Heart Murmurs, EKG, MI complications

Question 1

aortic stenosis

Answer 1

crescendo-decrescendo ejection murmur at right upper sternal border

soft S2 +/- ejection click

“pulsus parvus et tardus” (weak pulses with delayed peak)

in older patients, most commonly due to age-related calcification; in younger patients, most commonly due to early-onset calcification of a bicuspid aortic valve

Question 2

mitral regurgitation

Answer 2

holosystolic, high-pitched “blowing” murmur loudest at apex, radiates toward axilla

often due to ischemic heart disease, mitral valve prolapse, LV dilation, rheumatic fever, or infective endocarditis

Question 3

mitral valve prolapse

Answer 3

Midsystolic click followed by late systolic murmur

can predispose to infective endocarditis; can be caused by rheumatic fever, chordae rupture, or myxomatous degeneration

Question 4

ventricular septal defect

Answer 4

holosystolic, harsh-sounding murmur, loudest at tricuspid area

larger VSDs have lower intensity murmur than VSDs

Question 5

aortic regurgitation

Answer 5

early diastolic, decrescendo, high-pitched “blowing” murmur heard at the base (aortic root dilation) or left sternal border (valvular disease)

caused by bicuspid aortic valve, endocarditis, aortic root dilation, rheumatic fever

wide pulse pressure, pistol shot femoral pulse, pulsing nail bed (Quincke pulse); hyperdynamic pulse and head bobbing when severe

Question 6

mitral stenosis

Answer 6

follows opening snap (OS); delayed rumbling mid-to-late diastolic murmur (decreased interval between S1 and OS correlates with increased severity)

late and highly specific sequalae of rheumatic fever; chronic MS can => LA dilation and pulmonary congestion, atrial fibrillation, Ortner syndrome, hemoptysis, right HF

Question 7

patent ductus arteriosus

Answer 7

continuous machine-like murmur, best heart at left infraclavicular area, loudest at S2

often caused by congenital rubella or prematurity

Question 8

crescendo-decrescendo ejection murmur, loudest at heart base, radiates to carotids

Answer 8

aortic stenosis

Question 9

holosystolic, high-pitched “blowing” murmur loudest at the apex, radiates toward axilla

Answer 9

mitral regurgitation

Question 10

holosystolic, high-pitched “blowing” murmur loudest at tricuspid area

Answer 10

tricuspid regurgitation

Question 11

late crescendo murmur with midsystolic click that occurs after carotid pulse

Answer 11

mitral valve prolapse

best heart over apex, loudest just before S1

Question 12

holosystolic, harsh-sounding murmur loudest at tricuspid area

Answer 12

ventricular septal defect

Question 13

early diastolic, decrescendo, high-pitched “blowing” murmur best heart at base or left sternal border

Answer 13

aortic regurgitation

hyperdynamic pulse and head bobbing when severe and chronic

Question 14

opening snap followed by delayed rumbling mid-to-late murmur

Answer 14

mitral stenosis

late and highly specific sequelae of rheumatic fever

Question 15

continuous machine-like murmur, best heart at left infraclavicular area, loudest at S2

Answer 15

patent ductus arteriosus

Question 16

leads with ST-segment elevations or Q waves: V1-V2

Answer 16

anteroseptal (LAD)

Question 17

leads with ST-segment elevations or Q waves: V3-V4

Answer 17

anteroapical (distal LAD)

Question 18

leads with ST-segment elevations or Q waves: V5-V6

Answer 18

anterolateral (LAD or LCX)

Question 19

leads with ST-segment elevations or Q waves: I, aVL

Answer 19

lateral (LCX)

Question 20

leads with ST-segment elevations or Q waves: II, III, aVF

Answer 20

inferior (RCA)

Question 21

leads with ST-segment elevations or Q waves: V7-V9

Answer 21

posterior (PDA)

Question 22

Answer 22

atrial fibrillation: irregularly irregular rate and rhythm with no discrete P waves

risk factors = HTN and CAD; may predispose to thromboembolic events, particularly stroke

management: rate and rhythm control, cardioversion; ablation of pulmonary vein ostia or left atrial appendage; coagulation based on stroke risk

Question 23

multifocal atrial tachycardia

Answer 23

irregularly irregular rate and rhythm with at least 3 distinct P wave morphologies due to multiple ectopic foci in atria

associated with COPD, pneumonia, HF

Question 24

Answer 24

atrial flutter: rapid succession of identical, consecutive atrial depolarization waves => “sawtooth” appearance of P waves

treat like atrial fibrillation +/- catheter ablation of region between tricuspid annulus and IVC

Question 25

paroxysmal supraventricular tachycardia

Answer 25

due to reentrant tract between atrium and ventricle, most commonly in AV node sudden onset palpitations, lightheadedness, diaphoresis treatment: terminate reentry rhythm by slowing AV node conduction, electrical conversion if hemodynamically unstable; catheter ablation of reentry tract

Question 26

Answer 26

Wolff-Parkinson-White syndrome: abnormal fast accessory conduction pathway from atria to ventricle (bundle of Kent) bypasses rate-slowing AV node => ventricles partially depolarize earlier => characteristic delta wave with widened QRS complex and shortened PR interval may result in reentry circuit => supraventricular tachycardia treatment: procainamide; avoid AV nodal blocking drugs

