Cards (U.W.) Flashcards
which aortic arches don’t contribute to adult anatomy
1,2, and 5th
adult anatomy derived from 3rd aortic arch?
proximal internal and common carotid A
adult anatomy derived from 4th aortic arch?
true aortic arch and subclavian As
adult anatomy derived from 6th aortic arch?
pulmonary As and ductus arteriosus
explain Tetrology of Fallot?
cause?
4 associated defects
- deviation of the infundibular septum during development, causes VSD (1) and an overriding aorta (2)
other associated problems include RVOT obstruction (3) which causes (4) RVH
describe the location of the AV node
in the RA, near the septum of the tricuspid valve and coronary sinus orifice
low pitched holosystolic murmur at LLSB that increases with increased afterload
VSD
murmurs that are louder with increased handgrip
MR,AR, VSD
in a pacemaker where are the three leads placed and how?
- ) RA 2.) RV via the IVC and SVC
3. LV via coronary sinus which runs in the atrioventricular groove
describe the course of the saphenous V
starts at medial foot, runs anterior to medial malleolus and superficially on medial aspect of leg, reaches the femoral triangle inferolaterally to the PUBIC TUBERCLE
describe the blood supply of the retinal A (important in retinal artery occlusion)
ICA-> opthalmic A-> retinal A
lead 1, avL, and v5-v6 correlates to which part of the heart? which blood supply
lateral left ventricle,
supplied by L circumflex A
V1-V4 correlates to which part of the heart? which blood supply
anterior LV and interventricular septum supplied LAD (note distal LAD spares septum, and is V3-V4)
II, III, AVF correlates to which part of the heart
RV and inferior LV
RCA
calculate True Positive
SENSITIVITY *( # of people WITH disease)
calculate False Negative
(1- SENSITIVITY) * (# of people WITH disease)
Aschoff Bodies
granulomas of plump macrophages in cardiac tissue
pathognomonic for ARF induced carditis
Wet Beri Beri
thiamine B1 deficiency
peripheral neuropathy + CHF
Stanford Type A dissection originates near
Stanford Type B dissection originates near
A- ascending- sinotubular junction
B- descending- near L subclavian A
progressive heart failure shortly following viral infection is suspicious for what kind of HF
DILATED cardiomyopathy
Nonbacterial thrombotic endocarditis (NBTE)
platelet rich, sterile thrombi on cardiac valves
can be related to an advanced malignancy or a chronic inflamm condition (Lupus, Antiphospholipid)
Turner’s Syndrome is associated with what valvular deficiency
Bicuspid Aortic Valve
ACUTE pericarditis is associate w
pericardial friction rub
Pulsus Paradoxicus
upon INSPIRATION, SBP drop by 10+ mmHG
seen in cardiac tamponade, constrictive pericarditis, severe asthma/COPD
reason? bc if expansion of heart is impaired or prevented, inspiration which causes increase in R atrial/ vent filling will cause bowing of septum, decreased LV vol and decreased SV
the collagenous scar formed in the heart, post MI, is what kind of collagen?
Collagen type I
collagen type I found in
bone, tendons, ligaments,
collagen type II found in
cartilage, nucleus pulposis, vitreous humor
collagen type III found in
granulation tissue, skin, lungs
collagen type IV found in
basement membrane
coronary steal syndrome
in response to ischemia, local vasodilators cause coronary arteries supplying ischemic regions to preferentially dilate.
giving this patient a synthetic coronary artery dilator like adenosine or dipyramidole can shunt blood AWAY from ischemic areas making ischemia worse. this is bc a’s to ischemic areas are already max dilated, now these drugs are dilating other coronary a’s too
loss of palpable pulse during inspiration is a physical finding of what
pulsus paradoxus
Beck’s Triad includes what? is consistent with which diagnosis
1.) hypotension
2.) JVD
3.) diminished heart sounds
acute cardiac tamponade
varicose veins? what causes it? what does it cause?
dilated tortuous superficial veins of LE, due to incompetent valves/loss of wall strength
can cause skin ulcers, edema, stasis dermatitis, poor wound healing (note: major thrombotic events are rare bc its superficial veins.)
what is most susceptible to atherosclerosis
Lower abdominal aorta
coronary As
which arteritis’s involve granulomatous formation
GCA, takayasu
carcinoid heart disease
carcinoid syndrome( a neuroendocrine tumor producing excess 5HT, histamine, and VIP) can cause cardiac symptoms. the extra serotonin stimulates fibroblast growth, and fibrous plaque causing TR, pulmonic valvulopathy, and RHF
holosystolic murmur that increases in intensity upon inspiration
TR
Origin of middle meningeal A
ECA-> maxillary A->MM
what prevents edema in moderate elevations of central venous pressure?
increased lymph drainage. even though CVP is increasing, therefore capillary hydrostatic P is increasing, causing more fluid to be filtered into interstitial space, this is offset by increased lymph clearance
Osler- Weber- Rendu syndrome
autosomal dominant condition of hereditary hemorrhagic telengectasias
common presentation: nosebleeds+ pale pink spider like lesions
occlusion of RCA causes what kind of HF
RHF bc while yes, RCA supplies inferior LV via PDA it is not the only source of LV blood supply. Meanwhile, the RV is mainly only supplied by the RCA so RV failure is seen first. ( double check xray findings, and if lungs are clear you know this is only the RHF)
how to decrease LVOT HOCM murmur
increase the preload or afterload.
