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CV Test 3 > Ischemic Heart Disease > Flashcards

Ischemic Heart Disease Flashcards

1
Q

What does the left coronary supply?

A

LV anterior wall
LV anteroseptal wall
The largest part of the LV

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2
Q

What does the right coronary supply?

A

RV
SA, AV node
LV inferior wall

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3
Q

What is another name for the LV inferior wall?

A

The diaphragmatic wall

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4
Q

What are the main branches off of the left coronary artery?

A

Left anterior descending

Circumflex

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5
Q

What is the main branch off of the right coronary artery?

A

Posterior descending

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6
Q

What is the Sinus of valsalva?

A

A dilation about the aortic valve which allows the valve to open efficiently without occluding the coronary Ostia

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7
Q

What is another name for the innominate artery?

A

Brachiocephalic artery

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8
Q

What is another name for the innominate artery?

A

Brachiocephalic artery

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9
Q

Which coronary dominance is more common?

A

Right dominant

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10
Q

What does it mean to be right coronary dominant?

A

The RCA feeds the PDA

Taylor: More volume of blood flows through the right coronary than the left

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11
Q

What is the second most common coronary dominance?

A

Equal right and left blood flow

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12
Q

What is the least common coronary dominance?

A

Left coronary dominance

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13
Q

A lesion in the LAD causes an infarct where?

A

Anterior LV

Anteroseptal LV

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14
Q

In what leads will an anterior LV infarct be seen?

A

V3-V4

Co-existing: V3-V5
Barash: I, aVL, V1-V4

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15
Q

In what leads will an anteroseptal infarct be seen?

A

Anterior V3-V4
Septal V1-V2

Co-existing: V3-V5

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16
Q

A lesion in the RCA will cause an infarct where?

A

Inferior Wall LV
RV, RA
SA and AV node

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17
Q

In what leads will an inferior wall infarct be seen?

A

II, III, aVF

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18
Q

What else does the RCA supply that can cause dysrhythmias?

A

SA and AV nodes

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19
Q

A lesion in the circumflex causes an infarct where?

A

Posterior LV

Lateral LV

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20
Q

In what leads can a lateral infarct be seen?

A

I, aVL, V5-V6

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21
Q

What structure receives most of the coronary venous drainage?

A

Coronary sinus

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22
Q

Where is the coronary sinus located?

A

RA

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23
Q

What veins drain venous blood into the heart chambers?

A

Thebesian veins

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24
Q

Why does the blood that enters the aorta have just slightly lower PO2 than it did when it left the lungs?

A

Venous admixture from venous drainiage from heart and bronchial supply of the lungs

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25
Q

How much of CO goes to the coronaries?

A

4-5%

-225 mL/min

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26
Q

Does metabolism affect the amount of CO that flows to the coronaries?

A

Yes

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27
Q

What predominently increases blood flow to the coronaries when metabolism increases?

A

Local factors

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28
Q

What is the predominant substance released by the heart itself inorder to cause vasodilation when metabolism is increased?

A

Adenosine

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29
Q

What is the Vasodilator theory?

A

Tissues release vasodilator substance as a result of increased metabolism

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30
Q

Where do the tissue released vasodilator subastance act?

A

Precapillary sphincter

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31
Q

When does blood flow through the coronaries?

A

During diastole

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32
Q

Why does blood flow to the coronaries during diastole?

A

Ventricular pressure during systole compresses the coronaries

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33
Q

What causes blood to flow

A

Pressure gradients

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34
Q

What opposes the movement of blood in the coronary arteries?

A

Tissue pressure within the myocardium (systole)

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35
Q

During systole, where in the myocardium is the highest pressure?

A

Subendocardium

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36
Q

What layer of the maycardium is at greatest risk of not receiveing adequate blood flow?

A

The subendocardium, because it is under the most pressure during systole

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37
Q

What layer needs the most blood flow/O2?

A

Subendocardium

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38
Q

What is the heart’s main source of fuel for metabolism?

A

Fatty acids (stead of carbs)

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39
Q

Is the heart able to use anerobic metabolism?

A

Yes

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40
Q

What is released when tissues use anerobic metabolism?

A

Lactic Acid

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41
Q

How is lactic acid related to angina?

A

Lactic acid is a tissue irritant

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42
Q

How much oxygen does normal perfusion deliver to the heart?

A

8-10 mL/100g/min

-g of tissue

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43
Q

How efficient is the heart in extracting oxygen?

