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advanced bioscience > cardiac > Flashcards

cardiac Flashcards

1
Q

non modifiable risk fx heart disease

A

age, male, family history

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2
Q

modifiable risk fx heart disease

A

smoking, htn, diet, hyperlipidemia, physical inactivity, obesity DM, pvd, l ventricular wall motion dysfunction

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3
Q

majority mis caused by

A

atherosclerosis

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4
Q

patho MI

A

emoli–>ischemia–>acidosis–>inflammatory/cellular response–>preservation measures (collateral circ)–?zones of necrosis—>signs of MI

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5
Q

ami caused by

A

ruptured plaque emboli lodging in a coronary vessel

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6
Q

cessation of perfusion causes

A

aerobic production (38 ATP) to anaerobic (2ATP)

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7
Q

ischemia occurs when

A

ATP deman is greater than atp production

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8
Q

myocardial acidosis

A

first 6 hours of onset mi symptoms:

  1. H+accumulate
  2. ca++ displace from SR
  3. K= shift outside cell and NA+ inside, altered cell membrane action potential causing edema and arrhythmias
  4. myocardial acidosis
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9
Q

anerobic waste leads to

A

lactic acide, increased intracellular ph and inhibition of anaerobic atp production

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10
Q

continued hpoxia leads to

A

cell death and necrosis

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11
Q

necrotic myocardial cells release

A

cytokines that mediate acute inflamm process

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12
Q

what accumulates at infarct site- proteolytic enzymes that spills proteins into smaller peptides

A

this exacerbates injury

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13
Q

myocardial o2 reserve is gone within

A

8 seconds

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14
Q

immediaely after total occlusion how many normal heartbeats can be completed

A

sufficient o2 and atp in tissue to sustain 27

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15
Q

ecg changes in

A

30 seconds

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16
Q

pain with mi

A

60 seconds after ischemia

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17
Q

myocardial cells are irreversibly injured after

A

30-40 minutes of ischemia

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18
Q

zone of necrosis

A

center, contains dead tissue

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19
Q

zone of injury

A

inner ring- tissue cannot contract but not necrotic

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20
Q

zone of ischemia

A

inner and outer ring, superimposed upon the zone of injury, separates the other two zones from undamaged tissue

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21
Q

effects of MI

A

decrease ventricular stroke volume—> decreased CO

  1. increased LV filling pressure
  2. decreased cardiac output—> decreased compliance left ventricle= resultant stiff muyocardiam increases BP
  3. decreased CO and arterial pressure–> baroreceptor mediated
  4. pain stimulates vasoconstriction and HTN
  5. SNS increases o2 demand, enlarging the infarcted region and preciptating arrhythmias and impairing cardiac function
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22
Q

s/s AMI

A

substernal chest pain
progressing hypoxia
dizziness, nausea
itachycardia, increased resp and dyspnea

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23
Q

class i nyh assoc

A

no limit physical activity

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24
Q

class II (mild)

A

slight limitation activity, physical activity leads to fatigue, dyspnea, palpitation

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25
Q

class III (moderate)

A

marked limitation physical activity, ok at rest but less then ordinary physical activity causes fatigue, palp, dysp

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26
Q

class IV (severe)

A

unable to carry out any physical tast

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27
Q

what lead is most sensitive for detecting ischemia

A

V5

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28
Q

lead II can detect

A

ischemia of RCA distribution and most useful for monitroing p waves

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29
Q

V5 and lead II

A

highest sensitivity to detect ischemia

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30
Q

MI drugs of choice

A

fentanyl vs. inhaled

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31
Q

inhaled agents cause

A

vasodilation, decreased preload, decreased CO

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32
Q

o2 demand determined by

A

wall tension, hr and contractility

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33
Q

o2 delivery

A

determined by o2 content, coronary blood flow

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34
Q

increased wall tension factors

A

increased preload, increased afterload will increase o2 demand

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35
Q

increased contractility in response to sympathetic stim or inotropes will

A

increase o2 demand

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36
Q

increased heart rate

A

increases contractility but decreases ventricular diameter, decreases wall tension, decreases o2 demand

