP; septal bounce and thickened pericardium on echo are characteristic

C.  Dilated cardiomyopathy — radiation injury causing systolic dysfunction

D.  Superior vena cava syndrome — radiation causes mediastinal fibrosis compressing the SVC

14.  A patient with constrictive pericarditis is examined. During inspiration, instead of decreasing, his jugular venous pressure rises. The nurse documents this finding.

What is this physical examination finding and why does it occur in constrictive pericarditis?

A.  Beck's triad — hypotension, JVD, and muffled heart sounds occurring in tamponade

B.  KUSSMAUL'S SIGN — paradoxical RISE in jugular venous pressure (JVP) on INSPIRATION; normally JVP falls with inspiration because negative intrathoracic pressure increases right heart filling; in constrictive pericarditis, the rigid pericardium prevents accommodation of the increased venous return on inspiration, so JVP rises instead

C.  Pulsus paradoxus — abnormal decrease in systolic BP during inspiration seen in tamponade

D.  Pericardial knock — high-pitched sound heard in early diastole in constrictive pericarditis

15.  A student asks about the differences between constrictive pericarditis and restrictive cardiomyopathy, as both present with diastolic dysfunction and right-sided heart failure symptoms.

Which finding best helps DISTINGUISH constrictive pericarditis from restrictive cardiomyopathy?

A.  Bilateral leg edema is only seen in constrictive pericarditis, not restrictive cardiomyopathy

B.  THICKENED PERICARDIUM on echo/CT/MRI with SEPTAL BOUNCE is characteristic of constrictive pericarditis; LOW PULMONARY PRESSURES on catheterization favor constrictive pericarditis; restrictive cardiomyopathy has NORMAL pericardium but infiltrative myocardium (e.g., amyloidosis); treatment also differs: pericardiectomy for constrictive pericarditis vs. treat underlying cause or transplant for restrictive cardiomyopathy

C.  JVD is only present in constrictive pericarditis and not in restrictive cardiomyopathy

D.  Cardiac catheterization shows identical findings in both conditions and cannot distinguish them

16.  A patient with constrictive pericarditis has failed medical management with NSAIDs and diuretics.

What is the DEFINITIVE treatment for constrictive pericarditis?

A.  Long-term colchicine therapy indefinitely

B.  SURGICAL PERICARDIECTOMY — removal of the fibrotic, adherent pericardium; this is the DEFINITIVE treatment; NSAIDs and colchicine may provide some anti-inflammatory benefit but the constrictive physiology requires surgical correction when medical management fails

C.  Pericardiocentesis — drainage of pericardial fluid

D.  Cardiac transplantation — only option when pericardiectomy fails

17.  A 62-year-old patient presents with progressive dyspnea, edema, and hepatomegaly. He reports undergoing coronary bypass surgery 4 years ago and radiation therapy 10 years ago for lymphoma.

What are the TWO most clinically relevant causes of constrictive pericarditis to consider in this patient?

A.  Tuberculosis and viral infection — the two most common infectious causes in developed countries

B.  POST-CARDIAC SURGERY and RADIATION — both are major causes of constrictive pericarditis; post-surgical scarring and radiation-induced fibrosis are among the most important causes in developed countries; tuberculosis is the most common cause globally but less common in the US

C.  Uremia and autoimmune disease — most common causes in patients on dialysis

D.  Malignant pericardial metastasis causing constriction — lung and breast cancer

Section 3: Pericardial Effusion & Cardiac Tamponade (Questions 18–26)

18.  A 52-year-old woman with metastatic breast cancer presents with dyspnea and hypotension. CXR shows a large globular cardiac silhouette. ECG shows low-voltage QRS complexes with alternating QRS amplitude.

What ECG finding is described and what condition must be immediately considered?

A.  First-degree heart block — PR prolongation causing hemodynamic compromise

B.  ELECTRICAL ALTERNANS (alternating QRS amplitude) combined with LOW VOLTAGE and globular CXR silhouette = CARDIAC TAMPONADE until proven otherwise; electrical alternans results from the heart swinging back and forth within the pericardial fluid, changing its electrical axis with each beat

C.  Wolff-Parkinson-White — delta waves with alternating conduction pathways

D.  Atrial flutter with 2:1 conduction causing alternating QRS heights

19.  A patient with a known large pericardial effusion is brought to the ED in distress. Physical examination reveals hypotension (BP 78/50), elevated JVP to the jaw, and distant/muffled heart sounds.

What is this triad called and what does each component represent?

A.  Trousseau's sign — used for hypocalcemia testing; three findings indicate hypercalcemia

B.  BECK'S TRIAD of cardiac tamponade: (1) HYPOTENSION — low stroke volume and cardiac output from impaired filling; (2) JVD (jugular venous distension) — elevated venous pressure from impaired diastolic filling; (3) MUFFLED/DISTANT heart sounds — sound must pass through pericardial fluid before reaching the chest wall

C.  Virchow's triad — stasis, hypercoagulability, and endothelial injury for DVT/PE

D.  Cushing's triad — bradycardia, hypertension, respiratory depression in increased intracranial pressure

20.  During physical examination of a patient with suspected cardiac tamponade, the examiner measures blood pressure during inspiration and expiration. The systolic BP drops from 124 mmHg to 100 mmHg during quiet inspiration.

What is this finding called and what is the clinical threshold that defines it as abnormal?

A.  Kussmaul's sign — JVP rising with inspiration seen in constrictive pericarditis

B.  PULSUS PARADOXUS — an abnormally large decrease in systolic BP during inspiration; normal physiologic decline is <10 mmHg; pulsus paradoxus is defined as an inspiratory systolic BP drop of >10 mmHg; this patient's drop of 24 mmHg is markedly abnormal; the 'paradox' is that you can hear heart sounds on auscultation but cannot palpate the radial pulse during inspiration

C.  Pulsus alternans — alternating strong and weak pulses from heart failure with reduced EF

D.  Pulsus bisferiens — double-peaked pulse seen in hypertrophic obstructive cardiomyopathy

21.  A 45-year-old male is brought to the ED with hypotension and suspected cardiac tamponade. Bedside echocardiogram is obtained and shows a large circumferential pericardial effusion.

What is the GOLD STANDARD for diagnosing cardiac tamponade and what findings confirm the diagnosis?

A.  ECG showing electrical alternans and low voltage — confirmatory for tamponade without echo needed

B.  ECHOCARDIOGRAPHY is the GOLD STANDARD — shows: large pericardial effusion, RIGHT ATRIAL COLLAPSE (early finding), RIGHT VENTRICULAR DIASTOLIC COLLAPSE (highly specific), and respiratory variation in Doppler flow velocities; diastolic collapse of right-sided chambers indicates elevated intrapericardial pressure exceeding right-sided filling pressures

C.  Cardiac catheterization showing equalization of diastolic pressures — definitive invasive test

D.  CT scan of the chest with contrast — most sensitive imaging for pericardial effusion

22.  A patient with cardiac tamponade is brought to the ED. She is hypotensive (BP 70/40) and has a GCS of 13. She requires urgent intervention. The interventional cardiologist and cardiac surgeon are not immediately available.