A

Very. It can extract 65-75% of the oxygen

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44
Q

What occurs when the heart needs more oxygen?

A

The only way to increase oxygen is to increase blood flow

-the heart can not increase it’s extraction

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45
Q

Besides the vasodilator theory, what else could be the cause of coronary dilation in times on increased demand?

A

Oxygen demand theory

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46
Q

What is the oxygen demand theory?

A

Vasocontriction requires constant oxygen, so when oxygen is inadequate vessels passively dilate

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47
Q

What does SNS stimulation cause in the heart?

A

Increased HR and contractility

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48
Q

What are the indirect effects of SNS stimulation on the heart?

A

Due to SNS induced increased contractility and HR, the metobolic rate of the heart is also increased, so the vessels dilate to get more blood flow

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49
Q

Which effect during SNS stimulation of the heart predominants?

A

The dilation effects

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50
Q

What vascular response do alpha receptors have to SNS stimulation?

A

Vasoconstriction

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51
Q

What vascular response do beta receptors have to SNS stimulation?

A

B1 increased HR and contractility

B2 Vasodilation

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52
Q

What type of adrenergic receptors are present on the coronaries?

A

alpha and beta 2 receptors

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53
Q

What response does SNS stimulation have on beta 1 receptors?

A

Increase HR and contractility

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54
Q

How does SNS stimulation increase HR and contractility?

A

Through beta 1 receptors on the heart

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55
Q

Heart’s response to SNS activity

A 
Vasoconstriction due to alpha receptors
Increases HR and contractilty through B1
Increased metabolism and O2 demand
Local factors release Adenosine to cause vasodilation and increase blood flow
B2 stimulation causes vasodilation
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56
Q

What response does PSNS have on the heart?

A

Decreases HR > decreases metabolism, so the heart doesn’t need as much blood flow

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57
Q

What is vagospastic disease?

A

A strong alpha response in coronary arteries

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58
Q

What is occuring with vagospastic disease?

A

With SNS stimulation alpha vasoconstriction predominates > angina and ischemia

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59
Q

How is vagospastic disease treated?

A

Calcium channel blockers

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60
Q

In the cath lab a person with vagospastic disease may have what result?

A

Clean coronaries

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61
Q

What factors affects coronary blood flow?

A

Vessel patency
Perfusion pressure
Heart rate

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62
Q

What can affect vessel patency?

A

CAD and spasm

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63
Q

What determines perfusion pressure?

A

DBP and LVEDP

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64
Q

What about HR affects coronary perfusion?

A

Time spent in diastole

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65
Q

CPP =

A

CPP = DBP-LVEDP

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66
Q

What affects arterial oxygenation?

A

Hemoglobin

-quantity and quality

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67
Q

What affects saturation?

A

FiO2 and gas exchange

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68
Q

What supply factors affect myocardial oxygen balance?

A 
Vessel patency
Perfusion pressure
HR
O2 extraction 
-Hgb
-Saturation
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69
Q

What demand factors affect myocardial oxygen balance?

A

HR
Preload
Afterload
Contractility

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70
Q

What affects wall tension?

A

Preload and afterload

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71
Q

How does HR affect demand of O2?

A

Increased HR increases metabolism

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72
Q

How does contractility affect demand of O2?

A

Increased contractiity increases metabolism

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73
Q

How can contractility affect supply of O2?

A

If stronger contraction decreases LVEDV, this decreases wall tension and increases CPP

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74
Q

How does arterial hypertension affect O2 demand?

A

In order to overcome HTN metabolism is increased and so is demand

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75
Q

How can arterial hypertension affect O2 supply?

A

If the higher systemic BP also increases DBP, then CPP may improve

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76
Q

Does HR affect supply or demand? In what way?

A

Both

  • HR decreases supply
  • HR increases demand
77
Q

What is the number 1 thing to control in a patient that has ichemia heart disease?

A

HR

-do not allow tachycardia

78
Q

What affect does an increase in BP have on the supply and demand of O2 in the heart?

A

BP increases demand, but it may help increase supply (not always)

79
Q

What is more acceptable in a patient with ischemic heart disease hypotension or hypertension?

A

Hypertension

80
Q

What demand factors affect myocardial oxygen balance?

A

Wall tension
HR
Contractility
Systemic HTN

81
Q

High LVEDV increases risk of what?

A

Ischemia

-D/T increase in preload and wall tension

82
Q

What is tolerated better, hypertension or tachycardia

A

HTN

83
Q

Low DBP is a risk for what?

