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1
Q

In pt with suspected Stemi, what is initial treatment

A

Cath lab, percutaneous intervention…angioplasty vs stent

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2
Q

Mitral stenosis physiologic needs

A

Slow heart rate. Preload.

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3
Q

Is the PAP in mitral stenosis falsely estimating the left ventricle end diastolic pressure to high or too low

A

Falsely estimates it too hi. Real value is lower

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4
Q

Mitral stenosis vasopressor.

A

Phenylephrine

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5
Q

how long does ck and ckmb last in a MI patient

A

2 days

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6
Q

how long does troponin last in a MI patient

A

10 days

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7
Q

what is pulsus paradoxus

A

an exaggerated decrease in sbp on inspiration

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8
Q

what cardiac conditions cause pulsus paradox

A

tamponade, constrictive pericarditis, heart failure

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9
Q

what lung problems can cause pulsus paradox

A

emphysema, asthma, pneumothorax

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10
Q

what misc caues for pulsus paradox

A

obesity, PE

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11
Q

does pna cause pulsus

A

no

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12
Q

what is associated with arterial line occlusion

A

prolong line, non teflon, size of radial arter, ratio of cath to radial artery, increased attempts, hematoma formation

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13
Q

when is an radial artery considered a thromboocclusion

A

it is considered time after the cath has been removed and a thrombus forms

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14
Q

what is the time frame for thromboocclusion of radial artery s/p cath

A

occurs within 48 hours after decannulation

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15
Q

does transfixtion aka through and through methoid increase arterial aa occlusion

A

no

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16
Q

when has heparinization of cathethers been proven useful to prevent thromboocclusion of radial aa

A

it is beneficial in arterial lines kept in longer than 24 hours

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17
Q

following cardiothoracic surgery, how many patients develop afib

A

30 to 60%

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18
Q

what are electrolyte causes for afib in ct surg patients

A

hypokalemia and hypomag

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19
Q

besided elelctrolyte abnorm, what other risk factors for afib s/p ct surg

A

male, age above 60, preop tachycardia, reduced post op card output, post op increase in b naturetic peptide

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20
Q

What is the ACC and AHA recommened about pt who just got drug-eluting stents

A

wait for 1 year after placement for elective surgeries

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21
Q

how much risk reduction do we see with delaying elective surgerys s/p placement of drug eluting stents

A

50% reduction…from 6.4 to 3.3% of cardiac injury

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22
Q

what is the risk of having surgery after having a stent placed

A

the antithrombotic will be stopped and pt is at increased risk of thrombosing the stent

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23
Q

what is the moa of rethrombosing the stent

A

lack of time for re-endothilization, procoagulant state induced by stress of surgery, rebound of procoagulant state after stopping dual antithrombotic drugs

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24
Q

what drugs are used in dual antiplatelet therapy for stented patients

A

aspirin and clopidogrel

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25
Q

how long should dual antiplatelet therapy be used for metal stents

A

1 month

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26
Q

how long should dual antiplatelet therapy be used for drug-eluting stents

A

12 months

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27
Q

what if the surgery is an emergency and pt has a stent…what should be done to the antiplatlete drugs

A

continuation of asa and stop the clopidogrel

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28
Q

what if the surgery is urgent…how should the antiplatelet drugs be dealt with

A

continue of asa and stop the clopidogrel 5 days prior to surgery

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29
Q

in mitral prolapse, what can help you see if a normal ef is really normal

A

a decrease in cardiac output can tell you how severe the regurge is

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30
Q

is tachy or brady bad for mitral regurge

A

brady is bad because the heart spends more time in systole

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31
Q

what is the managment goal of mitral regurge

A

decrease svr, increase heart rate

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32
Q

what virus are tested in donated blood

A

hiv1 hiv 2 human tcell lymphocyte virus 1 and 2, westnile virus, hep b and c, syphillus

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33
Q

is cmv tested for in donated blood

A

no

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34
Q

what is the first line of screening of blood for infectious agents

A

pre donation period…by a questionaire…eliminates 90% of infected donnors

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35
Q

why do we not screen for cmv

A

50-80% adults carry cmv..sero conversion for cmv is 0.33% if infected w/ blood transfusion

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36
Q

which pt must require cmv screening of blood before transfusion

A

immunocomp, neonates and pregnant pt because of serious cmv mannifestation if infected

