Podcast Episode 81: Internal Medicine EOR Cardiology Questions

Answer: B, Infective endocarditis

Infective endocarditis (IE) is an infection of the endocardial surfaces of the heart, most commonly the heart valves. IE occurs when a microorganism begins to invade the heart valves causing an inflammatory reaction that damages the valve – sometimes leading to stenosis and sometimes leading to regurgitation. This patient developed a new cardiac murmur in recent weeks that is described as a faint systolic murmur heard over the lower left sternal border. This is most consistent with tricuspid regurgitation. She also has distended neck veins and hepatomegaly, both of which suggest right-sided heart failure, which can result from tricuspid regurgitation. Small infectious emboli can break away from the primary lesion on the tricuspid valve and go into the pulmonary vasculature causing shortness of breath and pleuritic chest pain. Most cases of IE are caused by Staphylococcus aureus and Viridans streptococci, and diagnosis is confirmed by obtaining multiple blood cultures that show that there is continuous bacteremia.

• Fat embolism to the pulmonary circulation almost always occurs with major trauma, including surgical procedures like intramedullary nailing of long bones. Fat emboli can occlude the microvasculature, triggering a systemic inflammatory response. The woman did not have recent trauma, and a fat embolism would not explain her cardiac murmur.
• Clinical presentation of myocardial infarction most often includes substernal crushing chest pain, radiation of pain to the arms, left shoulder, back, neck, and jaw, as well as shortness of breath, anxiety, and fatigue. A myocardial infarction would not explain her developing a new cardiac murmur in recent weeks.
• Rheumatic fever is an autoimmune inflammatory process that develops as a sequela of streptococcal infection. Clinical manifestations include polyarthritis, carditis, erythema marginatum, chorea, and subcutaneous nodules. Rheumatic fever can cause some of the symptoms seen in this case, but the acute onset makes this option less likely.
• Although small cell lung cancer can present with pulmonary symptoms and low grade fevers, it wouldn’t easily explain her new cardiac murmur or the signs of right-sided heart failure.

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The answer is A. Adenovirus

Myocarditis in the United States is most commonly caused by a viral infection, typically adenovirus, coxsackie B, parvovirus B19, or others. It often presents with systemic symptoms such as fatigue and chest pain, but may cause sudden death.

• Though coxsackie B virus is one of the most common causal pathogens of acute myocarditis, Coxsackie A causes herpangina, aseptic meningitis, and hand, foot, and mouth disease.
• Staphylococcus aureus is a common cause of bacterial endocarditis, not myocarditis. Endocarditis is more likely to present with a new murmur and signs of distant emboli such as nail-bed hemorrhage and Janeway lesions.
• Corynebacterium diphtheriae is the causal agent of diphtheria, which may involve myocarditis. However, the patient would then most likely have other symptoms of the disease, including pseudomembranous pharyngitis, lymphadenopathy, or an arrhythmia.

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The answer is C. Pericardial effusion

Pericardial effusions are associated with a variety of causes, including autoimmune disorders and infectious pericarditis. If pericardial effusion leads to cardiac tamponade, patients may have pulsus paradoxus, or a decrease in systolic blood pressure during inspiration of more than 10 mm Hg. Certain ECG findings are characteristic for pericardial effusion. In particular, electrical alternans (shown by arrows) is highly specific for pericardial effusion (usually in association with cardiac tamponade) but not particularly sensitive. This pattern, characterized by beat-to-beat changes in the QRS axis in the limb and precordial leads, is caused by swinging of the heart within the accumulated pericardial fluid. Other common findings on ECG include sinus tachycardia and low QRS voltage.

• Patients with aortic dissection classically present with a tearing or ripping pain in the chest or back and may have a significant variation in systolic blood pressure between arms (not across respirations).
• The severity of tricuspid regurgitation varies widely, ranging from asymptomatic disease to symptoms of right-sided heart failure (hepatosplenomegaly, ascites, peripheral edema).
• Patients with aortic stenosis, the most common cause of left ventricular outflow obstruction, typically present with exertional dizziness or angina. In end-stage disease, symptoms may progress to heart failure.
• Mitral stenosis obstructs the flow of blood from the left atrium to the left ventricle and typically manifests as exertional dyspnea and decreased exercise tolerance.

Review PAEA EOR Blueprint Pearls With Links to Topic Lesson: Internal Medicine Rotation: Cardiovascular (PEARLS) ⇒ Pericarditis

The answer is B. Immediately consult vascular surgery

Peripheral vascular disease with intermittent claudication and signs of decreased perfusion should be examined using Doppler ultrasound and the ankle-brachial index (ABI). An ABI of <0.41 is grounds for the immediate surgical consultation.

