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Flashcards in Cardio exam 5 Deck (76)
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1
Q

4 determinants of cardiac fxn

A

contractility
preload
afterload
HR

2
Q

Relationship b/t PCWP and PADP

A

PADP 1-4mmHg greater than PCWP

higher in pulmonary disease

3
Q

Test to determine b/t systolic and diastolic HF

A

echo

4
Q

Hypertrophy type and cause

A

concentric from pressure overload

eccentric from volume overload

5
Q

Division b/t nonprogressive and progressive shock pressure

A

45mmHg systolic

6
Q

Tx for anaphylatic/neurogenic shock

A

sympathomimetics

7
Q

Impact of increased preload on pressure cycle of heart

A

increased LVEDV

slight increase in afterload

8
Q

Impact of contractility on pressure cycle of heart

A

increased max LV pressure and stroke volume
no change in LVEDP
decreased LV end systolic volume

9
Q

Chronic HF treatment focus

A

neurohormonal modulation

10
Q

Side effects of diuretics with HF

A
overdiuresis
electrolyte imbalances (K+ and Mg2+)
11
Q

1st line tx for systolic HF

A

ACE-I’s

12
Q

3 drugs decreasing mortality with systolic HF

A

beta blockers
ACE-I’s
spironolactone

13
Q

Ejection fraction eqn

A

EDV-ESV/EDV

14
Q

CO and TPR relationship

A

CO=arterial BP/TPR

15
Q

Exercise and neurohormonal control

A

skeletal m. vasodilation causes decreased TPR
sympathetics cause increased HR, contractility and venoconstriction
increases arterial BP, increasing flow to muscle

16
Q

Intrapleural pressure and RA pressure relation with CO

A

breathing decreases intrapleural pressure, increasing RA pressure
cardiac output increases with more negative intrapleural pressure (due to increased RA pressure)

17
Q

Sympathetics role in shock

A

maintains normal BP/cardiac compensation
except in brain and heart (local mediators)
overwhelmed in shock and cannot compensate enough

18
Q

Cellular effects of progressive shock

A

lysosomal enzyme release
decrease in high energy phosphates (irreversible)
acidosis

19
Q

Cause of neurogenic shock

A

rapid loss of vasomotor tone

drops VR and CO

20
Q

Cause of anaphlyatic shock

A

Ab-Ag response via mass histamine release

causes massive vasodilation

21
Q

Difference b/t severe sepsis and septic shock

A

severe sepsis can be corrected by fluids

22
Q

Most common cause of septic shock with burn victims

A

Pseudomonas

23
Q

Bugs with early onset neonatal sepsis

A

Group B strep
E. coli
H. flu
Listeria

24
Q

Bugs with late onset neonatal sepsis

A

S. epidermidis
N. meningitidis
H. flu

25
Q

High and low pathogenic gram + bugs with sepsis

A

S. aureus/S. pneuno high

S. epidermidis/E. faecalis low

26
Q

Virulence factors for sepsis

A

gram (-) have LPS

gram (+) have peptidoglycan/teichoic acid/superantigens

27
Q

Peptidoglycan virulence with sepsis

A

activates defense pathways

28
Q

Superantigen virulence with sepsis

A

activates T cells nonspecifically (without Ag) by binding outside of HCM II and T cell receptor
examples: TSS1 and SPE

29
Q

LPS virulence with sepsis

A

cleaves C3 to C3b, causing C5 to be cleaved into C5a which attracts neutrophils
also lipid A is toxic, causing cytokines/coagulation

30
Q

Sepsis bug with increased risk with Sickle Cell

A

salmonella

31
Q

Pyogenic IL’s

A

IL1
IL6
TNF-alpha

32
Q

Chemoattractant molecules

A

IL8

C5a

33
Q

Breakdown of dorsal mesentery of heart

A

transverse pericardial sinus

34
Q

Endocardial cushion origin

A

in bulbus/truncus is neural crest

b/t A and V not neural crest

35
Q

Tetralogy of Fallot

A

Pulmonary obstruction
RVH
Overriding aorta
VSD

36
Q

Aortic arches and what they become

A
I-maxillary a.
II-hyoid/stapedial a.
III-internal and common carotid
IV-R subclavian and aortic arch
VI-R pulmonary a. and L pulmonary a./ducts arteriosus
37
Q

Veins obliterated with great venous shift

A

R umbilical

L cardinal/vitelline

38
Q

What does supracardinal v. become

A

azygos system

39
Q

What is Eisenmerger syndrome?