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37
Q

what is hcm

A

hypertrophich cardiomyopathy

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38
Q

should you use nitroglycerine on hcm

A

no, it vasodilates and decreases svr..drecreasing preload…causing lvot obstruction

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39
Q

should you use ephedrine in hcm

A

no, it increases svr and preload, but acutally also increases contractility and my worsen lvot obsruction

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40
Q

what is milrinone

A

phosphodiesterase III inhibitor

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41
Q

how does milrinone work

A

it increases contractility and decrease svr

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42
Q

would you use milrinone in hcm

A

no,

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43
Q

what is a good drug to tx hcm assoc hypotension

A

betablock

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44
Q

what is hcm aka

A

idiopathic hypertrophic subaortic stenosis, assymetrical septal hypertrophy and hcom,

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45
Q

how does hcm cause lvot obstruction

A

it is the anterior leaflet of the mitral tha comes into contact with the anterior segment of the left ventricle to cause obstruction

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46
Q

how to treat hcm

A

volume and increse svr w phenylephrine and betablockade

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47
Q

what are signs of arterial cannula induced dissection

A

high inflow arterial cath pressures, minimal

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48
Q

during a dissection 2ndry to cannula, how should bp be maintained?

A

lowest viable map should be done to prevent further dissection

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49
Q

what should be done after dissection is diagnosed

A

a distal cannulation should be done, usually at the femoral artery

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50
Q

after femoral cannulation is done, what is done next

A

systemic hypothermia and circulatory arrest and repair of the aortic dissection

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51
Q

xxxxxxxxxxxxxxxxxxxxxxxxxx

A

xxxxxxxxxxxxxxxxxxxxxxxxxx

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52
Q

what are the classifications for aortic dissection

A

stanford and debakey

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53
Q

what is the debakey classification of aortic dissection

A

I, II, IIIA, IIIB

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54
Q

what is debakey I aortic dissection

A

totall involvement of aorta

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55
Q

what is debakey II aortic dissection

A

ascending aorta involvement

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56
Q

what is debakey IIIA aortic dissection

A

originating at descending aorta, extends to diaphram or extends to arch of aorta

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57
Q

what is debakey IIIB aortic dissection

A

originating at descending aorta, extends past diaphram or extends to arch of aorta

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58
Q

how is the stanford classification of aortic dissection

A

type a and b

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59
Q

what is standford type a disscetion of aorta

A

involvement of aortic arch

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60
Q

what is standord type b dissection of aorta

A

confined to the descend aorta, not passing left subclavian

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61
Q

what is a common pathology of stanford type a

A

percardial effusion

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62
Q

does the pericardial effusion of stanford type a cause tamponade

A

not always lead to tamponade, effusion is more common

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63
Q

can you treat the pericardial effusion of stanford type a dissection with a pericardial centesis

A

no, not advised…because it will promot a pressure gradient…less in the pericardial space that may allow dissection to extend down further into the aortic root

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64
Q

what is the mainstay treatment for hcm in pregnant patients

A

metoprolol

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65
Q

are there risk with using beta blocker in hcm pregos?

A

there are concerns for IUGR and fetal bradycardia, however risk is low compared to benefit of controling maternal hcm

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66
Q

what is the goal for hcm treatment of pregos

A

prevent aortocaval compression, slow sinus hr, volume, maintain svr, prevent increase iontropy

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67
Q

can neuraxial approach be used in hcm pregos

A

yes…but careful titration of local anesthestic to prevent sympathectomy

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68
Q

which kind of neuraxia approach is better for hcm pregos

A

epidural bc that can be titraed…versus one shot spinal that can lead to decrease svr and reflexive tachycardia

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69
Q

what is the pressor of choice for hcg pregos

A

phenylephrine

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70
Q

what is added to blood during a TEG to get blood to clot

A

kaolin

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71
Q

how do you measure R time

A

from the beginning of the test to the start of coagulation

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72
Q

what does R time represent

A

coagulation factors

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73
Q

what is K time

A

it is the beginning of clotting time to the time where coagulation reaches 20mm amplitude

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74
Q

what does k time represent

A

clot kinetics

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75
Q

how is alpha angle measure

A

it is the angle made by the baseline and the line tangent to the coagulation curve

