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what is a centrifugal vs a roller pump in a CPB circuit?

roller pump - forward flow is produced with the partial compression of the tubing by two roller heads. it is not sensitive to preload or afterload (i.e. kinking, occlusion, increased SVR, clamp placement), can delivery pulsatile flow, and reliably produces a certain amount of flow based on pump speed. disadvantages include: increased damage to red blood cells, potential delivery of large quantities of air to the patient, risk of over-pressurization leading to subsequent tubing separation or rupture, lack of preload occlusion leading to negative-pressure induced cavitation (microscopic bubbles)

centrifugal - (kinetic) rotational force is responsible for forward flow. it is less damaging to red blood cells and sensitive to changes in preload/afterload. it will cease to function if a significant amount of air is entrained. it is incapable of delivery pulsatile flow and is only partially able to compensate for decreases in forward flow due to increased distal pressure


would alpha-stat or ph-stat management be preferable and why?

either strategy is likely acceptable, but the there may be some slight improvement in neuropsychologic outcomes with the use of alpha-stat management in adults. these two strategies describe different approaches to managing CO2 in a hypothermic patient. hypothermia leads to increase in the solubility of CO2 with subsequent reductions in the arterial pH and partial pressure of CO2 (it does not reduce CO2 content).

pH stat strategy would add CO2 to the oxygenator as necessary to maintain a PaCO2 of 40 mmHg and a pH of 7.4. a practitioner using alpha-stat management would not add CO2, maintaining electrochemical neutrality.

the primary mechanism of brain injury in adults is thought to be embolic rather than ischemic, thus the enhanced blood flow to the brain with CO2 addition may prove more harmful than helpful.


what about if the patient was pediatric?

the primary mechanism of brain injury in pediatric patients is thought to be ischemic in nature, therefore the addition of CO2 and then increase in CBF would be beneficial. additionally, the enhanced blood flow facilitates cerebral cooling prior to cardiopulmonary arrest and thereby decreases the cerebral metabolic demands. however, there is some evidence that pH stat may impair the cerebral metabolic recovery following CPB. some practitioners are utilizing a crossover strategy that employs pH stat during first 10 min of cooling and then alpha stat for the rest of the case.


how high would you like the ACT before initiating CPB? what if you are using aprotinin?

i would like the ACT to be >480 seconds.
in the presence of aprotinin, the celite ACT will have to be highter because aprotinin artificially prolongs the celite ACT through inhibitions of kallikrein and inhibition of XII to XIIa (intrinsic pathway).

ideally, a kaolin ACT can be obtained, but if not a celite ACT >700-750 secs is adequate.


how does ACT work?

it measures seconds needed for whole blood to clot after exposure to factor XIIa (intrinsic pathway). it can be prolonged due to heparinization, thrombocytopenia, or platelet dysfunction.


what is aprotinin? aminocaproic acid?

aprotinin: serine protease inhibitor - inhibits formation of factor XIIa, causing inhibition of intrinsic pathway and fibrinolysis

aminocaproic acid: inhibits fibrinolysis via inhibition of plasminogen activators


what difference does it make if the mitral regurgitation is acute or chronic? what is the pathophysiology of acute MR?

acute mitral regurgitation results in left atrial and ventricular volume overload without compensatory ventricular dilation. will have markedly increased left atrial/ventricular EDP with a decrease in CO, pulmonary edema and right ventricular failure.

the increase in LVEDP in combination with tachycardia places the patient at risk of severe myocardial ischemia.


what will the pulmonary capillary wedge tracing look like in MR?

in the presence of mitral regurgitation, there will be a prominent v-wave, demonstrating the inflow of regurgitant blood from the ventricle to the atrium during ventricular systole through the loose mitral valve. the x-descent is absent because while the atrium is relaxing, it is being filled with the regurgitant blood. the y-descent is quite sharp as the blood quickly flows from the overpressurized atrium to the ventricle when the ventricle is relaxing.


how will you monitor temperature?

both core and shell temp must be monitored while on CPB, due to the temp gradient that is created by cooling and rewarming. to monitor core temp you can place a NP or tympanic probe. shell temp can be accomplished by a rectal or toe probe. temperature monitoring is very crucial to ensure adequate cerebral cooling during bypass and to avoid large temperature gradients (greater than 10C) as this can lead to gas bubble formation in the blood.


you have an 128 kg, 68" patient for 4vCABG and MVR secondary to worsening CP. he has IDDM, severe GERD, chronic HTN, and is a smoker. he is on 10 L FM with SpO2 of 89% and SaO2 71 mmHg on ABG. how will you induce this man?