A

R to L shunt caused by a L to R shunt

irreversible pulmonary HTN

40
Q

Secundum ASD

A

asymptomatic till 30’s
RV volume overload/R axis deviation
RVH and failure eventually

41
Q

Sinus venosus ASD

A

R pulmonary v. connected to R atrium

42
Q

Assc of endocardial cushion defect

A

Trisomy 21

43
Q

Patent ductus arteriosus meds

A

NSAIDs close it

PGE2 keeps it open

44
Q

Assc with coarctation of aorta (8)

A
bicuspid aortic valve
Turner's syndrome
Berry aneuryms
ascending aortic aneurym
bacterial endocarditis
PDA
VSD
45
Q

Mitral valve abnormalities presenting as mitral stenosis

A

doulbe orifice MV
parachute MV
accessory MV

46
Q

What is Ebstein’s anomaly?

A

part of triscupid valve in apical RV

causes tricuspid regurg

47
Q

What is a Blalok-Taussig shunt and use?

A

subclavian v. to pulmonary artery connection

for tetralogy of fallot

48
Q

Goals of Tetralogy of Fallot surgery

A

remove pulmonary obstruction
closure of VSD/shunts
competent pulmonic valve

49
Q

Necessity for life with tricuspid atresia

A

patent ductus arteriosus

ASD

50
Q

What is a Fontan repair?

A

vena cava to pulmonary artery connection

to bypass R side of heart

51
Q

Conditions you see paradoxical emobli

A

R to L shunts

52
Q

5 R to L shunts

A
TOF
transposition of great arteries
patent truncus arteriosus
tricuspid atresia
TAPVC
53
Q

Pressures in TOF

A

R side greater than L side

54
Q

What sx do you see with R to L shunts?

A

cyanosis

55
Q

What is always present in total anomalous pulmonary venous connection?

A

ASD or patent foramen ovale

56
Q

L to R shunts (4)

A

ASD
VSD
PDA
AV defect

57
Q

VSD assc’s

A

Tetralogy of Fallot

Trisomy 21

58
Q

AV septal defect and assc

A

malformation of tricuspid and mitral valves

Down syndrome

59
Q

What are Quilty lesions seen with?

A

Cardiac transplant
overlies myocardium
mostly T cells

60
Q

Problem with long term cardiac transplant

A

stenosing intimal proliferation of coronary arteries

silent MI’s

61
Q

Post op problems with cardiac transplant

A

infection/malignancy

EBV assc with B cell lymphoma

62
Q

What are heart failure cells?

A

hemosiderin deposition in macrophages

due to congested capillaries leaking into alveolar spaces

63
Q

Impact of placenta removal from fetal circulation

A

increased resistance in umbilical vein

flow stops in umbilical vein and arterty

64
Q

Impact of first breath on neonatal circulation

A

decreased resistance of lungs
closure of foramen ovale
ductus arteriosus close with oxygen exposure

65
Q

Timeframe of closure/stopped flow in fetal circulation loops

A

umbilical v./ductus venosus-days
foramen ovale-minutes
ductus arteriosus/umbilical a.-hours

66
Q

Pathologies increasing cardiac output

A

Beri beri
AV shunts
hyperthyroidism
anemia

67
Q

Pathologies decreasing cardiac output

A

MI
shock
severe valve disease

68
Q

1st degree heart block

A

fixed PR interval greater than 200ms

69
Q

2nd degree type 1 heart block

A

lengthening PR interval with a dropped QRS

70
Q

2nd degree type 2 heart block

A

fixed PR interval with more P than QRS

71
Q

R bundle branch block

A

lead V1 has slurred S and wide QRS
lead I has wide QRS
both deflected up

72
Q

L bundle branch block

A

lead V1 is downwardly deflected and wide QRS

lead I has wide QRS

73
Q

LVH on EKG

A

V1/V2 down + V5/V6 up is over 35mm

deep S wave on V1

74
Q

RVH on EKG

A

R axis deviation
R/S over 1 on V1
deep S wave on V6

75
Q

R atrial abnormality

A

V1 P wave over 1.5mm OR

II P wave over 2.5mm

76
Q

L atrial abnormality

A

V1 P wave over 1mm deep and wide OR

II P wave longer than 120ms