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  3. Air Embolism – Case 1

Air Embolism – Case 1

Clinical Presentation

  • 55-year-old male who presented to the hospital with dyspnea and exertional intolerance.

Past Medical History

  • NSCLC (s/p Neoadjuvant Chemotherapy/XRT, R Pneumonectomy in 2008), Myocarditis
  • LVEF 50%

Clinical Variables

  • Stress MPI: Mild infero-apical wall segment stress inducible myocardial ischemia.


  • Home Medications: Isosorbide Mononitrate, Digoxin, Albuterol, Budesonide-Formoterol, Montelukast
  • Adjunct Pharmacotherapy: None

Pre-procedure EKG


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Left coronary artery angiography
  • no significant disease in the left anterior descending (LAD) and left circumflex (LCx) coronary arteries.
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Left coronary artery angiography

  • no significant disease in the left anterior descending (LAD) and left circumflex (LCx) coronary arteries.
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Right coronary artery (RCA) angiography

  • mild diffuse disease in the proximal right coronary artery (RCA) and 50-60% stenosis in the mid segment of the RCA.
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Right coronary artery angiography with presence of contrast dye ‘hang-up’ distally due to presence of air embolism.

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Rapid aspiration and aggressive saline flushing was followed by administration of IC vasodilators through the guide catheter, which caused the patient to become hypotensive. IV Epinephrine 1mg and phenylephrine 0.5mg was administered through the guide catheter. However, the patient went into ventricular tachycardia, which was successfully treated with a single defibrillator shock of 200 J. Angiography showing restoration of flow (TIMI 3) and contrast clearing from the distal vessel and microvasculature.

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Angiography showing restoration of flow (TIMI 3) with clearing of contrast from the distal vessel and microvasculature.

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Final angiography of the RCA after successful treatment of abrupt vessel closure (AVC) due to air embolism.

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Patient continued to have refractory chest pain with hemodynamic instability, and an intra-aortic balloon pump (IABP) was placed.

Post-procedure EKG

Case Overview

  • Underwent cardiac catheterization with procedure being complicated by RCA abrupt vessel closure (AVC) due to air embolism.
  • While preparing the manifold for injection, air entered the system and inadvertently injected into the RCA.
  • Patient became hemodynamically unstable with ischemic changes on the EKG.
  • Rapid aspiration and serial saline flushing was performed using the manifold.
  • IC vasodilators were also administered and the patient became hypotensive.
  • IV neosynephrine 0.5mg and Epinephrine 1mg was given and shortly after, patient developed ventricular tachycardia which was successful treated with a single defibrillator shock of 200 J.
  • Follow-up RCA angiography showed restoration of flow without contrast dye ‘hang-up’.
  • Patient continued to have ongoing chest pain with persistence of hypotension and ischemic changes on the EKG and an IABP was placed.
  • Troponin-I peaked at 1.7 ng/mL and CK-MB peaked at 6.2 ng/mL.
  • He was discharged home 2 days later without further sequelae.

