Heart Murmurs, EKG, MI complications Flashcards
aortic stenosis
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
mitral regurgitation
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
mitral valve prolapse
Midsystolic click followed by late systolic murmur
can predispose to infective endocarditis; can be caused by rheumatic fever, chordae rupture, or myxomatous degeneration
ventricular septal defect
holosystolic, harsh-sounding murmur, loudest at tricuspid area
larger VSDs have lower intensity murmur than VSDs
aortic regurgitation
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
mitral stenosis
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
patent ductus arteriosus
continuous machine-like murmur, best heart at left infraclavicular area, loudest at S2
often caused by congenital rubella or prematurity
crescendo-decrescendo ejection murmur, loudest at heart base, radiates to carotids
aortic stenosis
holosystolic, high-pitched “blowing” murmur loudest at the apex, radiates toward axilla
mitral regurgitation
holosystolic, high-pitched “blowing” murmur loudest at tricuspid area
tricuspid regurgitation
late crescendo murmur with midsystolic click that occurs after carotid pulse
mitral valve prolapse
best heart over apex, loudest just before S1
holosystolic, harsh-sounding murmur loudest at tricuspid area
ventricular septal defect
early diastolic, decrescendo, high-pitched “blowing” murmur best heart at base or left sternal border
aortic regurgitation
hyperdynamic pulse and head bobbing when severe and chronic
opening snap followed by delayed rumbling mid-to-late murmur
mitral stenosis
late and highly specific sequelae of rheumatic fever
continuous machine-like murmur, best heart at left infraclavicular area, loudest at S2
patent ductus arteriosus
leads with ST-segment elevations or Q waves: V1-V2
anteroseptal (LAD)
leads with ST-segment elevations or Q waves: V3-V4
anteroapical (distal LAD)
leads with ST-segment elevations or Q waves: V5-V6
anterolateral (LAD or LCX)
leads with ST-segment elevations or Q waves: I, aVL
lateral (LCX)
leads with ST-segment elevations or Q waves: II, III, aVF
inferior (RCA)
leads with ST-segment elevations or Q waves: V7-V9
posterior (PDA)
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
multifocal atrial tachycardia
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
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
paroxysmal supraventricular tachycardia
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
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
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
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
ventricular fibrillation: disorganized rhythm with no identifiable waves
fatal without immediate CPR and defibrillation
first-degree heart block: prolonged PR interval (>200 ms)
benign and asymptomatic
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
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
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
bundle branch block
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
premature atrial contraction
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
premature ventricular contraction
ectopic beats arising from ventricle instead of SA node; shortened diastolic filling time => decreased SV; wide QRS complex with no preceding P wave
Brugada syndrome
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
congenital long QT syndrome
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)
sick sinus syndrome
age-related degeneration of SA node => ECG shows bradycardia, sinus pauses, sinus arrest, junctional escape beats
MI complications: cardiac arrhythmia
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
MI complications: peri-infarction pericarditis
1-3 days
pleuritic chest pain, pericardial friction rub, ECG changes, and/or small pericardial effusion
usually self-limited
MI complications: papillary muscle rupture
2-7 days
can result in acute mitral regurgitation => cardiogenic shock, severe pulmonary edema
posteromedial»_space; anteromedial papillary muscle rupture (posteromedial has single blood supply (PDA), anterolateral has dual (LAD, LCX)
MI complications: interventricular septal rupture
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
MI complications: ventricular pseudo-aneurysm
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
MI complications: ventricular free wall rupture
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
MI complications: true ventricular aneurysm
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
MI complications: postcardiac injury syndrome
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
Aortic regurgitation
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)
