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Cardiac > Heart Rotation Questions - General > Flashcards

Heart Rotation Questions - General Flashcards

1
Q

When do we bolus heparin and what is the dose

A

300-500 units/kg of patients weight

Prior to cannulation

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2
Q

Protamine reversal dosing

A

1mg for every 100 units of heparin

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3
Q

Why do we use insulin for CPB?

A

Bc insulin resistance occurs when the body temp drops ➡️ hyperglycemia

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4
Q

What do you need to redose during the rewarming phase? (3)

A

Benzos, narcs, and NMBs

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5
Q

What is cardioplegia?

A

A potassium solution administered by the perfusionist to arrest the heart for surgery

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6
Q

Difference between anterograde and retrograde cardioplegia cannulation

A

Anterograde > placed in ascending aorta b/t aortic valve and cross clamp to deliver cardioplegia down the coronary arteries

Retrograde > placed into the coronary sinus and delivers cardioplegia into the coronary veins

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7
Q

Valves of the heart; how many leaflets do each have?

A

Tricuspid, pulmonic, mitral, aortic

Mitral is the only one that has 2 leaflets

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8
Q

Most diseases of the aortic valve are due to what?

A

People being born with a bicuspid aortic valve

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9
Q

Coronary Artery Anatomy:

A

Left Main spilts into Left circ & LAD

Right Main splits into marginal and right posterior descending artery (PDA)

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10
Q

What do TEGS test?

A

The efficiency of blood coagulation

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11
Q

How many phases of diastole and what are they?

A

(1) > Isovolumetric relaxation
(2) > Rapid filling phase
(3) > slow filling “diastasis”
(4) > final filling during atrial systole - atrial kick

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12
Q

How does heparin work?

A

It binds to Antithrombin III to inhibit the conversion of fibrinogen to fibrin which prevents fibrin from participating in clot formation

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13
Q

What pathway(s) does Heparin work on?

A

Intrinsic and Final Common

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14
Q

How does protamine work?

A

It neutralizes heparin
>heparin is a negatively charged acid + protamine is a positively charged base
> they bind together and neutralize out

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15
Q

T/F- protamine technically also has an anticoagulant effect

A

True - protamine overdose will result in increased ACT

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16
Q

3 contraindications to protamine vs 3 cautions

A

3 contraindications > allergy, vasectomy, NPH insulin users
3 cautions > pulmonary HTN, previous exposure to protamine, previous CABG

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17
Q

3 types of reactions to protamine

A

Type 1 = anaphylactic
>IgE mediated reaction where mast cells release histamine
> previous exposure results in an antigen (foreign protein) that stimulates the production of antibodies against that foreign protein. (“Pt develops antibodies from a previous exposure”)
> when body is exposed again to this antigen, it attacks and causes the mass histamine release > hypotension
>NOT dose dependent

Type 2 = anaphylactoid
>Immune mediated reaction where mast cells release histamine
>dose dependent

Type 3 = pulmonary HTN and RV failure
> Protamine binds to heparin, thromboxane is released > pulmonary vasoconstriction

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18
Q

5 things to look for when giving protamine

A
  1. Allergic reaction
  2. Pulmonary HTN
  3. Hypotension
  4. Bradycardia
  5. Bronchoconstriction
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19
Q

What is the treatment for any adverse reactions to protamine?

A

Epi is the best treatment for each reaction, each for different reasons

Type 1 & 2 (anaphlyactic & anaphylactoid)
>Epi- good for it’s mast cell stabilizing properties, also increases afterload, vascular tone, & pulmonary vasodilation)

Type 3 (pulmonary vasoconstriction)
> Epi- dilates the pulmonary vasculature, increases CO, contractility, and HR

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20
Q

Aortic insufficiency anesthetic goals:

A

Full, Fast, Forward

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21
Q

Aortic Stenosis: normal AV vs severe AS

A

Normal AV = 2.5-3.5cm
Severe AS = <0.8 cm

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22
Q

Mitral Stenosis:
Goals:
Normal valve area:
Severe MV stenosis

A

-Full, slow (more time for LV filling), constricted
-normal valve area 4-6cm
-Severe MV stenosis < 1cm

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23
Q

Anesthetic goals for mitral and aortic regurgitation/insuffiency

A

FULL , Fast, Forward

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24
Q

CPP calculation

A

Aortic diastolic pressure - LVEDP (or PAOP)

-I think I saw pulmonary artery diastolic pressure can be used as a surrogate for LVEDP but is PADP the same as PAOP?