Learning Objectives

  • What is the likely explanation or reason why the complication occurred?
    • Air embolism due to inappropriate guide catheter and manifold preparation.
  • How could the complication have been prevented?
    • Properly preparation of the guide catheter and manifold.
    • Do not engage the coronary ostium when you pull out the guiding wire unless the patient has excessive aortic tortuosity or an enlarged aortic root.
    • Do not connect the manifold to the catheter with the flush running. This may lead to an air embolism if the catheter has a column of air already in it.
    • It is essential to properly prepare and de-air all catheters, especially diagnostic/guide catheter prior to connecting them with the manifold:
      • Draw back at least 2 ml of continuous blood into the injection syringe, which should be filling with saline. If you see a large amount of air in addition to blood being drawn back, pull back the catheter until there is only free flowing blood being drawn back.
      • Discard the saline/blood mixture into the one-way waste bag. Draw back saline and discard into the waste bag until there is no air in the system.
      • Draw back dye into the syrine for injection.
      • Attempt to inject a few ml of dye into the ascending aorta before engaging the coronary ostium.
      • Once engaged, continue with cine acquisition and angiography by injecting contrast.
    • Proper handling of the manifold to prevent inadvertent air injection.
      • Hold the manifold at 45° and assure no air is within the syringe prior to injecting.
      • Never fully inject all the contents within the 10 cc syringe (leave 1-2cc).
      • If there are minimal air bubbles with in the syringe, gently tap the syringe to allow them to ascend to the top.
      • If air is in the manifold, disconnect the syringe from the manifold and empty it, back flush the manifold with saline continuously flushing and then reconnect the syringe to the manifold.
    • Pay attention to the entire system (tubing, contrast bottle etc.) to assure no air is within the circuit.
  • Is there an alternate strategy that could have been used to manage the complication?
    • There are various management strategies aimed at restoring blood flow in the affected coronary and depend on the patients hemodynamic status, and include the following:
      • 1st: Vigorous saline flush into the coronary arteries and aspirate blood via guide catheter and inject forcefully back into the coronary artery.
        • Assure catheterization system is air tight and allow bleed-back from the catheter to clear any residual air in the system prior to performing this.
        • Air aspiration should be performed quickly using the catheter which is already being used to cannulate the vessel (diagnostic catheter, guide catheter or thrombectomy catheter etc.).
      • 2nd: Hemodynamic support to increase perfusion pressure to assure adequate coronary perfusion.
        • Blood pressure management:
          • If hypotension and SBP is 50-90 mmHg give IV phenylnephrine 200 ug push and followed by flush with saline, repeat as needed every minute
          • If blood pressure is non-measureable give IV epinephrine 1cc of [1:10,000 dilution] push and followed by flush with saline, repeat as needed every 2 minutes
        • Bradycardia Management:
          • IV atropine 0.5-1mg (up to a dose of 3mg), Dopamine 2-10 ug/kg/min gtt, and/or epinephrine 2-10 ug/min gtt
          • Transcutaneous pacing or temporary venous pacer
      • 3rd: Dissolving or passage of the air embolism by transient elevation of intra-atrial pressure by use of inotropes and intra-aortic balloon pump.
      • 4th: 100% oxygen to promote nitrogen diffusion.
      • 5th: Use of vasodilators (adenosine, CCB, nitrates) for treatment of slow flow/no-reflow.
    • What are the important learning points?
      • Air embolism is almost always iatrogenic and may result from inadequately flushed catheters, introduction or withdrawal of balloon catheters and guidewires, rupture of the balloon, defective manifold systems, leaky equipment.
      • Air embolism can cause acute chest pain, loss of consciousness, hypotension, arrhythmias, bradycardia, conduction blocks, ST-segment elevation myocardial infarction (most common EKG finding), discreet vessel cutoff (most common angiographic finding), slow flow/no-reflow phenomenon, and death.
      • Signs and symptoms are dependent on the amount of air introduced into the coronaries, number of vessels affected, baseline cardiac function) and vascular response to symptoms.
      • Guidelines for management of coronary air embolism are lacking. Emphasis should be on prevention by thoroughly flushing cardiac catheterization equipment and carefully aspirating the catheters. Early recognition is very important. In this case we noted dye ‘hang-up’ in the RCA, raising our suspicion for coronary air embolism. When suspicion for coronary air embolism is high or confirmed NO FURTHER angiographic images should be acquired.
      • In hindsight the RCA lesion intervention could have been considered once the patient is stabilized and flow was established in the RCA.
Educational Content


  • AVC is the commonest major complication of PCI1
  • Incidence: 0.3% [used to be 3% in pre-stent era]2
  • Risk factors:3
    • Proximal vessel tortuosity
    • Diffuse lesion
    • Pre-existing thrombus
    • Degenerated vein graft
    • Extremely angulated lesion
    • Unstable angina
    • Multivessel disease
    • Female gender
    • Chronic renal failure
  • Common causes:3
    • Coronary dissection
    • Intracoronary thrombus formation
    • Native thrombus (or atheroma) embolization
    • Air injection
    • Coronary no-reflow
    • Coronary vasospasm

In the current DES era, commonest causes of AVC are stent edge dissection and acute stent thrombosis. However, the cause is indeterminate in almost 50% of patients.2