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37
Q

tee can detect with mi

A

new segmental wall motion abnormalities

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38
Q

goal periop

A

maintain supply and demand

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39
Q

what should be avoided with mi

A

ketamine

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40
Q

muscle relax with mi

A

vec, roc (pan increases hr)

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41
Q

malignant hypertension

A

systolic greater than 200 or dbp>120

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42
Q

stage 1 htn

A

140-159 or 90-99 confirm in 2 months

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43
Q

stage 2 hypertension

A

> 160 or >100

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44
Q

htn during anesthesia may be due to

A

depth of anesthesia, hypoxia, hypercarbia

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45
Q

systolic dyfunction

A

reduced ability for heart to eject, lvef <40%

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46
Q

factors affecting CO

A

preload, contractility, afterload,(stroke volume), heart rate

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47
Q

compensatory mech co

A

neurohormonal, frank starling, inflammatory cytokines, ventric remodeling

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48
Q

neurohormonal activation sns- adaptive

A
  1. catecholamine induced augmentation ventricular contractility and hr
  2. systemic and pulmonary vasoconstriction leads to enhanced venous tone, leads to increased preload, maintains blood pressure
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49
Q

maladaptive neurohumoral activation

A

elevation catechoamine, leads to direct myocyte toxicity leads to apoptosis and myocardial removeling

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50
Q

RAAS

A

angiotensin II leads to vaocostriction leads to increased preload
aldosterone leads to increase NA resorption, leads to increased preload

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51
Q

maladaptive RAAs

A

angiotensin II lacts directly on myocytes to promote pathologic removeling leading to decreased contractility

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52
Q

release of atrial and brain natriuretic peptides released following

A

atrial and ventricular vent, decreased perivpheral vascular resistance and promote sodium excretion

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53
Q

one of fist signs heart failure

A

increased BNP

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54
Q

frank starling curve

A

increased sarcomere length, increased CO to a point

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55
Q

ventricular remodeling-

A

hemodynamic stresses on the heart lead to this, changes compensatory initially to increase ventricular volume, greater stroke volume, higher CO, then ventricle continues to enlarge and myocardium hypertrophies, leading to impaired ontractility

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56
Q

s/s systolic dysfunction

A

dyspnea, orthopnea, paroxysmal nocturnal dyspnea, dry/nonprod cough, fatigue and weakness, nocturia, decreased exercise toleratnce

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57
Q

systolic dysfunction clinical signs

A

caxechia, ansious, expir wheeze and rhonchi, cough, tachypnea, laterally displaced PMI, S3, cool and pale extremitie

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58
Q

Stage A

A

risk factors present, no heart failure

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59
Q

stage b

A

structural heart disease, no smptoms heart failure

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60
Q

stage c

A

structural disease with prior or current symptoms of heart failure and lv dyfunction (high risk of decompensation)

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61
Q

stage d

A

refractory end stage heart disease (highest risk anesthesia)

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62
Q

intraop with systolic dysfunction

A

avoid nitrous, etomidate for induction, opiods, positiove pressure and peep

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63
Q

hemodynamic goals systolic dyfunction

A

maintain co, o2 delivery, tissue perfusion, maintain contractility, avoid increases in afterloa

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64
Q

maintain contractiity and co with

A

epinephrine, dobutamine, milrinone, iabp, vad

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65
Q

diastolic dysfunction

A

functional abnormality of diastolic relaxation (lusitropy), filling or distensibility of the left ventricle, regardless of ejection fraction. abnormal cardiac relaxation stiffness and filling

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66
Q

diastolic heart failure

A

diastolic dysfuction with s/s of heart failure, having anormal EF

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67
Q

dyastolic dysfunction vs. systolic dysfunction

A

diastolic (can’t relax and fill), systolic (too relaxed, cant contract)

