Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Surgery > Cardiovascular Surgery Lecture > Flashcards

Cardiovascular Surgery Lecture Flashcards

1
Q

what is the purpose of the CPB machine?

A

to replace the heart and lungs during surgery so you can turn the heart and lungs “off” during surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

why is there risk of thrombosis with CPB and how do you deal with this

A

because blood exposed to foreign surfaces (ie plastic) and to liquid-air interfaces, is prone to clotting

therefore must use heparin to conduct CPB (doses up to 30 000 IV before CPB and measure activated clotting time to make sure its thin enough)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is the MOA of heparin

A

binds to antithrombin III allosterically to increase its activity by about 1000x (therefore thins blood)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

how do you reverse heparin after cardiac sx

A

administer antidote which is protamine sulfate (dosed 1:1)

forms salt pair and cleared renally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are the names of the three “laws” of cardiac surgery

A

Ohm’s law

Poiseuille’s law

Law of LaPlace

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is Ohm’s law

A

I equals V/R -or- V equals IxR

describes current flow between two points in a conducting circuit

in CV system…
V is pressure differential between two points in a circuit

I is flow between two points

R is resistance to flow (i.e systemic or pulmonary vasc resistance)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is poiseuilles law

A

flow through a tube is proportional to the pressure drop across the tube and inversely proportional to the resistance

Q equals (P2-P1)/R

also….
R equlas (8nl)/pie x r^4
R is directly proportional to the length and resistance of the tube and inversely proportional to the radius ^4
(therefore small change in radius has big change in resistance)

thus….
Flow (Q) equals (P2-P1)pie x r^4/8nl

therefore, radius reduction decreases flow by ALOT comparatively so pressure needs to go up

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is Law of LaPlace

A

wall stress (T) equals (cavity pressure)x(radius) /2(wall thickness)

helps explain why a ventricle changes in response to pressure and volume loads and aneurysmal dilatation and risk of rupture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how do you measure RA pressure

A

central line into neck—> jugular vein to RA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how do you measure RV and PA pressure

A

swan ganz catheter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how are cardiac volumes derived?

A

echocardiographically …usually use pressure as a volume surrogate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how do you assess cardiac function?

A
  1. ejection fraction (most common way of assessing ventricular fxn)
  2. cardiac output (stroke volume x HR)
  3. Guyton curves (describe a given hearts performance under various filling conditions)
  4. pressure volume loops with preload occlusion (best assessment of cardiac function but most often performed in lab setting)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

define ischemia

A

inadequate blood flow

think in terms of myocardial O2 supply and demand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

define hypoxia

A

low tension of O2 in the blood

in and of itself, does not necessarily result in ischemia

–> ischemia reduces oxygen delivery to cells because reduces blood flow–thus by definition, ischemia causes cellular hypoxia but reverse is not true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

which is worse, hypoxia or ischemia?

A

ischemia–because reduced blood flow causes anaerobic byproducts to not be washed out and impair metabolism

(hypoxia still has normal blood flow and washout, though may get local injury due to low O2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

determinants of myocardial oxygen supply

A

blood flow and oxygen content

oxygen content is determined by hemoglobin and tension of O2 in blood

requires functional lung units, adequate blood oxygen tension and functional Hb molecules at adequate levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

determinants of myocardial oxygen demand

A

HR

contractility (vigor with which is pumps)

myocardial wall stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what causes cardiac ischemia

A

coronary causes–
most common–> thrombosis superimposed on atherosclerotic CAD

embolism
spasm
dissection
ostial narrowing due to aortitis

also…
HOCM
AS
AI

these two normally wouldnt cause demand ischemia in a normal heart but can in a heart that already has disease
anemia
hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how do the following average diameter losses translate to cross sectional area losses

A

33% diameter–> 50% cross sectional area

50% diameter–> 75% cross sectional area…at this or above, SIGNIFICANT
–in case of the left main coronary artery (before splits into LAD and circumflex) 50% is significant because occlusion here really fucks the heart

67% diameter–> 90% cross sectional area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what amount of stenosis is significant in the left main coronary artery?

A

50%–supplies so much heart that we tolerate less stenosis in it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what condition causes more death, disability and economic cost than any other illness in the world?

A

ischemic heart disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

is primary prevention effective in ischemic heart disease

A

yes–delays disease in all groups

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

risk factors for ischemic heart disease

A 
HTN
DM
dyslipidemia (high LDL, low HDL)
smoking
family history

plus…
coexisting vascular disease
previous strokes/TIAs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what does the presence of angina mean?