  • Classification of coronary perforation: As per the National Heart, Lung and Blood Institute scheme, types A–F classification remains useful to describe the severity of luminal injury:4
Type AMinor radiolucency within the coronary lumen without dye persistence
Type BParallel tracks or double lumen separated by a radiolucent area during angiography without dye persistence
Type CExtraluminal, persisting extravasation of contrast
Type DSpiral luminal filling defects
Type EPersistent lumen defect with delayed antegrade flow
Type FFilling defect accompanied by total coronary occlusion
  • Prevention:
    • Maintain ACT > 300 throughout procedure
    • Make sure interface is free of air
    • Avoid high-pressure balloon dilatation or stenting
    • Avoid unnecessary post-dilatation and very long stents
    • Use distal protection devices in vein graft PCI
    • Be careful when retrieving delivery after stent implantation
    • Avoid geographical miss during stenting
    • Avoid aggressive post-dilatation at the stent edges
    • Be careful while positioning wire distal tip in tortuous vessel
  • Management: Abrupt closure results in acute ischemia manifesting as ECG changes, hypotension, bradycardia, chest pain and ventricular arrhythmias. The first step is to identify the underlying cause of AVC and then treat it accordingly.
    • Immediate priority should be to ensure intraluminal position of coronary guidewire and, if in doubt, an over-the-wire balloon catheter or Twin-Pass or other microcatheter should be advanced distal into the target vessel to allow minimal contrast media injection and confirm wire position.
    • If intraluminal guidewire position is confirmed, the most likely mechanism underlying AVC is dissection or intraluminal thrombus. Prompt balloon

inflation should be attempted to establish antegrade flow. If flow returns immediately after balloon inflation the likely cause of AVC is dissection and urgent stenting is useful for stabilizing.

    • If the distal flow after balloon inflation is sluggish (TIMI 0 or 1), the likely cause of AVC is distal thromboembolism. Using a Twin-Pass or microcatheter to administer distal vasodilators can help reestablish flow.
    • If initial contrast agent injection reveals guidewire position within a false lumen, careful exploration of the occluded segment using a second guidewire must be performed.
    • Aspiration thrombectomy and Glycoprotein IIb/IIIa antagonists may be helpful if acute closure is due to

thrombus. Control of anticoagulation is of paramount importance to avoid thrombotic occlusion of stented artery. ACT should be measured every ~30 minutes to keep ACT > 300 throughout the procedure and dose of anticoagulation is adjusted accordingly. If ACT is not reaching therapeutic levels consider resistance to anticoagulant and a possible reason for suspected thrombus formation causing AVC.

    • Intravenous fluids, vasopressors, inotropes and intra-aortic balloon pump (IABP) should be considered for unstable hemodynamics.
    • Emergency CABG should be considered if patient have persistent AVC depending on the location of the occlusion, patient’s clinical condition and assessment of risks and benefits.

Coronary slow flow/no-reflow phenomenon

Slow flow/No-reflow is an acute reduction in coronary flow (TIMI grade 0–1) in a patent vessel with absence of dissection, thrombus, spasm, or high-grade residual stenosis at the original target lesion.5 The underlying mechanism is complex and not completely understood, but some proposed mechanisms include distal embolization of calcium, plaque or thrombus and microvascular spasm caused by release of vasoconstrictor substances like serotonin and thromboxane, oxidative stress, and reperfusion injury.6 Clinical and lesion characteristics associated with higher incidence of no-reflow include left ventricular systolic serotonin and thromboxane, oxidative stress,and reperfusion injury.6 Clinical and lesion characteristics associated with higher incidence of no-reflow include left ventricular systolic dysfunction or hemodynamic instability, long calcified lesions, ostial lesions, chronic total occlusion of right coronary artery, thrombotic lesions, and vein graft lesions. Use of rotational atherectomy is also associated with a higher incidence of no-reflow.
    • Direct stenting whenever feasible
    • Use of distal embolic protection devices for vein graft interventions.
    • Aspiration thrombectomy in STEMI cases if there is large thrombus burden
    • For cases involving rotational atherectomy, the use of rota flush, small

initial burr sizes, shorter rotablation runs, avoiding drops in rotations per minute (RPMs), and prevention of hypotension/bradycardia

Management: Coronary no re-flow must be immediately differentiated from AVC due to dissection as placement of stent in a vessel with no reflow may worsen the situation. Exclusion of dissection, thrombus, spasm, or high-grade residual stenosis at the original target lesion suggests no-reflow.
    • Stabilize hemodynamics with medications/intra-aortic balloon pump (IABP)
    • IC verapamil (100–200 μg)
    • IV adenosine (10–20 μg)
    • IC nitroprusside (50–200 μg)
    • Moderately forceful injection of blood or saline through the manifold
    • GPIIb/IIIa agents, IV cangrelor may also be helpful

Air Embolism

Intracoronary air embolism is a potentially lethal but rare complication. It could result in hypotension, hemodynamic collapse, cardiac arrest, and in rare cases death. Coronary air embolism is almost always iatrogenic. It occurs mostly when
    • Catheters are not adequately aspirated and flushed
    • During introduction or withdrawal of a guidewire, balloon catheter or other interventional devices
    • Rupture of a balloon during high inflation
    • During intracoronary medication injection