Question 27

Answer 27

ventricular tachycardia: regular rhythm, rate >100, QRS > 120 ms due to structural heart disease (cardiomyopathy, scarring after myocardial infarction) high risk of sudden cardiac death

Question 28

Answer 28

torsades de pointes: polymorphic ventricular tachycardia; shifting sinusoidal waveforms; may progress to ventricular fibrillation long QT interval predisposes to torsades de pointes; caused by drugs that decreased K+, Mg++, and Ca++ treatment: magnesium sulfate drugs that induce long QT: Ia and III antiarrhythmics, arsenic, macrolides, fluoroquinolones, haloperidol, chloroquine, TCAs, thiazides, ondansetron, fluconazole, protease inhibitors, methadone

Question 29

Answer 29

ventricular fibrillation: disorganized rhythm with no identifiable waves fatal without immediate CPR and defibrillation

Question 30

Answer 30

first-degree heart block: prolonged PR interval (>200 ms) benign and asymptomatic

Question 31

Answer 31

second degree heart block type I: progressive lengthening of PR interval until a beat is "dropped" (P wave not followed by QRS complex); variable RR interval with a pattern (regularly irregular) usually asymptomatic

Question 32

Answer 32

second degree heart block type II: dropped beats that are not preceded by a change in PR interval; may progress to 3rd degree block usually indicates a structural abnormality (ischemia, fibrosis, sclerosis) treatment: pacemaker

Question 33

Answer 33

third degree heart block: P waves and QRS complexes rhythmically dissociated; atria and ventricles beat independently of each other; atrial rate > ventricular rate may be caused by Lyme disease treatment: pacemaker

Question 34

bundle branch block

Answer 34

interruption of conduction of normal left or right bundle branches; affected ventricle depolarizes via slower myocyte-to-myocyte conduction from the unaffected ventricle, which depolarizes via faster His-Purkinje system commonly due to ischemic or degenerative changes

Question 35

premature atrial contraction

Answer 35

extra beats arising from ectopic foci in atria instead of the SA node; often secondary to increased adrenergic drive (caffeine consumption); narrow QRS complex with preceding P wave benign, but may increase risk for atrial fibrillation and flutter

Question 36

premature ventricular contraction

Answer 36

ectopic beats arising from ventricle instead of SA node; shortened diastolic filling time => decreased SV; wide QRS complex with no preceding P wave

Question 37

Brugada syndrome

Answer 37

AD loss of function mutation of Na+ channels => pseudo-right bundle branch block and ST segment elevations in leads V1-V2 treatment: prevent sudden death with ICD

Question 38

congenital long QT syndrome

Answer 38

mutations of KCNQ1 => loss of function of K+ channels => affects repolarization Romano-Ward syndrome (AD, pure cardiac phenotype), Jervell and Lange-Nielsen syndrome (AR, sensorineural deafness)

Question 39

sick sinus syndrome

Answer 39

age-related degeneration of SA node => ECG shows bradycardia, sinus pauses, sinus arrest, junctional escape beats

Question 40

MI complications: cardiac arrhythmia

Answer 40

first few days to several weeks supraventricular arrhythmias, ventricular arrhythmias, or conduction blocks due to myocardial death and scarring; important cause of death before reaching the hospital and within the first 48 hours post MI

Question 41

MI complications: peri-infarction pericarditis

Answer 41

1-3 days pleuritic chest pain, pericardial friction rub, ECG changes, and/or small pericardial effusion usually self-limited

Question 42

MI complications: papillary muscle rupture

Answer 42

**2-7 days** can result in acute **mitral regurgitation** => cardiogenic shock, severe pulmonary edema posteromedial >> anteromedial papillary muscle rupture (posteromedial has single blood supply (PDA), anterolateral has dual (LAD, LCX)

Question 43

MI complications: interventricular septal rupture

Answer 43

3-5 days mild to severe sxs with cardiogenic shock and pulmonary edema macrophage-mediated degradation => VSD => increased O2 saturation and increased pressure in RV

Question 44

MI complications: ventricular pseudo-aneurysm

Answer 44

3-14 days asymptomatic or chest pain, murmur, arrhythmia, syncope, HF, embolus from mural thrombus; rupture => tamponade more likely to rupture than true aneurysm because it does not contain endocardium or myocardium

Question 45

MI complications: ventricular free wall rupture

Answer 45

5-14 days free wall rupture => cardiac tamponade; acute forms usually leads to sudden death LV hypertrophy and previous MI protein against free wall rupture

Question 46

MI complications: true ventricular aneurysm

Answer 46

2 weeks to several months similar to pseudoaneurysm: chest pain, murmur, arrhythmia, syncope, HF, embolus from mural thrombus; rupture => cardiac tamponade outward bulge with contraction ("dyskinesia"); associated with fibrosis

Question 47

MI complications: postcardiac injury syndrome

Answer 47

weeks to several months fibrinous pericarditis dye to autoimmune reaction aka Dressler syndrome; cardiac antigens released after injury => deposition of immune complexes in pericardium => inflammation

Question 48

Aortic regurgitation

Answer 48

High-pitched “blowing”, diastolic, decrescendo murmur at left upper sternal border (valvular) or right upper sternal border (aortic root) Due to Marfan syndrome (aortic root dilation) or bicuspid aortic valve, rheumatic heart disease (valvular)