• Statin therapy has shown to be effective in treating intermittent claudication. However, this intervention is appropriate only when the patient is deemed to be stable, and the risk of limb ischemia has been addressed.
• Alteplase (tPa) has been used to treat intermittent claudication, but its use is outside the scope of the emergency room. Treatments initiated in the emergency department are unfractionated heparin, aspirin, pain control, and positioning of the leg to maintain perfusion.
• The patient has significant impairment of perfusion to his legs. Discharge and vascular surgery follow-up as an outpatient would be inappropriate and likely to result in morbidity or mortality.
• While this leg should be rested, compression and elevation are the opposite of what is needed. These therapies will further decrease the blood flow to the leg and put the patient at increased risk of complications.

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The answer is B. Long-term penicillin

Rheumatic heart disease is caused by autoimmune cross-reactivity following a Streptococcal infection. Development of antibody-mediated mitral valve damage is common. Long-term penicillin is suitable for acute treatment and prophylaxis from complications.

• Digoxin is a purified cardiac glycoside that is typically used in the treatment of various heart conditions, such as atrial fibrillation, atrial flutter, and heart failure that cannot be controlled by other medication. It is not recommended for use in rheumatic fever.
• Clindamycin is an antibiotic used to treat middle ear infections, bone or joint infections, pelvic inflammatory disease, strep throat, pneumonia, and endocarditis. Clindamycin is typically used as endocarditis prophylaxis for patients that are already receiving penicillin for secondary rheumatic fever prophylaxis.
• This patient is suffering from rheumatic fever, which can lead to rheumatic heart disease. This can cause significant carditis which manifests as congestive heart failure.
• Ceftriaxone is an antibiotic used to treat numerous bacterial infections, such as pneumonia, ear infections, skin infections, urinary tract infection, and meningitis. It is not used in the treatment of rheumatic fever.

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The answer is C. Labetalol

Chronic hypertension in pregnancy can be treated with some medications and labetalol is recommended as a first-line therapy for treatment of hypertension during pregnancy. Angiotensin-converting enzymes (ACE) inhibitors and angiotensin II receptor blockers (ARBs) should be avoided.

• Atenolol is a β-blocker medication, which decreases blood pressure by decreasing heart rate and stroke volume. It is contraindicated in pregnancy because it has been associated with fetal growth restriction. β-blockers considered safe in pregnancy are metoprolol and labetalol.
• Hydrochlorothiazide is a thiazide diuretic which decreases blood pressure via volume depletion. Diuretics do not cause fetal malformations but are generally avoided in pregnancy, as they prevent the physiologic volume expansion seen in normal pregnancy. They may be used in states of volume-dependent hypertension, such as renal or cardiac disease.
• Lisinopril is an angiotensin-converting enzyme (ACE) inhibitor which decreases blood pressure through inhibition of the renin-angiotensin-aldosterone system. ACE inhibitors and the closely related angiotensin-receptor blockers are contraindicated in pregnancy because of the risk of birth defects including renal dysgenesis and oligohydramnios.
• Losartan is an angiotensin II receptor blocker (ARB) which decreases blood pressure through inhibition of the renin-angiotensin-aldosterone system. ARBs and the closely related angiotensin converting enzyme (ACE) inhibitors are contraindicated in pregnancy because of the risk of birth defects including renal dysgenesis and oligohydramnios.

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Answer: A. Enalapril

Hypertension in the setting of diabetes should be treated, with a goal systolic blood pressure of <130 mm Hg. The best first choice of medication is an angiotensin-converting enzyme inhibitor (ACEi).

Incorrect Answers:

• Furosemide is a loop diuretic that can be used to treat hypertension but it is not a first line agent. Unlike ACE inhibitors, loop diuretics have no renoprotective qualities and therefore are a worse initial choice in a hypertensive diabetic patient.
• Hydrochlorothiazide is a thiazide diuretic and a first-line agent for the treatment of hypertension in non-diabetic patients. It is relatively contraindicated in diabetes because it has the potential adverse effect of hyperglycemia. It may also precipitate attacks of gout by increasing uric acid concentrations.
• Metoprolol is a β-blocker that is used for the treatment of hypertension but is not a first line treatment. Also, β-blocker are contraindicated in asthma, as well as in diabetic patients due to its potential to mask signs of low blood sugar.
• Nifedipine is a calcium channel blocker that is used in the treatment of hypertension but it is not a first line therapy. It has no renoprotective effects, and commonly causes peripheral edema as an unwanted adverse effect.

Review PAEA EOR Blueprint Pearls With Links to Topic Lesson: Internal Medicine Rotation: Cardiovascular (PEARLS) ⇒ Hypertension

The answer is C: add ezetimibe 10 mg

If LDL-C is not at goal after 6-12 weeks the next best step for the treatment of familial hypercholesterolemia is to add ezetimibe 10 mg daily and check again in 6-12 weeks. If at that time the patient’s LDL is still not at goal (ideally < 150) refer to lipid specialist to consider adding a PCSK9 inhibitor.