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68
Q

systolic dysfunction

A

decreased EF, progressive chamber dilation eccentric remodeling EF <50

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69
Q

diastolic dysfunction

A

normal EF, normal LVEDV, abnormal diastolic function, concentric remodeling/hypertrophy

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70
Q

grading system diastolic dysfunction

A

I-relaxation abnormality
II psudonormal
III- restrictive (reversible)
IV- irreversible

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71
Q

dyastolic heart failure

A

ef>50

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72
Q

etiology diastolic ysfunction

A

abn stiffness left vent
abn relaxation left vent
abn filling left vent

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73
Q

isovolumetric relaxation

A

period between aortic valve closre and mitral valve opening, no change in volume, lv pressure declines

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74
Q

increase in LV diastolic pressure causing and increase in pulm venous pressure can cause

A

heart failure

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75
Q

hypertrophic remodeling

A

caused by hypertension

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76
Q

concentric hypertrophy

A

lv muscle mass thicker, diminishing volume while maintaing a normal ef of blood

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77
Q

anesthesia contraindications

A

severe aortic or mitral valve stenosis
uncontrolled heart failure
mi less than 1 month

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78
Q

prevent intraop diastolic heart failure

A

keep HR within narrow range (allow filling)
tachycardia bad
bp withina narrow range
careful with volume
careful with volatile agents and induction as they may decrease inotropy

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79
Q

complication of stenosed valves

A

obstructed blood flow forward, pressure overload

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80
Q

stenosed valve can lead to

A

compensation via increas in chamber wall thickness (concentric hypertrophy)

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81
Q

stenosis implications

A

slow and steady heart rate
maintain preload
maintain SVR

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82
Q

regurgitation problem

A

back flow of blood, volume overload

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83
Q

regurgitation leads to

A

compensation via chamber dilation (eccentric hypertropy)

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84
Q

implications of regurgitation

A

after load reduction for fast, full, forward flow

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85
Q

MR TRAPS

A

systole

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86
Q

MS. PARTS

A

diastole

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87
Q

tricuspid stenosis leads to

A

right sided heart failure- hepatomegaly, ascies, peripheral edema, fatigue, dyspnea

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88
Q

tricuspid regurgitation- r

A

right atrial volume overload

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89
Q

tricuspid regur leads to

A

a fib, rv systolic dysfunction, rv hypertrophy, r sided heart failure, dyspnea

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90
Q

serous pericarditis

A

non infectious

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91
Q

fibrinous

A

dry with a fine granulare roughening (friction rub)

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92
Q

serofibrinous

A

more intense inflammatory process with cloudy pericardial fluid d/t leukoscytes/red blood cells fibrin

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93
Q

purulent/suppurative

A

invasion of the pericardial space with microbes

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94
Q

hemmorhagic

A

blood with a fibrous/serious mix

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95
Q

caseous

A

most often with tb, direct spread from TB foci

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96
Q

most common pericarditis

A

serofibrinus

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97
Q

friction rub assoc with

A

fibrinous pericarditis

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98
Q

caseous necrosis is

A

a form of cell death when tissue maintains a cheese like appearance

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99
Q

acute pericarditis clinical presentation

A

sharp peuritic pain ant chest, increasing pain with recumbent position (may be leaning forward), low grade fever, malaise, tachycardia, ecg, duration hours to days, elevated wbc, troponin may be elevated

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100
Q

pericardial friction rubs are

A

present throughtout the cardiac cycle

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101
Q

normal pericardium

A

intrathroacic pressure decreases during inspiration, leading to an increas in venous return to the right heart and increase in right ventricular chamber size. b/c normal pericardium accomodates the increased venous return, return does not impair left vent filling

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102
Q

pericardium

A

anchors, reduces friction, acts as a barrier, limits acute dilation of ventricles, promotes diastolic coupling

