causes, prevention and management of coronary air embolism

1. CORONARY AIR EMBOLISM
Dr Siva Subramaniyan
PGIMER &Dr.RML Hospital
New Delhi

2. INCIDENCE
• Coronary air embolism is an uncommon complication encountered
during cardiac catheterization
• No randomized trail to evaluate incidence
• a reported incidence of 0.1 to 0.3%

3. • Sequelae range from a clinically insignificant event to an acute
coronary syndrome and death
• Catastrophic hemodynamic compromise can occur within seconds
after introduction of air emboli within the coronary arteries and may
resolve within a few minutes if prompt treatment is undertaken.

4. CAUSES

5. • Most often, air embolization occurs when catheters used for vascular
procedures have not been adequately aspirated and flushed
• The introduction of air into catheters can also occur by entrainment
during balloon catheter or guide wire
• Air embolization can also result from the rupture of balloon catheters,
although in the case of coronary dilatation balloons, the amount of
air is generally quite small.

6. Mechanisms - air embolism during PTCA.
• Not flushing the catheter before introduction into vasculature.
• Incomplete aspiration of guiding catheter upon introduction into the
vasculature.
• Balloon leakage or rupture if balloon is not adequately prepared.

7. • Removal of balloon catheters from deeply seated guiding catheters - during
catheter exchanges when balloon catheter is removed and haemostatic
valve is left open, causing air to enter the potential space left behind by
balloon catheter if the operator fails to purge the air from the guide
catheter coronary air embolism may occur during coronary injection.
• Structural failure of catheter

8. • A paradoxical embolism arises when air/gas entrained in the venous
circulation manages to enter the systemic arterial circulation causing
symptoms of end-artery obstruction.
• The passage of gas across a patent foramen ovale to the systemic
circulation.
• A patent foramen ovale is detectable in about 30% of the population
and makes right-to-left shunting of gas bubbles possible.
PARADOXICAL EMBOLISM

9. • Elevated pulmonary arterial pressure due to a venous gas embolism
may be reflected in elevated right atrial pressures predisposing to
bubble transport across a patent foramen.
• In addition, the decrease in left atrial pressure caused by controlled
ventilation and use of positive end-expiratory pressure may create a
pressure gradient across the patent foramen ovale favouring passage
of gas into the systemic circulation.

10. • venous gas may enter the arterial circulation by overwhelming the filter
capacity of the lungs normally in place to prevent arterial gas emboli.
• overexpansion of the lung through decompression barotraumas in diving,
pulmonary barotraumas in the ventilatory therapy for critical care patients,
can cause paradoxical embolism.
• Insertion or removal of central line.

11. • Rupture of balloon catheters used for peripheral vascular intervention
and valvuloplasty procedures are more likely to result in greater
volume of air released into the blood stream.
• This can especially occur if they have not been properly prepared
prior to introduction into the bloodstream.

12. IABP rupture
• Arterial helium gas embolism has been reported in the setting of
rupture of an intra-aortic balloon pump

13. ABLATION OF AF

14. A 30-year-old male with a history of rheumatic mitral valve disease presented with progressive exertional
dyspnoea. Echocardiography revealed a mitral valve area of 1 cm2, and absence of mitral regurgitation.
Percutaneous mitral valvuloplasty was performed.
Unexpectedly, one balloon suddenly ruptured during a second inflation. The patient experienced severe chest
pain and shock.
The electrocardiogram showed ST-segment elevation in leads II, III, and aFV.

15. • Prompt resuscitation was performed and right coronary angiography
showed a bubble of air trapped at the crux of the right coronary artery.
• The operator injected 100 mcg of nitroglycerin inside the right coronary,
followed by intracoronary infusion of normal saline.
• Ultimately, right coronary angiography revealed that the air was
successfully cleared off the artery, with TIMI grade 3 flow and, return of
myocardial blush. Eventually, chest pain disappeared, with a favourable
haemodynamic condition

18. IN MITRAL VALVULOPLASTY
• Although rare but in a series of 161 pt who underwent Percutaneous
mitral valvuloplasty with double balloon technique 14 patient (8.7%)
has coronary air embolism due to balloon rupture.
• Virtually all cases of coronary embolism as a complication of
percutaneous mitral valvuloplasty affected the right coronary artery

19. • Usually procedure done in supine position
• RCA ostium is anterior, and air bubble being lighter rises against
gravity so preferentially goes in to RCA.