A

angina IS ischemic pain

therefore angina means active ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

how do patients describe angina

A

OPQRST

central retrosternal or epigastric heaviness, squeezing or smothering pain

often radiates to left shoulder, arm, neck, jaw

can be variable presentations

*atypical–can present with dyspnea alone–atypical is more common in diabetics and elderly women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what specifically should you look for in a patient with angina/ischemic heart disease

A

xanthelasmas
arcus senilis
fundal exam
evidence of thyroid disease

volume status exam

cardiac exam–EHS/murmus?

nicotine stains
pulse exam
tendinous xanthomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is important to look for on physical exam from a surgeons standpoint when assessing a patient with ischemic heart disease

A

baseline neuro exam including gait and mobility

examine incisional sites

assess bypass conduits (i.e vascular in/sufficiency)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what initial treatment can you initiate almost right away in a patient with suspected ACS (in the CCU)

A

aspirin
oxygen
morphine
heparin drip

*talk to senior cardio before starting other antiplatelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what workup should you do for suspected ACS

A

coags
troponin
ABG

ECG
CXR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

give an example of a Class I indication for a CABG

A

Left main artery occlusion/stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what vessels/conduits can be used for CABG

A

saphenous vein grafts

internal mammary arteries (left most commonly)

radial arteries (either..preferentially non dominant hand radial artery)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

saphenous vein graft patency rate

A

60% patent at 10 years

33
Q

internal mammary artery graft patency rate

A

LEFT artery–95% patent after 15 years

34
Q

radial artery grafts patency rate

A

89% patent at 5 years

35
Q

which conduit/vessel is most commonly used in CABG

A

left internal mammary–reduced symptoms of ischemic heart disease and also improves survival

*left internal mammary to LAD is one of most significant grafts

36
Q

common indications for CABG

A
  1. left main stenosis above 50%–class I indication
  2. 3 system disease–class I indication (i.e all 3 coronary artery territories)
  3. 2 system disease with important proximal stenosis (i.e LAD)–class I indication
37
Q

what is aortic stenosis

A

incomplete AV opening–> fixed LV obstruction

restricts blood flow out of LV

38
Q

what causes aortic stenosis

A 
congenital--
unicuspid
bicuspid
quadracuspid
sub/supravalvular AS

acquired–
degenerative/calcific AS**most common cause
rheumatic AS(uncommon in western countries…rarely presents in isolation)

39
Q

what is the pathophysiology of aortic stenosis

A

significant obstruction to LV outflow increases LV pressure

increased pressure increases LV wall stress

40
Q

how does the LV respond to a pressure overload

A

pressure overload–> increases systolic stress–> wall thickening (replicates sarcomeres in parallel)–> CONCENTRIC hypertrophy (helps to reduce wall stress)… this leads to a decreased radius to wall thickness ration–thicker wall for the same radius

41
Q

what is the natural history of AS

A

concentric hypertrophy–> less compliant LV–> diastolic dysfunction–> increased end diastolic pressure impairs maximal coronary flow

this causes–>
slower rhythm
poorly tolerated Afib
increased myocardial oxygen demand and impaired oxygen supply (thus angina with activity)

42
Q

why do you want a slower HR in a stenotic lesion heart?

A

you want longer diastolic filling times because of diastolic dysfunction caused by less compliant LVs

43
Q

how do we classify aortic stenosis severity

A
  1. the difference between the peak LV pressure and the peak aortic pressure
    - -> “peak to peak gradient”
    - -> measure by catheter
    - -> one of the best ways to measure severity of aortic stenosis
  2. aortic valve area on echo
    - -> severe AS aortic valve area of less than 1cm square, mean gradient over 40 mmHg and jet velocity above 4 m/s
44
Q

what is the most prevalent valvular heart disease

A

aortic stenosis

2% of people over age 65 have isolated calcific AS

45
Q

how do aortic valve area, jet velocity and mean pressure gap progress generally in AS

A

MPG increase 7mmHg/yr

JV increase 0.3 m/s/yr

AVA decrease 0.1cmsquared/yr

46
Q

what are the cardinal manifestations of aortic stenosis

A

Angina

syncope

CHF–> dyspnea**, orthopnea, PND

can also present–fatigue, decreased exercise tolerance, GI bleeding (rare, advanced disease)

47
Q

what does the onset of severe symptoms suggest in aortic stenosis

A

that death will be soon–> there is a latent period that lasts a while during which there is increasing obstruction, myocardial overload etc…

once severe symptoms start, its near the end of life

  • anginal presentation–> average survival of 5 years
  • syncope presentation–> 3 years
  • dyspnea–> 2 years
48
Q

what is a way to remember the cardinal symptoms of aortic stenosis and their survival rates

A

ASD-532

angina–5 year survival

syncope–3 year survival

dyspnea–2 year survival

49
Q

what might you expect to see on physical exam for a patient with aortic stenosis

A
  1. JVP/CVP–> prominent a wave
  2. carotid “bruits”
  3. carotid pulse–small volume, delayed systolic peak (pulses parvus et tardus)
  4. systolic crescendo decrescendo murmur at RUSB
  5. delayed S2, single or paradoxic split S2
50
Q

what tests would you order to work up AS

A

blood work

CXR

ECG

ECHO!! key test

51
Q

are there medical tx for aortic stenosis

A

no–its a purely structural disease

52
Q

what is the gold standard tx for aortic stenosis

A

surgical aortic valve replacement

53
Q

how should you manage severe, symptomatic aortic stenosis

A

intervene surgically with valve replacement

54
Q

what are the options for surgical valve replacements

A
  1. mechanical
    –advantage–> good long term durability
    BUT increased risk of thrombosis and must be lifelong anticoagulated with warfarn
  2. bio-prosthetic valves
    - -less durable especially in younger patients but have lower thromboembolic risk so only need ASA

*generally recommend biological valves for over age 65 and younger than that we discuss risk factors etc

55
Q

what do you recommend for a young woman who has not had kids yet for aortic valve replacement?

