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Cath Sap 5 board prep > stats/ structural/ IVUS-oct > Flashcards

stats/ structural/ IVUS-oct Flashcards

1
Q

precision in improved as _____. _____increased

how is prcision estimated in stats terms

A

sample size

tighter CI’s

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2
Q
  1. when there are big outliers or the distribution isnt normal what is better median or mean.
  2. MC used meaure of variabilty for a guassian aa nomral distribution
  3. when filling in missing data with multiple imputation what is key assumption
  4. internal vs. external validity?
  5. how can one determine external validity?
  6. Why is ITT so favored?
  7. do rcts established causation?
A
  1. median

2 standard deviation

  1. That the missing data must be missing at random.
  2. internal vs. external validity? internal-> sound study design and results. external generalizaiblity
  3. use registry data to confirm an RCTs result
  4. It is the only method to gaurantee and ubiased estimate of treatment effect. bc altering treatment group after randomization inherently biasisi the results.
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3
Q

by statistical dogma should you compare baseline charateristics in an RCT by p value

A

No, bc of some bullshit about source derivation

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4
Q

3 factors that go into making a balanced trial

A
  1. randomization
  2. outcome detection are done in a balanced manner between the groups. (ie blinding )
  3. missing data must be minimzed.
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5
Q

How do determine noninferiority statistically

A

The upper 95% CI cannto include the noniferiority boundary. Setting these boundaries are controveral.

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6
Q
  1. How is bayseanstatistics different fromStandard?
A
  1. Baysean Analysis Utilizes prior probability distribution based on what is known And reCalbraith these probabilities in light of experimental results
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7
Q

False positive rate pneumonic

False negative trial

A

alpha error (FAST) - Fasle Alpha statisitcal test - alpha is first so this is type one error.

False negative trial –> beta error…(type II error the other one is the other one)

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8
Q

alpha error

A

false positive test (FAST)

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9
Q

type I error =

What is it preset as in trials

How do you thing of it?

A

alpha error - False positive staisitical test

0.05 althought it looks like the p value it is a different concept, it is the probablity before the trial starts that the result would be a false positive

If you repeated the trial 100 x then 95% of the time or more the result would be the same

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10
Q

Beta error what is it

A

false negative rate (probablity of a false negative trial). This is also type II error.

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11
Q

power is what

A

1-Beta error aka ture postive rate

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12
Q

True postive rate

A

1-Beta error or Power

Power is the abillty to show a difference when one exists.

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13
Q

RR calc

A

(control relative risk - exper RR)/ CRR

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14
Q

SIHD major updates.

  1. prior to PCI for SICHD need to do this?
  2. Rule of thumb regarding deferring intervention?
  3. Rule of thumb regarding FFR of a lsions
  4. when to do stress after cabg per guidelines in asx. overall exercise and imaging studies should only be done when therre is a change in clinical status not annualy.
A
  1. trial medical therapy
  2. choose it.
  3. choose it.
  4. after 5 years its reasonable
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15
Q

change in GL on aspiration thrombectomy and embol

A
  1. total increase in stroke now class III
  2. embolic protection still reasonable in SVG Ib (european gl dropped it but not ours, bc the data that causes the european gl didnt make sense. )
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16
Q

GL changes non infacrt artery at time of STEMI

A

now pci should not be performed in seeting of shock

Can perform in STEMI as long as not as in shock (hasnt made guidleins)

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17
Q

AUC NSTEMI/US what constitute high risk features for nonfateal MI or death

A

TIMI/GRACE risk score

accelerating sx

age

character of pain

ecg change

bio markers

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18
Q

What does fred welt do regarding pt with lysis and 50% reduction in stemi and imrpvoed paoin

A

he calls in the team and waits the 3 -12 hours post (he’s lying).

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19
Q

CCS class in most trecent gl

A

now lumped together.

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20
Q

determing Stress test risk category high risk (5

A

High risk

  • LV EF < 35%
  • resting perfousion abn > 10%
  • stress ECG including > 2 mm ST depression at low workload or presisting into recovery or STE
  • TID
  • WMA/ ischemia 2 oronary beds or LM

CAC > 400

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21
Q

CAC score impt high risk

A

400

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22
Q

400

A

CAC score high risk

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23
Q

to be fully appropriate for p lad in SCIHD with pLAD + another vessel need what for PCI

A

basically need to have high risk stress or DM and need to be sx or ffr +

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24
Q

LM disease PCI for boards

A

generally for ostial or midvessel -otherwwise be conservative

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25
Q

2 high risk surgerys

A

cross clamp aortas asnd substantial bleeding.