What is the appropriate immediate intervention for this hemodynamically UNSTABLE patient with cardiac tamponade?

A.  Emergent intubation with positive pressure ventilation to support oxygenation and allow time for the cardiologist to arrive

B.  BEDSIDE PERICARDIOCENTESIS — for hemodynamically UNSTABLE tamponade, bedside pericardiocentesis is performed emergently; AVOID positive pressure ventilation if possible (increases intrathoracic pressure, decreases venous return and cardiac output, worsening tamponade); IVF bolus to maintain a perfusing blood pressure while preparing for pericardiocentesis

C.  Immediate electrical cardioversion for suspected arrhythmia

D.  IV furosemide to reduce preload and relieve cardiac compression

23.  A stable patient with a moderate pericardial effusion and no hemodynamic compromise is admitted. The echocardiogram shows no right atrial or right ventricular collapse.

What is the appropriate management for a STABLE pericardial effusion without tamponade physiology?

A.  Urgent pericardiocentesis regardless of stability — all pericardial effusions require drainage

B.  MONITOR conservatively: serial ECG, serial pulsus paradoxus measurement, and serial echocardiograms; treat with NSAIDs, corticosteroids, and/or colchicine (note: GI side effects common with colchicine); TREAT UNDERLYING CAUSE (e.g., hypothyroidism, autoimmune, malignancy)

C.  Immediate surgical pericardial window — safer than pericardiocentesis for all effusions

D.  IV antibiotics for presumed infectious cause without culture results

24.  A 62-year-old woman with known hypothyroidism presents with progressive dyspnea and pitting edema over 8 weeks. CXR shows marked cardiac enlargement. Echo shows a large pericardial effusion without tamponade physiology.

What is the most likely underlying cause of her pericardial effusion and what treatment addresses both the effusion and the root cause?

A.  Malignant pericardial effusion — metastatic breast cancer is the most likely cause in this demographic

B.  HYPOTHYROIDISM — a recognized cause of pericardial effusion (along with the chronic gradual onset); TREATING HYPOTHYROIDISM with thyroid hormone replacement often resolves the effusion without the need for drainage; other causes of effusion include inflammation post-op/ACS, autoimmune disease, metastatic cancer (lung, breast), radiation/chemo, uremia, and trauma

C.  Post-viral pericarditis — the most common cause of all pericardial effusions

D.  Uremia — confirmed only by finding elevated BUN/Cr requiring dialysis

25.  A patient with a large pericardial effusion develops cardiac tamponade. After emergency pericardiocentesis, 400 mL of serosanguineous fluid is removed. The team notes the patient's blood pressure immediately improves.

What is the physiological reason that removing even a SMALL amount of pericardial fluid causes rapid hemodynamic improvement in cardiac tamponade?

A.  The removed fluid was compressing the coronary arteries, causing ischemia

B.  Because of the pressure-volume relationship of the pericardium: the pericardial sac has a STEEP pressure-volume curve — when maximally distended, a small increase in fluid causes a LARGE increase in intrapericardial pressure; therefore, removing even a SMALL amount of fluid can cause a LARGE drop in intrapericardial pressure, immediately improving cardiac filling and stroke volume

C.  The fluid contained inflammatory cytokines that were causing myocardial depression

D.  The procedure itself activates baroreceptors that increase sympathetic tone

26.  A 22-year-old presents to the ED with chest pain, dyspnea, and palpitations following a viral URI 2 weeks ago. His ECG shows sinus tachycardia. Troponin is 1.2 ng/mL. Echo shows an ejection fraction of 35% with diffuse hypokinesis.

What is the most likely diagnosis and what organism is the most common cause?

A.  Acute STEMI — troponin elevation with decreased EF indicates coronary artery occlusion

B.  MYOCARDITIS — inflammation of the myocardium; VIRAL is the most common cause; COXSACKIE VIRUS B is the most common specific viral cause; presentation: preceding viral illness + dyspnea + chest pain + palpitations + ELEVATED TROPONIN + decreased EF on echo; common cause of dilated cardiomyopathy and sudden cardiac death in young people

C.  Hypertrophic cardiomyopathy — genetic condition causing hypertrophy and outflow obstruction

D.  Acute pericarditis — pericarditis does not cause elevated troponin or decreased EF in isolation

Section 4: Myocarditis (Questions 27–31)

27.  The gold standard for diagnosing myocarditis has traditionally been myocardial biopsy. However, an emerging non-invasive modality is increasingly becoming the preferred study.

What imaging study is emerging as the preferred diagnostic modality for myocarditis and what does it show?

A.  CT angiography — shows coronary anatomy to rule out ischemic cause

B.  CARDIAC MRI — T1 and T2 MAPPING demonstrates myocardial EDEMA and INFLAMMATION consistent with myocarditis; cardiac MRI is non-invasive and can detect diffuse myocardial involvement; myocardial biopsy is the TRADITIONAL gold standard but is invasive and limited by sampling error; cardiac MRI is replacing biopsy as the study of choice

C.  Technetium-99m pyrophosphate scan — used for amyloid diagnosis

D.  Stress echocardiography — assesses wall motion abnormalities during exercise

28.  A 19-year-old athlete with myocarditis is treated with supportive care. He asks when he can return to competitive sports.

Which treatment considerations are important for myocarditis management?

A.  Discharge home with oral antibiotics targeting viral causes and follow-up in 4 weeks

B.  ADMIT for SUPPORTIVE CARE: standard heart failure therapy (diuretics, ACE inhibitors), supplemental O2 and NIPPV, pacing if needed, antidysrhythmics; antivirals (interferon-alfa or ribavirin) in acute phase; antimicrobial therapy for bacterial/parasitic causes; ECMO, intra-aortic balloon pump, or LVAD if cardiovascular collapse; strict ACTIVITY RESTRICTION until recovered

C.  Colchicine and NSAIDs — same as pericarditis treatment protocol

D.  Aspirin and beta-blockers as the primary treatment regimen

29.  A 25-year-old with myocarditis develops cardiogenic shock despite supportive care.

What mechanical circulatory support options are available for refractory cardiovascular collapse in myocarditis?

A.  Immediate heart transplantation — only option for refractory myocarditis

B.  ECMO (extracorporeal membrane oxygenation), INTRA-AORTIC BALLOON PUMP, or LVAD (left ventricular assist device) — these mechanical circulatory support devices are used as a bridge to recovery or transplantation; myocarditis can occasionally cause severe cardiogenic shock requiring mechanical support

C.  Positive pressure ventilation and IV vasopressors alone are sufficient for all cases of cardiogenic shock in myocarditis

D.  Pericardiocentesis — draining the pericardial space to relieve cardiac compression

30.  A provider is explaining a complication of myocarditis to a cardiology fellow.

What are the two most important long-term sequelae of myocarditis?