A

Ischemia

-because there is not enough driving perfusion

84
Q

Causes of ischemia heart diease?

A 
Artherosclerotic plaque
Vascular disease
Coronary artery lesions
Coronary stenosis
CAD
85
Q

What are the major risk factors for ischemic heart disease?

A

Male gender

Age

86
Q

What are the nother risk factors for ishemic heart disease?

A 
Obesity
Sedentary life style
HLD
HTN
DM
Smoking
Family Hx
PVD
87
Q

Where can angina be located?

A 
Sternal
Left arm/shoulder
Face, neck, jaw
Right arm/shoulder
GI distress
88
Q

What things distinguish angina from infarct?

A

Angina is transient ischemia that can be relieved

  • rest
  • NTG
89
Q

What is the most common cause of an acute occlusion in a coronary artery?

A

Vessel with preexisting plaque is narrowed and a clot gets stuck

90
Q

Coronary vessels with obstructive plaque are more prone to what?

A

Spasm

91
Q

How does the body attest to compensate to ischemic heart disease, angina and transient ischemia?

A

Collateral circulation

92
Q

What is the stimulus for collateral vessels to grow?

A

Long standing ischemia and hypoxia

93
Q

How does infarct differ from angina?

A

Prolonged ischemia
Eventual necrosis
Persistent unrelieved pain
May be asymptomatic

94
Q

Diagnostics for MI

A 
12 lead
Pathologic Q wave
ST segment changes
PVCs are common
Elevated temperature from inflammatory response
Troponin
95
Q

How much oxygen does myocardial tissue usually require?

A

8 mL/100g/min

96
Q

Necrosis occurs when myocardial oxygen falls to less than what?

A

< 1.3 mL/100g/min

97
Q

What is stunned myocardium?

A

Tissue that is ischemic without cell death

98
Q

Is stunned myocardium reversible?

A

Yes

-but there is contractile dysfunction

99
Q

Where is stunned myocardium located?

A

In the area around the central necrosis (central part of the infarct)

100
Q

What does MI extension mean?

A

The infarct has extended into the stunned myocardium

101
Q

What is ischemic preconditioning?

A

Inhalation agents have a protective effect on stunned myocardium

102
Q

Why is the subendocardial layer the most vulnerable to ischemia?

A

It is the area that receives the least supply from max compression and it has the most demand because it has the highest oxygen need

103
Q

What is another name for a subendocardial MI?

A

Non Q wave MI

-more minor since it has not gone all the way through the layers, but indicates something needs to occur

104
Q

What is the formula for coronary perfusion pressure?

A

CPP = DBP-LVEDP

105
Q

How does decreased DBP affect CPP?

A

decreases CPP

106
Q

How does increased LVEDP affect CPP?

A

Decreases CPP

107
Q

What is the risk with a decreased CPP?

A

Ischemia and infarct

108
Q

What may an elevated DBP be needed/helpful?

A

In patients with CAD

109
Q

How can LVEDP be measured?

A

PCWP

PAD - pulmonary artery diastolic pressure

110
Q

Why do MIs cause decreased CO?

A

Loss of muscle and contractility

111
Q

Why is there risk of cariogenic shock with an MI?

A

Poor tissue perfusion due to decrease SV from loss of contractility
-Increased risk with larger infarcted areas

112
Q

What happens with blood flow due to an MI?

A

Damming of blood occurs

  • lack of forward flow
  • accumulates in lungs and periphery
  • renal fluid retention
113
Q

What is systolic stretch?

A

Infarcted area bulges outward with each contraction (instead of the normal inward)

114
Q

What is a possible consequence of systolic stretch?

A

Area may rupture

115
Q

How does vasodilation cause coronary steal?

A

Vasodilation in health tissue pulls blood flow from ischemic area

116
Q

What causes coronary steal?

A

Activity or vasodilating drugs

117
Q

What is the treatment for chest pain in preop?

A 
O2
Rest
NTG
BB
Thrombolytic
Surgical revascularization or angioplasty
118
Q

Does NTG dilate veins or arteries more?

A

Veins

119
Q

With NTG is preload or afterload decreased?

A

Preload

120
Q

With NTG decreasing preload is O2 demand decreased or supply increased?

A

Demand is decreased

121
Q

What affect do BB have on the O2 supply and demand?

A

BB decrease demand by decreasing HR and increases supply by decreasing HR

122
Q

What affect does thrombolytics have on the O2 supply and demand?

