Cardio 1 - Valve disease, heart sounds, MI

gsafsaf's version from 2015-05-28 18:49

Valve disease + their mmmurmurs

Question Answer
High-pitched "blowing" early diastolic decrescendo murmurAR
Widened pulse pressure (increased SBP, decreased DBP)AR
Bounding/hyperdynamic pulseAR
Pulsating nail-bed/Quincke's sign of alternate blanching + reddening of the lightly compressed nail-bedAR
Head bobbingAR
Aortic root dilationAR
Bicuspid aortic valveAR
Bicuspid aortic valveAS
Predisposes to endocarditisMVP
ECCENTRIC LV hypertrophyAR
ECCENTRIC LV hypertrophyMR
ECCENTRIC LV hypertrophyDilated cardiomyopathy
ECCENTRIC LV hypertrophyMI
CONCENTRIC LV hypertrophyChronic HTN
Progresses to L HFAR
Isolated aortic root dilationAR
Syphilitic aortic root dilationAR
Marfans aortic root dilationAR
Prominent carotid pulse (may be seen at bedside)AR
May palpate a mid-systolic dip in carotid pulse pressure due to high velocity AR
Increases stroke volumeAR
Crescendo-decrescendo systolic ejection murmur (note: not holosystolic, even tho long)AS
Ejection clickAS
LV >> aortic pressure during systoleAS
Loudest at the base (R sternal border)AS
"Pulsus parvus et tardus" Weak, delayed peripheral pulsesAS
SAD - syncope, angina, dyspnea on exertionAS
Age-related calcificationAS
Early-onset calcification of bicuspid valveAS
Prolonged asymptomatic phaseAS
Microaangiopathic hemolytic anemiaAS
Radiates to carotidsAS
Late systolic crescendo murmur w midsystolic clickMVP
Most frequent valvular lesionMVP
Best heard over apexMVP
Best heard over apex + radiates toward axillaMR
Usually benignMVP
Can be caused by myxomatous degeneration MVP
Ehlers-Danlos MVP
Chordae rupture MVP
Chordae ruptureMR
Can be caused by MVPMR
Can be caused by LV dilationMR
Can be caused by RV dilationTR
Holosystolic harsh-sounding murmur, loudest at tricuspid areaVSD
Holosystolic high-pitched blowing murmur, loudest over tricuspid areaTR
Holosystolic high-pitched blowing murmur, loudest at apexMR
Delayed rumbling late diastolic murmurMS
Follows opening snapMS
What would indicate increased severity of MS?Decreased interval between S2 and OS correlates with increased severity
Can result in LA dilation --> pulm. congestionMS
Edema, alvolar hemorrhage, hemosidering laden macrophagesPulm. congestion 2ndary to MS
Atrial fibrilationLA dilation 2ndary to MS
Continuous machine-like murmurPDA
Loudest at S2PDA
Often due to congenital rubella or prematurityPDA
Best heard at left infraclavicular areaPDA
Early rheumatic fever lesionMR
Late rheumatic fever lesion MS
Assctd w rheumatic feverPretty much all valve related murmurs: MR + MS most common; but also AR, AS, TR, MVP
Systolic murmur at left sternal borderhypertrophic cardiomyopathy
Presence of S3 gallop with left ventricular overload = best indicator of this valvular lesion's severityMR

Murmur maneuvers

Question Answer
What does handgrip do to circulation?Increases after load
Handgrip increases intensityMR
Handgrip increases intensityAR
Handgrip increases intensityVSD
Handgrip decreases intensityHCM
Causes later onset of click in MVPHandgrip
What does inspiration do to circulation?Increases venous return to RA
Inspiration increases intensityR sided valve murmurs
Inspiration increases intensitySplitting of S2
What does valsalva do to circulation?Increases intrathoracic pressure - reduces venous return to RA; also reduces systemic pressure if held long enough; Decreases preload and after load
Valsalva decreases intensitymost murmurs
Valsalva increases the intensityHCM
Causes earlier onset of click in MVPValsalva
What does rapid squatting do to circulation?Increases venous return, increases preload
Rapid squatting decreases intensityHCM
Rapid squatting increases intensityAS
Causes later onset of click in MVPRapid squatting
Heard best in left lateral decubitus positionMS
Heard best in left lateral decubitus positionMR
Heard best in left lateral decubitus positionLeft sided S3
Heard best in left lateral decubitus positionLeft sided S4
Enhanced by expirationMS

More on <3 sounds

Question Answer
Increased filling pressuresS3
Mid diastolic heart soundS3
Rapid ventricular fillingS3
Assctd. w dilated cardiomyopathyS3
Assctd. w CHFS3
Assctd. w MRS3
Assctd. w L->R shunt like VSD, ASD, PDAS3
Normal in children + pregnant womenS3
Late diastolic heart sound right before S1S4
Assctd. w LV hypertrophyS4
Assctd. w ASS4
Assctd. w chronic HTN (+ resultant LV hypertrophy)S4
Assctd. w hypertrophic cardiomyopathyS4
Commonly heard post-MIS4
Heard on inspiration, NOT expirationSplitting of S2
Assctd. w Pulmonic stenosisWide splitting of S2
Assctd. w RBBBWide splitting of S2
Heard on both inspiration and expirationWide splitting of S2
Assctd. w ASDFixed splitting of S2
Heard on both inspiration and expirationFixed splitting of S2
Assctd. w delay in aortic valve closureParadoxical splitting of S2
Assctd. w ASParadoxical splitting of S2
Assctd. w LBBBParadoxical splitting of S2
Heard on expiration, NOT inspirationParadoxical splitting of S2
Considered benign when there is no evidence of diseaseSplit S1
Considered benign when there is no evidence of diseaseSplit S2 on inspiration
Considered benign when there is no evidence of diseaseS3 in pt. <40yo
Considered benign when there is no evidence of diseaseEarly, quiet systolic murmur
Diastolic murmurMS
Diastolic murmurTS
Diastolic murmurAR
Diastolic murmurPR
Systolic murmurMR
Systolic murmurTR
Systolic murmurAS
Systolic murmurPS
Systolic murmurMVP
Systolic murmurMVP
Continuous murmurPDA

MI over time

Question Answer
0-4hrs histominimal change
0-4hrs risk ofarrhythmias
4-12 hrs histoearly coagulation necrosis, edema, punctate hemorrhages, wavy fibers, cytoplasmic hypereosinophilia
4-12 hrs risk ofarrhythmias
12-24 hrs histocoagulation necrosis and marginal contraction band necrosis aka neutrophilic infiltration of the zone of dead myocardium
12-24 hrs risk of arrhythmias
1-5 days histocoagulation necrosis and neutrophilic infiltrate and hyperemia (redness)
1-5 days risk ofarrhythmias
5-10 days histomacrophage phagocytosis of dead cells (acute inflammatory infiltrate recedes) and yellow tan softening grossly
5-10 days risk ofventricular aneurism, wall rupture, papillary muscle rupture
10-14 days histofibrovascular granulation tissue and neovascularization
10-14 risk ofventricular aneurism, wall rupture, papillary muscle rupture
2 weeks to 2 months histocollagen deposition/scar formation/decreased cellularity in the zone of infarced myocardium
>2weeks risk ofDressler syndrome (pericardial friction rub + fever), ventricular aneurysm