A.  Aortic stenosis and mitral regurgitation — valvular destruction from myocarditis

B.  DILATED CARDIOMYOPATHY (common long-term sequela from ongoing myocardial damage and remodeling) and SUDDEN CARDIAC DEATH (from ventricular arrhythmias during the acute phase or from dilated cardiomyopathy) — both are major complications; myocarditis is one of the leading causes of dilated cardiomyopathy and sudden cardiac death in young people

C.  Pericardial constriction and cardiac tamponade — from pericardial involvement

D.  Infective endocarditis — from bacteremia associated with myocarditis

31.  A 28-year-old IV drug user presents with 3 days of high fever (39.8°C), rigors, and a new regurgitant heart murmur. Blood cultures grow Staphylococcus aureus.

What is the diagnosis and what organism is MOST COMMONLY responsible for ALL cases of infective endocarditis?

A.  S. viridans — most common overall cause, especially in IV drug users

B.  INFECTIVE ENDOCARDITIS from S. AUREUS — S. aureus is the most common cause in ALL cases of endocarditis regardless of setting; IV drug use is a major risk factor; presents acutely with HIGH FEVER, rigors, and new murmur; right-sided valves (tricuspid) are preferentially affected in IVDU

C.  Strep viridans is the most common cause, and this presentation is consistent with subacute endocarditis

D.  Coagulase-negative Staphylococci are the most common cause in all settings

Section 5: Infective Endocarditis (Questions 32–45)

32.  A 68-year-old male presents with 6 weeks of fatigue, low-grade fever, night sweats, and a 10-pound weight loss. He had a dental procedure 8 weeks ago. On exam: mildly elevated temperature, new heart murmur, pale conjunctiva, and painful nodular lesions on his fingertips.

What is the diagnosis and what are the two peripheral vascular findings that suggest it?

A.  Acute leukemia — painful fingertip lesions and anemia; bone marrow biopsy is needed

B.  SUBACUTE ENDOCARDITIS (S. viridans after dental procedure) — the PAINFUL fingertip nodular lesions are OSLER NODES (immune complex deposition); JANEWAY LESIONS (non-tender, hemorrhagic, flat lesions on palms and soles) are also associated with endocarditis; these peripheral stigmata are classic exam findings

C.  Rheumatoid arthritis with Felty's syndrome — anemia and painful nodular lesions

D.  Polyarteritis nodosa — vasculitis causing nodular skin lesions

33.  An emergency physician is evaluating a patient with suspected endocarditis. She explains the diagnostic approach.

What are the three components of the diagnostic workup for infective endocarditis?

A.  CBC, blood urea nitrogen, and urinalysis — standard sepsis workup

B.  CLINICAL CRITERIA (modified Duke criteria) + BLOOD CULTURES (multiple sets; note: results take DAYS) + TRANSTHORACIC ECHOCARDIOGRAPHY (TTE) — the modified Duke criteria use major and minor criteria; blood cultures are essential but slow; TTE is the initial imaging; TEE (transesophageal) is used when TTE is non-diagnostic or for prosthetic valves

C.  CT scan of the chest/abdomen/pelvis + lumbar puncture + skin biopsy

D.  Cardiac catheterization + cardiac MRI + PET scan — advanced imaging modalities

34.  A patient with suspected endocarditis arrives in the ED. You decide to start empiric antibiotics before blood culture results return.

What is the recommended EMPIRIC antibiotic regimen for a patient with suspected endocarditis on a NATIVE VALVE before culture results are available?

A.  Ceftriaxone 2g IV daily alone — adequate coverage for all endocarditis organisms

B.  VANCOMYCIN or DAPTOMYCIN PLUS a BETA-LACTAM — empiric therapy consists of: Vancomycin (or daptomycin) PLUS ceftriaxone or cefazolin for NATIVE VALVE; the combination provides broad-spectrum coverage including MRSA (vancomycin), gram-negatives (beta-lactam), and streptococcal species; treatment course is 4-6 weeks; repeat blood cultures every 24-48 hours after starting antibiotics

C.  Ampicillin-sulbactam alone covers all organisms including MRSA

D.  Piperacillin-tazobactam monotherapy is sufficient for all native valve endocarditis

35.  A 52-year-old woman has confirmed Staphylococcus aureus endocarditis. She develops a new complete heart block and cardiogenic shock.

What are the cardiothoracic surgery consultation indications in infective endocarditis?

A.  Only heart failure — all other complications can be managed medically without surgery

B.  CARDIOGENIC SHOCK OR CHF, HEART BLOCK, and TREATMENT-REFRACTORY INFECTION — these three are the primary indications for cardiac surgery in endocarditis; other indications include: paravalvular abscess, large mobile vegetations (>10 mm), persistent bacteremia after 7 days of appropriate antibiotics, and heart failure from valvular destruction

C.  Bacteremia lasting more than 48 hours after starting antibiotics

D.  Presence of Osler nodes or Janeway lesions indicating embolic complications

36.  A 65-year-old man with rheumatic heart disease needs a dental extraction. He has a known history of endocarditis.

What antibiotic prophylaxis should be given, when should it be administered, and what is the first-line agent?

A.  No prophylaxis is needed — antibiotic prophylaxis for endocarditis prevention is no longer recommended

B.  AMOXICILLIN 2g PO/IV/IM, administered 30-60 MINUTES BEFORE THE PROCEDURE — this patient has a history of endocarditis (high-risk individual) undergoing a high-risk dental procedure (manipulation of gingiva, tooth extraction); PCN ALLERGY alternatives: cephalexin 2g PO, azithromycin 500 mg PO, clarithromycin 500 mg PO, or doxycycline 100mg PO

C.  Vancomycin 1g IV started 2 hours before the procedure for all dental prophylaxis

D.  Metronidazole 500 mg PO — covers oral anaerobes responsible for endocarditis

37.  A provider is counseling a patient about who does NOT need antibiotic prophylaxis before a dental procedure.

Which of the following individuals does NOT require endocarditis antibiotic prophylaxis before dental extraction?

A.  Patient with a bioprosthetic aortic valve replacement — prosthetic valves always require prophylaxis

B.  PATIENT WITH ISOLATED MITRAL VALVE PROLAPSE — mitral valve prolapse is EXPLICITLY EXCLUDED from endocarditis prophylaxis indications; however, patients with prosthetic heart valves, history of endocarditis, congenital heart disease, rheumatic heart disease, PWID, and cardiac transplant with valvulopathy DO require prophylaxis

C.  Patient with a history of bacterial endocarditis 2 years ago — prior endocarditis history requires prophylaxis

D.  Patient with rheumatic heart disease and mitral regurgitation — requires prophylaxis

38.  A patient is being evaluated for possible infective endocarditis. Vital signs show: T 39.6°C, HR 118 bpm, BP 94/60 mmHg, RR 22 breaths/min, WBC 18,500.

What syndrome do these vital signs fulfill and what does it suggest about this patient's systemic status?