Hernias

cataracts low risk

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26
Q

functional capactiy able to send to surgery if intermediate risk

A

4 mets

A few stairs, light running, golf, dancing, doubles

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27
Q

Dicrotic notch represents what

A

Dicrotic notch is Ao closure.

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28
Q

AS gradient wiggins diagram

A

Big gradient, loss of anacrotic notch (point C), delacyed upstroke from C to peak in diagram

c= Ao opending and end of isovolumetric contraction.

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29
Q

Gorlin

and

HAaki

A

Gorlin

AVA = CO/Systolic ejection time *HR*44.3* sq root of mean gradient

Haaki

CO/ sq of p-p gradien

ie 6/ sq of 36 = 1

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30
Q

give hakki again

exclusion of haaki

A

CO/ Sq peak to peak

Need HR to be normal.

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31
Q

Big hint on hemodynamics that there is a hug prob after tavr

A

matching of LV end diastolic pressure. and aortic diastolic

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32
Q

Charterisks of hocm on wiggins (2)

A

spike and dome, early ejection and delayed obstruction. (very strange systolic upstroe)

Brunwald braunbraun - increase in gradient and spike and dome on the aortic tracing. in AS have increase in both Ao and LV gradients but no change in p-p

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33
Q

Braunawauld brokenbrough

A

PVC AS no change in peak to peal gradient (both trancing increase due to increase contractilituy on post pvc beat due to delay and increased calcium

in HOCM get a big increase in gradient with spike and dome on aortic (lower tracing.

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34
Q

Summaries gradient and areas for vavle lesions

AS

MS

PS

TS (mean)

Coarc (mean)

subas (mean)

A

AS - 40 mmHG mean, AVA <1

MS 10 mean, 1.5 mVA

PS > 30 and 60 peak if sx, 40 and 70 if no sx

TS >5 mean

coarc 20

Sub as 30

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35
Q

TS mean gradient for intervention

A

5 mmhg

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36
Q

coarc p-p for intervention

A

20 mmhg mean change

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37
Q

subAS mean gradient need surgery

A

30 mmHG

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38
Q

Tamponade hemodynamic findings

A

pericardial pressure approches RA pressure

pulsus paradox on Ao tracing

Intraventicular interdendence. however no dip and platau in constriction.

39
Q

intracardiac shunt math

A

Qp = Sat ao- sat VC/ Sat PV - Sat PA

Higher sats go infrom, Q p terms go in denominator despite p bing in numberator

40
Q

normal pericardial pressure

A

-5 to +5 mmHg

41
Q

pulsus that is sig\

tamponade RA pressure tacing

A

10 mmg, 10 mmg drop with inspriation

big X drop with no y descent.

42
Q

Where dont wire with pericardial tap

A

exiting the pericardium into the pulmonary tree

43
Q

Kussmals sign

A

increased JVP with inspiration - reflective wave bc heart cant relax with incrased volume with insp.

44
Q

How to tell constriction and restriction

A

draw lines and they should be going oppositie from the peaks of the wave tracings.

45
Q

buzz word for constricution (2)

A

dip (y decentl/ late) and platau aka square root sign

46
Q

dip and platau

A

constriction

47
Q

RR calc

OR calc

A

divid the two probablities of events fro the two groops

prob of an outcome occuring in one groop divided by the prob of the event not occuring in the same group then dividing this by the same in the other group.

48
Q

RR what is in numberator

RRR

A

experimaental in general

100*1-RR

49
Q

RRR calc

A

100*1-RR

when RR = Exp pro/control exp

50
Q

When is OR used

A

retrospective studys when number of people exposed unkonw.

51
Q

def power

A

1-B

probablity of detecting a difference if one does exist try to do at 80% power.

52
Q

sensitivity

Specifiity

PPV

NPV

A

4 x 4 with positives in the right hand coroncer and disease on top

DZ

test A B

C D

sens - pos test in someone with dz

spe neg test witout dz

ppv detecting dz in someone with a pos test

NPV non detectivn dz in those with a negative test

Sens A/A+C

spe D/D+B.

