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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

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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)

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3
Q

what is the MOA of heparin

A

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

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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

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5
Q

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

A

Ohm’s law

Poiseuille’s law

Law of LaPlace

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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)

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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

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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

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9
Q

how do you measure RA pressure

A

central line into neck—> jugular vein to RA

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10
Q

how do you measure RV and PA pressure

A

swan ganz catheter

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11
Q

how are cardiac volumes derived?

A

echocardiographically …usually use pressure as a volume surrogate

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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)
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13
Q

define ischemia

A

inadequate blood flow

think in terms of myocardial O2 supply and demand

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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

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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)

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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

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17
Q

determinants of myocardial oxygen demand

A

HR

contractility (vigor with which is pumps)

myocardial wall stress

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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

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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

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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

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21
Q

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

A

ischemic heart disease

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22
Q

is primary prevention effective in ischemic heart disease

A

yes–delays disease in all groups

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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

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24
Q

what does the presence of angina mean?

A

angina IS ischemic pain

therefore angina means active ischemia

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25
how do patients describe angina
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
26
what specifically should you look for in a patient with angina/ischemic heart disease
xanthelasmas arcus senilis fundal exam evidence of thyroid disease volume status exam cardiac exam--EHS/murmus? nicotine stains pulse exam tendinous xanthomas
27
what is important to look for on physical exam from a surgeons standpoint when assessing a patient with ischemic heart disease
baseline neuro exam including gait and mobility examine incisional sites assess bypass conduits (i.e vascular in/sufficiency)
28
what initial treatment can you initiate almost right away in a patient with suspected ACS (in the CCU)
aspirin oxygen morphine heparin drip *talk to senior cardio before starting other antiplatelets
29
what workup should you do for suspected ACS
coags troponin ABG ECG CXR
30
give an example of a Class I indication for a CABG
Left main artery occlusion/stenosis
31
what vessels/conduits can be used for CABG
saphenous vein grafts internal mammary arteries (left most commonly) radial arteries (either..preferentially non dominant hand radial artery)
32
saphenous vein graft patency rate
60% patent at 10 years
33
internal mammary artery graft patency rate
LEFT artery--95% patent after 15 years
34
radial artery grafts patency rate
89% patent at 5 years
35
which conduit/vessel is most commonly used in CABG
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
common indications for CABG
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
what is aortic stenosis
incomplete AV opening--> fixed LV obstruction restricts blood flow out of LV
38
what causes aortic stenosis
``` 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
what is the pathophysiology of aortic stenosis
significant obstruction to LV outflow increases LV pressure increased pressure increases LV wall stress
40
how does the LV respond to a pressure overload
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
what is the natural history of AS
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
why do you want a slower HR in a stenotic lesion heart?
you want longer diastolic filling times because of diastolic dysfunction caused by less compliant LVs
43
how do we classify aortic stenosis severity
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
what is the most prevalent valvular heart disease
aortic stenosis 2% of people over age 65 have isolated calcific AS
45
how do aortic valve area, jet velocity and mean pressure gap progress generally in AS
MPG increase 7mmHg/yr JV increase 0.3 m/s/yr AVA decrease 0.1cmsquared/yr
46
what are the cardinal manifestations of aortic stenosis
Angina syncope CHF--> dyspnea**, orthopnea, PND can also present--fatigue, decreased exercise tolerance, GI bleeding (rare, advanced disease)
47
what does the onset of severe symptoms suggest in aortic stenosis
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
what is a way to remember the cardinal symptoms of aortic stenosis and their survival rates
ASD-532 angina--5 year survival syncope--3 year survival dyspnea--2 year survival
49
what might you expect to see on physical exam for a patient with aortic stenosis
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
what tests would you order to work up AS
blood work CXR ECG ECHO!! key test
51
are there medical tx for aortic stenosis
no--its a purely structural disease
52
what is the gold standard tx for aortic stenosis
surgical aortic valve replacement
53
how should you manage severe, symptomatic aortic stenosis
intervene surgically with valve replacement
54
what are the options for surgical valve replacements
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
what do you recommend for a young woman who has not had kids yet for aortic valve replacement?
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
what is mitral regurgitation
inappropriate reflux of blood through the MV apparatus retrograde systolic flow
57
what is the structure of the mitral valve
"valvar-ventricular complex" composed of left atrium, annulus, leaflets, chordae, papillary muscles, LV
58
what are the 4 types of structural changes that can cause mitral regurgitation
1. leaflet retraction 2. annular dilatation 3. chordal abnormalities 4. LV dysfunction
59
what is type I mitral regurgitation
normal leaflet motion--> cardiomyopathic process or perforation of one of the leaflets causes the mitral regurgitation
60
what is type II mitral regurgitation
leaflet prolapse, or excessive leaflet motion i.e floppy mitral valve or CAD with elongated chords or ruptured papillary muscles
61
what is type III mitral regurgitation
restricted leaflet motion in diastole or systole i.e rheumatic heart disease, cardiomyopathy
62
what is the most common cause of mitral regurgitation in the patients undergoing surgical intervention in the USA
myxomatous degeneration
63
can people tolerate acute mitral regurgitation
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
can people tolerate chronic mitral regurgitation
yes --> symptoms may not develop for years because left atrium and pulm veins can adapt but eventually LV contractility often becomes impaired
65
how do heart chambers adapt to a volume overload
volume overload--> increased diastolic stress--> increased LV volume--> in series replication of sarcomeres--> eccentric hypertrophy---> preserved radius to wall thickness ratio
66
in mitral regurgitation can you have normal indices of LV function (i.e EF/SV etc) but still have significant ventricular dysfunction?
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
what do the symptoms of mitral regurgitation reflect when they do arise?
decreased cardiac output and pulmonary congestion ``` i.e dyspnea weakness fatigue palpitations may have R sided HF symptoms-->are a late symptom ```
68
how does acute mitral regurgitation present
marked pulmonary edema, marked symptoms
69
what signs on physical exam would you expect in mitral regurgitation
S1 diminished S2 single--> widely split S3 characteristic murmur is apical holosystolic
70
list types of aortic disease
aneurysmal disease (down to abdominal aneurysm) pseudoaneurysms traumatic aortic disease/disruption
71
what are the two major classification schemes of aortic dissection
Debakey Stanford
72
define Stanford A aortic dissection
dissection involving ascendig aorta
73
define Stanford B aortic dissection
dissection that originates in the descending aorta and doesn't involve the ascending
74
pathogenesis of aortic dissection
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
risk factors for aortic dissection
HTN connective tissue disease pre-existing aneurysmal disease
76
how does aortic dissection present
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
assessment of patient with aortic dissection
head to toe exam and vitals neuro, abdo, vasc exam etc
78
diagnosis of aortic dissection
CT angio from circle of willis to femoral run off CXR, ECG, echo, routine bloods
79
treatment of aortic dissection
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)

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