Intracardiac Flashcards

1
Q

The determinants of Myocardial Oxygen Demand (MVO2) are:

A

Wall Tension

Contractility

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2
Q

What are the determinants of coronary blood flow?

A
  1. Perfusion pressure and vascular tone of the coronary arteries (duh)
  2. The time available for perfusion (since perfusion only happens during diastole, perfusion time with decrease with an increase in HR)
  3. Severity of intraluminal obstructions (blockages)
  4. Presence or absence of collateral circulation
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3
Q

The area of the heart most vulnerable to ischemia is:

A

the subendocardium of the LV

It has the highest intracavitary pressure and the greatest metabolic requirements

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4
Q

LV coronary perfusion pressure is determined by:

A

The aortic diastolic pressure and the LV diastolic pressure (LVDP)

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5
Q

What is the MOST important cause of intraoperative and perioperative ischemia?

A

Tachycardia

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6
Q

What is the coronary vascular reserve?

A

The difference between the auto regulated flow through the coronary arteries and the amount of flow it CAN acheive under maximal vasodilation

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7
Q

Supply Ischemia results from:

A

transient coronary occlusion (like from a clot or vasospasm)

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8
Q

Demand Ischemia results from:

A

the inability to increase coronary blood flow and oxygen delivery in response to an increased MVO2

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9
Q

Coronary goals for patients with CAD are:

A

Slow (heartrate)

Small (ventricle size)

Well Perfused

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10
Q

To maintain MVO2 you’re aiming for ______ heart rate and _____ Blood Pressure

A

Slow heartrate

High blood pressure (vs hypotension)

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11
Q

What do the a and v waves of a PAOP waveform indicate?

A

A is for atrial systole

V is for ventricular systole

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12
Q

If you see an elevated a wave on a wedge, what does that tell you?

A

Primary Diastolic Dysfunction

There is decreased LV compliance. The LA is having to work very hard to pump into the LV

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13
Q

If you see an elevated V wave on a wedge waveform, what does that tell you?

A

There is pressure building up in the LA during LV contraction

This means there is mitral regurgitation or papillary muscle disfunction due to ischemia

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14
Q

Why would you run nitroglycerin and a pressor together?

A

If you want to increase the BP to improve perfusion pressure, but want to mitigate the increase in preload a pressor will cause

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15
Q

Which CCB has the largest negative inotropic effect?

Which one has the least?

A

Verapamil has the most

Nicardipine has the least

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16
Q

What is the normal area of the AV?

A

2 - 4 cm2

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17
Q

What is the normal diameter of the LVOT?

A

2 - 2.4 cm

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18
Q

What are the classic symptoms of AS?

A

Angina

Syncope

Dyspnea

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19
Q

AS usually becomes symptomatic when the orifice is reduced to:

A

0.8 - 1 cm2

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20
Q

How is atrial kick impacted by aortic stenosis?

A

Normally atrial kick only accounts for about 10% of ventricular filling, but as the LV gets stiffer and less compliant, filling becomes more dependent on atrial contraction

In AS, the atrial kick may account for up to 30-40% of LVEDP

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21
Q

What are the three big goals for hemodynamic management of a patient with AS?

A

Avoid Hypotension (their coronary perfusion pressure is already marginal)

Maintain sinus rhythm (they need atrial kick and an adequate stroke volume)

Avoid heart rate extremes (bradycardia will decrease CO and tachycardia will cause ischemia)

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22
Q

What are the three big goals for hemodynamic management of patients with HOCM?

A
  1. Avoiding extreme HR
  2. Maintain or increase preload (to prevent LVOT obstruction)
  3. No increase in contractility
  4. Maintain sinus rhythm (rely on atrial kick)

NOTE: very similar to AS, because similar problems with both

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23
Q

What causes acute aortic insufficiency?

A

bacterial endocarditis

aortic dissection

trauma

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24
Q

What the difference between eccentric and concentric hypertrophy?

A

Eccentric means the intraventricular size is increasing

Concentric means the ventricle thickness is increasing

They often occur together. Any amount of eccentric hypertrophy will usually cause some amount of concentric hypertrophy

25
Q

What BP alterations would you see in a patient with AI?

A

An increased pulse pressure: increased systolic, decreased diastolic, which ultimately leads to aortic dilation and increased LV systolic pressure

26
Q

When should patients with aortic insufficiency ideally receive a new valve?

