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First Aid > CARDIO > Flashcards

CARDIO Flashcards

1
Q

Truncus arteriosus gives rise to

A

ASCENDING AORTA

and

Pulmonary Trunk

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2
Q

Bulbus cordis gives rise to ?

A

smooth parts (outflow tract) of Left and Right ventricles

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3
Q

Endocardial cushion

give rise to?

A

atrial septum

membranous interventricular septum

AV and Semilunar valves

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4
Q

primitive Atrium

gives rise to?

A

trabeculated part of :left and right Atria

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5
Q

primitive Ventricle

gives rise to

A

Trabeculated (muscular) part of left and right Ventricles

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6
Q

Primitive pulmonary vein gives rise to

A

smooth part of left atrium

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7
Q

LEFT horn of sinus venosus

gives rise to?

A

Coronary sinus

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8
Q

RIGHT horn of sinus venosus

A

Smooth part of rigjt atrium (sinus venarum)

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9
Q

Right Common Cardinal vein and right anterior cardinal vein

give rise to

A

superior vena cava

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10
Q

pt with down syndrone and Atrial septal defect

this is commonly due to?

A

endocardial cushion defect

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11
Q

what is responsible for development of the outflow tract formation? for example the aorticopulmonary septum

A

Neural crest and endocardial cell migrations –> truncal and blbar ridges that spiral and fuse to form aorticopulmonary septum –> ascending aorta and pulmonary trunk

note the ascending aorta will be posterior

and the pulmonary trunk will be anterior.

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12
Q

conotruncal abnormalities associated wtih failure of neural crests cells to migrate (problem w/ developing spiral septum) ?

A

transposition of great vessels (RV –> aorta, LV –> PA)

tetraology of fallot

Persistent truncus arteriosus ( = partial spiral development)

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13
Q

mitral/tricupsid valves are derived from

A

fused endocardial cushions of the AV canal

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14
Q

what virus is associated with a continous machine-like murmur (during diastole and systole)

whats the mechanism of the virus?

treatment MOA?

A

Congenital Rubella

the virus infects smooth muscle cells that are needed for contraction of teh patent ductus arteriosus

Indomethacin: inhibits the formation of PGE2, via COX1 and 2 inibition.

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15
Q

what forms the mediaN umbilical ligament?

A

​AllaNtois –> Urachus

the urachus is part of allantoic duct bw bladder and umbilicus.

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16
Q

the L recurrent laryngeal n. passes udner the ligamentum arteriosum which is a derivative of?

A

ductus arteriosus

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17
Q

what forms the MediaL umbilical ligament?um

A

umbiLical arteries

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18
Q

if given an MRI of a spin with an acute disc herniation, and you see a torn anulus fibrosus allowing the nucleus pulposes to herniate. what did the nucleus pulposes derive from?

A

Notocord.

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19
Q

occlusion of the RCA can lead to?

A

Nodal dysfunction –> bradycardia or heart block, fatal arrthymias

bc the RCA supplies the SA and AV nodes

20
Q

pt has RCA infarct or Posterior descending A occlusion –> posteromedial papillary muscle rupture –> ?

A

new onset mitral regurgitation

21
Q

54 yo F presents with Hoarsenss and dysphagia, hx of RHD whats the cause of the hoarseness and dysphagia?

A

RHD –> Mitral valve stenosis –> inc in LA size –> compression of esophagus (dysphagia) and compressed left recurrent laryngeal nerve (hoarsenss) which innvervates the intrinsic muscles of the larynx.

22
Q

describe the antaomy position in terms of the aorta and esophagus and the laryngeal nerve position.

A

left atrium sits directly infront of esophagus

left recurrent laryngeal nere loops under the ligamentum arteriosum.

23
Q

normal splitting of A2 P2 is caused by?

A

during inspiration –> inc in intrathoracic volume –> drop (-) intrathoracic pressure –> inc venous return –> inc RV filling (inc EDV) —> inc RV stroke volume –> inc RV ejeciton time –> delayed closure of pulmonic valve

24
Q

Wide splitting is caused by

A

conditions that delay RV emptying (pulmonic stenosis, RBBB), anything that caused delayed contraction of RV

25
Q

what is the most common cause of splitting that doesnt change regardless if your in expiration or inspiration.

A

ASD

ASD–> left -to - Right shunt –> Inc RA and RV volumes –> inc flow through pulmonic valve.

26
Q

what is it called when listening to the heart you hear splitting of P2 and A2 on expiration but not on inspisiration

A

paradoxical splitting

this is caused by delay in aortic valve closure.

the reason why its eliminated during inspiration is that you still get your delayed closure of P2 during inspiration moving it close to A2 sound.

