Cards (F.A.) Flashcards
what is the embryological derivative of the Ligamentum Teres? (Round ligament(
Umbilical Vein
Where is the Ligamentum Teres found
Falciform ligament
What is the embryological derivative of the MediaN ligament and the MediaL ligament
MediaN- Allantois/urachus
MediaL- Umbilical A
an RCA infarction will present in which EKG leads?
II, III, avF
a LCX infarction will present in which EKG leads?
I, V5, V6, avL
an LCA infarction will present in which EKG leads
V1,V2 - interventricular septum
V3, V4- anterior LV
what are the (2) equations to determine Cardiac Output?
CO= HR * SV CO = rate of O2 consumption/ (arterial O2 - venous O2)
what are (2) equations to calculate MAP
MAP= 2/3 DBP + 1/3 SBP MAP = CO * TPR
how to calculate Pulse Pressure
SBP- DBP
how to calculate Stroke Volume?
SV= EDV- ESV
what 3 factors affect SV
contractility, afterload, preload
how do you calculate wall tension
wall tension = pressure * radius
hence, tension increases with increasing radius
how do you calculate wall stress
Pressure * radius / 2* wall thickness
wall tension/ 2* wall thickness
Driving Pressure in a vessel=
P= Q * R Pressure= Flow rate * Resistance
how are size of the vessel and flow through the vessel related
Q= (P1-P2/ nL) * r^4
so in radius is cut in half (1/2), flow decreases by (1/16)
what is an S3 sound related to
dilated ventricle or increased filling pressure (like bc of MR)
think- SYSTOLIC dysfunction
what is an S4 sound related to
stiff ventricle
think - DIASTOLIC dysfunction
JVP tracing: a wave (1)
absent in??
R. atrial contraction
absent in Afib
JVP tracing: c wave (2)
R. ventricular contraction
JVP tracing: x descent (3)
ventricular ejection, caused by downward motion of Tricuspid
JVP tracing: v wave (4)
“villing” -increase in atrial pressure due to diastolic filling
JVP tracing: y descent (5)
absent in??
RA emptYing into RV
absent in constrictive pericarditis
normal splitting
what is it?
why does it happen?
a normal split in S2, with P2 coming after A2 during inspiration
- increased VR in inspriration causes delayed Pulmonic valve closing
Wide splitting
what is it?
why does it happen?
an abnormal split in S2- with P2 coming MUCH after A2 in inspiration due to conditions that delay P2 closure
- RBBB or pulmonic stenosis which is exaggerated by the increased VR in inspiration causes wide split
Fixed Splitting
what is it?
why does it happen?
- an abnormal split in S2- with P2 coming after A2 in inspiration and expiration
- ASD, causes Right heart volume overload all the time, so always causing delayed pulmonic valve closure
paradoxical splitting
what is it
why does it happen
- an abnormal split in S2- with A2 coming before P2 usually. But on inspiration, the split is actually reduced bc P2 closure is delayed
- caused by delays in aortic valve closure-LBBB and aortic stenosis
AS- describe the murmur
crescendo- decrescendo systolic ejection murmur, with presence of possible ejection click
MR/TR- describe the murmur
holosystolic, high pitched, blowing murmur
MVP - desrcibe the murmur
late crescendo murmur with midsystolic click
VSD- describe the murmur
holosystolic, harsh sounding murmur
AR - describe the murmur
early diastolic decrescendo murmur, blowing, high pitched
MS - describe the murmur
diastolic, OS followed by diastolic delayed rumble
PDA- describe the murmur
constant and machine like
pulsus parvus et tardis is associated with which murmur
AS
inspiration makes which murmurs louder?
why?
all right heart murmurs
- bc increased VR to RH
handgrip makes which murmurs louder?
why?
- MR, AR, and VSD
- because increase in afterload
handgrip softens or delays which murmurs
- AS, and click of MVP as well as HOCM
- it increases afterload, which increases LV vol
valsalva/standing up does what to HOCM murmur?
it increases HOCM murmur because it decreases preload
valsalva does what to MVP click
it makes MVP click earlier bc it decreases preload making LV vol smaler
what does rapid squatting do? whats the murmur it makes better?
it increases preload and afterload.