A.  Only bacteremia criteria — not enough findings to suggest more severe illness

B.  SIRS CRITERIA (Systemic Inflammatory Response Syndrome) — temperature >38°C , HR >90 , RR >20 , WBC >12,000 ; the lecture states 'these patients present very ill — remember your SIRS criteria'; endocarditis patients can develop sepsis and septic shock from bacteremia; this patient meets SIRS and has borderline hypotension (BP 94/60) suggesting early septic shock

C.  This represents normal variation seen in all febrile patients with murmurs

D.  ARDS criteria — bilateral lung infiltrates with hypoxemia in mechanical ventilation

39.  A 45-year-old male with a history of IV drug use presents with fever, a new holosystolic murmur heard at the left lower sternal border that increases with inspiration, and multiple septic pulmonary emboli on CT.

Which valve is most commonly affected in IV drug users with endocarditis, and why do the septic pulmonary emboli occur?

A.  Mitral valve — left-sided endocarditis is equally common in IV drug users

B.  TRICUSPID VALVE — right-sided endocarditis (TRICUSPID VALVE) is preferentially affected in IV DRUG USERS; injected bacteria enter the venous system directly → right heart → tricuspid valve; SEPTIC PULMONARY EMBOLI occur because vegetations on the tricuspid valve embolize to the PULMONARY CIRCULATION (right-sided circulation goes to lungs); murmur of tricuspid regurgitation = holosystolic, left lower sternal border, increases with INSPIRATION (right-sided murmurs increase with inspiration)

C.  Aortic valve — most common in elderly patients; aortic stenosis is a risk factor

D.  Pulmonic valve — rarest affected valve

40.  A patient with Streptococcus bovis bacteremia and endocarditis is identified. The infectious disease consultant recommends further workup beyond treating the endocarditis.

What additional evaluation is indicated and why?

A.  HIV testing — S. bovis endocarditis is associated with immunocompromise

B.  COLONOSCOPY — S. bovis (S. gallolyticus) bacteremia is classically associated with COLORECTAL CANCER; any patient with S. bovis bacteremia or endocarditis requires colonoscopy to evaluate for underlying colon pathology; this is a high-yield board examination pearl

C.  Echocardiography is sufficient — no additional workup beyond treating the endocarditis

D.  Thyroid ultrasound — S. bovis has a known association with thyroid malignancy

41.  The provider is reviewing the complications of infective endocarditis with medical students.

Which of the following is a RECOGNIZED complication of infective endocarditis?

A.  Primary hypertension — endocarditis causes chronic afterload increase

B.  SYSTEMIC EMBOLI (stroke from left-sided vegetations, renal emboli, splenic emboli), HEART FAILURE (from valvular destruction/regurgitation), PARAVALVULAR ABSCESS (especially in aortic valve endocarditis), SEPTIC SHOCK, CONDUCTION ABNORMALITIES (heart block from abscess extending into conduction system), METASTATIC INFECTION (septic joints, meningitis)

C.  Primary pulmonary hypertension — a rare but recognized complication

D.  Constrictive pericarditis — from pericardial involvement by endocarditis

42.  A 55-year-old presents with chest pain that worsens with deep inspiration and improves when sitting up and leaning forward. ECG shows diffuse ST elevation in multiple leads with PR depression. He is on procainamide for a cardiac arrhythmia.

What is the most likely diagnosis and what role does his medication play?

A.  STEMI from acute coronary occlusion — diffuse ST elevation indicates multivessel disease

B.  DRUG-INDUCED PERICARDITIS from PROCAINAMIDE — procainamide and hydralazine are the classic drug-induced causes of pericarditis; ECG shows diffuse ST elevation + PR depression consistent with pericarditis; positional pleuritic chest pain + medication history + ECG pattern = drug-induced pericarditis; management includes stopping the offending drug + dual anti-inflammatory therapy

C.  Pulmonary embolism — S1Q3T3 pattern is the classic PE ECG finding, not diffuse ST elevation

D.  Constrictive pericarditis — presents as right-sided heart failure, not acute chest pain with ECG changes

43.  A 35-year-old male marathon runner presents to the ED with progressive dyspnea and near-syncope. Physical exam reveals: hypotension, JVD, muffled heart sounds, and pulsus paradoxus of 22 mmHg. He had a 'chest cold' 3 weeks ago. ECG shows tachycardia, low voltage, and electrical alternans.

What is the diagnosis and what is the sequence of management steps?

A.  Massive pulmonary embolism — treat with systemic thrombolytics and anticoagulation

B.  CARDIAC TAMPONADE — Beck's triad (hypotension + JVD + muffled sounds), pulsus paradoxus >10 mmHg, electrical alternans, and low voltage on ECG; management sequence: (1) CALL FOR HELP; (2) IVF bolus to maintain perfusing BP; (3) AVOID positive pressure ventilation (worsens tamponade); (4) EMERGENT PERICARDIOCENTESIS (hemodynamically unstable → bedside; stable → cath lab); gold standard confirmation = ECHOCARDIOGRAPHY

C.  Tension pneumothorax — absent breath sounds and tracheal deviation expected

D.  Cardiogenic shock from myocarditis — treat with diuretics and ACE inhibitors

44.  You are managing three patients simultaneously: Patient A has confirmed cardiac tamponade with BP 86/50 and needs positive pressure ventilation. Patient B has subacute endocarditis with S. viridans and needs antibiotic therapy determined. Patient C has constrictive pericarditis unresponsive to NSAIDs and diuretics.

What is the MOST immediately life-threatening concern about PPV in Patient A, and what definitively treats Patient C?

A.  PPV is beneficial in tamponade by improving oxygenation; Patient C needs pericardiocentesis

B.  PPV in tamponade = DANGEROUS because increased intrathoracic pressure DECREASES VENOUS RETURN → further REDUCES cardiac output → worsens hemodynamic compromise → may precipitate cardiac arrest; manage with bedside pericardiocentesis and IVF instead. Patient C (constrictive pericarditis unresponsive to medical management) requires SURGICAL PERICARDIECTOMY — definitive treatment for constrictive pericarditis

C.  PPV is the preferred treatment for tamponade; Patient C needs pericardiocentesis for drainage

D.  PPV has no effect on tamponade physiology; Patient C needs prolonged colchicine therapy

45.  A 30-year-old male presents with chest pain after a recent GI viral illness. He has elevated troponin (0.95 ng/mL), persistent resting tachycardia (HR 110), normal ECG except for sinus tachycardia, and an echocardiogram showing EF of 40% with global hypokinesis.

How does this presentation differ from isolated pericarditis, and what condition does the combination suggest?

A.  This is typical isolated acute pericarditis — troponin can be elevated up to 2 ng/mL without myocardial involvement

B.  MYOPERICARDITIS (pericarditis WITH myocardial involvement) — isolated pericarditis: normal troponin, normal EF, pleuritic positional pain; this patient has: ELEVATED TROPONIN (myocardial damage), PERSISTENT TACHYCARDIA (another red flag), DECREASED EF (systolic dysfunction), GLOBAL HYPOKINESIS — all indicating MYOCARDIAL INVOLVEMENT; myopericarditis = hospital admission criteria; treatment includes heart failure therapy in addition to anti-inflammatory treatment

C.  Stress cardiomyopathy (Takotsubo) — apical ballooning is characteristic

D.  NSTEMI from multivessel disease — global hypokinesis indicates three-vessel disease

Section 6: Integrated High-Yield Clinical Scenarios (Questions 46–50)

46.  A medical student is asked to compare and contrast acute pericarditis, cardiac tamponade, and constrictive pericarditis in terms of key physical examination findings.