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103
Q

acute pericarditis

A

acute inflammation of the pericardial layers

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104
Q

constrictive pericarditis

A

chronic inflammation can lead to fibrosis and calcification and eventually impaired diastolic filling

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105
Q

st elevation with pericarditis

A

widespread, concave, t waves inverted when st segments have normalized

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106
Q

result of scarring with constrictive pericarditis

A

adhesion of pericardium to epicardium

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107
Q

constrictive pericarditis is

A

typically chronic, can be acute, transient, occult constriction

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108
Q

constrictive pericarditis leads to

A

diminished elasticity of pericardium, prevents the normal inspitory decrease in intrathoracic pressure, rapid early diastolic filling, ultimately reduced SV

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109
Q

s/s constrictive

A

fluid overload- peripheral edema, ascites, jvd, fatique, pericardial knock

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110
Q

pericarditis diagnosis

A

TEE- pericardial thickening, atrial enlargement, abn septal movement, echo with doppler, ct/mri, coronary angiography

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111
Q

cardiac tamponade

A

cardiac filling is impeded by external foce, ventricular interdependence, decrease in stroke volume and CO

112
Q

in chronic tamponade symptoms may not occur until

A

effusion>2L

113
Q

s/s tamponade

A

cp, tachypnea, dyspnea, increased JVP, muted heart sounds, hypotension, tachycardia, pulsus paradoxus, cyanosis, decreased UO, pericardial rubb

114
Q

constrictive pericarditis treatment

A

nsaids, steroids, chemotherapy, ace plus diuretics, pericardiectomy only definitive tx option

115
Q

cardiac tamponade

A

pericardiocentesis

116
Q

acute pericarditis in the absence of assoc pericardial effusion or scarring does

A

not alter cardiac function

117
Q

surgery and acute pericarditis

A

focus on underlying disease, case cancelled if possible,

118
Q

pericardiotomy

A

large bore IV, CPB available, arterial monitoring, ketamine/etomidate/nitrous/benzos, vaa with caution avoid ppv if possible

119
Q

goal with hemodynamics in pericardiotomy

A

preserve contractility, hr, preload and afterload

120
Q

cardiac tamponade and anesthesia

A

optimize clinical status, cvc/art line, local infiltration anesthesia only, no positive pressure vent, inotrope if needed

121
Q

after pericardiocentesis

A

preserve hr, co, preload, afterload, myocardial contractility

122
Q

primary cardiac tumors are

A

rare

123
Q

clinical manifestation of cardiac tumors

A

location

124
Q

obstruction of circulation thru heart valves leads to

A

heart ailure sysmptoms

125
Q

interference with heart falves

A

regurgitation

126
Q

direvt infasion of myocardium

A

impaired heart

127
Q

invasion of adjacent lung

A

pulm symptoms

128
Q

left atrial tumors

A

mimic symptoms of obstructing AV flow or causing mitral regurgitation

129
Q

direct invasion of myocardium leads to

A

impaired contractility, arrhythmias,heart block, or pericardial effusion with or without tamponade

130
Q

s/s heart tumor

A

fever, malaise, arthralgias, raynauds, rash, clubbing

131
Q

lab findings heart tumor

A

increased igm, increased ESR

132
Q

tumor embolism

A

tumor fragments. systmic- mi, cva, pe- pah, cor pulmonale

133
Q

majority of benign cardiac tumors are

A

myxomas

134
Q

where are most tumors

A

left atrium

135
Q

myxomas

A

produce vascular endothelial growth factor. 35% are friable or billous.