21. • 56-year-old man with symptomatic paroxysmal atrial fibrillation
refractory to both conventional antiarrhythmic drug therapy and
ablation
• He was referred for transcatheter left atrial appendage (LAA) closure.
• he is also K/C/O HCM

22. • The presence of hypertrophic cardiomyopathy with enlarged left
atrial diameter (50 mm), heart failure, recurrent episodes of
refractory atrial fibrillation, previous transient ischemic attacks, and
hypertension led to a high annual predicted risk of stroke based on
CHADS2 and HAS-BLED
• The patient also experienced gastrointestinal bleeding. Therefore, a
transcutaneous LAA occlusion was attempted with the AMPLATZER
Cardiac Plug (ACP) system.

24. • The patient received 100% oxygen administration and intravenous
atropine, after which his blood pressure increased and stabilized.
• Two rapid, forceful injections of contrast medium administered with
great caution into the coronary arteries resulted in immediate
resolution of the ECG abnormalities and transient atrial fibrillation ,
which began from the anterior leads because the left coronary artery
was injected first

26. • A 35-year-old male patient was admitted because of dysphagia and
odynophagia
• A chest X-ray showed multiple cavitary lesions in both lungs and a CT-
guided lung biopsy was requested for histopathological diagnosis.

28. Mansour et al recognise three possible causes for air embolism:
• communication between the pulmonary vein and the atmosphere;
• bronchovenous fistula or other communication between air-
containing spaces and pulmonary veins;
• air from the pulmonary arterial system reaching the pulmonary
venous circulation by traversing the pulmonary microvasculature

31. • In this patient, hyperbaric therapy was applied and he recovered
from the near fatal condition

32. OTHER CAUSES
• The application of tissue vaporization techniques such as excimer
laser can result in excimer laser-induced cavitation bubbles but these
are more significantly associated with localized dissection rather than
distal embolization

33. PATHOPHYSIOLOGY

34. PATHOPHYSIOLOGY
• An intracoronary air dose of 0.02 ml/kg was associated with 28%
mortality in a study conducted in a canine model .
• Porcine studies have demonstrated that injection of air bubbles with
diameters of 75, 150, or 300 micro M each in a volume of 2 micro l/kg
resulted in transient depression of regional myocardial function
characterized by decreased systolic segment shortening despite
maintenance of heart rate, left ventricular pressure, and mean
arterial pressure.

35. • The decrease in indices of cardiac function was directly related to the
size of the bubbles injected into the coronary arteries

36. • The effects of air embolism in the coronary circulation depend on two
factors: the volume of air entrapped and the rate of accumulation
• In humans, lethal volume of air has been shown to be about 200-300 ml
i.e. 3-5 ml/kg
• A pressure decrease of 5 cm H2O across a 14-gauge needle is capable of
transmitting approximately 100 ml of air per second . Accumulation at this
rate can be lethal. Conversely, the heart is able to tolerate large quantities
of air if entrainment occurs over a prolonged period

37. • The volume of air trapped and the rate of accumulation depend upon
the size of vascular lumen as well as the pressure gradient across the
blood-air interface
• Vascular air embolism increases micro vascular permeability . In
addition, platelet aggregation occurs due to turbulent flow. this in
turn may lead to a systemic inflammatory response

38. • The diagnosis of coronary air embolism is made angiographically by
the visualization of air bubbles traversing the coronary arteries on
fluoroscopy.
• Air bubble may occlude the artery but the occluded artery appear
vaguely defined rather than as the discrete vessel cut off typically seen
when vessel is occluded by thrombus.
• Air embolism can also cause no reflow or slow flow.
DIAGNOSIS

39. • Majority of cases are asymptomatic
• Rapid onset of chest pain.
• Electrocardiographic evidence of myocardial ischemia or injury
• Systemic blood pressure may be unaffected or may decline.
• The effects clear spontaneously within 5 to 10 minutes in most
part of the cases
SIGNS AND SYMPTOMS

40. Rare Signs and Symptoms
• Bradycardia
• Complete heart block
• Hypotension
• Asystole
• Ventricular tachycardia/ fibrillation

41. • There is no established consensus on the adequate management of air
embolism and its complications. The principal management is
PREVENTION
• The vast majority of observed emboli are extremely small volumes of
air that do not result in symptoms or hemodynamic consequences;
therefore, they require no therapy.
TREATMENT

42. • Once patient develops sign and symptoms 100% oxygen by face mask
should be given.
• This aids in eliminating nitrogen by diffusion down its concentration
gradient and out of the embolus leading to significant reduction in
the size of the air bubble.
A Case Report and Review of the Literature. Catheter Cardiovasc Interv 68: 897-900.