Which of the following correctly matches each condition with its KEY distinguishing physical examination finding?

A.  Acute pericarditis = Kussmaul's sign; Tamponade = pericardial friction rub; Constrictive = electrical alternans

B.  ACUTE PERICARDITIS = PERICARDIAL FRICTION RUB (scratchy, transient, best heard sitting up and leaning forward); CARDIAC TAMPONADE = BECK'S TRIAD (hypotension + JVD + muffled heart sounds) + PULSUS PARADOXUS (>10 mmHg systolic BP drop with inspiration); CONSTRICTIVE PERICARDITIS = KUSSMAUL'S SIGN (paradoxical rise in JVP on inspiration)

C.  Acute pericarditis = pulsus paradoxus; Tamponade = Kussmaul's sign; Constrictive = friction rub

D.  All three conditions have identical physical examination findings — ECG is the only distinguishing modality

ANSWER KEY

Myo-Pericardial Syndromes & Infective Endocarditis

#

Correct Answer & Clinical Explanation

1. B

ACUTE PERICARDITIS cardinal features: sharp pleuritic POSITIONAL chest pain (worse supine, better leaning forward), low-grade fever, tachycardia, and a preceding viral illness (viral is the MOST COMMON cause — echovirus and coxsackievirus). It mimics ACS but the positional nature and pleuritic quality are distinguishing features.

2. B

PERICARDIAL FRICTION RUB: The pathognomonic finding of acute pericarditis. Scratchy/leathery sound with up to 3 components: ventricular systole (most common), early diastole, and late diastole/atrial systole. TRANSIENT — comes and goes. Best heard with the patient sitting up and leaning forward, pressing the diaphragm firmly against the left lower sternal border. Persists with breath-holding (distinguishes from pleural rub, which disappears when breathing stops).

3. B

PERICARDITIS ECG vs. STEMI: PERICARDITIS = DIFFUSE ST elevation (multiple leads, multiple territories simultaneously), PR DEPRESSION in the same leads as ST elevation, SPODICK SIGN (down-sloping TP segment), and NO reciprocal ST depression. STEMI = ST elevation in one coronary territory, reciprocal ST DEPRESSION in opposite leads, NO PR depression, evolution over hours. The Spodick sign is the downsloping of the TP segment seen in pericarditis.

4. B

MYOPERICARDITIS indicators in pericarditis: Elevated TROPONIN indicates myocardial involvement (myocarditis component). PERSISTENT TACHYCARDIA is another red flag. Both are HOSPITAL ADMISSION CRITERIA. Other admission criteria: associated myocarditis, cardiomegaly/pericardial effusion, uremia, hemodynamic instability, failure to respond to outpatient treatment. Troponin is normally NORMAL in isolated pericarditis.

5. B

ACUTE PERICARDITIS TREATMENT: DUAL THERAPY is required. (1) COLCHICINE: continued for 3 months after first episode and 6 MONTHS after recurrence. 15-20% of patients NOT treated with colchicine will have RECURRENCE — this is the key reason to add it. (2) HIGH-DOSE NSAIDs (Indomethacin is preferred) OR ASPIRIN if patient has concomitant ischemic heart disease (e.g., Dressler's syndrome). NSAIDs are started initially and TAPERED after symptoms resolve AND inflammatory markers normalize. Steroids are SECONDARY — only if NSAIDs/Aspirin are contraindicated.

6. B

DRESSLER'S SYNDROME: Post-MI pericarditis, typically appearing 1-8 weeks after an acute MI (or cardiac surgery). Autoimmune mechanism — pericardial antibodies form against damaged myocardial tissue. Fever, pleuritic chest pain, friction rub, elevated inflammatory markers. TREATMENT: ASPIRIN (preferred in this population over other NSAIDs) + colchicine. Aspirin provides anti-inflammatory benefit while also being cardioprotective. Indomethacin/ibuprofen can reduce coronary blood flow and impair scar formation after MI.

7. B

RECURRENT PERICARDITIS TREATMENT ESCALATION: First-line = Colchicine + NSAIDs/Aspirin. If corticosteroids are needed: taper is required (rapid taper is associated with recurrence). For REFRACTORY/RECURRENT/INCESSANT PERICARDITIS after failure of first-line AND/OR corticosteroids: ANTI-IL-1 AGENTS — anakinra (IL-1β receptor antagonist) and rilonacept (IL-1 trap). These target interleukin-1β, the key cytokine driving autoinflammatory recurrent pericarditis. Colchicine duration: 3 months for first episode, 6 MONTHS for recurrence.

8. B

PERICARDITIS ACTIVITY RESTRICTION: Exercise restriction for AT LEAST 1 MONTH after acute pericarditis. Rationale: physical exertion increases inflammation, can trigger arrhythmias, and may worsen subclinical myocardial involvement. Athletes (competitive sports) require even more caution — many guidelines recommend return to sport only after complete symptom resolution with normalized inflammatory markers, typically 3 months. This is an exam-high-yield fact.

9. B

PERICARDITIS WHEN NSAIDs ARE CONTRAINDICATED: TAPERED CORTICOSTEROIDS (prednisone) are the secondary/alternative treatment. Important caveat: corticosteroids are associated with a HIGHER RECURRENCE RATE than NSAIDs — this is why they are not first-line. The rapid tapering of steroids also increases recurrence risk; a slow taper is required. Colchicine should still be maintained alongside steroids to reduce recurrence risk.

10. B

CXR IN PERICARDITIS: NORMAL unless pericardial effusion is present. The cardiac silhouette only appears enlarged (water bottle/globular heart shape) when significant pericardial effusion develops. Therefore CXR is NORMAL in isolated acute pericarditis. Primary diagnostic modality is the ECG (diffuse ST elevation, PR depression, Spodick sign). Echo or CT is ordered to EVALUATE FOR EFFUSION. Labs show elevated WBC, CRP, and ESR.

11. B

NSAIDs TAPERING IN PERICARDITIS: NSAIDs are started at high dose and TAPERED AFTER BOTH: (1) Symptoms resolve AND (2) Inflammatory markers NORMALIZE (primarily CRP, but also ESR). This typically takes several weeks. Using CRP to guide treatment duration reduces recurrence risk. Tapering too early — especially with steroids — is a major cause of recurrence. Colchicine is continued separately for 3 months (first episode) or 6 months (recurrence).

12. B

PERICARDITIS CAUSES: Most common VIRAL causes = ECHOVIRUS and COXSACKIE VIRUS. Drug-induced causes (classic exam question) = PROCAINAMIDE and HYDRALAZINE (both can also cause drug-induced lupus). Other causes: malignancy (LUNG and BREAST most common), post-MI Dressler's syndrome, uremia (requires dialysis as treatment), autoimmune, radiation/chemotherapy, post-cardiac surgery, tuberculosis.