136
Q

myxoma patho

A

obstruct pulm or systemic venous drainage, impair av flow

137
Q

s/s myxoma

A

fever, weight loss, raynauds, myalgia, etc

138
Q

tx myxoma

A

surgical resection

139
Q

carney omplex- inherited autosomal dominant disorder hcar by multiple tumors including atrial, extracardiac myxomas

A

true

140
Q

2nd most common cardiac tumor

A

papillary fibroelastomas 80% in heart valves- usually left side heart

141
Q

fibroelastoma most common presentation

A

stroke or tia, angina, sudden death hf, pe

142
Q

cardiac lipoma

A

benign fatty cells, mainly in adults, half in subendocardial regions

143
Q

cardiac lipoma

A

not a true tumor, exxagerated growth of normal fat in septum

144
Q

rhabdomyomas

A

exclusively in children less than 1 year old

145
Q

location rhabdomyoma

A

ventricular walls or av valves

146
Q

s/s rhabdomyomas

A

rhythm disturbances, heart block, v tach

147
Q

second most common pediatric tumor

A

cardiac fibromas- ventricular muscle 5x more in left then right

148
Q

teratomas

A

benign tumors located in the pericardium, mainly in peds

149
Q

purkinje cell tumors/hamartomas

A

benign tumors, small, flat sheets cells, usually young children

150
Q

purkinje cell tumors located

A

left ventrical endocardial and epicardial surfaces

151
Q

s/s purkinje cell tumors

A

incessant V tach

152
Q

can you se epurkinje cell tumor on echo

A

no

153
Q

mesothelioma

A

most arise in pleura, can arise from pericardium

154
Q

mesothelioma

A

malignant

155
Q

location mesothelioma

A

av node, may produce heart block

156
Q

s/s mesothelioma

A

cardiac tamponade, constriction

157
Q

sarcomas

A

primary malignant tumors- proliferate rapidly and invade myocardium, obstruct blood flow to heart

158
Q

la tumors

A

pulm congestion, s4, loud s1, diastolic murmur

159
Q

ra tumors

A

r sided congestion, diastolic mumur, tricuspid regurg

160
Q

rv tumors

A

r sided chf, s3

161
Q

lv tumors

A

positional changes of murmur and bp, buaortic hypertrophic cardiomyopathy

162
Q

outflow obstruction causes

A

hypotension d/t posture

163
Q

hypotension during induction avoid

A

epinephrine

164
Q

left atrium myxoma may mimic

A

mitral stenosis with pulmonary hyptertension

165
Q

what needs to be avoided in cardiac tumor surgery

A

tachycardia, max. vent filling- slow HR, high afterload to maintain perfusion setting, adequate preload

166
Q

3 layers aorta

A

tunica intima, tunica media, tunica dventitia

167
Q

localized abnormal dilation of a blood vessel or the wall of the heart.

A

aneurysm

168
Q

most common cause aneurysm

A

aaa, htn, older age

169
Q

patho aortic aneurysm

A

degeneration and wekening of the normal elastic medial layer from constant stress, arterial wall thinning secondary to plaque that originates in the intima, dilation from effect of blood stream across obstructive vascular plaque, causes turbulance and weakens wall

170
Q

laplace and aneurysm

A

aneurys will get progressively larger regardless of cause. as radius expands, wall tension increases

171
Q

true aneurysm

A

bounded by arterial wall components

172
Q

false aneurysm

A

breach in vascular wall

173
Q

fusiform aneurysm

A

make up majority, uniform dilation involves entire vessel

174
Q

saccular

A

less common- localized, balloon shaped outpoutching that involves only portion of vessel wall

175
Q

crawford1

A

originates distal to subclavian artery

176
Q

crawford 2

A

involves entire aorta distal left subclavian

177
Q

crawford3

A

involves distal half of descending thoracic aorta and entire abd aorta

178
Q

crawford4

A

involves infradiaphragmatic aorta

179
Q

dissection

A

an expanding hematoma within aortic wll, caused by either an intimal tear or degeneration of media

180
Q

4 major inherited disorders that are known to effect major arteries

A

marfans, ehlers-danlos, biscupid aortic valve, nonsyndromic familial aortic dissection

181
Q

marfans

A

most prevelent connective tissue disorders- mutations in fibrillin-1 gene

182
Q

ehlers danlos

A

group connective tissue disorders, syndrom type IV only type with increased risk death- mutations type III procollagen gene

