Coronary Artery Disease Flashcards

1
Q

Describe the anatomy of the coronary blood vessels.

A

Blood flow to the heart is supplied by the right and left coronary arteries. The LCA becomes the left anterior descending and circumflex arteries. The LCA supplies the left atrium and anterolateral LV.
The RCA supplies the RA and RV. Blood to the SA node comes from the LAD (60%) or the RCA (40%). Blood to the AV node comes from the RCA (90%) or circumflex (10%).

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2
Q

What supplies blood to the SA node?

A

Blood to the SA node comes either from the LAD (60% of people) or the RCA (40% of people).

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3
Q

What supplies blood to the AV node?

A

The RCA supplies blood to the AV nodes in 90% of people. The remaining 10% of people have the AV node supplied by the circumflex coronary artery.

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4
Q

What is the O2 extraction ratio of the heart as compared to the rest of the body?

A

The O2 extraction ratio of the heart is approximately 65% versus 25% for the body with a coronary sinus saturation of 30% vs an average of 75% for the MvO2.

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5
Q

How does myocardium increase O2 delivery in periods of higher demand?

A

The myocardium is unable to extract more O2 because O2 is essentially maximally extracted from Hgb, thus the only way it can increase O2 delivery is by inducing coronary artery dilation.

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6
Q

What is the formula for coronary perfusion pressure?

A

CPP = AoDBP - LVEDP

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7
Q

What layer of the heart is most susceptible to ischemia and why?

A

The endocardium is exposed to the greatest pressure and is farthest from the coronary arteries and is thus most susceptible to ischemia (ST segment depression).

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8
Q

How does tachycardia cause LV ischemia?

A

Since LV perfusion primarily occurs during diastole, tachycardia (HR > 120) decreases diastolic filling time.

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9
Q

How does severe bradycardia cause ischemia of the heart?

A

Severe bradycardia can cause ischemia by allowing diastolic runoff and reducing coronary perfusion pressure.

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10
Q

What is the formula for O2 content of blood?

A

O2 content = (1.34 x [Hgb] x [saturation] ) + (0.003 x PaO2)

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11
Q

What is the primary determinant of coronary blood flow?

A

Changes in coronary artery tone (diameter) is the primary determinant of coronary blood flow.

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12
Q

What is the law of Laplace?

A

The law of Laplace defines the relation of wall tension as: Tension = Pressure x radius / (2 x thickness)

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13
Q

What is stable angina?

A

Chest pain that is usually exertional with substernal or radiating pain; however non-exertional and silent (especially with DM) can occur; vasospasm can also occur especially in areas with an epicardial plaque exists.

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14
Q

What is unstable angina?

A

Defined as abrupt increase in severity of angina, frequency ( >3x/day) or duration, or new onset (within past two months); usually not associated with precipitating factors; often associated with severe disease and may precede MI.

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15
Q

What is the progression of detectable changes due to myocardial ischemia?

A
Wall motion abnormalities
Increases in filling pressures (diastolic dysfunction)
Decreases in EF
ST segment changes
CHF
Cardiogenic shock
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16
Q

What is the mortality of myocardial infarction?

A

Overall 25% (mostly due to dysrhythmias); 50% mortality if occurs perioperatively.

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17
Q

What type of MI is caused by an LAD lesion?

A

Anterior, apical, septal

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18
Q

What type of MI is caused by a circumflex lesion?

A

lateral, posterior

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19
Q

What type of MI is caused by an RCA lesion?

A

RV and posterior-inferior

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20
Q

What vessel is involved if an MI affects the RV?

A

RCA

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21
Q

What vessel is involved if an MI affects the posterior-inferior walls of the heart?

A

RCA

22
Q

What vessel is involved if an MI affects the lateral and posterior walls of the heart?

A

Circumflex

23
Q

What vessel is involved if an MI affects the anterior or apical portion of the heart?

A

LAD

24
Q

What vessel is involved if an MI affects the septum of the heart?

A

LAD

25
Q

What causes a non-Q wave MI?

A

Subendocardial ischemia usually occurring with sustained high demand and severe coronary artery stenosis.

26
Q

What is the difference between a non-Q wave MI and a Q-wave MI?

A

Non-Q-wave MIs are characterized by remaining viable myocardium, whereas a Q-wave MI is transmural.

27
Q

When is coronary artery stenosis considered significant?

A

When it reaches 70 - 80%.

28
Q

What is the Bowditch effect?

A

The increase in contractility caused by increase in HR.

29
Q

Why has ischemia due to tachycardia been said to be a “supply side effect”?

A

Tachycardia increases myocardial contractility and thus demand but increasing contractility improves myocardial emptying which can decrease LVEDP and wall tension which decreases demand and perhaps increases supply. Thus if one assumes that these effects cancel each other, then what is left is the decrease in diastolic filling time (and thus decrease in time for perfusion of the LV).