makes HOCM better, because it increases preload, it also makes MVP happen later for same reason
Romano Ward Syndrome
congenital QT prolongation
AD
pure cardiac phenotype
Jervell and Lange-Lielsen
congenital QT prolongation
AR
accompanied by sensineural deafness
Brugada syndrome
AD in asian males
pseudo RBBB and St elevations in V1-V3
risk of V tach and SCD
1st degree AV block
prolonged PR (>200 msec) benign
2nd degree AV block, type I (Mobitz I)
regularly irregular
progressive PR lengthening until dropped beat
asymptomatic
2nd degree AV block, type II ( Mobitz II)
randomly dropped beats, theres no change or progressive PR interval length preceding it
may become type 3 heart block, may need pacing
3rd degree AV block
atria and ventricles beat separately
capillary fluid exchange formula
Flow out of capillary = ( hydrostatic capillary P - oncotic capillar pressure) - (hydrostatic interstitial P- oncotic interstitial P)
hyperplastic arteriosclerosis seen in
extreme hypertension
hyaline arteriosclerosis seen in
diabetes, maybe low levels of hypertension
list most common sites of atherosclerosis
abdominal aorta > CORONARY As > popliteal A > carotid As
claudication symptoms caused by
atherosclerosis
what is AAA associated with, how about Thoracic Aortic Aneurysm?
AAA- atherosclerosis
TAA- cystic medial degeneration
unstable angina vs NSTEMI vs STEMI
UA- no cardiac biomarker elevation
NSTEMI- cardiac biomaker elevation but ST DEPRESSION due to SUBendocardial infarct
STEMI- cardiac biomarker elevation but ST ELEVATION due to TRANSmural infarct
MI: first 4 hours
no change
MI: 4-12 hours
wavy fibers w/ edema, hemorrhage, and start of coag necrosis
MI: 12-24 hr
cytopia and neutrophils begin to appear
MI: 1-3 days
extensive coagulative necrosis
acute inflammation with neurtophil abundance
MI: 3- 14 days
granulation tissue (collagen III) macrophages
MI: 2 wks- months
scar tissue complete (collagen I)
an infarct in PDA will show changes in which EKG leads?
V7-V9 has elevations ( note depression in V1-V3)
MI complication: within the first few days
arrhythmia (death before 24 hr) postinfarction pericarditis (1-3 days) - note this is not autoimmune, and it only overlies area of necrosis
MI complication: before first week
Papilary Muscle Rupture - usually posteromedial papillary and will cause MR
Interventricular septal rupture - causes VSD, is macrophage mediated
MI complication: within first two weeks
ventricular pseudoaneurysm - contained free wall rupture
free wall rupture- causes cardiac tamponade
Mi complication: several weeks following
true ventricular aneurysm- outward bulge w contraction and assn with fibrosis
Dressler Syndrome- autoimmune fibrinous pericarditis
Kussmaul Sign
increase JVP on inspiration
sign of constrictive pericarditis, restrictive cardiomyopathy, or ventricular tumor
you would expect JVP to decrease on inspiration bc drop in transthoracic pressure, but an increase suggests that the drop in transthoracic pressure is not transmitted to heart
vasculitides with focal granulomatous inflammation
Large Vessel- GCA and Takayasu
vasculitides affecting Medium size vessels
Polyarteritis Nodosa, Thromboangiitis Obliterans (Buerger) and Kawasaki
PAN key features?
segmental transmural inflammation with fibrinoid necrosis
spares pulmonary As
Hep B assn
renal microaneurysms form
Kawasaki key features?
risk of: coronary artery aneurysms CRASH& BURN C- conjunctival injection R- rash A- adenopathy S- strawberry tongue H- hand and foot changes BURN- fever
Thromboangiitis Obliterans (Buerger) key features?
young male HEAVY smoker
- gangrene and Raynaud’s
“segmental thrombosing vasculitis”
What are the small vessel vasculitides?
- Wegener’s
- Churg- Strauss
- Henoch Schonlein
- Microscopic Polyangitis
Wegener’s (Granulomatosis with Polyangitis) Vasculitis
granulomas in lung+ glomerulonephritis + “focal necotizing vasculitis”
c-ANCA (aka pr3 ANCA)
Churg Strauss (Eosinophilic Granulomatosis with polyangitiis)
asthma + peripheral neuropathy (foot drop)
p-ANCA (MPO ANCA)
Henlock Schonlein Vasculitis
triad: GI disturbance + Arthralgia + palpable purpura on legs and butt
IgA complex deposition
Osler-Weber- Rendu syndrome
AD disorder of blood vessels. Telengiectasias (blanching), recurrent nosebleeds/ GI bleeds/ hematuria, AVMs
Leukocytoclastic Vasculitis
a drug response (penicillin)
nonblanching palpable purpura
sm vessel vasculitis
which vasculitis are p-ANCA (MPO ANCA) positive?
microscopic polyangitis
churg strauss
Ranolazine
used in refractory angina
inhibits late phase sodium current without affecting contractility or HR
Ivabradine
selective inhibition of funny Na+ current which slows phase 4 depol in nodes WITHOUT ionotropy
used for stable angina for pts who cant take B blockers
ae: visual brightness, htt, bradycardia
How to calculate Flow Rate?
Q= CSA * velocity of flow
