Cardiopulmonary Bypass Study Facts Flashcards
Two difference Oxygenators avilable
Membrane oxygenator–sheaves of hollow fibers (120 to 200 um) with 0.3-0.8 um pores. produce less particular and gaseous micro-emboli, less reactive to blood elements, and allow superior control of blood gases
Bubble oygenators–cheaper, produce more gaseous micro-embolic and therefore rarely used.
Two main types of Venous reservoir
1) Open reservoirs (rigid, hard plastic canisters)–Large capacity for storage of circulating volume, allow vacuum-assisted venous drainage, easier to prime, aless expensive, can incorprorate filters and allow for volume measurements and management of venous air
2) Close reservoirs (collpasible, soft plastic bags)–less versatile, eliminating the blood-gas interface, able to reduce the systemic inflammatory response, lower risk for producting gas micro-emboli
Types of Cardiopulmonary bypass pumps
Roller Pumps–produce flow by compression of the heparin-coated tubing using two rollers 180 degrees apart. The flow rate is determined by
a) rate of rotation of the rollers
b) degree of compression
c) length and diameter of the tubing being compressed
Centrigular pumps–flow by using a rotating impeller. The flow rate is determined by
a) speed of rotation of the impeller
b) afterload within the circuit, distal to the pump
Name 3 filters available within the CPB system
1) Arterial line filters (40um) used to reduce the cerebral embolic load
2) Leucocyte depleting filters removed activated neutrophils and therefore may reduce the system inflammatory response
3) Ultrafiltration and modified ultrafiltation, which remove excess fluid. Also good for filtering cytokines.
How does Protamine work
Protamine is a cation (comes from salmon sperm) that binds with the anion, to form stable heparin-protamine complexes
For each 100U of heparin given then 1mg of protamine should be injected IV.
Should be given over 15 minutes
Describe Horrow Classification of Protamine Reaction
Class 1: Hypotension–caused by rapid administration of protamine. Triggered by a histamine release and can usually be treated by fluid resuscitation and vasopressor
Class 2:
IIa (true anaphylaxis)–hypotension, brochospasm and angioedema—mediated by anti-protamine immunoglobine E antibody, histamine, prostaglandins, and kinins. Patients with fish allergies and those exposed to protamine.
IIb (immediate anaphylactoid) and IIc (delated anaphlactoid) less severe–mediated by complement
Class 3: Catastrophic pulmonary vasoconstriction–complement activation and release of thromboxane A2 (RV failure, circulatory shock, severe broncospam)
5 Complication of CPB
Systemic inflammatory response Coagulopathy Hemolysis Renal and splanchnic hypoperfusion Cerebrovascular accident
5 things to check before going on CPB
arterial line pressure decompression of heart venous drainage systemic arterial and venous pressure arterial blood oxygen cocentration
once bypass is started should wait 2 minutes to make sure that hemodynamic factors are stable, lung ventilation is off, systemic cooling is happening, and then cross clamp aorta
Principles of managing an IVC tear during venous cannulation
Advance the venous cannula into the IVC beyond the tear to obtain venous drainage along with cardiotomy suction return
use additional purse string to secure the venous cannula
cool to 18 degrees
during circulatory arrest the IVC can be repaired by direct suture or using a bovine pericardial patch
Management of massive airlock in venous line
Stop CPB
separate the venous cannula from the venous line
manually fill the venous line with saline
reconnect the venous cannula to the venous line
If there is a small to moderate amount of air it can be chased back into the reservoir by progressively lifting the venous line
management of massive arterial air embolism
Stop CPB—clamp both arterial and venous lines
place pt in steep Trendelenburg position
Remove arterial cannula and aspirate any air at the site of entry
Remove the venous cannula
Place the arterial cannula via the right atrium into the SCV and snare
Start retrograde cerebral perfusion at 400 to 500 ml/min for 3 minutes
Mannitol, dexamethasone, and ice packs around the head
Antegrade circulation is then recommenced withe DHCA for 30 minutes
The perfusion pressures are kept relatively high (70 to 80 mmHg) and 100% Fio2
TEE to look for residual air
Hyberbaric chamber/disclose to family
Management when arterial cannula falls out
Stop CPB
Clamp venous line
Flush the arterial line and forward flow from pump
Replace the arterial cannula
Reconnect the arterial line and the arterial cannula, ensuring the absence of air bubbles
Signs of iatrogenic aortic dissection
Spreading hematoma with bleeding at point distal to the cannulation site
Classically a boggy mass may be palable
failure of blood to rise to the top of arterial cannula
Poor swing on the arterial line following removal of the line clamp
High line pressure when fluid is infused via the arterial cannula
Profound hypotension with poor venous return
Principles of managing iatrogenic aortic dissection
Stop CPB and clamp both arterial and venous lines Insert the aortic cannula into the right atrium and rapidly infuse volume as required Inset an arterial cannula into a peripheral artery or uninvolved distal aorta Following DHCA (18) the ascending aorta is opened and inspected for dissection at the orginal site of cannulation The aorta can then be repaired using a direct suture, patch, or interposition graft depending on the extent of the dissection It is important to recognise and treat iatrogenic aortic dissection immediately, to limit the extent of the injury and restore the systemic perfusion--when recongnised early survival rates are 66-85% but when discovered late its only 50%.
Describe de-airing routine for AVR
Prior to tying down the aortotomy suture
1) patient in Trendelenburg position
2) venous line is partially occluded to fill the heart
3) heart is gently agitated while keeping the aortotomy open with forceps to allow release of trapped air
4) lung are inflated to displace any air in the pulmonary veins
5) aortic cross clamp is removed and the aortotomy suture is tied
6) aortic root is turned onto suction
TEE to confirm de-airing process
Indications for Deep Hypothermic Circulatory Arrest
Aortic dissection Arch aneurysms Thoraco-abdominal aneursyms Renal tumors invading the IVC and right atrium Complex congenital cardiac surgery Porcelain aorta Pulmonary thromo-endarterectomy Blood loss during resternotomy Repair of ruptured thoracic aorta
What are safe periods of circulatory arrest
Temp Duration of safe CA (min) 36 1 32 5 28 10 24 20 20 30-40 16 45-60
What strategies exist in the management of acid-base metabolism during DHCA
pH stat
- -adding CO2 to keep the PaCo2 and pH at 7.4 which are normal levels in arterial blood at 37 degrees
- advantage of a more rapid and homogenous cooling but an increased risk of cerebral embolism
alpha- stat
- -- not adding CO2 thereby allowing the pH and PaCO2 to drift as dictated by the solubility at a given temperature, producing alklotic blood during the cooling process.
- -- has the advantage of reducing the risk of cerebral embolism and the alkalosis produced may also be beneficial in terms of reducing cerebral and mycardial metabolism.
pH stat on cooling enhances cerebral perfusion by maintaing PaC02 and facilitates cooling and alpha stat on rewarming to reduce the miroemboli load on the circulation.
Names different options for blood conservation
Pharmacological
Tranexamic acid
recombinant EPO
delaying surgery in patients on ASA/Plavix.
Autologous pre-donation
Intra-operative cell salvage
Auto-transfusion of washed shed post operative mediastinal fluid
Meticulous hemostasis
consider fibrin glue
Low threshold for resternotomy for bleeding
2 studies examining Aprotinin
IMAGE trial showed aprotinin:
reduces postoperative mediastinal blood loss
reduces the need for postoperative blood transfusions
reduces the need for post operative platelets
reduces the resternotomy for blooding
possible reduction of graft patency when you have poor run off
BART
Increased incidence of mortality
renal impairment
heart failure and myocardial infarction