A

They increase supply by restoring blood flow

123
Q

What surgical sites increase risk of cardiac complications?

A

Thoracic

Upper abdominal

124
Q

What type of procedures increase risk of cardiac complications?

A

Vascular procedures

125
Q

What clinically can be used to assess LV function?

A 
Activity tolerance
-SOB
Breath sounds
Peripheral edema
Neck vein distention
126
Q

What diagnostic tests can be used to assess LV function?

A

Echocardiogram
Ejection fraction
Cardiac cath
-Wall motility

127
Q

What is the number 1 predictor of cardiac complications in surgery?

A

Symptomatic CHF

128
Q

Is current, symptoms CHF a contraindication to elective surgery?

A

Yes

129
Q

What is the goal during anesthesia for a patient with poor LV function, but no acute CHF?

A

Optimal LV function

  • fluid balance
  • optimal filling pressure
  • +/- invasive monitoring
  • avoid drug induced myocardial depression
130
Q

What questions do you ask about chest pain?

A 
Duration
Frequency
Precipitating factors
At rest - non cardiac vs vasospastic
Relief measures
131
Q

History of MI increases risk of complications, especially with what surgical location?

A

Thoracic or upper abdominal

132
Q

What is the importance of timing of an MI and an elective procedure?

A

If less than 30 days since MI, postpone elective procedures

133
Q

What constitutes stable angina?

A

No change in 60 days

134
Q

What is the anesthetic goal in a patient with angina?

A

Maintain myocardial oxygen supply and demand

135
Q

If angina is unstable or accelerating what should be obtained?

A

Cardiac consult

  • stress test
  • cardiac cath
136
Q

What is unstable coronary syndrome?

A

Acute MI
Recent MI
Unstable angina

137
Q

Is the risk of recent subendocardial MI different from the risk of recent transmural MI?

A

No, risk is the same

138
Q

What are the postop cardiac complications associated with risk of unstable coronary syndrome?

A 
MI
Pulmonary edema
CHF
Arrhythmias
Thromboembolism
139
Q

What is THE most common cause of myocardial ischemia?

M&M

A

Atherosclerosis of coronary arteries

140
Q

Major preop risk factors for CAD?

A 
Hyperlipidemia
Hypertension
Diabetes
Smoking
Increasing age
Male
Family Hx
141
Q

Other preop risk factors for CAD

A

Hx of cerebrovascular or peripheral vascular disease
Menopause
High-estrogen oral contraceptives by smokers
Sedentary lifestyle

142
Q

What is unstable angina?

A

An abrupt increase in servity, frequency or duration
Angina at rest
New onset with severe or frequent episodes

143
Q

What is Chronic Stable Angina?

A

Relieved by NTG or rest

144
Q

What patients are at increased risk for silent ischemia?

A

Diabetics

145
Q

Before what percentage of occlusion of coronaries are patients generally asymptomatic?

A

50-75%

146
Q

At what percentage of occlusion is maximum compensatory dilation usually present distally in the coronaries?

A

70%

147
Q

What factors may precipitate vasospastic episodes?

A

Emotional stress or upset

Hyperventilation > hypocapnia > coronary artery vasoconstriction

148
Q

How do beta blockers help ischemic heart disease?

A

They decrease O2 demand by decreasing HR and contractility, and in some cases afterload

149
Q

What affects can occur with B2 blockade?

A

Mask hypoglycemic symptoms
Delay metabolic recovery from hypoglycemia
Impair the handling of large K+ loads

150
Q

How do calcium channel blockers help ischemic heart disease?

A

They reduce myocardial oxygen demand by decreasing cardiac afterload and augment myocardial oxygen supply via coronary vasodilation

151
Q

What CCBs also reduce demand by decreasing HR?

A

Verapamil and diltiazem

152
Q

What class and specific drug is used primarily in preventing cerebral vasospasm following subarachnoid hemorrhage?

A

Nimodipine - CCB

153
Q

What affect if any do CCB have on NMB?

A

All CCB potentiate depolarizing and nondepolarizing NMB agents

154
Q

What affect is potentiaed by CCB with inhalation agents?

A

Circulatory effects

155
Q

Verapamil and diltiazem can potentiate what affects of VAs?

A

Depression of cardiac contractility and conduction in the AV node

156
Q

Nifedipeine and similar agents can potentiate what affects of volatile and IV agents?

A

Systemic vasodilation

157
Q

How do nitrates help with ischemic heart disease?