183
Q

bicuspid aortic valve

A

most common congenital anomaly resulting in aortic dilation/dissection

184
Q

nonsyndromic familial aortic dissection

A

no criteria marfans,

185
Q

dissection usually

A

in right lateral wall of ascending aorta or close to ligamentum arteriosum

186
Q

patho dissection

A

tear in intima, inflow of blood along aortic media, separates intima and media, creates false lumen

187
Q

debakey type 1- dissection

A

intimal tear originates in prox ascenting aorta- involves variable lenghts of arch, descending and abd aorta

188
Q

debakey type 2-dissection

A

contained to ascending aorta

189
Q

type 3

A

confined to desending thoracic aorta

190
Q

type iiib

A

extends into abd aorta and iliacs

191
Q

dissection and anesthesia

A

minimize increases blood pressure

192
Q

perfusion pressures distal to the clamp in aortic surgery are

A

directly dependent on proximal aortic pressures (above the clamp) not CO or intravascular volume

193
Q

goal in aortic surgery is to

A

maintain distal aortic pressures (permissive hypertension), decrease afterload, normalize preload, coronary blood flow and contractility

194
Q

hemodynamic responses to aortic unclamping

A

decreased SVR and bp, CO no change, LVEDP decreases, Myocardial blood flow increases, hypotension (hypoia mediate, central and vasoactive

195
Q

clamping aorta hemodynamics

A

increased filing pressures- cvp, lvedp, pcwp, increased SVR and BP, decreased CO, increased pulm vascular resistance, systemic hypertension causes increased afterload,

196
Q

risks with aortic surgery

A

spinal cord ischemia, mi and heart failure, hypothermia, coagulopathy, renal insufficiency, pulm complications

197
Q

if la is used during aorta it may

A

produce sensory and motor anesthesia which delays the recognition of anterior and spinal artery syndrome

198
Q

primary cardiomyopathy

A

genetic, mixed, acquired

199
Q

genetic cardiomyopathy

A

hypertrophi, arrhythmogenic, left ventricular noncompaction

200
Q

mixed cardiomyopathy

A

dilated cardiomyopathy, primary restrictive nonhypertrophic cardio

201
Q

acquired cardiomyopathy

A

myocarditis, peripartum, stress

202
Q

secondary cardiomyopathies

A

toxic, inflammatory, infiltrative, storage, endomyocardial, endocrine, neuromuscular, autoimmune

203
Q

hypertrophic cardiomyopathy

A

genetic- autosomal dominant. lv hypertrophy (most common anterolateral)

204
Q

s/s hypertrophic cario

A

fatigue, dyspnea, chest pain, palpitations, syncopeecho lv wall thick>15mm, ecg, mri, myocardial biopsy

205
Q

diagnosis HCM

A

diagnosis, ef>80, lv wall>15

206
Q

manifestations HCM

A

myocardial hypertrophy, lv outflow tract, diastolic dysfunction, myocardial ischemia, dysrhythmias

207
Q

most common arrhythmias with HCM

A

a fib

208
Q

tx HCM

A

beta blockers, CCB, diuretic, amiodarone, ICd

209
Q

anesthesia and hypertropic cardiomyopathy

A

avoid increase LVOT obstruction

210
Q

what increases LVOT

A

increase in myocardial contractility, decrease in preload, decrease in afterload

211
Q

what decreases preload

A

vasodilators, hypovolemia, tachycardia

212
Q

what decreases afterload

A

hypotension, vasodilators

213
Q

what increases myocardial contractility

A

beta adrenergic stim, digitalis

214
Q

hypertrophic cardiomyopathy avoid

A

atropin/glyco b/c increase HR

215
Q

goal anesthesia hypertorophic cardiomyopathy

A

avoid tachycardia, maintain preload, maintain afterload, maintain contractiity, maintain NSR do not inactivate DDD pacemaker if placed for gradient reduction