13. B

CONSTRICTIVE PERICARDITIS: Thickened, fibrotic, adherent pericardium reduces elastic properties → RESTRICTS DIASTOLIC FILLING → produces ELEVATED VENOUS PRESSURES. Causes: TUBERCULOSIS (global most common), RADIATION, viruses, histoplasmosis, surgery. Presents like RIGHT-SIDED HEART FAILURE: DOE, fatigue, weakness, edema, hepatomegaly, JVD. ECG: KUSSMAUL'S SIGN (JVP rises on inspiration — paradoxical). Diagnostics: Echo/CT/MRI (thickened pericardium, septal bounce); cardiac catheterization = CONFIRMATORY.

14. B

KUSSMAUL'S SIGN: PARADOXICAL RISE in JVP on INSPIRATION. Normally: inspiration → negative intrathoracic pressure → increased venous return to right heart → JVP falls. In CONSTRICTIVE PERICARDITIS: the rigid pericardium cannot accommodate increased right heart filling on inspiration → blood backs up → JVP RISES with inspiration. Kussmaul's sign is characteristic of CONSTRICTIVE PERICARDITIS (and occasionally cardiac tamponade). Also seen in right ventricular failure and restrictive cardiomyopathy.

15. B

CONSTRICTIVE PERICARDITIS vs. RESTRICTIVE CARDIOMYOPATHY: Both cause severe diastolic dysfunction and restrictive filling. KEY DIFFERENTIATORS: Constrictive = THICKENED PERICARDIUM on imaging + SEPTAL BOUNCE + LOW pulmonary pressures on cath. Restrictive = NORMAL pericardium + infiltrative myocardium (amyloidosis, sarcoidosis). TREATMENT: Constrictive → diuretics + surgical PERICARDIECTOMY (definitive). Restrictive → treat underlying disorder (amyloidosis treatment) or cardiac transplant.

16. B

CONSTRICTIVE PERICARDITIS TREATMENT: NSAIDS + colchicine for anti-inflammatory management. SURGICAL PERICARDIECTOMY is the DEFINITIVE treatment for constrictive pericarditis. Pericardiectomy = surgical removal of the thickened fibrotic pericardium to restore normal diastolic filling. Diuretics are used for symptomatic management of venous congestion. Pericardiocentesis is used for EFFUSION (fluid drainage), NOT constrictive pericarditis (where the problem is a fibrotic rigid pericardium, not fluid).

17. B

CONSTRICTIVE PERICARDITIS CAUSES: TUBERCULOSIS (most common cause WORLDWIDE/globally). In DEVELOPED COUNTRIES: IDIOPATHIC (most common), POST-CARDIAC SURGERY, RADIATION THERAPY, viral pericarditis, histoplasmosis, connective tissue disorders, malignancy. This patient has BOTH post-cardiac surgery (CABG 4 years ago) AND radiation therapy (lymphoma 10 years ago) — both are major risk factors for constrictive pericarditis development.

18. B

ELECTRICAL ALTERNANS: Beat-to-beat alternation of the QRS AMPLITUDE (and sometimes P wave) on ECG. MECHANISM: The heart literally swings back and forth within the pericardial fluid like a pendulum, changing its electrical axis with each beat → alternating QRS amplitude. Highly specific for CARDIAC TAMPONADE when combined with LOW VOLTAGE QRS + TACHYCARDIA + globular cardiac silhouette on CXR. GOLD STANDARD for tamponade diagnosis = ECHOCARDIOGRAPHY.

19. B

BECK'S TRIAD (Cardiac Tamponade): (1) HYPOTENSION — ↓ stroke volume and cardiac output from pericardial fluid under pressure compressing the heart; (2) JVD — elevated venous pressure because blood cannot adequately fill the compressed right heart → backs up into the venous system; (3) MUFFLED HEART SOUNDS — sound must pass through the pericardial fluid before reaching the chest wall. Tamponade = pericardial fluid UNDER PRESSURE leading to impaired cardiac filling and hemodynamic COMPROMISE.

20. B

PULSUS PARADOXUS: Abnormally LARGE decrease in systolic BP (>10 mmHg) during INSPIRATION. Normal physiologic drop = ≤10 mmHg. Tamponade: >10 mmHg drop (often 20-40 mmHg). MECHANISM: In tamponade, the pericardial fluid constrains the heart. Inspiration increases right heart filling but the increased RV size compresses the LV (interventricular interdependence) → ↓ LV stroke volume → ↓ systolic BP on inspiration. PARADOX: heart sounds audible on auscultation but radial PULSE NOT PALPABLE during inspiration.

21. B

CARDIAC TAMPONADE GOLD STANDARD = ECHOCARDIOGRAPHY. Echo findings: (1) Pericardial EFFUSION (confirms fluid); (2) RIGHT ATRIAL COLLAPSE in systole (early/sensitive finding); (3) RIGHT VENTRICULAR DIASTOLIC COLLAPSE (most SPECIFIC finding); (4) Respiratory variation in mitral/tricuspid Doppler velocities (>25% decrease in mitral E velocity with inspiration). ECG: low voltage + electrical alternans + tachycardia. CXR: water bottle heart/globular silhouette (may be present). Remember: tamponade is a CLINICAL diagnosis — treat before waiting for full workup if hemodynamically unstable.

22. B

CARDIAC TAMPONADE TREATMENT EMERGENCY ALGORITHM: (1) CALL FOR HELP; (2) IVF BOLUS (to maintain perfusing BP); (3) AVOID positive pressure ventilation (PPV increases intrathoracic pressure → ↓ venous return → ↓ cardiac output → WORSENS tamponade); (4) HEMODYNAMICALLY STABLE → pericardiocentesis in cath lab or pericardial window in OR; (5) HEMODYNAMICALLY UNSTABLE → BEDSIDE PERICARDIOCENTESIS. PPV is particularly dangerous in tamponade. Never give furosemide — these patients are preload-dependent!

23. B

STABLE PERICARDIAL EFFUSION MANAGEMENT: Monitor if stable. Monitor with: serial ECG, serial pulsus paradoxus measurements, and serial echocardiograms. Pharmacologic treatment: NSAIDs, corticosteroids, and/or COLCHICINE (note: GI side effects are common with colchicine). Treat the UNDERLYING CAUSE — effusions can result from pericarditis, autoimmune disease, malignancy, hypothyroidism, uremia, trauma, or radiation. Only drainage is needed when tamponade develops or is imminent.

24. B

PERICARDIAL EFFUSION CAUSES (key list): Inflammation (post-op, ACS), AUTOIMMUNE, METASTATIC CANCER (lung and breast most common), RADIATION/CHEMOTHERAPY, UREMIA, HYPOTHYROIDISM, TRAUMA, INFECTION. HYPOTHYROIDISM is a classic cause of pericardial effusion — the slow, gradual fluid accumulation allows the pericardial sac to stretch over time (gradual accumulation = less hemodynamic compromise than rapid accumulation). Treating the underlying hypothyroidism with thyroid hormone replacement resolves the effusion.