assuming his airway exam was reassuring, i would move the difficult airway cart into the room and place the appropriate monitors (SASAM, pre-induction arterial line), place him in reverse-trendelenberg and apply cricoid pressure. i would induce with etomidate and fentanyl to achieve sufficient depth of anesthesia during laryngoscopy while also avoiding hypotension and bradycardia.

my goals:
1. safely secure the airway in this obese patient who may be difficult to ventilate or intubate
2. avoid aspiration with his severe GERD
3. ensure adequate depth of anesthesia to avoid hypertension and tachycardia that can worsen MR, ischemia, and pulm edema
4. avoid hypotension that would lead to inadequate coronary perfusion
5. avoid brady that will worsen MR
6. avoid bronchospasm in his smoking-induced hyperactive airway


during laryngoscopy, the patients blood pressure spikes and he goes into atrial fibrillation. what happened?

it could be related to ischemia or atrial dilation from worsening mitral regurgitation. this could be from:
1. inadequate anesthesia leading to hypertension and tachycardia (worsens mitral regurg and increases myocardial oxygen demand)
2. overdose of anesthesia leading to bradycardia with worsened mitral regurgitation


what will you do?

since atrial contribution to preload is less critical in patients with mitral regurgitation (vs those with stenosis), i may just ensure ventricular rate control with BB, CCB, or digoxin and monitor the BP closely. however, given his CAD and potential for worsening regurgitation and heart failure, i would have a low threshold for amiodarone or even DC cardioversion. additionally, i would alert the surgeon and suggest rapid preparation of the patient for CPB.


CPB is initiated. the perfusionist notes a falling level of the venous reserve. what do you do?

have the perfusionist turn down the flow rates and add fluid to the blood volume as necessary to prevent reservoir emptying and entrainment of a massive amount of air. at the same time, i would look for potential causes such as elevation of the heart by the surgeon, or venous cannula kinking, air lock, inadequate diameter, or obstruction by thrombosis.


where does the venous cannula go?

RA and IVC. if bloodless heart is required, it can be placed in SVC and IVC.


where does the oxygenated blood go?

1. aortic cannula which is after the cross clamp, it provides systemic blood and pressure
2. anterograde cardioplegia into the pre-clamp aorta
3. retrograde cardioplegia into the coronary sinus


what vents are required?

all cases require a LV vent because there will be a small amount of venous return via the thesbian veins, bronchial veins, aortic insufficiency, etc.

if IVC/SVC are cannulated and RA is not, an atrial vent is required to capture blood that returns from the coronary sinus


following the surgical repair, the surgeon askis you to vigorously inflate the lungs. why? is de-airing the heart important for this procedure?

first, this will recruit collapsed alveoli. second, the positive pressure results in increased flow through the pulmonary vasculature, displacing air into the left heart where it can be more easily removed with the vent. de-airing of the heart is crucial to prevent end-organ damage from air emobli in the coronary arteries or cerebral vasculature. TEE can aid in ensuring adequate de-airing of the LV prior to LV ejection.


normothermia is achieved and the patient is attempted to be weaned from CPB, however the pulmonary artery pressure increases and the systemic pressure decreases. what do you think is happening?

these are signs that the LV is not producing adequate CO. this could be from many factors, such as:
1. increased afterload secondary to MVR (low resistance flow back into the atrium is no longer available)
2. graft failure (kinking, air, clot)
3. inadequate myocardial preservation during CPB
4. inadequate coronary blood flow (hypotension, emboli, spasm, tachycardia, decreased diastolic perfusion)
5. myocardial infarction
6. valve failure
7. hypoxemia
8. inadequate preload (hypovolemia, loss of atrial kick)
9. reperfusion injury
10. acidemia
11. electrolyte abnormalities


how does recent MVR contribute to LV failure when coming off bypass? what is the treatment?

it results in the loss of the low resistance outflow tract into the left atrium and as a result leads to increased LV afterload. the increased afterload can unmask LV dysfunction. it can be treated with inotropes, vasodilators (to reduce afterload) or fluids (increase preload)


what increase the risk of needing postbypass inotropes?

severity of regurgitation, pulm htn, low pre-op LVEF, prolonged aortic cross clamp


would an intra-aortic balloon pump help wean this patient from CPB?

possibly. it can improve coronary perfusion during diastole and reduce afterload during systole. it will decrease myocardial oxygen demand and simultaneously increase myocardial oxygen supply.


how does milrinone work?