216
Q

what do you use for hypotension with HCM

A

phenylephrine, not ephedrine, dopamine, dobutamine

217
Q

most common cardiomyopathy

A

dilated

218
Q

s/s dilated cardiomyopathy

A

heart failure (initial), chest pain on exertion, dyspnea

219
Q

dilated cardiomyopathy diagnosis

A

echo: ef<40%, ecg- lbbb, s segment abn, r heart cath- increased wedge pressure, increased SVR, decreased CO

220
Q

tx dilates cardiomyopathy

A

gen supportive measures- adequate weight loss, na and diet, fluid restriction

221
Q

anesthetic management dilated cardiomyopathy

A

ppv and peep may be beneficial, fluid management, monitoring

222
Q

stress induced cardiobyopathy mimics

A

signs of mi

223
Q

cardiac transplant patient reminders

A

aseptic technique, these pateints are denervated- no sympathetic innervation, no parasymp innervation, no sensory

224
Q

consequences denervation

A

loss of vagal tone, carotid massage and valsalva have no effect, nod irect symp restponse to DL or TE, blunt hr response to pain, no immed response to hypovolemia

225
Q

pvd

A

slow, progressive circulatory disorder may involve arteries, veins, lymphatics

226
Q

PAD

A

atherosclerosis major

227
Q

progression of atherosclerosis

A 
endothelial injury
accumulation of LDL
monocyte adhesion to endothelium
transformation of monocytes into macrophages and foam cells
platelet adhesion
smooth muscle cell recruitment, prolif
lipid acumulation extra and intra cell
228
Q

progression atherosclerosis

A

damaged endothelium, fatty streak and lipid core, fibrous plaque, complicated lesion, trhombus, plaque is complicated by red thrombus depositoin

229
Q

most commonly effected vessles pad

A

pelvis, le

230
Q

assessment findings

A

diminished/absent pulses, dry/shiny/hairless skin, pallor on elevation, dusky pale mottled skin, cool or cold limb, deep small, round ulcers

231
Q

s/s pad

A

intermittent claudication (main), pain, burning, tightening, cramping, fatigue, lower extrem- triggered by activity and relieved by rest

232
Q

diagnosis pad

A

doppler, abi, angiography ratio is less than 0.9 with claudication

233
Q

abi normal

A

1.0-1.2

234
Q

severe pad 0-0.4

A

true

235
Q

rutherford scale

A

o- asymptomatic
1-mild claudication
2-moderate
3-severe claudication
4-rest pain
5- ischemic ulceration not exceeding ulcer of digits foot
6- severe ischemic ulcers or frank gangrene

236
Q

when pad present

A

6-7x higher risk MI, CVA

237
Q

intraop

A

avoid/limit pure alpha agonists aggressive hr and bp control

238
Q

virchows triad in thrombosis

A

endothelial injury,, hypercoagulability, abnormal blood flow

239
Q

endothelial injury

A

loss of endothelium>exposure of subendothelium>adhesion platelets>release tissue factor>local depletion of prostacylin>plasminogen activators

240
Q

abnormal blood flow

A

promotes endothelial activation and enhances procoagulant activity, disrupts laminar flow and brings plt in contact with endothelium

241
Q

turbulence

A

primary causative factor in arterial and cardiac circulation, causes endothelial injury and pockets of stasis