43. • Hyperbaric oxygen therapy for cases of massive arterial air emboli
• Analgesics
• Monitor and treat arrhythmias
• Attempts to maintain coronary blood flow should be instituted. These
may include the use of inotropes and intra-aortic balloon pump.
MASSIVE EMBOLI

44. • Other manoeuvres such as intracoronary injection of vasodilators
(adenosine, nitroprusside, calcium channel blockers) may be
attempted.
• It has been proved that nitroglycerin causes dilatation of the
epicardial coronary artery and microcirculation.

45. • Thus, a more dilated coronary vessel could have a higher coronary driving force
and much more surface contact between the inhaled 100% oxygen and the air
emboli.
• These effects facilitate the passage and absorption of the air bubbles.
• Intracoronary nitrates may lower the blood pressure excessively and should be
used with utmost caution.
Korean Circulation J 2007;37:334-336

46. • Intracoronary adenosine has proven vasodilatory effect through the
release of nitric oxide.
• Adenosine cause vasodilatation of the vessel and accelerate the
clearance of the air bubble through the vessel while the nitric oxide
effect can overcome the microvascular dysfunction.

47. • Also the use of guide wire to disrupt the air bubbles can be
performed.
• Intracoronary thrombus aspiration catheter systems which are the
best options to resolve intracoronary air embolisms safely and
harmlessly.
• Haraphogse M, Rossall RE (1989) Large air embolus complicating coronary angioplasty.
Cathet Cardiovasc Diagn 17: 168-171.

48. • Pushing method
• Balloon method
• Suction methods

49. PUSHING METHOD
• Disruption or dislodgement by the guidewire and the forceful
injection of saline are aimed at fragmenting the air embolus to allow
dispersal or to force it distally.
• Such interventions may result in main vessel patency
• but clearly such techniques have a potential to damage the main
vessel during aggressive manoeuvres and to damage the distal
microvasculature due to widespread, smaller embolisations

50. BALLOON METHOD
• the balloon method is simple
• Inflate the balloon in the air bubble, so that bubble get fragmented
into pieces
• But it may damage the coronary site without lesion by inflating the
balloon inside the bubble.

51. SUCKING METHODS
• One more mechanical methods is aspiration of the bubbles by
aspiration catheters
• It is safe method
• It will not damage the vessel wall
• It will not cause distal embolization

53. • Patient was undergoing left coronary angiography
• After 2 coronary angiography shots of the left coronary system, there were
slow coronary flow down the LAD, inferior leads ST segment elevation,
bradycardia with complete atrioventricular block and mild chest
discomfort.
• There was slow flow down the RCA with multiple bead-like shadow defects
oscillating in the RCA with Thrombolysis In Myocardial Infarction (TIMI)
grade 2 flow.

55. • The intra-arterial blood pressure (IBP) was 81/60 mm Hg and heart rate
was 34 beat per min (bpm).
• Intracoronary 1 mg of atropine was given.
• The whole guiding catheter (GC) system was carefully prepared with
adequate back bleeding.
• A coronary wire was tracked down the RCA and multiple passages of
intracoronary aspiration were done with a Thrombuster II aspiration
device. The hemodynamics slowly improved.

56. • There are only 2 reported cases of contralateral CAE in the literature
with one postulation mentioned being about the possible mixture of
the culprit blood–air-contrast bouncing off from the left cusp towards
the right cusp and into the RCA.

60. • Place the patient in the Trendelenburg position when possible. If
not possible, the supine position is sufficient.
• Position the catheter exit site (e.g., neck, arm) at a height lower
than the height of the patient’s heart.
• Cover the exit site with gauze and apply gentle pressure while
removing the catheter in a slow, constant motion.
REMOVAL OF CENTRAL VENOUS ACCESS DEVICES

61. • Instruct the patient to hold his or her breath, and perform a Valsalva maneuver as
the last portion of the catheter is removed; if unable to do so, time the removal
during patient expiration.
• Place pressure on the site until hemostasis is achieved. One to five minutes is
suggested.
• Apply a sterile occlusive dressing, such as gauze impregnated with petroleum jelly
and covered with a transparent film dressing.
• Leave dressing in place for at least 24 hours.

62. • Change the dressing every 24 hours until the exit site has healed. (Plain
gauze dressings have been associated with air passing through a persistent
catheter tract into the bloodstream, resulting in air embolisms, as have
occlusive dressings left in place for shorter periods of time.)
• Instruct the patient to remain lying flat for 30 minutes after removal of the
catheter.

63. conclusion
• Coronary air embolism almost always iatrogenic
• Most of the these are small and spontaneously resolved, but
sometimes it may be life threatening
• Prevention is the treatment