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76
Q

what are the things that alpha angle measure

A

acceleration of fibrin formation and the fibrin crosslinking process

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77
Q

what is the max amplituide of the TEG measure

A

clot stregnth, aka, platelet funx

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78
Q

what is the ly30

A

it is the max amplitude minus the amplitude s/p 30 mins

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79
Q

what does ly30 mean

A

it measures fibrinolysis

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80
Q

how many pacemaker codes are there

A
  1. XXXXX
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81
Q

what is the first code of the pacemaker

A

which chambers are paced. A, V, D, or O (none)

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82
Q

what is the second code of the pacemaker

A

it is which chamber is sensed AVD or O

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83
Q

what does sensed mean

A

if the pacemaker recognizes the intrinsic rate of the chamber

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84
Q

what is the third code of the pacemaker

A

it is the response to the sensed chamber

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85
Q

what are the 3 responses of a pacemaker to the sensed chamber

A

I for inhibit, T for trigger, or O for no response

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86
Q

what happens when there is a D in the third code of the pacemaker, such as DDD

A

if there is a sense of atrial activity, there will be inhibition of the atrium

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87
Q

what is the 4th code of the pacemaker

A

it is the rate modulation of the pacemaker

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88
Q

what is rate modulation

A

it allows the rate of the paced chamber to change to vibration, motion, and minute ventilation

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89
Q

what are the 2 values of the 4th pacemaker code

A

R or O

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90
Q

what equation do you use to understand cardiac wall tension

A

LaPlace’s law

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91
Q

what is Laplaces law

A

Tension = Pressure x Radius /2Wall thickness

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92
Q

if a mycardium is thickened, is tension increase or decrease

A

decrease, because it is inversely proportional to tension

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93
Q

why is understanding wall tension for heart important

A

because increase tension increases o2 consumption

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94
Q

what cardiac pathology has a treatment dependant on laplace’s law

A

dilated cardiomyopathy 2ndry chf

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95
Q

what is the goal of treating chf?

A

diuresis and venodilation to decrease cardiac radius and prevent further thining of cardiac wall

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96
Q

What to do in vtach

A

Determine if it is stable or not.

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97
Q

What to do in stable v tach

A

Administer IV Amiodarone

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98
Q

What use to be the recommended med for stable v tach

A

Lidocaine

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99
Q

At what point does vtach become unstable.

A

When there is no pulse

100
Q

What is the treatment of choice for pulseless vtach

A

Synchronized cardio version

101
Q

What is a vtach that is polymorphic rather than monomorphic

A

Torsades

102
Q

How do you treat torsades

A

Magnesium

103
Q

What is another name for torsades

A

Polymorphic ventricular tachycardia

104
Q

What is the danger sign when ventricle tachycardia becomes unstable

A

One ventricle fibrillation occurs

105
Q

Why do you have to use synchronized cardioversion for ventricle tachycardia

A

Synchronizing your shock will prevent shocking during the refractory phase

106
Q

What happens if shocks are delivered during the refractury phase

A

Ventricular fib

107
Q

What kind of shock is used for vfib

A

Defibrillation, a higher current requiring shock, not synchronized

108
Q

What to do if defibrillation is used for v fib and it fails

A

Give vasopressin

109
Q

Where is the arterial and venous cannulations in a cabg

A

The aorta after the aortic clamp is the arterial cannulation. The right atrial appendage is the venous cannulation.

110
Q

Where is the anterograde cannulation of cabg

A

It is between the aortic valve and the aortic clamp. This will give paraplegic medications to the coronary arteries

111
Q

What valvular abnormalities will make the anterograde cannulation inefficient

A

Aortic insufficiency. The valve does not close and all the cardioplegic meds go to the left ventricle instead of the coronary arteries

112
Q

What is the retrograde cannulation.

A

It is through the right atrial into the coronary sinus

113
Q

Where is the cannula during retrograde infusion if you loose pressure

A

It is in the right ventricle….out of the coronary sinus

114
Q

What happens to the arterial like systolic pressure as you move more peripherally