242
Q

primary causative factor in venous circulation for thromboembolism

A

stasis

243
Q

risk thromboembolism

A

age,metabolic syndrome, trauma, surgery, immobiliation, cancer, pregnancy

244
Q

arterial thromboembolism form in

A

areas of turbulence and endothelial injury

245
Q

myocardial infarction is main cause of

A

intracardiac thrombi by causing dyskinetic wall motion and damage to endocardium

246
Q

venous thromboembolism

A

occur at sites of stasis, primarily lodge in pulm capillary beds

247
Q

arterial thromboemoblism most arise from

A

mural thrombi- 2/3 left vent infarct, 1/4 left atrial dilation and fibrillation

248
Q

most common severe manifestations of atherothrombosis

A

mi and stroke

249
Q

most common source of cerebral artery thromboemb

A

cardiac mural thrombi or a fib and valve disease

250
Q

where is most often affected in cerebral artery thromboemb

A

middle cerebral artery

251
Q

mi most common source

A

ruptured atherosclerotic plaques

252
Q

venous thromboembolism triggered by

A

procoag activity on intat endothelium from inflammation and/or stasis

253
Q

what is most significant clinical manifestation of venous thromboembolism

A

pulm embolism

254
Q

2 main pathophysiologic consequences pe

A

respiratory compromise from non-perfused, ventilated alveoli, circulatory compromise from increased resistance in pulm blood flow

255
Q

clinical manifestation pe

A

dyspnea, chest pain, fever, tachypena, cough, blood tinged sputum, coarse breath sounds, new s4

256
Q

regional and decreased incidence dvt

A

sympathectomy- increased lower extrem. blood flow, decreased plt activity, faster ambulation post op,

257
Q

acyanotic heart defects

A

vsd, asd, coarc of aorta

258
Q

cyanotic defects

A

tetrology, total anomolous pulm vascular connection

259
Q

left to right shunt

A

not initially assoc with cyanosis, increased pulm blood flow can lead to pulm htn and rv hypertrophy. potential for rv hf

260
Q

what does l to r shunt lead to

A

eventually pvr increases above svr which will reverse shunt right to left (unoxygenated blood will enter the ystemic circ)

261
Q

ostium secundum

A

located near intrarterial septum most

262
Q

ostium primum

A

large opening in the interatrial septum, adjacent to av valve

263
Q

sinus venosus

A

located near entracnce SVC

264
Q

ASD s/s

A

dyspnea, supravent dyshryth, r heart failure, paradoxical embolism, recurrent pulm infections, systolic ejection murmur

265
Q

asd large shunt

A

2 cm left to right

266
Q

small asd

A

0.5cm- no hemodynamic compromise

267
Q

if pulm blood flow is 1.5x systemic blood flow

A

asd should be closed to prevent rv dysfunction adn irreversible pulm htn

268
Q

ASD anesthetic managment

what not to do

A

avoid increased SVR, avoid decreased PVR b/c leads to increased L-R shunting
avoid high fio2- decreases pvr and increases pulm blood flow
no air bubbles

269
Q

what to do with asd and anesthesia

A 
decrease left to right shunt-
decrease SVR (VA)
increase PVR (ppv)
270
Q

antibiotic prophylaxis

A

valve with artifical material, hx of endocarditis, heart transplant, certain congenital defects- cyanotic not repaired, or congentital repaired with artificial material or a device for the fist 6 monts after procedure

271
Q

3 types VSD

A

membranous, supracristal, muscular

272
Q

VSD s/s

A

small- may not have s/s

large- svr exceeds pvr left to right shunting

273
Q

diagnosis vsd

A

systolic holistic murmur, enlarged l atria/vent on ecg/ xray with atrial/vent enlargement, echo, heart cath

274
Q

VSD surgery what not to do

A

avoid increase in svr, avoid decrease pvr b/c leads to increased shunting, avoid hypovolemia, avoid increased myocardial contractility

275
Q

coarctation of aorta

A

preductal- proximal to ductus arteriosus or ligamentum arteriosum, ductal occurs at the insertion of ductious arteriosus, postductal- distal to ductus arteriosus

276
Q

s/s coarctation of aorta

A

htn with absent femoral pulse, headache, dizziness, palpitations, harsh systolic ejection murmur

277
Q

tet anesthesia managment

A

avoid decreased SVR, avoid increased PVR avoid increased myocardial contractility…. why? increased right to left shunt, increased arterial hypoxemia

advanced bioscience (2 decks)

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