Heart Rotation Questions - General Flashcards
When do we bolus heparin and what is the dose
300-500 units/kg of patients weight
Prior to cannulation
Protamine reversal dosing
1mg for every 100 units of heparin
Why do we use insulin for CPB?
Bc insulin resistance occurs when the body temp drops ➡️ hyperglycemia
What do you need to redose during the rewarming phase? (3)
Benzos, narcs, and NMBs
What is cardioplegia?
A potassium solution administered by the perfusionist to arrest the heart for surgery
Difference between anterograde and retrograde cardioplegia cannulation
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
Valves of the heart; how many leaflets do each have?
Tricuspid, pulmonic, mitral, aortic
Mitral is the only one that has 2 leaflets
Most diseases of the aortic valve are due to what?
People being born with a bicuspid aortic valve
Coronary Artery Anatomy:
Left Main spilts into Left circ & LAD
Right Main splits into marginal and right posterior descending artery (PDA)
What do TEGS test?
The efficiency of blood coagulation
How many phases of diastole and what are they?
(1) > Isovolumetric relaxation
(2) > Rapid filling phase
(3) > slow filling “diastasis”
(4) > final filling during atrial systole - atrial kick
How does heparin work?
It binds to Antithrombin III to inhibit the conversion of fibrinogen to fibrin which prevents fibrin from participating in clot formation
What pathway(s) does Heparin work on?
Intrinsic and Final Common
How does protamine work?
It neutralizes heparin
>heparin is a negatively charged acid + protamine is a positively charged base
> they bind together and neutralize out
T/F- protamine technically also has an anticoagulant effect
True - protamine overdose will result in increased ACT
3 contraindications to protamine vs 3 cautions
3 contraindications > allergy, vasectomy, NPH insulin users
3 cautions > pulmonary HTN, previous exposure to protamine, previous CABG
3 types of reactions to protamine
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
5 things to look for when giving protamine
- Allergic reaction
- Pulmonary HTN
- Hypotension
- Bradycardia
- Bronchoconstriction
What is the treatment for any adverse reactions to protamine?
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
Aortic insufficiency anesthetic goals:
Full, Fast, Forward
Aortic Stenosis: normal AV vs severe AS
Normal AV = 2.5-3.5cm
Severe AS = <0.8 cm
Mitral Stenosis:
Goals:
Normal valve area:
Severe MV stenosis
-Full, slow (more time for LV filling), constricted
-normal valve area 4-6cm
-Severe MV stenosis < 1cm
Anesthetic goals for mitral and aortic regurgitation/insuffiency
FULL , Fast, Forward
CPP calculation
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?
Induction goals for patients with cardiac tamponade
- 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? - 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
Normal Tricuspid valve area
7-9cm
Normal Pulmonic valve area
2.5-4cm
What else will you do if the surgery involves the aortic arch? (2)
- Deep hypothermia protocol - 15-20 degrees for cerebral protection
- B/L A-lines
What is the coronary sinus?
Where is it located
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
Is the coronary sinus the only drainage system of the heart?
No- coronary sinus drains deoxygenated blood into RA
The Thebasian veins and anterior cardiac veins drain deoxygenated blood into the LA (anatomic shunt)
Why do we do radial a-lines over brachial?
Lower complications (bleeding/hematoma)
What are the 3 branches off the aortic arch?
“I Can Ski”
Innominate (Brachiocephalic) > Right SC & Right common carotid
Common Carotid (Left)
Subclavian (Left)
What is your major concern with acute pulmonary vasoconstriction/pulmonary HTN?
Right heart failure
How does Amicar work?
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)
Why do we give Amicar on bypass?
It prevents the breakdown of clot formation intraop which decreases the risk for bleeding
What is plasmin? What does it do?
It helps break down fibrin (clots)
What happens in sepsis physiologically?
Why do you have massive vasodilation?
What will you see clinically?
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
What does cellsaver not have? Why?
Clotting factors
It undergoes a washing process that removes heparin and clotting factors
Why do we mainly take autologous blood at the start of some cardiac cases?
Bc cellsaver washes the blood of clotting factors
Which organs have the hardest time on bypass?
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
Contraindications for swan (3)
- Clot/mass
- Endocarditis - vegetations on the valve can break off and cause a PE or stroke
- LBBB- can send them into CHB
Hemodynamic management of HOCM
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
Hemodynamic management of CAD
Avoid tachycardia > it increases o2 demand while reducing supply
*add more
What is the catheter called that you put in the large port of the IJ?
Cordis
Where should the brown EKG lead be placed?
5th ICS, MCL
Where should you never put IV’s A-lines when working with Dr. Husain
In the patients dominant hand/arm
With Dr. Husain, what do you need to do right away when bringing pt into the room if you gave them versed?
Put o2 on them
Coronary Blood Flow and O2 supply and demand
*Apex chart
Basics of how the bypass circuit works
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
BP management goals for CABG when patient has carotid stenosis
*
What is the coronary sinus
Venous drainage system for the coronary arteries
*does not drain the entire heart
Why is heparin used for cardiac cases rather than Agatraban or Bivalirudin?
They have longer half lives and no reversals
Anesthetic management of carotid artery disease
*
Coagulation cascasde- explain process
What does thrombin do? What does AT3 do?
Why dont we have fibrinogen circulating all the time?
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
Why do we have conversion steps in the clotting cascade rather than just synthesizing fibrinogen when we need it ?
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
?
Is diastole an active or passive process?
Both- Passive and active filling- active requires ATP
MOA of Levophed vs Epi vs Neo
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
What drugs/things can cause hyperglycemia? (6)
- Beta-2 agonists
- Surgical stress
- Steroids
- Heparin (impairs glucose uptake into the muscles by inhibiting insulin from binding to the insulin receptor)
- Hypothermia (increases insulin resistance)
- Non-pulsatile flow to the pancreas while on pump alters insulin secretion
What’s in cryo? (5)
Fibrinogen (factor 1)
Factor 8
Factor 13
Fibronectin
& VWF
How much does 5 pool bag of cryo increase fibrinogen?
By 50mg/dl
What does FFP contain
Indications?
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)
Indications for cryo
Low fibrinogen, VWD, and hemophilia