A

bioprosthetic

because warfarin is teratogenic

(but will require re-operation at some point in time because the valve will be put under lots of stress)

56
Q

what is mitral regurgitation

A

inappropriate reflux of blood through the MV apparatus

retrograde systolic flow

57
Q

what is the structure of the mitral valve

A

“valvar-ventricular complex”

composed of left atrium, annulus, leaflets, chordae, papillary muscles, LV

58
Q

what are the 4 types of structural changes that can cause mitral regurgitation

A
  1. leaflet retraction
  2. annular dilatation
  3. chordal abnormalities
  4. LV dysfunction
59
Q

what is type I mitral regurgitation

A

normal leaflet motion–> cardiomyopathic process or perforation of one of the leaflets causes the mitral regurgitation

60
Q

what is type II mitral regurgitation

A

leaflet prolapse, or excessive leaflet motion

i.e floppy mitral valve or CAD with elongated chords or ruptured papillary muscles

61
Q

what is type III mitral regurgitation

A

restricted leaflet motion in diastole or systole

i.e rheumatic heart disease, cardiomyopathy

62
Q

what is the most common cause of mitral regurgitation in the patients undergoing surgical intervention in the USA

A

myxomatous degeneration

63
Q

can people tolerate acute mitral regurgitation

A

no it is poorly tolerated… normal LA that has not had time to adapt (low compliance)–> reflux of blood means higher LA pressures so higher pulmonary veins pressures –> transudates

leads to PULMONARY EDEMA

64
Q

can people tolerate chronic mitral regurgitation

A

yes –> symptoms may not develop for years because left atrium and pulm veins can adapt

but eventually LV contractility often becomes impaired

65
Q

how do heart chambers adapt to a volume overload

A

volume overload–> increased diastolic stress–> increased LV volume–> in series replication of sarcomeres–> eccentric hypertrophy—> preserved radius to wall thickness ratio

66
Q

in mitral regurgitation can you have normal indices of LV function (i.e EF/SV etc) but still have significant ventricular dysfunction?

A

yes

because in mitral regurgitation blood flow out of ventricle now has two paths to follow–> thus overall the LV sees less impedance to blood flow so may still get reasonably good end systolic volume/good stroke volumes

67
Q

what do the symptoms of mitral regurgitation reflect when they do arise?

A

decreased cardiac output and pulmonary congestion

i.e 
dyspnea
weakness
fatigue
palpitations
may have R sided HF symptoms-->are a late symptom
68
Q

how does acute mitral regurgitation present

A

marked pulmonary edema, marked symptoms

69
Q

what signs on physical exam would you expect in mitral regurgitation

A

S1 diminished

S2 single–> widely split

S3

characteristic murmur is apical holosystolic

70
Q

list types of aortic disease

A

aneurysmal disease (down to abdominal aneurysm)

pseudoaneurysms

traumatic aortic disease/disruption

71
Q

what are the two major classification schemes of aortic dissection

A

Debakey

Stanford

72
Q

define Stanford A aortic dissection

A

dissection involving ascendig aorta

73
Q

define Stanford B aortic dissection

A

dissection that originates in the descending aorta and doesn’t involve the ascending

74
Q

pathogenesis of aortic dissection

A

often a primary tear can be identified–>aortic flow creates a cleavage plane within the MEDIA

end result is a true lumen and a false lumen

75
Q

risk factors for aortic dissection

A

HTN

connective tissue disease

pre-existing aneurysmal disease

76
Q

how does aortic dissection present

A

about 40% die immediately
–> type A, 50% die within 48 hours if untreated

1/3 of patients are thought to have another diagnosis

  • *severe, unrelenting chest pain**–> usually mid sternal for ascending and mid scapular in the back for descending
  • -ripping/tearing pain
  • -pain usually constant and greatest at onset
  • -nitro provides no relief

can also have symptoms of consequences of the dissection like poor downstream perfusion

77
Q

assessment of patient with aortic dissection

A

head to toe exam and vitals

neuro, abdo, vasc exam etc

78
Q

diagnosis of aortic dissection

A

CT angio from circle of willis to femoral run off

CXR, ECG, echo, routine bloods

79
Q

treatment of aortic dissection

A

early treatment goal is to lower BP if hypertensive and reduce wall stress and shear stress in the aorta
–> beta blocker with short half life would be good

surgical–>
Type A is surgical repair
surgery not indicated for Type B unless presentation is complicated (i.e malperfusion)

Surgery (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions