EMBOLIC EVENTS IN

CPB
-Dr Rheecha Joshi
CONTENT
• INTRODUCTION

• TYPES OF EMBOLI

• PATHOPHYSIOLOGY

• PREVENTION

• TREATMENT
• Embolus : two Greek words en (in) and ballein (to throw)

• medical definition of embolism is "a sudden blocking of an artery by

a clot or foreign material which has been brought to its site of
lodgment by the blood current

• The production of emboli during CPB, whether gross or microscopic,

has been linked to numerous perioperative and postoperative
complications
TYPES OF EMBOLI
• Blood born

• Foreign substance

• Gaseous emboli
Blood born
• consist primarily of autologous cellular products or aggregates of various cell types

• Cellular products include microthrombi containing fibrin/fibrinogen, lipid material,

protein (denatured or not), bone or muscle fragments,platelet, neutrophil, and red cell
aggregates

• Fibrin formation occurs when inadequately anticoagulated blood contacts a foreign

surface, thereby activating factor XII to factor XIIa and thus initiating the coagulation
cascade

• Fibrin deposits likely form in areas of stagnant blood flow or where turbulence or
cavitation phenomena exist and on roughened surfaces
• Specific sites of emboli formation include oxygenator connectors ,
within bubble oxygenators or within arterial line filters

• Systemic heparinzation

• ACT 300 -400 seconds is considered adequate for prevention of fibrin

formation within circuits
• Macroembolic and microembolic particles of fat (denaturation of plasma
lipoproteins and lipids )

• may vary from 4 to 200 um in diameter

• are found in capillaries of the kidneys, lungs, heart, brain, liver, spleen and in
pericardial blood

• are released as a result of trauma to the fat cells in the epicardium and surgical
wound and can occur without CPB after median sternotomy or thoracotomy
• It has been estimated that two thirds of the fat emboli developed
within a CPB circuit enter via cardiotomy suction

• are commonly observed with bubble oxygenators and to a lesser

degree with membrane-type oxygenators
Foreign Material
• consist of cotton fibers, plastic or metal particles from connectors or
housings of disposable devices, filter material, tubing, talc, or surgical
thread

• Pulmonary embolism from bone wax has been suggested as a

potential contributor to pulmonary complications after open heart
surgery blood

• reports of elevated serum aluminum levels postoperatively in patients

who had undergone CPB ( aluminum heat exchangers)
• Microemboli (greater than 300 um) may be released into the circuit from
tubing (e.g., by spallation)

• Spallation is defined as the release of fragments (often >300 µm diameter) of

tubing into the circuit that can potentially embolize into the patient

• These emboli are more common with silicone-based rubber tubing than with
tubing of polyvinyl chloride or polyurethane base

• Another known foreign material is microfibrillar collagen used for surgical

hemostasis
Gaseous Emboli
• oxygen microbubbles generated by bubble oxygenators : the most
commonly source

• Gaseous microemboli produced in these devices are usually 400 um

or less in diameter and consist primarily of oxygen, other gases like
carbon dioxide, nitrogen, or nitrous oxide

• Bubbles with diameters greater than 35 to 40 um are reportedly

associated with CPB morbidity, unlike those of smaller diameters
• Chemical defoaming agents and arterial line filtration, significantly
reduced the numbers and sizes of gaseous microemboli produced by
bubble oxygenators

• Gaseous microemboli with diameters below 40 um are still reported

even with arterial line filtration
• Production of gaseous microemboli depends in part on the methods of operation
of bubble oxygenator

• Maintaining a low gas-to-blood flow ratio --> reduce the number of microbubbles
released into the arterial line

• Arterial and venous blood reservoir levels

• With increased fluid levels, the time available for gas dissipation and defoamer
action increases

• any unnecessary jarring or abrupt shock releases bubbles into the arterial line
• Regardless of oxygenator type, the colder the solution, the greater the number of
molecules dissolved within the liquid phase

• While warming from hypothermia, gaseous microemboli will form in the blood if the
warming gradient exceeds a certain critical threshold

• the greatest chance of gaseous microemboli production as a result of temperature

changes most likely occurs during the cooling phase, where bubbles are released
directly into the patient's circulation

• the actual determinative gradient site for the formation of gaseous microemboli is in
the aortic arch where the blood and perfusate first mix
• Gaseous and particulate emboli are commonly reported with cardiotomy suction

• the mixing of air with the blood, forms relatively large bubbles, consist of air
(mostly nitrogen) and hence are more stable

• The increased stability is due to the larger volume of gas in the bubble and the
differences in solubility of nitrogen in blood as compared with oxygen or carbon
dioxide

• The process of suctioning also results in significant blood trauma, which causes
cellular aggregation
• Gaseous emboli also can be produced by processes known as gaseous
or vaporous cavitation

• Cavitation involves hydrodynamic phenomena that consist of bubble

nucleation, growth in volume, and then ultimate collapse

• Vaporous cavitation occurs when a vacuous space is created in blood,

for example, within the negative pressure regions behind the roller
pump heads
• Air emboli can be introduced into the patient's arterial blood when
the cardiac chambers are opened to the atmosphere

• "surgical air" is characterized as that air entering the arterial

circulation from cannulation of the heart and aorta, after removal of
the aortic clamp, air entrainment at the site of venous cannulation,
after restoration of cardiac function, and during left atrial
catherization
• animals embolized intravascularly with gases of high solubility, such as
carbon dioxide or oxygen, tolerate the insult better than those
embolized with air or nitrogen bubbles

• In the case of oxygen bubbles, the diffused gas will combine with
unsaturated hemoglobin while carbon dioxide may be absorbed
within the plasma
Bubble in blood showing the effects of gas diffusion on size
Major mechanisms of gas embolism
 PATHOPHYSIOLOGY
• postoperative diffuse cerebral dysfunction

• Histologic studies have shown embolic material in the kidneys, heart, liver,
lungs, and spleen after CPB

• the period of greatest risk of cerebral injury is at the beginning of CPB when
the patient is susceptible to both hypotension and microemboli initially
released from the perfusion circuit

• Cerebral pathology may include hemorrhage, edema, astrocyte and neuronal

swelling, vacuolation, and necrosis
• Cerebral gas embolism can cause transient changes in the EEG that may persist from
seconds to hours and neurologic dysfunction

• Visual abnormalities as occult visual field defects after cardiac surgery : ocular
embolization with subsequent microvessel obstruction of the retina

• Coronary air is associated with impaired left and right ventricular function and with ECG
changes ventricular dysrhythmias, atrioventricular dissociation, QRS complex widening,
and ST segment and T wave changes

• Clearance of coronary air while on CPB can be accomplished with the use of certain drugs,
aortic clamping with ventricular or aortic compression, or retrograde cerebral perfusion
Prevention
• It is unlikely that all embolic events can be totally eliminated

• A variety of safety devices with proven efficacy is available for the circuit and
includes arterial line filters, bubble traps, air bubble detectors, low-level alarms,
and one-way valves for the vent or arterial filter purge line

• Pharmacologic interventions to minimize emboli during bypass consist primarily

of ensuring adequate heparin anticoagulation

• Decreased transmission of microemboli per unit volume of blood flow favors the
alpha-stat approach to minimize the embolic "load" in perfused tissue beds
• Cardiac ejection should be avoided until complete blood filling occurs

• Prevention of systemic air embolism by insertion of a vent into the

left ventricle or needle aspiration of the pulmonary veins and cardiac
chambers

• flooding the surgical field with carbon dioxide, closure of the left
atrium under blood, lung expansion to clear pulmonary venous blood,
and placement of the patient in the Trendelenburg position
• Another source of emboli during cardiac surgery relates to the status
of the patient's ascending aorta

• the presence of proximal aortic atherosclerosis is a strong predictor of

stroke

• Atheromatous plaques may be dislodged during cannulation, cross-

clamped, and manipulation during the procedure
Treatment
• Hyperbaric oxygenation is considered the most effective treatment of gross air
embolism although access to such a treatment facility is limited

• postsurgical hyperbaric oxygenation treatment may remain effective even

hours or days after the initial insult

• hemodilution with perfluorocarbon emulsions, which aids in the absorption of

the vascular bubbles

• induction of hypothermia for cerebral protection, or retrograde cerebral or

retrograde coronary perfusion
• use of nitrous oxide should be discontinued to avoid bubble growth

• Use of the Trendelenburg position .These techniques, however, have been shown
experimentally using in vivo and in vitro techniques to offer little or no protection

• The use of transesophageal echocardiography and transcranial Doppler has been

reported to aid in the identification of intraventricular or intravascular bubbles

• Rigorous deairing techniques may be assessed in this manner to decrease the

persistence of entrapped surgical air emboli
INTRAOPERATIVE AND POSTOPERATIVE MANAGEMENT OF AIR EMBOLISM

1. Stop CPB immediately, clamp arterial and venous lines, and notify surgeon
and anesthesiologist.

2. Locate and confirm source of air; if due to pressurized CPB component;

isolate component from patient before relieving pressure.

3. Perfusionist: Purge air from CPB systemic flow line and refill with fluid.

4. Surgeon: Aspirate air (if present) from arterial cannula; if possible, initiate
cardiac massage until CBP restarted
5. Anesthesiologists: Place patient in steep head-down position; be prepared
to temporarily occlude carotid arteries

6. Confirm sufficient volume in CBP reservoir and resume CPB with active
aortic root venting

7. Administer vasopressors to raise perfusion pressure

8. If suspected cerebral air embolism, cool patient on CBP and consider

instituting retrograde cerebral perfusion; consider packing patients head in ice
9. Anesthesiologists: Ventilate lungs vigorously with 100% oxygen;
administer corticosteroids (2-4 g methylprednisone and/or 20 mg
dexamethasone, and continue for 72-96 hr postoperatively)

10. Administer 25 g mannitol and maintain for 48 hr postoperatively

11. Aim for early patient arousal and assess for return of normal
mentation

12. Consult a neurologist if central nervous system damage is suspected

13. Consider computed tomography or magnetic resonance imaging if
patient fails to awaken or develops delayed mental deterioration

14. Consider hyperbaric oxygen treatment and repeat hyperbaric

therapy as necessary

15. Do not give up resuscitative efforts unless patient expires or is

diagnosed brain dead
REFERENCES
• Cardiopulmonary Bypass: Principles and Practice
• Massive air embolism during cardiopulmonary bypass. Causes,
prevention, and management
THANK YOU …..