25. B

PERICARDIAL PRESSURE-VOLUME CURVE: The pericardium has LIMITED distensibility. When a large effusion has slowly stretched the pericardium, the sac is at the 'flat' portion of its pressure-volume curve. However, as tamponade develops, the pericardium reaches its maximum distensibility and the curve becomes STEEP — small additional fluid = large pressure increase. CONVERSELY: removing even a SMALL amount of fluid (50-100 mL) can cause a large DROP in intrapericardial pressure → immediate hemodynamic improvement. This explains why 'just a little drainage' can be lifesaving.

26. B

MYOCARDITIS: Inflammation of the MYOCARDIUM. MOST COMMON CAUSE = VIRAL; MOST COMMON SPECIFIC ORGANISM = COXSACKIE VIRUS B. Other causes: other viruses, Borrelia burgdorferi (Lyme disease), Trypanosoma cruzi (Chagas disease — parasitic), autoimmune, toxins. Presentation: preceding respiratory/GI viral illness, dyspnea, chest pain, palpitations, myalgias, fever, UNRESOLVING TACHYCARDIA (key red flag). ELEVATED TROPONIN (myocardial damage), decreased EF. Severe cases → CHF, cardiovascular collapse. Common cause of dilated cardiomyopathy.

27. B

MYOCARDITIS DIAGNOSIS: Traditional GOLD STANDARD = ENDOMYOCARDIAL BIOPSY (Dallas criteria: lymphocytic infiltration + myocyte necrosis). EMERGING PREFERRED STUDY = CARDIAC MRI — T1 and T2 MAPPING shows myocardial EDEMA and INFLAMMATION. Advantages: non-invasive, no sampling error, can show diffuse involvement. ECG: often NORMAL or sinus tachycardia (nonspecific ST-T wave changes). CXR: ± cardiomegaly, pulmonary edema. Echo: ↓ EF, wall-motion abnormalities, hypokinesis. Troponin elevated (though not always).

28. B

MYOCARDITIS TREATMENT: ADMIT for supportive care. Standard HEART FAILURE THERAPY (ACE inhibitors, diuretics, beta-blockers). Supplemental O2 and NIPPV. Transcutaneous/transvenous PACING if significant conduction abnormalities. ANTIDYSRHYTHMICS for arrhythmias. ANTIVIRALS (interferon-alfa or ribavirin) in acute phase. ANTIMICROBIAL THERAPY for bacterial (Borrelia) or parasitic (Chagas) causes. For cardiovascular COLLAPSE: ECMO, intra-aortic balloon pump, LVAD. Activity restriction is critical — strenuous exercise during myocarditis can precipitate sudden cardiac death.

29. B

MYOCARDITIS MECHANICAL SUPPORT for cardiovascular COLLAPSE: (1) ECMO (extracorporeal membrane oxygenation) — provides full cardiopulmonary support; (2) INTRA-AORTIC BALLOON PUMP — reduces afterload and improves coronary perfusion; (3) LVAD (left ventricular assist device) — provides mechanical unloading of LV. These devices are used as a BRIDGE to recovery (myocarditis can improve with time) or as a bridge to cardiac TRANSPLANTATION in severe cases. Myocarditis is a reversible cause of cardiomyopathy in many cases.

30. B

MYOCARDITIS COMPLICATIONS: (1) DILATED CARDIOMYOPATHY — ongoing inflammation and myocyte necrosis leads to ventricular dilation, wall thinning, and systolic dysfunction; myocarditis is a MAJOR CAUSE of DCM; (2) SUDDEN CARDIAC DEATH — from ventricular arrhythmias (VT/VF) in the acute phase or from DCM-related arrhythmias. This is why activity restriction is so important — exercise increases arrhythmia risk in myocarditis. Also: CHF, heart block requiring pacing, and cardiogenic shock are additional complications.

31. B

INFECTIVE ENDOCARDITIS MICROBIOLOGY: S. AUREUS = MOST COMMON ORGANISM in ALL cases. Key additional organisms: S. VIRIDANS (tooth extraction, dental procedures — produces glucan allowing adherence to heart valves), Strep bovis (colorectal cancer association — order colonoscopy), Enterococcus (GI/GU procedures), Coagulase-negative Staph (prosthetic valve, after cardiac surgery), HACEK organisms (subacute). IV DRUG USERS: S. aureus + right-sided endocarditis (tricuspid valve). FUNGI: Candida in immunocompromised patients.

32. B

ENDOCARDITIS PERIPHERAL STIGMATA: OSLER NODES = TENDER, painful, nodular lesions on TIPS OF FINGERS AND TOES (immune complex deposition → small vessel inflammation). JANEWAY LESIONS = NON-TENDER, hemorrhagic, FLAT lesions on PALMS AND SOLES (septic emboli). Memory: Osler = 'Ouch!' (tender); Janeway = 'Just painless' (non-tender). Other peripheral signs: Splinter hemorrhages (under nails), Roth spots (retinal hemorrhages), petechiae. SUBACUTE endocarditis = OLDER patients, fatigue, anemia, low-grade fever; S. VIRIDANS most common after dental procedure.

33. B

INFECTIVE ENDOCARDITIS DIAGNOSIS: (1) MODIFIED DUKE CRITERIA — clinical scoring system using major criteria (positive blood cultures, evidence of endocardial involvement on echo, new valvular regurgitation) and minor criteria (fever, predisposing condition, vascular phenomena, immunologic phenomena); definite IE = 2 major, 1 major + 3 minor, or 5 minor criteria; (2) BLOOD CULTURES — multiple sets, RESULTS TAKE DAYS; (3) TRANSTHORACIC ECHOCARDIOGRAPHY — initial imaging; transesophageal echo (TEE) for prosthetic valves or inconclusive TTE. Note: 'You won't get culture results back for days' — from lecture.

34. B

EMPIRIC ENDOCARDITIS TREATMENT: 'Think VANCO + BETA LACTAM.' VANCOMYCIN or DAPTOMYCIN PLUS: NATIVE VALVE = Ceftriaxone or Cefazolin; PROSTHETIC VALVE (<3 months) = Ceftriaxone, Cefepime, Zosyn (piperacillin-tazobactam), or Carbapenem; PROSTHETIC VALVE (>3 months) = Ceftriaxone, Cefazolin, or Unasyn. Treatment duration = 4-6 WEEKS. Repeat blood cultures every 24-48 hours after starting therapy. ALL patients need ADMISSION + Infectious Disease consult if available. May require transfer to tertiary center.

35. B

SURGERY INDICATIONS IN ENDOCARDITIS: From lecture: (1) CARDIOGENIC SHOCK or CHF (from valvular destruction/regurgitation); (2) HEART BLOCK (from paravalvular abscess extending into conduction system); (3) TREATMENT-REFRACTORY INFECTION (persistent bacteremia despite appropriate antibiotics). Additional indications: paravalvular ABSCESS, large mobile VEGETATIONS (>10 mm, high embolic risk), prosthetic valve dehiscence, fungal endocarditis. PROGNOSIS: Untreated endocarditis is FATAL; even with treatment, mortality is significant. All require ADMISSION + ID consult.