27
Q

what are two caused of Paradoxical splitting

A

aortic stenosis

LBBB

anything that delays aortic valve closure.

28
Q

rapid squatting causes inc or dec in

Venous return

preload

afterload

A

Inc venous return (bc squatting the muscels of lower extremities are compressing the vein inc VR)

inc preload (same as VR)

inc afterload (compressing the arteries in lower limbs inc afterload

29
Q

rapid squatting increases what murmurs

A

inc AS, MR, and VSD murmurs

DEC: hypertrophic cardiomyopathy murmur

30
Q

if someone is rapidly squatting when will you hear the clickl in MVP

A

Later onset of click/murmur

31
Q

handgrip causes and inc in afterload

what murmurs will be increased vs dec

A

increased: MR, AR, VSD
dec: hypertophic cardiomyopathy, AS murmurs

MVP LATER onset of click

32
Q

valsalva (phase II) standing up leads to a decrease in preload.

via inc in intrathoracic pressure –> dec venous return –> dec preload.

what murmurs will be inc and dec?

A

ALL MURMURS WILL BE DECREASED except

HYPERTROPHIC CARDIOMYOPATHY murmur increased

MVP will have an EARILER onset click **** ( Uworld)

33
Q

in a Pacemaker AP (SA and AV nodes) what is phase 0 (upstroke) caused by

in contrast to ventricular Myocardial AP occuring in myocytes, bundle his and Purkinje fibers?

A

Ca influx (opening of voltage gated Ca2+ channels) causes the phase 0 upstroke. and the fast voltage gated NA channels are permanently inactivated bc of thee less negative resting potential of these cells.

in contrast to the fast voltage gated NA channels in phase 0 of Ventricular AP

34
Q

the upstroke caused by influx of CA2+ allows for in pacemaker cells?

A

slow conduction velocity that is used by the AV node to prolong transmission from the atria to ventricles.

35
Q

phase 1 and 2 of AP is absent in?

A

Pacemaker AP

36
Q

what phase accounts for the automaticity of SA and AV nodes.?

A

phase 4 = slow spontaneous diastolic depolarizatiion due to If (“funny current”)

If channels responsible for a slow mixed NA/K inward current.

37
Q

abnormal fast accessory conduction pathway from atria –> ventricle (bundle of Kent) bypasses the rate slowing AV node –> ventricles begin to partially depolarize.

most cocmmon type of ventricular pre excitation syndrome.

Diagnosis

A

WPW

38
Q

Delta wave with widen QRS complex. and shortened PR interval

on ECG.

this may result in?

A

re-entry circuit –> supraventricular tachycardia

tx with procainamide or amiodarone

not adenosine

WPW

39
Q

name some of the drugs that cause long QT (ABCDE)

A

AntiArrhythmics (class IA, III)

AntiBiotics (marcorlides)

anti Cychotics (haloperidol), risperidone

antiDepressants (TCAs)

AntiiEmetics (ondansetron)

40
Q

what Congenital long QT syndrome

is autosomal Dominant

pure cardiac phenotype (only K channels in heart effected)

.NO deafness

A

Romano-Ward syndrome

41
Q

what congenitial Long QT syndrome (disorder of myocardial repolarization)

is autosomal Recessive

Cardiac K+ channels + sensorineural deafness

A

Jervell and Lange- Nielsen syndrome

42
Q

NA channel abnormality inherited in Asians (usually MALES)

ECG: pseduo-RBBB (QRS widen), ST elevations V1-V3

inc risk for sudden ventricular tachyarrrhythmias and SCD.

what is this syndrome and what parts of the -cardium does it effect?

A

Brugada syndrome

dec NA influx in Epicardium and Endocardium.

43
Q

Asian decent with Pseudo RBBB and ST elevations iin V1-V3. what is the tx

A

Implantable cardioverter-defibrillator (ICD)

44
Q

In stable angina what is your classic ECG findings

A

ST DEPRESSION

it resolves with rest, or nitroglycerin

45
Q

pt is triggered by smoking, triptans, coccaine

occurs at rest

ECG: TRANSIENT ST ELEVATIONS.

what would you tx with and whats the diagnosis?

A

variant (prinzmetal) angina

tx: Ca channel blockers, nitrates, and smoking cessation

46
Q

what is unstable angina due to?

A

unstable atherosclerotic plaque thats gonna rupture.

leads to thrombosis w/ incomplete coronary artery occlusion

47
Q

what are the classic ECG and BIomarkers for unstable angina

A

+/- ST depresions, and or T-wave inversion

biomarkers: no cardiac biomarker elevation (unlike NSTEM)

pt will complain of inc frequency, duration, or intensity of chest pain, or chest pain at rest.

First Aid (15 decks)

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