- ex: squat/passive leg raise and handgrip
hyperplastic arteriosclerosis vs hyaline arteriosclerosis?
describe each
what is each associated with
hyperplastic- onion skin like concentric thickening–> hypertensive crisis
hyaline- homogenous acellular thickening–> lower levels of hypertension
murmur at RSB (w/ radiation to carotids) cresecendo decrescendo
AS
where is angiotensinogen made
liver
where is ACE found
pulmonary endothelial cells
how does squatting help in a tet spell
it increases SVR, making the blood want to flow through stenotic pulmonary circulation instead of going into systemic
after how long of ischemia do the cardiac myocytes stop contracting
1 minute due to ATP depletion and cellular toxins
till how long after ischemia is injury reversible for the cardiac myocytes
30 minutes- until the adenosine is depleted
what is normal LA max pressure
10 mmhg
increase in LA max pressure and peaked, early, tall “v” waves in pressure tracing of LA is
mitral regurg
severe MR can be indicated by what heart sound
S3- S3 is an indicator of LV dilation or increased blood flow into LV
irregularly irregular rhythm
a-fib
AAA pathogenesis
chronic transmural inflammation leads to weakening and progressive expansion of aortic wall due to MMPs released by inflamm cells
Concentric hypertrophy of LV
- caused by chronic increase in afterload – like aortic stenosis and chronic HTT
liofuscin
yellow brown perinuclear pigment seen in aging/cachetic pts due to lipid peroxidation and free radical buildup
why is it advisable to give aspirin before Niacin t(x) for hyperlipidemia
niacin (aka nicotinic acid) decreases LDL and TGs and increases HDL. However it also releases prostaglandins which causes the unwanted side-effect of flushing and itching. Aspirin which ihibits PGE production can help
DIFFERENTIAL clubbing/cyanosis of LE only, without any discrepency in pulse or BP is what disease?
large PDA that has reversed from L->r flow to r–>L flow (eisenmenger)
Rheumatic heart disease causes what patholologically
chronic inflamm and scarring of valve
Infective endocarditis pathology
disruption of endocardial surface–> sterile platelet and fibrin attaches (nidus)–> after bacterial infection, bacteria colonize nidus
enterrococcus endocarditis is usually preceded by what procedures
- GU related or GI related
cystoscopy, obstetrics, colonoscopy
isoproterenol
non selective B agonist. B1- increased contractility; B2- decreased TPR
claudication caused by
atherosclerosis
loss of what can make systolic HF significantly worse??
loss of atrial kick
what is INR
patient’s PT/ control PT
- we are measuring PT bc Warfarin inhibits carboxylation of vit K dependent coag factors like Factor VII and remember factor VII is in extrinsic pathway (measured by PT)
myxomatous changes in media are found in
“cystic medial degeneration” aka aortic aneurysm (often seen in Marfan’s)
what jvp waveform is missing in an a-fib pt
“a” wave, first wave, has to do with atrial contraction
adenosine side effects
flsuhing, chest burning, hypotension, high grade AV block
most serious complication of kawasaki
coronary artery aneurysm
where is cardiac action potential speed the fastest
purkinje cells
where is cardiac action potential speed the slowest
AV node
from fastest to slowed name the cardiac action potential cells
park at venture ave
purkinje, atrial, ventricular, AV node
how does a cardiac myocyte relax after excitation and contraction
well it has to get the Ca2+ out of the cytoplasm in one of two ways
(1) Na+/Ca2+ exchanger
(2) SERCA- Ca2+ ATPase - this one brings Ca2+ back into SR
how do you best listen to S3/S4?
- use bell at apex
- lateral decubitus & end expiration to bring heart closer to chest
nitrates work by
primarily venodilation
causes decreased preload, so reduces myocardial work and therefore myocardial oxygen demand
what predisposes to IE in developed countries
MVP
Cilastazol
- phosphodiesterase inhibitor
- inhibits platelet aggregation and acts as arterial vasodilator
wide fixed splitting of S2
ASD
S3 is what kind of dysfuntion? S4?
S3- systolic
S4- diastolic
how do mineralocorticoid receptor antagonists (spironolactone, eplerone) improve survival/mortality in HF
the K+ sparing dieuretics are aldosterone inhibitors
VSD sounds like
holosystolic murmur over LLSB
when is peak intensity of AR
right after aortic valve closure
