cardio Flashcards
cannon a-wave
3rd degree block
A and V contract together, so atrial pressure sky-rockets
c-v wave
mitral regurg
no x because when atria relax, the back flow of blood form the ventricles keeps the pressure up
flat y
cardiac tamponade (as blood passively leaves A into V, pressure in A should decrease, but ventricular filling pushes pericardial fluid around A and increases A pressure)
Sharp y-descent
constrictive pericarditis (atria start emptying but ventricle can't expand very much so puts back pressure on atria quickly)
Left sternal boarder: which sounds
Aortic regurg
Pulonary regurg
hypertrophic cardiomyopathy
holosystolic:
crescendo-decrescendo =
harsh =
high-pitched and blowing =
crescendo-decrescendo = Aortic stenosis
harsh = VSD
high-pitched and blowing = MR/TR
high-pitched and blowing murmurs
systolic = TR/MR diastolic = AR/PR
mid systolic click with late crescendo murmur
MVP
MC valve lesion
best @ apex
via myxomatous degeneration (1’ or 2’ to EDS or marfans), rheumatic fever, chordae rupture (post-MI)
Predisposes to IE (damaged valve)
Phase 2 of myosin AP
Ca in via L-type VG ca++ channels
causes CICR from SR
Phase 4 of pacemaker cells
controlled by funny Na+ channels
they control the HR
ACh and adenosine decrease opening .: decrease HR
catecholamines increase opening .: increase HR
[different than inward Na+ channels which are permanently inactivated in pacemaker cells via higher RMP (-70 vs. -85)]
Torsades ppt factors
congenital: romero-ward, jervell and lange-nielsen - K+ ion channel defects, risk of SCD
Low K+, Mg++, Ca++
Drugs:
Antiarrytmics (Ia + III - K+ blockers) antiBiotics (macro) antiCychotics (haloperidol) antiDepressants (TCA) AntiEmetics (ondansetron)
SCD via:
Congenital torsades: romero-ward and jervell/lang-neilsen Brugada: pseudo-RBBB and STE V1-V3 Hypertrophic caridomyopathy (b-myosin-HC)
speed of conduction
purkinje > atria > ventricles > AV
Causes of A. fib
HTN CAD RHD HF binge drinking hyperhtyroidism
F-waves
a flutter