36. B

ENDOCARDITIS PROPHYLAXIS: HIGH-RISK INDIVIDUALS: congenital heart disease, rheumatic heart disease, PROSTHETIC HEART VALVES, HISTORY OF ENDOCARDITIS, PWID, cardiac transplant with valvulopathy. Note: MITRAL VALVE PROLAPSE is NOT an indication. HIGH-RISK PROCEDURES: dental procedures with gingival manipulation, tooth extraction, abscess drainage, invasive respiratory procedures, invasive procedures involving infected skin/soft tissue. NOT GI/GU procedures. TIMING: 30-60 MINUTES BEFORE procedure. AGENT: AMOXICILLIN 2g PO/IV/IM preferred. Vancomycin if MRSA concern (120 minutes prior).

37. B

ENDOCARDITIS PROPHYLAXIS — NOT indicated for MITRAL VALVE PROLAPSE (explicitly stated in the lecture). Required for: congenital heart disease, RHEUMATIC HEART DISEASE, PROSTHETIC HEART VALVES, HISTORY OF ENDOCARDITIS, PWID (persons who inject drugs), cardiac transplant with valvulopathy. Dental procedures requiring prophylaxis: manipulation of gingiva, tooth extraction, abscess drainage. NOT required for: GI or GU procedures (does not apply to colonoscopy, cystoscopy), routine dental cleaning in low-risk patients.

38. B

SIRS CRITERIA (from lecture: 'remember your SIRS criteria'): ≥2 of: Temperature >38°C or <36°C , HR >90 bpm , RR >20 or PaCO2 <32 mmHg , WBC >12,000 or <4,000 or >10% bands . Endocarditis patients are systemically ILL. Bacteremia from valve infection can progress to SEPSIS and SEPTIC SHOCK. Presentation: ACUTE endocarditis = YOUNGER patients, HIGH FEVER, murmur, flu-like symptoms (often S. aureus). SUBACUTE = OLDER patients, FATIGUE, ANEMIA, S. viridans.

39. B

ENDOCARDITIS IN IV DRUG USERS: Preferentially affects the TRICUSPID VALVE (right-sided). Mechanism: injected bacteria enter venous circulation → right atrium → tricuspid valve → vegetations form. Septic PULMONARY EMBOLI: tricuspid vegetations embolize to the PULMONARY ARTERIES (right-sided circulation drains to lungs) causing multiple pulmonary nodules/abscesses on CT. Murmur: tricuspid REGURGITATION (holosystolic, left lower sternal border, increases with INSPIRATION — all right-sided murmurs increase with inspiration).

40. B

S. BOVIS (S. GALLOLYTICUS) ENDOCARDITIS: Classic board pearl — S. bovis bacteremia or endocarditis is STRONGLY ASSOCIATED WITH COLORECTAL CANCER. Every patient with S. bovis endocarditis requires COLONOSCOPY to rule out underlying colon pathology (cancer, polyps). Mechanism: colorectal cancer disrupts the mucosal barrier → S. bovis from gut flora enters bloodstream. This association is tested on almost every board exam. Other organism associations: S. viridans → dental procedures; Enterococcus → GI/GU procedures; HACEK → subacute endocarditis.

41. B

ENDOCARDITIS COMPLICATIONS: (1) SYSTEMIC EMBOLI — vegetations embolize from left-sided valves (aortic, mitral) → STROKE (most feared), renal infarcts, splenic infarcts; right-sided (tricuspid) → PULMONARY EMBOLI; (2) HEART FAILURE — from valve destruction/regurgitation; most common indication for surgery; (3) PARAVALVULAR ABSCESS — especially aortic valve, can cause HEART BLOCK from extension into conduction system; (4) SEPTIC SHOCK; (5) METASTATIC INFECTION (septic arthritis, meningitis, brain abscess); (6) IMMUNE COMPLEX DEPOSITION → glomerulonephritis, Osler nodes.

42. B

DRUG-INDUCED PERICARDITIS: Classic causative agents = PROCAINAMIDE and HYDRALAZINE (both can also cause drug-induced lupus/lupus-like syndrome). Management: STOP the offending drug + DUAL anti-inflammatory therapy (colchicine + NSAIDs). Other drug causes: isoniazid, minoxidil, phenytoin. ECG of pericarditis: DIFFUSE ST elevation (not in one coronary territory) + PR DEPRESSION in the SAME leads + SPODICK SIGN (down-sloping TP segment). This combination distinguishes pericarditis from STEMI (which has reciprocal changes and no PR depression).

43. B

CARDIAC TAMPONADE DIAGNOSIS and MANAGEMENT: Beck's TRIAD = Hypotension + JVD + Muffled heart sounds. ECG = tachycardia + LOW VOLTAGE + ELECTRICAL ALTERNANS. Pulsus PARADOXUS >10 mmHg. Gold standard = ECHO. MANAGEMENT: (1) Call for help; (2) IVF to maintain BP; (3) AVOID PPV; (4) Hemodynamically stable → pericardiocentesis in cath lab or pericardial window in OR; (5) Hemodynamically UNSTABLE → BEDSIDE PERICARDIOCENTESIS. NO furosemide (preload-dependent). NO negative inotropes.

44. B

PPV IN TAMPONADE: Positive pressure ventilation INCREASES intrathoracic pressure → DECREASES venous return (preload) to the right heart → further REDUCES stroke volume and cardiac output (already critically reduced by tamponade) → worsens hemodynamic collapse → cardiac arrest. TAMPONADE MANAGEMENT: AVOID PPV; IVF bolus; bedside pericardiocentesis if unstable. CONSTRICTIVE PERICARDITIS DEFINITIVE TREATMENT = SURGICAL PERICARDIECTOMY. NSAIDs, colchicine, and diuretics are palliative — pericardiectomy is the only definitive treatment.

45. B

MYOPERICARDITIS vs. ISOLATED PERICARDITIS: ISOLATED PERICARDITIS = normal troponin, normal EF, pleuritic positional pain, ECG with diffuse ST elevation and PR depression. MYOPERICARDITIS = ELEVATED TROPONIN + DECREASED EF + PERSISTENT TACHYCARDIA + wall motion abnormalities. The lecture explicitly states: 'If troponin + or persistent tachycardia: think myocarditis.' MYOPERICARDITIS = HOSPITAL ADMISSION. ECG in myocarditis is often normal or shows only sinus tachycardia. Cardiac MRI is the preferred diagnostic modality for myocarditis.

46. B

KEY PHYSICAL EXAM FINDINGS: ACUTE PERICARDITIS = PERICARDIAL FRICTION RUB (pathognomonic; scratchy/leathery; transient; comes and goes; best heard sitting up and leaning forward). CARDIAC TAMPONADE = BECK'S TRIAD (hypotension + JVD + muffled heart sounds) + PULSUS PARADOXUS (>10 mmHg drop). CONSTRICTIVE PERICARDITIS = KUSSMAUL'S SIGN (JVP RISES with inspiration — paradoxical). Additional: Constrictive can also have a PERICARDIAL KNOCK (early diastolic high-pitched sound). ECG: Pericarditis = diffuse ST elevation + PR depression; Tamponade = low voltage + electrical alternans.