A

Increase in pulse pressure - increase in sbp

115
Q

What happens to more peripheral a line upstrokes

A

Delayed

116
Q

What happens to the dicrotic notch in more peripheral a lines

A

Delayed, more slurred

117
Q

What happens to the diastolic wave of a more peripheral a line

A

More prominent

118
Q

How many types of shock are there

A

4

119
Q

What are the 4 types of shock

A

Cardiogenic, hypovolemic, distributive, obstructive

120
Q

What are 3 numbers to look for to determine shock

A

Cvp, paop, svr

121
Q

What numbers would you see in hypovolemic shock

A

Low cvp, low paop, high svr

122
Q

What numbers would you. See in right sided heart failure shock

A

Normal cvp, normal paop, high svr

123
Q

What numbers would you see in left sided heart failure

A

Elevated cvp, elevated paop, high svr

124
Q

What numbers in biventricular failure

A

Everything is elevated

125
Q

What numbers do you see in distributive shock

A

Look at the svr. It is always decreased

126
Q

What are examples of distributive shock

A

Anaphylaxis, spinal shock, sepsis, corticosteroid insufficiency…all lead to peripheral vasodilation

127
Q

What are examples of obstructive shock

A

Tamponade, pulm embolism, tension pneumo

128
Q

What happens when the diastolic pressure equal that of the chamber pressures

A

Sign of cardiac tamponade

129
Q

Cardiac tamponade…what is severely reduced in tamponade

A

Diastolic filling.

130
Q

Cardiac tamponade…what is the result of decrease diastolic filling in tamponade on a cvp line

A

Decrease in y descent or even absent

131
Q

Cardiac tamponade…what happens to the pressures on a cvp

A

Equalization of right atrial pressure, pulm artery diastolic pressure, and pcwp.

132
Q

Cardiac tamponade…what is the triad we see

A

Becks triad….hypotension, increase cvp,and distant heart sounds

133
Q

Cardiac tamponade…what happens to systolic pressure on inspiration

A

Decrease on inspiration,,,aka…pulsus paradoxus

134
Q

Cardiac tamponade…what are the EKG findings

A

Low voltage on qrs and electrical alternans

135
Q

Cardiac tamponade…can you give the patient opiod or benzo before the pericardial centesis

A

No…they will have sympathy lysis and thus decease heart rate and then hypotension. These patients are dependent on tachycardia

136
Q

Cardiac tamponade….what is a safe form of sedation for tamponade

A

Ketamine…it will increase sympathetic…as well as as maintains pts ability to creative negative pressure inspiration…positive pressure ventilation has a tendency to decrease preload and cause arrest

137
Q

What is the most common cause do sudden cardiac death in teens

A

Hypertrophic cardiac myopathy

138
Q

Hcm…what is the inheritance pattern

A

Autosomal dominance

139
Q

Hcm…what kind of murmur do u have.

A

Left lower stern all border murmur. And apex murmur.

140
Q

Hcm…what increases the murmur

A

Decease preload by Valsalva maneuver.

141
Q

Hcm…what decreases the murmur.

A

Increase preload aka squatting position.

142
Q

Hcm…how do u diagnose it

A

Tte…left ventricular wall greater than 15mm without enlarged ventricle cavity

143
Q

Hcm…should you pretreat the patient with benzo

A

Yes…it will blunt sympathetics and allow for slow heart rate and maintained svr

144
Q

Mitral stenosis. What is the physiologic goals for anesthesia

A

Slow heart rate and increased svr

145
Q

Mitral stenosis. Why do u want high svr

A

Because a drop in svr will cause a reflex tachycardia

146
Q

Mitral stenosis. What is the problem with tachycardia

A

Poor time for ventricular filling.

147
Q

Mitral stenosis. What can tachycardia lead to

A

Atrial fibrillation.

148
Q

Mitral stenosis. What is the problem with atrial fibrillation..

A

It leads to decrease in cardiac output because there is little ventricular filling

149
Q

Mitral stenosis. What cans atrial fibrillation lead to.

A

Atrial fibrillation with rvr.

150
Q

Mitral stenosis. What is the volume resuscitation goal for mitral stenosis

A

Euvolemia. Do not cause too high in central blood volume or else you can overload the right ventricle

151
Q

Mitral stenosis. What is the metabolic goals for ms

A

Prevent hypoxia and hypercapnia. These can lead to pulmonary hypertension and then lead to right sided heart failure. This would worsen the pulmonary hypertension that is already associated with mitral stenosis.

152
Q

intraop cardiac arrest. what is the most common prodromal sign

A

bradycardia…shows up 67% of the time

153
Q

intraoperative cardiac arrest. what is the common spo2 reading before arrest

A

below 90 on the spo2

154
Q

intraoperative cardiac arrest. what are 3 indicators of a possible cardiac arrest

A

hypotension, bradycardia, hypoxia

155
Q

intraoperative cardiac arrest. what is the first step in management

A

cardiac compression

156
Q

protamine. what side effects can it cause

A

severe hypotension, right sided heart failure, pulm htn, bronchospasm

157
Q

protamine. what are independant risk factors to get allergic rxn to it

A

history of nph use, fish allergy, history of allergies in general

158
Q

protamine. what are theoretical risks are prior use of protamine or history of vasectomy

A

theoretical risks are prior use of protamine or history of vasectomy

159
Q

protamine. can a protamine reaction be prevented by preadmin with histamine

A

no

160
Q

protamine. what to do if you only see hypotension

A

use vasopressors and fluids

161
Q

protamine. what differentiates severe hypotension from non severe

A

check the cvp…if it is elevated, then there is significant right sided involvement

162
Q

protamine. what vasopressor is used for severe hypotension in protamine reaction

A

epinephrine

163
Q

protamine. what side effect seen with hypotension should also be treated with epinephrine

A

bronchospasm

164
Q

protamine. when should fluids not be used to treat hypotension

A

when you see right vent failure on TEE…heart is dilated already, so the increase in fluids will cause worsening clinical picture.

165
Q

protamine. what should be done if right heart failure is seen after protamine reaction

A

reinstitution of cardiopulmonary bypass

166
Q

intraop mi. what is seen first, increase in pa pressures or systemic hypotension

A

increase in PA pressure is seen before systemic hypotension

167
Q

intraop mi. why is the pa increase seen before hypotension

A

because diastolic dysfunction during mi occurs before systolic dysfunction. decrease cardiac compliance occurs and back pressure into the pulm artery occurs

168
Q

intraop mi. what valvular lesion may be seen.

A

mitral regurge…bc papillary muscles may infarc and cause mitral regurge.

169
Q

intaop mi. when the mitral regurge happens, what do u see on cvp tracing

A

prominent a and v waves

170
Q

intraop mi. what is the most sensitive indicator of MI

A

TEE

171
Q

intraop mi. if ekg changes is seen and pap increase…but no hypotension…what drug is given

A

nitroglycerin…to decrease preload to heart to decrease right ventricle straing…and secondly, it dilates coronary arteries to increase coronary blood flow

172
Q

pacemakers with defibrillators. what does placing the magnet do to it

A

it will stop the defibrilator from functioning

173
Q

pacemaker with defibrillators. so what happens to a ddd pacemaker with defibrillator function

A

it will become ddd without a defibrillator function

174
Q

pacemaker with defibrillators. what should you look at first to know what to do.

A

look at the interrogation…see if the patient is pacemaker dependant (seen in pts with no intrinsic cardiac conduction left)

175
Q

pacemaker with defibrillators. what mode should the patient be placed in if they are pacemaker dependant

A

asynchronous mode…like doo or voo

176
Q

pacemaker with defibrillators. how is a pacemaker placed in doo or voo

A

magnet does not do this…magnet only turns off the defibrillator…the pacemaker must be reset by cardiology to go into voo or doo

177
Q

pacemaker with defibrillators. why should a pacemaker dependant pt be placed into asynchronous mode

A

assuming that the magnet has turned off the defibrillator, the pacemaker could still be in a mode where the inhibitor function may still function and get electrocautery interference …such as ddd modes of pacemaker that still has inhibition function after a magnet is placed

178
Q

mediastinoscopy. what must be available for all these cases

A

blood for transfusion

179
Q

mediastinoscopy. what is the biggest risk for these cases

A

bleeding.

180
Q

mediastinoscopy. what may be the cause of bleeding

A

pulm vv, pulm aa, thoracic duct, innominate vv

181
Q

mediastinoscopy. what nerve injury may be seen

A

phrenic nerve or recurrent laryngea nerve injury

182
Q

mediastinoscopy. what lung injury may be seen

A

pneumothorax, or air embolism

183
Q

mediastinoscopy. what limb should be monitored by what

A

pulse ox or arterial line should be placed on the right side because the innominate compression is commonly compressed during the case.