PPCV a/A+b

NPV D/D+c

53
Q

NPV and PPV are demendent on

Sens and spe depend on

A

the prevalence (think of the indiviular), this varies bacsed on prevalence

nothing, spe and sens are fixed for the test

54
Q

Angio type ABC lesion: Describe

A
  1. Type A: Less than 10 mm Non-angulated no thrombusNo side branch smoothNot totally included.
  2. Type B: Moderate to heavy calcium, nRhombus, Fabrication angulated
  3. Type C: (low success), long >20 mm. inability to protect side branch vein graph, excessive toruositiy., long < 20 mm, CTO
55
Q

SYNTAX SCORE WHAT LEVEL SEND TO CABG

A

>33 BYPASS BETTER THAN PCI

56
Q

OCT MOA

A

near infra red

57
Q

IVUS vs. OCT

  1. Wavelenght
A

IVUS OCT

Wavelenght 35-80 vs. 1.3

Resolution 100 um vs. 15 um (so OCT at least 10 x better)

frame rate 30 vs. 100

pull bac rate 1 mm/s vs. 20

penetration max 10 vs. 2.35 mm (IVUS can penetrate further except in ca)

58
Q

What has better tissue penetration IVUS or OCT

A

IVUS

59
Q

IVUS vs. OCT measurements

A

IVUS estimates 8% bigger.

60
Q

IVUS MLA for stenting

A

5.9 (litro study)

61
Q

What is the 8765 rule

A

> 8 mm LM, poc 7mm, LAD 6, LCX ostium 5 mm

  • all LM need IVUS.
62
Q

3 impt trials with improved outcomes with IVUS

A

Ultimate and IVUS XPL –> MACE and TLR,

also metaanalysis

63
Q
  1. Exposure equation
  2. New II form
A
  1. mA*KVP*pulse width
  2. Thin film transistor array
64
Q

mag views raditaion

A

greater

65
Q

ionizing radiation def

A

raditatoin enrought energy to eject at leat one orbiatl elevtron.

66
Q

radiation terms

  1. stochastic -
  2. nonstochastic –
  3. ALARA
  4. effectvie dose-
A
  1. stochastic - all on non effect from radiation (dna injry that leas to cancer/mutation
  2. nonstochastic –> dna injuery that lead to cell dealb
  3. ALARA
  4. effectvie dose- stochastic reisk derived from weighted sums of estimates for indivisl organs.
67
Q

exposure is measured how?

absorbed dose

equivalnt dose

effective dose

A

air erma measured in gy , 1 kg of air relaseas 1 joule of energy

amt of energy deposited in tissue gy/kg (depends on tissue gy/g)

equivalent dose- ionizing radiation cuasing varying injury depending on type ED=AD *weighting factor (siverts) –> biologic effects is seiverst

Effecitve dose - estimate of stochastic risk per obsorbed unit. Depensd on depth of beam from the the entrence point.

68
Q

sieverts

A

think of biologic as biologive effect –dna damage etc.

69
Q

direct skin eposure

A

250 cxr per minut 10 mSV per minute cine increase 10x

70
Q

osmolality

A

molecules per volume

increase osmolality increased SE

71
Q
  1. current contrast ionic or non?
  2. acute hypersensiticivty anaphylactic
  3. Arterial vs. venous
  4. shellfish
  5. people with allergies
A
  1. nonionic
  2. no anaphylactoid non-IGE
  3. venous
  4. dont pretreat. allergies to shellfish are not to iodine they are to other proteins.
  5. allergies - more liely to have reaction than non allergenic individuals
72
Q
  1. ACC recd for pretreatment
  2. Rx of anaphylaxis
  3. Rash rx
A
  1. 50 mg pred 13,7,1 hr before can also give 200 mgiv 200 2 hours before. Benadryl and other antihistamines
  2. fluids fluids fluids

epi

  1. steroids and antihistamines
73
Q
  1. delayed hypersens and cath
  2. delayed is mostly manifested as a -
  3. hyperthroidroid and contrast
A
  1. can happen its IgE mediated (up to 4%), dont forget about this bc freq blame on new drug added.
  2. rash.
  3. board question but quite rate (would have a goiter or a hx of issues.
74
Q

Nephrotox

  1. when?
  2. hydration
  3. if op when check
  4. metformin
A
  1. 48-72 hours
  2. 1.5 to 1 ml/g/hr 3-12 hours prior and 6-12 hours post.
  3. 48-72 hrs
  4. lactic acidosis, hold on day of procedure
75
Q

stochastic effects thing

A

dna damage leading to cancer and genetic risks (all or none)

76
Q

Increasing mA of xray generator

what has more xrays crani or caudal

A
  1. mA is current–> current is number of electrons, number of xrays emitted for the catholode

crani has more

77
Q

femoral instead of dual lumen

A

overshoot and delated (wave expansion. will falsly decrease gradient.