Pearls

• Familial hypercholesterolemia (FH) is the most common autosomal dominant genetic disease. The clinical syndrome (phenotype) is characterized by extremely elevated levels of low-density lipoprotein cholesterol (LDL-C) and a propensity to early-onset atherosclerotic cardiovascular disease. In general, homozygotes manifest the disease at a much earlier age than heterozygotes and the disease is more severe.
• Homozygous FH patients are rare and have an estimated prevalence of approximately 1:300,000 to 1:400,000
• Heterozygous FH is estimated to occur in 1 in 200 to 250 individuals in the United States.
• It is estimated that about 7 percent of American adults have an untreated lipoprotein cholesterol ≥190 mg/dL but only 1.7 percent carry an FH mutation
• Patients with undiagnosed homozygous familial hypercholesterolemia (FH) develop severe, premature, atherosclerotic cardiovascular disease and die before age 20 in many cases.
• In patients with a negative or unknown family history, an untreated LDL-C level of ≥190 mg/dL (4.9 mmol/L) suggests FH. This value is greater than the 90th percentile for age and sex.

Diagnosis

• The diagnosis of heterozygous familial hypercholesterolemia (FH) is made with genetic testing or clinical criteria. A causative mutation in the LDLR, APOB, or PCSK9 gene(s) secures this diagnosis
• When genetic testing is not available or not felt to be necessary, you can use the Dutch Lipid Clinic Network criteria, which assigns points based on low-density lipoprotein cholesterol (LDL-C) levels, personal history of early atherosclerotic cardiovascular disease (ASCVD), family history of early ASCVD, or high cholesterol in a first-degree relative, and personal and physical examination finding

Treatment

• Patients with homozygous familial hypercholesterolemia (FH) – intensive LDL-C lowering, which targets a minimal value of <150 mg/dL (3.9 mmol/L)
• In addition to a high-dose statin (atorvastatin 80 mg daily or rosuvastatin 40 mg daily), most homozygous patients will require additional therapies such as ezetimibe, a PCSK9 inhibitor, or potentially LDL-C apheresis

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The answer is C. Mitral valve regurgitation

Mitral valve regurgitation is defined as an incompetent closure of the mitral valve. Classically patients will present with a pansystolic heart murmur over the mitral area. Posterior myocardial infarction is the second most common cause of mitral valve regurgitation. Mitral valve regurgitation is characterized by an incompetent closure of the mitral valve. This condition causes retrograde blood flow into the left atrium during systole. The most common cause of mitral regurgitation is mitral valve prolapse, followed by a dysfunction of the posteromedial papillary muscle due to posterior myocardial infarction. Other causes may include, endocarditis or stretching of the mitral valve ring.

• Aortic stenosis is the reduction of the valvular orifice (<2 cm) with left ventricular outflow obstruction. Patients with aortic stenosis present with chest pain, syncopal episodes, and dyspnea. Here, the patient has progressive dyspnea (NYHA II), and a pansystolic murmur (mitral area), which relates to mitral valve regurgitation
• Aortic valve regurgitation (AOR) is described as an inefficient closure of the aortic valve leading to a retrograde blood flow into the left ventricle during diastole. Patients will present with a wide pulse pressure (Corrigan hammer pulse) or an Austin-Flint murmur (severe), none of which are present in this case.
• Mitral valve stenosis (MVS) is the reduction of the mitral valve orifice (<2.5cm). The left atrium becomes dilated and hypertrophied because of increased work of the left atrium. Patients with MVS present with dyspnea, rust-colored sputum, atrial fibrillation, and a diastolic heart murmur (diastolic rumble and opening snap).
• Pulmonary stenosis is an uncommon valvular lesion. It is commonly associated with congenital heart disease and carcinoid heart disease. Patients present a systolic ejection murmur in the left second intercostal space.

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The answer is C. Standing

The ‘click’ of mitral valve prolapse, caused by the tightening of the chordae tendinae, moves closer to S2 with increased preload. Increased preload causes the left ventricle to stretch, as a result, the chordae tendinae are stretched as well. This makes it harder for the mitral valve to prolapse until the ventricles shrink enough to allow the chordae tendinae to let the mitral valve prolapse. Since there is more blood in the ventricles, it takes them longer to pump it out and shrink to a point at which MVP can occur, hence it occurs later in systole. Thus, the click will get closer to S2 with increased preload. Hand grip, rapid squatting, and inspiration all increase preload. Standing decreases preload and will cause an earlier onset of the click.

• The click of mitral valve prolapse is heard closer to S2 in the event of increased preload. Preload is increased by hand grip, squatting and inspiration.
• Placing the patient in the left lateral cubitus position will not affect preload and will have no effect on the timing of the click in mitral valve prolapse.

Review PAEA EOR Blueprint Pearls With Links to Topic Lesson: Internal Medicine Rotation: Cardiovascular (PEARLS) ⇒ Heart murmurs