184
Q

valsalva maneuver. how many phases are there for hemodynamic changes

A

four

185
Q

valsalva maneuver. what happens in phase 1

A

the maneuver is initiated with increase in intrab pressure causing increase in preload…the heart reflex bradys

186
Q

valsalva maneuver. what happens in phase 2

A

valsalva is maintained and now there is a decrease in preload and reflex tacycardia occurs

187
Q

valsalva maneuver. what happens in phase 3

A

valsalva maneuver is stopped and now pulm vv capacitance is increased….less go to the left atrium and even more tachycardia occurs

188
Q

valsalva maneuver. what happens to phase 4

A

over shoot. now massive tachycardia and preload occurs and cardiac out and bp are at its highest

189
Q

valsalva maneuver. what medical condition can u diagnose using this

A

diabetic autonomic dysfunction. they wouuld not be able to do the reflex tachycardia. heart failure pt would also not show the overshoot

190
Q

Mitral stenosis. What is the heart sound that you hear.

A

Loud s1 (opening snap) and a mid diastolic rumble.

191
Q

Mitral stenosis. What diseases can cause this.

A

Rheumatic fever, sle, amyloidosis.

192
Q

Mitral stenosis. What is the best physiologic conditions for this disease.

A

Slow and squeeze.

193
Q

Mitral stenosis. What can cause chf in mitral stenosis.

A

Disease states that cause tachycardia and hypotension. Like thyrotoxicosis, anemia, or sepsis.

194
Q

Mitral stenosis. What is the danger in tachycardia in mitral stenosis.

A

atrial fibrillation

195
Q

cardiogenic shock. what is the most common risk factor

A

myocardial infarction…mainly ST elevated MI!

196
Q

cardiogenic shock. when does it occur after mi

A

50% of patients show shock signs at 6hrs…and 75% show it within 72hrs

197
Q

cardiogenic shock. at what age are pt more prone to get card shock

A

71 years old

198
Q

cardiogenic shock. males vs females…who are more prone

A

females

199
Q

cardiogenic shock. what infarc is more prone to shock

A

anterior infarct

200
Q

cardiogenic shock. what kinda ekg finding makes pt risk for shock

A

left bbb

201
Q

cardiogenic shock. what is necessary for diagnosis

A

you need evidence of end organ hypoperfusion…oliguria, altered mentation, severe peripheral vasoconstriction

202
Q

cardiogenic shock. what value of cardiac index dictates cardiogenic shock

A

end organ hypoperfusion must be diagnosed first….then cardiac index can be used to help establish the diagnosis. with no pressor, a CI less than 1.8, with pressors, a CI less than 2

203
Q

cardiogenic shock. if you already have signs of hypoperfusion. what bp reading can establish the diagnosis

A

for 30min or greather, sbp 80-90 or less,…or map in 30s

204
Q

cadiogenic shock. what must u not have to diagnose cardiogenic shock

A

there must be no hypovolemia

205
Q

cardiogenic shock. what is the foundation treatment for this

A

intaaortic ballon pump

206
Q

cardiogenic shock. balloon pump. when does it inflate

A

during diastole to increase systemic diastole pressure

207
Q

cardiogenic shock. balloon pump. when will it not improve coronary perfusion

A

if there was coronary stenosis

208
Q

cardiogenic shock. what does balloon pump do to afterload

A

it decreases it

209
Q

Prophylaxis infective endocarditis . What is the purpose of prophylaxis.

A

It is to prevent infections in those who would have great medical detriment if infection happens

210
Q

Prophylaxis infective endocarditis. What is better at preventing infection in pt getting oral procedures.

A

Oral hygiene is better than antibiotics itself. The risks of of antibiotics is greater than that of the benefits of just prophylactically getting it

211
Q

Prophylaxis infective endocarditis . What cardiac condition that has not had intervention should get prophylaxis.

A

Those of cyanosis disease should get it because these patients would die if infection occurs.

212
Q

Prophylaxis infective endocarditis. What cardiac conditions that has had intervention done need prophylaxis.

A

Those who have valvular hardware or valvulopathy or prosthetics or those who had congenital heart problems that still have residual defects.

213
Q

Prophylaxis infective endocarditis. What pmhx would indicate prophylaxis.

A

If the patient has history of infective endocarditis

214
Q

Prophylaxis infective endocarditis. What 2 kinds of surgery do not need prophylaxis

A

Gu and gi interventions do not need prophylaxis for infective endocarditis purposes

215
Q

Prophylaxis infective endocarditis. What are the 3 types of surgeries most associated with bacteremia

A

Skin musculoskeletal surgeries, oral surgeries, lung surgeries

216
Q

Prophylaxis infective endocarditis. If a cyanosis heart disease was repaired but without hardware placement. Should u still prophylax

A

Only if the intervention has been less than 6 months ago.