A

Reduce myocardial O2 demand by:

  • decrease venous and arteriolar tone
  • increase vascular capacitance
  • reduce ventricular wall tension
158
Q

Where does nitrite-induced coronary vasodilation preferentially increase blood flow?

A

In the subendocardial ischemic areas

159
Q

Where in epicardial vessels do obstructions most commonly occur and why?

Nagelhout

A

Areas of bifurcation, because flow is turbulent

160
Q

Coronary artery dominance %

A

RCA 50%
LCA 10-15%
Mixed R and L 35-40%

161
Q

What factors determine myocardial oxygen supply?

A 
Arterial blood content
DBP
Diastolic time as determined by HR
Oxygen extraction
Coronary artery blood flow
162
Q

What determines myocardial oxygen demand?

A

Preload
Afterload
Contractility
HR

163
Q

What is the most important factor that negatively affects MVO2?

A

HR, doubling HR doubles MVO2

164
Q

How can oxygen delivery to the myocardium increase?

A

Only by increasing blood flow

165
Q

What vasodilator substances have been identified and are released from the myocardium?

A 
Adenosine
Adenosine phosphate compound
Potassium ions
Hydrogen ions
Carbon dioxide
Bradykinin
Prostaglandins
166
Q

How is oxygen extraction in the coronaries determined?

A

By measurement of the difference between the oxygen tension in the pulmonary arterial blood and that in the coronary sinus

167
Q

What is the equation for arterial oxygen content?

A

CaO2 = (SaO2 x Hgb x 1.34) + (0.003 x PaO2)

168
Q

Coronary blood flow is autoregulated through what range?

A

MAP range of 60 to 140 mmHg

169
Q

What determines coronary blood flow if MAP is outside of autoregulated range?

A

Coronary blood flow becomes pressure dependent

170
Q

During hypotension, coronary arteries are maximally dilated, what equation determines blood flow?

A

MAP - RAP

171
Q

CPP =

A

DBP - LVEDP

172
Q

What is the major determinant of CPP?

A

DBP, because under normal conditions it is significantly higher than LVEDP

  • N: DBP 80
  • N: LVEDP 10
173
Q

What is coronary vascular reserve?

A

The difference between the maximal flow and the autoregulated flow
-closer the two values, the lower the reserve

174
Q

What decreases coronary reserve flow?

A

Factors that increase myocardial oxygen demand and limit supply

175
Q

What is coronary steal?

A

If a patient has a stenotic coronary vessel with collateral flow and a vasodilator is given, only the autoregulated vessel dilates and receives preferential flow over the stenotic area

176
Q

What is at coronary steal-prone anatomy?

A

Completely occlusion of one artery and at least 50% of a second artery that supplies collateral blood flow to the occluded area

177
Q

How are volatile anesthetics myocardial preconditioners?

A

Decrease the formation of free radials, preserving myocardial ATP stores and inhibiting intracellular calcium

178
Q

What is the most useful measure of CPP in the clinical setting?

A

MAP

179
Q

In patients with CAD, what happens to coronary autoregulation just after the partial obstruction?

A

It becomes pressure dependent, especially with MAP below 70

180
Q

What is the most significant cause of peri operative ischemia?

A

Increased HR

181
Q

Ideally what is the best HR for patients with CAD or elevated LVEDP?

A

It’s determined on an individual basis, but less than 70 is a good guide

182
Q

With myocardial ischemia, what occurs first systolic or diastolic dysfunction?

A

Diastolic

183
Q

What is the most sensitive intraoperative monitor for detecting myocardial ischemia?

A

TEE

184
Q

What is experienced with brief periods of myocardial ischemia (< 20 minutes)?

A

Necrosis does not occur, but reversible contractile dysfunction (stunning) can

185
Q

What is stunning? How long can it last? Treatment?

A

Stunning is reversible contractile dysfunction

  • 12-24 hours
  • inotropic support
186
Q

What is ischemic preconditioning?

A

Phenomenon whereby a short period of ischemia improves the heart’s ability to tolerate subsequently longer periods of ischemic insult

187
Q

What causes/is hibernation?

A

A state of left ventricular dysfunction at rest caused by reduced coronary blood flow, which can be reversed by restoring myocardial oxygen supply or reducing demand

188
Q

Besides patient’s with CAD, who else will benefit from high perfusion pressure and low HR?

A

Chronic HTN
Aortic stenosis
Obstructive cardiomyopathy

189
Q

What determines coronary dominance?

A

Which main coronary artery supplies the PDA

CV Test 3 (3 decks)

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