78
Q

thermodilation - bad with

co equation (simple)

how can use above for angiographic co

A
  1. TR and PR, error 5-10%,

Co = HR x SV

SV =EDV-ESV CO=HR*SV

Fick method= PV-PA O2 difference PBF = SBF

79
Q

fick eq

A

125/13.4*hb*PaO2 difference X100

80
Q

LV and Ao pressure are the same

A

acute AI

81
Q

peal tp peak for haaki for mv?

A

dont use, check mean. (doesnt work if out of nomral HR.

82
Q

question to look for after mital BAV

A

big V wave…

83
Q

shunts key

QP:Qs

A

find step up

Ao-SVC/Ao-Pa

84
Q
  1. WHO groups for PHTN
  2. defined ph based on 2018 world symposium
  3. who group 1 is only?
  4. female to male
A
  1. PAH one is primary, term is reserved for those with who group 1.
  2. LHC
  3. PH due to lung disease
  4. CTEPH
  5. multifactorial
  1. mean pa of >= 20 mmHg with a pcwp or edp <=15 and PVR >=3 woods uints.
  2. PAH or primary
  3. 2:1
85
Q

primary PAH can be cause by what

A

-most commonly Systemic sclerosis, also other collegen vac disease, 30% of sclerodema -patients have pah 3:1 female:male ratio.

86
Q
  1. cirrhosis and pah is called what and this is caused by what
  2. trick quation on RHC and Portopulmonary ph
  3. HIV related phtn is usually what?
  4. drug associated with PAH
  5. PAthologic findings of PAH this is forally called what?
  6. what does above look like on path with eosin staining
  7. exception to above is what?
A
  1. still type I and is called portopulmonary htn. this cause by pulmonary avm development
  2. They can have elevated CO raising pulmonary pressures but resulting in near normal PVRs. so need to use pvrs. (from pulm avms)
  3. type one PAH

4,. methaphetamine-–> fenflarmine to amiorex

  1. pathologic findings of pah –> hyperplasia of all the vessels in the lung. sm hyperplasion , plexogenic hyperplasia
  2. whorls of smppth muscle cells. also insitu thrombosis.
  3. SSclerodema which sohows fibrosis but no plegogeic changes.
87
Q

where is congental heart disease induced PH categorized in the who system

schistosomiasis

MC gene assocaited with PAH

Why does lung parencyhyma dz lead to pah

hat is the median survival of type I pah?

AC with group 4 PAH?

when to consider IV drugs rx for PAH?

A

1 or 4….

1

bone morphogenic progtein gene

bc it leads to HPV

7 years (this has increased sig)

life long

consider if sycnope or stage IV sx.

88
Q

what is considered an appropriate respons e to vasodilater rx on RHC for PH

A

drop of >= 10 mmHg to a mean pa <- 40 ith unchanged Or increased CO….

89
Q

PVR calc

normal\

Svr formula and nomrla

A

Mean PAP-LAP/CO*80 = take away the 80 and you have woods

20 and 130

SVR is mean Ao - RA pressure/ CO *80 ; normal is 600 to 1400

90
Q

6 min walk test associated ith class iv sx

A

less than 150 m is class IV, 150-300 is class III

91
Q

RX for primary pHNT what are the mainstays and MOA of each

common se

1/2 epo vs. trepo

A
  1. PDE-5 breakdon cGMP and improve no signalling, sildenaphil and tedalaphil are approved
  2. ricociguat is a direct cgmp agoinst is approved for pah and cteph
  3. prostanoids - epoprostinol IV or SQ, treprostinil and iloprost, oral optoions: selexipag is a prostcyclin receoptro agonsit, and trepostinil, thes acto on PDE-3 (inibiting their breakdon)
  4. endothelin receptor agonists (bosentan, amrisentan, macitentn (only macitentin is not generic)

Think vasodilator –> HA, flushing, ja pain, edema (edema most common with endothelin antagonistis), prostacyclins masseter pain and diarreha\

IV epo min, treop hrs

92
Q

ambition trial in primary ph

what is most potent

A

ambersantan (endotherlin) and tadalfil as better than either alone)

so this is the susal

prostacyclins

93
Q
A

Cath Sap 5 board prep (12 decks)

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