217
Q

Cardiac transplant. How should the volume status of the pt be kept under ga

A

The patients heart are de-enervated. They usually can’t raise heart rate sufficiently to compensate for hypovolemia. They are volume dependent pts. Keep them euvolemic. Do not restrict fluids and treat them like heart failure pts.

218
Q

Cardiac transplant. How do u increase the heart rate in these patients.

A

Epinephrine or isoproterenol.

219
Q

Cardiac transplant. Why do u have to monitor st-segment during surgery for these patients.

A

Bc transplant pt is very prone to getting cad. Their chronic steriods for immunosuppression may pedispose them to htn and diabetes.

220
Q

Cardiac transplant. If a pt is on immunosuppressants, should u avoid giving them steriods in the case?

A

No. Some of the immunosupressants are steriods to prevent rejection of the heart. Avoiding steriods will not improve their infection rate…actually they may require stress dose steriods bc they are usually. Chronic steroid users.

221
Q

mitral regurgitaiton. if there was an ischemic event. what is the most common mechanism of action for mitral regurge to develop

A

after cardiac infarc…remodeling occurs and causes distortion of the myocardium and annulus of the mitral valve…this causes mitral regurg…this mech is more common than papillary rupture

222
Q

mitral regurgitaiton. ischemic form. what is the severity of mitral regurge needed to have exercise induced pulmonary edema

A

any amount of mitral regurge can cause pulm edema associated with exercise. any high level of catecholamine states may cause dysrythmia that can cause mr to be exacerbated

223
Q

mitral regurgitation. ischemic form. what are good medications to use to prevent remodeling

A

beta blockers and ace inhibitors.

224
Q

mitral regurgitation. ischemic form. what interventions can be done to reduce mr

A

biventricular pacing can help reduce distortion upon the mitral valve

225
Q

lbbb. what do u look out for first on ekg.

A

must look for qrs greater than 0.12 seconds

226
Q

lbbb. where is st depression and twave inversion

A

I v5 v6

227
Q

lbbb. where is st elevation upright t wave

A

v1 v2

228
Q

rbbb. what do u look out for first on ekg

A

qrs greater than 0.12

229
Q

mitral stenosis. what is the normal valve area

A

4-6 cm2

230
Q

mitral stenosis. what is considered mild stenosis

A

any value between 2 and 4 cm2

231
Q

mitral stenosis. what is considered severe mitral stenosis

A

less than 1cm 2

232
Q

mitral stenosis. what are they at risk for

A

since there is low forward flow, the stasis makes clots can can make emboli

233
Q

aortic stenosis. valve area. mild/mod/sever

A

> 1.5cm2, 1.5-1.0, <1.0

234
Q

aortic stenosis. gradient mmHg. mild/mod/severe

A

40

235
Q

aortic stenosis. jet velocity. m/s mild/mod/severe

A

4

236
Q

persistent left SVC. where does this left svc drain into

A

directly into the coronary sinus

237
Q

peristent left svc. why does it drain into the coronary sinus

A

because this is a where embryonically at 8 weeks it is joined to drop venous drainage to the right side of the heart

238
Q

perisstent left svc. where does the left side of the svc drain in normal people

A

in normal people, an innominate vv would form at 8 weeks…connecting both right and left caval viens. the left svc that would connect to the coronary sinus would then dissentegrate

239
Q

persistent left svc. what happens to cardioplegia

A

cardioplegia placed for retrograde cannula might not work so well because blood would rather go up toward the left svc rather than down the coronary sinus

240
Q

oxygen consumption. what is oxygen delivery

A

DO2

241
Q

oxygen consumption. what is the equation for oxygen delivery

A

DO2 = CO X CaO2 X10

242
Q

oxygen consumption. if u plug in all normal values for calculating oxygen delivery, what is the average value u get

A

about 988ml O2/min

243
Q

oxygen consumption. what does an SVO2 of 75% mean

A

that your consumption of oxygen is only 250cc/min…aka 25% of your DO2 because 250cc/988cc is roughly 25%

244
Q

oxygen consumption. how does cyanide affect svo2

A

it increases SVO2 because mitochondria are not able to utilize oxygen and extract it off the rbc

245
Q

oxygen consumption. what kind of shunt will cause a decrease in svo2

A

a left to right shunt …

246
Q

oxygen consumption. what does an av fistula do to svo2

A

decreases it

ACE (18 decks)

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