A

BEFORE EF is less than 50% and BEFORE any LV dilation

27
Q

What is the main hemodynamic goal in patients with AI?

A

Avoid any increase in LV wall stress:

  1. Slightly increase preload so that you can decrease afterload without causing problems
  2. Decrease afterload
  3. Increase HR (to reduce ventricular volume)
28
Q

Why does aortic insufficiency alter the way we administer cardioplegia?

A

When we’re giving cardioplegia, we’re pouring it into the aorta. Ordinarily this flows into the coronary arteries, but with an incompetent valve it flows into the ventricle instead

WIth AI, they inject the solution directly into the coronary ostia or do it retrograde through the coronary sinus

29
Q

What is the most common cause of mitral stenosis?

A

atherosclerosis-associated calcification and endocarditis

30
Q

Mitral stenosis can cause regurgitation in which valve?

A

Tricuspid (Because the RV is working so much harder)

31
Q

What kind of anesthetic would be ideal for a patient with mitral regurgitation?

A

one that promotes vasodilation and tachycardia

32
Q

What’s the difference between an aneurysm and a dissection?

A

An aneurysm is a bulging

a dissection is a tear

34
Q

Which type of Aortic Dissection is a surgical emergency?

35
Q

Which type of Aortic Dissection can be managed medically?

36
Q

What are the hemodynamic goals with an aortic dissection?

A

Low and Slow (keep preload and afterload low, keep HR 60-80)

37
Q

When they’re large, aortic aneurysms can cause:

A

dysphagia (esophageal compression)

cough (tracheal compression)

hoarseness (RLN compression)

38
Q

Aortic root aneurysms may cause:

A

Aortic Insufficiency (regurg)

39
Q

Surgery is indicated for aneurysms greater than:

A

5.5 cm Ascending

6 cm Descending

40
Q

What percentage of patients who undergo CPB develop subtle cognitive deficits?

41
Q

What is believed to be the predominant cause of perioperative neurologic complications after CPB?

A

Emboli, NOT hypoperfusion

42
Q

When there’s hypotension before CPB, what is usually the cause?

A

Usually it’s from direct manipulation of the atria during cannulation

The more common problem is preventing hypertension during sternotomy etc

43
Q

How can you tell if you have adequate venous drainage on CPB?

A

There should be no pulsatility on your CVP or PA

44
Q

What is the most profound and devastating reaction to protamine reversal after CPB?

A

Profound pulmonary hypertension mediated by thromboxane

Leads to elevated CVP, RV failure, and systemic hypotension

USUALLY SHORT LIVED

45
Q

The S1 is caused by the closure of the ______ valves

The S2 is caused by the closure of the _______ valves

A

S1: AV

S2 Semilunar

47
Q

What are the cardioaccelerator fibers and where do they originate?

A

The preganglionic SNS fibers

T1-T4

48
Q

Where the do the preganglionic ParaSNS fibers originate?

A

the motor nucleus of the medulla

49
Q

How does ParaSNS alter cardiac cellular membranes?

A

Hyperpolarizes by increasing K transport INTO the cell

50
Q

Why does the SA node have a different resting membrane potential than the rest of the myocardium?

A

Leaky sodium channels hypopolarize the membrane

51
Q

What is the primary substance responsible for autoregulatory vasodilation in the myocardium?

52
Q

What is the autoregulatory range of the myocardium?

A

MAP of 60-140

54
Q

Hypertensive patients are volume up or volume down?

A

Generally, volume down (hypovolemic)

Either through renal compensation, extreme vasoconstriction that reduces preload, or from diuretics

55
Q

Why is induction difficult with hypertensive patients?

A

They have a strong hypotensive response to induction agents (because they’re already fluid down) but they have an exaggerated hypertensive response to noxious stimuli (intubation etc)

56
Q

Which is more dangerous in hypertensive patients: the hypotensive response to anesthetics or the hyperdynamic response to stimuli?

A

The hypotensive response

They’ll probably be okay having a high blood pressure during manipulation

They probably wont’ be okay if they have severe hypotension from the meds intended to blunt that hypertensive response

57
Q

What is Beck’s Triad?

A

The triad of symptoms of cardiac tamponade

Hypotension, JVD, Muffled Heart Sounds

58
Q

Which medications will not be effective in effecting the heart rate of a patient with a new transplant?

A

Anything that acts through the sympathetic or parasympathetic stimulation: ephedrine, atropine etc.

Only direct acting medications like epinephrine that have direct-acting effects on catecholamines will work