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25
Q

Induction goals for patients with cardiac tamponade

A
  1. Increase CO by increasing HR, decreasing afterload, and decreasing right atrial pressures
    *Fast, Full, Right (tachy, hypervolemia, increased SVR) - dont get this , decrease afterload but increase SVR?
  2. Maintain spontaneous ventilation as long as possible - the negative intrathoracic pressure with inspiration helps draw volume into the RA and aid in maintaining CO; once PPV occurs, the positive intrathoracic pressure reduces preload and can cause hemodynamic collapse in this patient
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26
Q

Normal Tricuspid valve area

A

7-9cm

27
Q

Normal Pulmonic valve area

A

2.5-4cm

28
Q

What else will you do if the surgery involves the aortic arch? (2)

A
  1. Deep hypothermia protocol - 15-20 degrees for cerebral protection
  2. B/L A-lines
29
Q

What is the coronary sinus?

Where is it located

A

A Large vein responsible for collecting deoxygenated blood from the myocardium (muscle) and depositing it into the RIGHT atrium

Located posteriorly b/t right atrium and ventricle

30
Q

Is the coronary sinus the only drainage system of the heart?

A

No- coronary sinus drains deoxygenated blood into RA
The Thebasian veins and anterior cardiac veins drain deoxygenated blood into the LA (anatomic shunt)

31
Q

Why do we do radial a-lines over brachial?

A

Lower complications (bleeding/hematoma)

32
Q

What are the 3 branches off the aortic arch?

A

“I Can Ski”
Innominate (Brachiocephalic) > Right SC & Right common carotid
Common Carotid (Left)
Subclavian (Left)

33
Q

What is your major concern with acute pulmonary vasoconstriction/pulmonary HTN?

A

Right heart failure

34
Q

How does Amicar work?

A

It prevents the breakdown of clots by inhibiting the conversion of plasminogen to plasmin

(Plasmin is needed to break down fibrin/clots)
(On the other side, t-PA and streptokinase enhance the conversion of plasminogen to plasmin, accelerating the breakdown of clots)

35
Q

Why do we give Amicar on bypass?

A

It prevents the breakdown of clot formation intraop which decreases the risk for bleeding

36
Q

What is plasmin? What does it do?

A

It helps break down fibrin (clots)

37
Q

What happens in sepsis physiologically?
Why do you have massive vasodilation?
What will you see clinically?

A

An exaggerated inflammatory response to bacteria
>activation of complement system and release of a ton of inflammatory mediators such as cytokines & nitric oxide > which dilates the vessels dropping your SVR systemically > hypotension
>inflammatory mediators and ROS injure the vessels, causing the vessels to leak
>accumulation of fluid into the tissues worsens tissue perfusion
>signals further vasodilation (nitric oxide and more inflammatory mediators) to try and improve blood flow
>anaerobic metabolism leads to acidosis, impairs heart contractility, further reducing CO & BP

38
Q

What does cellsaver not have? Why?

A

Clotting factors

It undergoes a washing process that removes heparin and clotting factors

39
Q

Why do we mainly take autologous blood at the start of some cardiac cases?

A

Bc cellsaver washes the blood of clotting factors

40
Q

Which organs have the hardest time on bypass?

A

All of them? Lol ; protective strategies for brain and kidneys

Lot of evidence talking about inflammatory lung injury with CPB; older people with pre-existing lung disease are of higher concern with postop resp vailure.