PDE inhibitor. works directly on the cardiac myocytes. stimulates myocardial contractility and acceleration of myocardial relaxation. causes equal arterial and venous dilation. CO improves with improved contractility and decrease in afterload.


where is ideal positioning of IABP?

at the junction of the aortic arch and the descending aorta, below the left subclavian artery to prevent cerebral emboli.


how does it work?

it should by synchronized with the cardiac cycle using the arterial pressure waveform or ECG QRS. balloon inflation should occur with aortic valve closure/start of diastole (dicrotic notch of arterial waveform or middle of T-wave with ECG). this increases aortic diastolic pressure and improves coronary perfusion. balloon should be rapidly deflated just prior to ventricular contraction. this promotes forward flow by reducing afterload (vacuum effect). to start, it should be set at a ratio of 1:2 to allow for comparison of natural ventricular beats to augmented beats. the ratio can be further adjusted.


what happens if the IABP is inappropriately timed?

it can lead to increased afterload and no augmentation of coronary perfusion.


is IABP contraindicated in a patient with a pacemaker?

no, but i can interfere with synchronization when using older systems. current IABP are able to distinguish QRS from pacer spike. another option would be to use the arterial waveform as the trigger.


you are transporting the pt to ICU and someone asks you to explain the difference between radial arterial pressure and central aortic pressure just after CPB.

peripheral vasodilation occurs as a result of rewarming. as such, radial artery pressure can be as much as 30 mmHg less than central aortic pressure just after CPB. it should be noted that femoral artery catheters will correlate well. the pressure gradient usually resolves within 45 min of separation from CPB. if central aortic pressure is necessary, a transducer can be connected to an aortic vent or a needle inserted in the aorta.


a few hours later, the BP is 76/43. what is your ddx?

1. myocardial ischemia/infarction
2. LV/RV failure
3. continued myocardial stunning
4. IABP malfunction/complication if still in place
5. tension PTX from CVL placement
6. hypo/hypervolemia
7. dysrhythmia
8. cardiac tamponade
9. metabolic distrubance (electrolytes, acid-base, hyper/hypoglycemia)
10. CV depression due to pain meds/sedation

to establish diagnosis, i would look at ECG, CVP, and PAC if present. could possibly utilize TEE.


how does cardiac tamponade manifest?

in an awake pt, not recently undergoing cardiac surgery: SOB, increased HR, decreased BP, JVD, muffled heart sounds, pulsus paradoxus.

however, in a mechanically ventilated postop patient the presentation can be more confusing. the atypical presentation is partially due to the fact that the pericardium is left open following cardiac surgery, resulting in regional vs homogenous compression of the heart. a loculated or localized hematoma can cause regional compression that is inconsistent with classic tamponade physiology with equalization of diastolic pressures throughout the heart. the picture may look more like RV/LV failure. high degree of clinical suspicion and TEE can facilitate the diagnosis.

signs on TEE: diastolic collapse of RA, RV, LV


what is pulsus paradoxus?

abnormally large decrease in arterial BP during inspiration. a small drop (10 mmHg) in systolic BP will be seen in normal patients due to the negative intrathoracic pressure generated during inspiration. this increases venous return to the heart, which increases RV volume and bulging of the septum into the LV. this reduces LV capacity and filling volume, which reduces SV. additionally, blood pools in the pulmonary vasculature and thereby decreases venous return to the heart. a reflexive increase in heart rate will be seen as well (baroreceptor reflex)

this is seen with cardiac tamponade, airway obstruction, COPD, pulm embolism


how does tamponade occur if the pericardium is not in tact?

loculated or localized hematoma.


tamponade is confirmed on TEE. what do you do?

if patient was relatively hemodynamically stable, i would alert surgeon, deliver 100% O2, administer fluids for volume expansion, consider administration of catecholamines, treat any bradycardia, correct metabolic acidosis (which can contribute to cardiac depression) and transport patient to OR with full monitoring and emergency CV drugs.

if however, the patient was too unstable, i would consider reopening his chest in the ICU. i would like avoid anesthesia to avoid the attenuation of compensatory mechanisms that are sustaining vital cardiac output and organ perfusion. however i would administer anesthetic drugs as soon as pericardial pressure was relieved and fxn improved.


could you perform needle decompression?

as pericardium is already open and it is unknown where the hematoma is developing, i would not choose to do this.


where do you perform needle decompression?

lateral 5th intercostal space