30
Q

What is the mechanism of nitrates when used in patients with CAD?

A

Nitrates dilate subendocardial vessels, increasing blood flow to ischemic areas. They also dilate systemic veins more than arterioles thus decreasing preload (demand). The caveat is that in high-risk patients, the reduction in preload and blood pressure may actually make the ischemia worse. The majority of controlled studies do not recommend its prophylactic use.

31
Q

How do calcium channel blockers affect the heart with CAD?

A

They reduce HR, BP (via vasodilation), contractility (especially diltiazem and verapamil), and vasospasm. They may pontentiate the effects of NDNMBs.

32
Q

What data supports the use of alpha-agonists in patient’s with CAD?

A

Clonidine and mivazerol have been shown to reduce the rate of periop myocardial ischemia, MI, and death. They may be used for control of HTN and reduction of adverse cardiac events.

33
Q

How do alpha-2 agonists work?

A

They attenuate sympathetic outflow, reducing HR, BP, anesthetic requirements, and provide sedation.

34
Q

What anesthetics are superior for the patient with CAD?

A

No single anesthetic has been shown to be clearly superior to another. Desflurane has been shown to be associated with more myocardial ischemia than patients receiving a narcotic-based technique during CABG. Ultimately the differences among the various anesthetic agents appears to be subtle.

35
Q

When in the perioperative period is the highest incidence of MI?

A

The postoperative period.

36
Q

How does exercise tolerance assist your assessment of a patient’s cardiac status?

A

It helps to determine the severity of the disease. Inability to exercise may be due to the cardiac disease or it may be due to other factors, but if the patient is able to exercise vigorously it suggests (in most cases) that the cardiac condition is not severe.

37
Q

How do you know when a disease is optimized for a surgery?

A

When it’s signs and symptoms are controlled to minimize surgical complications without in the process causing harm or incurring undue cost.

38
Q

What is a metabolic equivalent?

A

It is the VO2 of a 70kg, 40 year old man in a resting state which equals 3.5cc/kg/min.

39
Q

A patient has new ST-segment changes but the surgeon, noticing no Q waves wishes to proceed with elective surgery. What would you say?

A

Q waves suggest the presence of a transmural infarct and do not develop until muscle necrosis occurs - a process that takes days. If the ST-changes are new, then myocardial ischemia may be occurring whether or not the patient is symptomatic. Because perioperative MIs are associated with a mortality of 50% I would consider delaying the surgery and ruling out an MI.

40
Q

What is a high therapeutic index?

A

Median lethal dose much higher than median effective dose.

41
Q

What is coronary steal?

A

Steal is a diversion of blood from a post-stenotic ischemic region with maximal post-stenotic coronary artery dilation to a non-ischemic region with still dilatable coronary arteries through post-stenotic collateral vessels.

42
Q

What is the most sensitive ECG lead for detecting ischemia?

A

V5 (lateral). V4 is 2nd most sensitive. Leads II and V5 are often chosen to optimize detection of both ischemia (lateral ischemia with V5 and inferior ischemia with lead II) and dysrhythmias (lead II).

43
Q

What does the V-wave on the PCWP tracing suggest?

A

Mitral regurgitation from papillary ischemia

44
Q

What does an exaggerated a-wave suggest on a PCWP tracing?

A

Ventricular stiffening

45
Q

What is the most sensitive indicator of myocardial ischemia?

A

segmental wall motion abnormalities on TEE

46
Q

What is the earliest change associated with myocardial ischemia on TEE?

A

Systolic thickening

47
Q

Why might a TEE be considered “too sensitive” in its detection of myocardial ischemia?

A

Due to the high frequency of intraoperative changes lacking any postoperative sequelae.

48
Q

What are the goals of GA induction in a patient with severe CAD?

A

Optimization of myocardial supply and demand via the avoidance of tachycardia, hypotension, hypertension, hypoxia, and excessive contractility and filling pressures.

49
Q

Does it matter whether ST segment changes are down-going depressions or elevations?

A

ST segment depression suggest subendocardial myocardial ischemia. If they are down sloping or horizontal they are more specific for ischemia than up-sloping changes. ST elevations are rare during noncardiac surgery, but suggest epicardial ischemia (severe ischemia, vasospasm, or infarction). Changes are only signficant if they are 1mm in size for depressions, 2mm for elevations, and occur 80msec after the J-point (QRS-ST junction).

50
Q

Does intraoperative stability correlate with a lower likelihood of postoperative ischemia?

A

Not really. In setting of CPB, 50% of the episodes of ischemia (preop and intraop) are not accompanied by episodes of hemodynamic instability. So stable vital signs intraop do not mean that postop ichemia will not or did not occur.

51
Q

When is the risk of periop MI the greatest?

A

Postop days 1 - 2 (not 2 - 3 as was formerly thought), emphasizing the importance of adequate pain and HR control.