The pancreas doesn’t do well with non-pulsatile flow > decreased insulin secretion > no insulin to get glucose into the cells > hyperglycemia

41
Q

Contraindications for swan (3)

A
  1. Clot/mass
  2. Endocarditis - vegetations on the valve can break off and cause a PE or stroke
  3. LBBB- can send them into CHB
42
Q

Hemodynamic management of HOCM

A

So of the hypertrophy of the intraventricular septum causes a LVOT - we treat it similarly to AS
-Need to maintain a full ventricle is key to decrease the LVOT
-increase preload
-Slower HR to improve diastolic filling
-Maintaining SR & atrial kick
-Maintaining afterload

*main difference is you want to decrease contractility - the more profound the contraction of the hypertrophied ventricle = worsened LVOT obstruction

43
Q

Hemodynamic management of CAD

A

Avoid tachycardia > it increases o2 demand while reducing supply
*add more

44
Q

What is the catheter called that you put in the large port of the IJ?

A

Cordis

45
Q

Where should the brown EKG lead be placed?

A

5th ICS, MCL

46
Q

Where should you never put IV’s A-lines when working with Dr. Husain

A

In the patients dominant hand/arm

47
Q

With Dr. Husain, what do you need to do right away when bringing pt into the room if you gave them versed?

A

Put o2 on them

48
Q

Coronary Blood Flow and O2 supply and demand

A

*Apex chart

49
Q

Basics of how the bypass circuit works

A

Blood drains out through the venous return line > blood reservoir
> pump which has the motor > heat exchanger to regulate the temp of the blood
> oxygenation which works as the lungs, oxygenating the blood and removing CO2
>oxygenated blood returns to the heart

50
Q

BP management goals for CABG when patient has carotid stenosis

A

*

51
Q

What is the coronary sinus

A

Venous drainage system for the coronary arteries
*does not drain the entire heart

52
Q

Why is heparin used for cardiac cases rather than Agatraban or Bivalirudin?

A

They have longer half lives and no reversals

53
Q

Anesthetic management of carotid artery disease

A

*

54
Q

Coagulation cascasde- explain process
What does thrombin do? What does AT3 do?

A
55
Q

Why dont we have fibrinogen circulating all the time?

A

I think we do? Did they mean fibrin?

Bc fibrinogen is always circulating, it only is activated into fibrin when it needs to form a clot in an acute process

*Vascular injury > vasoconstriction > platelet aggregation > platelet plug > thrombin is released converting fibrinogen to fibrin

  • Fibrin reinforces the platelet plug, finalizing the clot
56
Q

Why do we have conversion steps in the clotting cascade rather than just synthesizing fibrinogen when we need it ?

A

Protein synthesis is a longer process than enzyme activation & the coat cascade is an acute process that you need to occur quickly when an injury happens

?

57
Q

Is diastole an active or passive process?

A

Both- Passive and active filling- active requires ATP

58
Q

MOA of Levophed vs Epi vs Neo

A

Neo- pure alpha 1 vasoconstriction
>Gq receptor - phospholipase converts PIP to IP3 and DAG which increases intracellular calcium

Epi >
-Low doses (2mcg/min) Beta 2 effects - pulmonary and coronary vasodilation
- Moderate doses - alpha & beta 1 predominately

Levophed> alpha 1 and beta 1 agonism predominately ; the mild beta 1 effects reduce the BRR seen with neo

59
Q

What drugs/things can cause hyperglycemia? (6)

A
  1. Beta-2 agonists
  2. Surgical stress
  3. Steroids
  4. Heparin (impairs glucose uptake into the muscles by inhibiting insulin from binding to the insulin receptor)
  5. Hypothermia (increases insulin resistance)
  6. Non-pulsatile flow to the pancreas while on pump alters insulin secretion
60
Q

What’s in cryo? (5)

A

Fibrinogen (factor 1)
Factor 8
Factor 13
Fibronectin
& VWF

61
Q

How much does 5 pool bag of cryo increase fibrinogen?

A

By 50mg/dl

62
Q

What does FFP contain

Indications?

A

All the coagulation factors, fibrinogen, and plasma proteins

Indications: coagulopathy (elevated PT/PTT, acute warfarin reversal, antithrombin deficiency, massive transfusion protocol, DIC, C1 esterase deficiency (angioedema)

63
Q

Indications for cryo

A

Low fibrinogen, VWD, and hemophilia

Cardiac (7 decks)

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