Diagnosis: Coronary air embolism is detected fluoroscopically as intracoronary filling defects during dye injection. It could also be seen as abrupt cutoff of a vessel secondary to occlusion of distal circulation with air column. Clinically small air embolism may be asymptomatic. Larger air embolism may present as chest pain, hypotension, ischemic EKG changes, or cardiac arrest.
    • Do not engage the left main coronary when pulling out the guiding wire unless the patient has excessive aortic tortuosity or an enlarged aortic root.
      • Do not connect the manifold to the catheter with the flush running. This may lead to an air embolism if the catheter already has a column of air inside it.
      • Draw back at least 2 cc of blood into the injection syringe and make sure that the interface is free of air prior to injection.
      • Inject some dye into the ascending aorta prior to engaging left main.
      • Always ensure that all the catheters and tubings are aspirated, flushed and free of air.
      • Take adequate care when prepping stents or balloons and ensure that the syringe tip is facing downwards.
      • Always inject with the syringe tip facing downwards


        • Put patient on 100% oxygen.
        • Flush air free saline vigorously into the coronary arteries. Aspirate blood and air column via guide catheter and reinject saline forcefully back into coronary arteries.
        • Administer IV phenylephrine 200 μg for hypotension. Repeat, as needed every minute. If significant hypotension or hemodynamic collapse is present, push IV 1 cc epinephrine (1:10,000 dilution).
        • Intracoronary injection of vasodilators (adenosine, nitroprusside, verapamil) may be attempted.
        • Supportive measures should be instituted (IABP for persistent hypotention) and patient admitted to intensive coronary care unit for further monitoring

      Coronary Vasospasm

      Coronary vasospasm can be induced by PCI secondary to endothelial denudation and nitric oxide loss.
        • Some cases are catheter-induced which is caused by a contact of a catheter without balloon deployment. It is usually short-lived and is most prone to occur at the ostium of the right coronary artery (RCA). The left main is less susceptible to ostial spasm
        • Rotablator cases are more prone to vasospasm
        • Coronary vasospasm is detected by presence of EKG changes of ST segment elevation in association with angina, and then EKG completely returns to baseline upon resolution of symptoms.
        • The definitive diagnosis of coronary vasospasm is made angiographically by demonstration of reduction of luminal diameter in a discrete segment of the vessel, which is proven reversible by the administration of intracoronary vasodilators.
        • Initial step is intracoronary vasodilatation with IC calcium channel blockers and/or nitrates [nitroglycerin 100-300 mcg, verapamil 100 mcg/min, up to 1.0-1.5 mg, nicardipine 100-300 mcg, nitroprusside 100-300 mcg]
        • IV atropine can be useful if there is associated hypotension of bradycardia
        • If vasospasm persists, remove all hardware and leave the guide wire in place to maintain position. This may

      If vasospasm persists, remove all hardware and leave the guide wire in place to maintain position. This may minimize distal vessel spasm

        • Repeat prolonged PTCA for 2-5 minutes at low pressures (1-4 atmospheres)
        • Stenting should be reserved in cases if all the above measures have failed, as it may lead to propagation of spasm to a new location
        • Refractory vasospasm may be indicative of dissection, which is also an indication for stenting

      Abrupt Vessel Closure Summary

      • Dissection
        • Minor dissections - usually heal without clinical sequelae, no treatment required
        • Major dissections - repeated prolonged low-pressure balloon [distal vessel], stenting [Proximal/mid vessel segment or impaired flow due to dissection]
      • Thromboembolism
        • Twin-Pass or microcatheter to administer vasodilators distally
        • Check ACT to keep > 300. Consider starting IV Cangrelor or bailout GPIs
        • Balloon dilatation and/or thrombus aspiration in case of stent thrombosis
        • Stenting on case of thrombosis in in unstented vessel segment
      • No-reflow
        • Intracoronary Adenosine, Nitroprusside, Nicardipine, Verapamil, or GPI’s
        • A transit catheter or over-the-wire balloon should be used to deliver the vasodilators to the distal microvasculature
        • Insertion of IABP to improve flow
      • Air embolism
        • Start 100% oxygen
        • Flush air free saline vigorously into the coronary arteries. Aspirate blood via guide catheter and reinject forcefully back into coronaries
        • IV phenyl epinephrine or epinephrine as needed
        • Intracoronary injection of vasodilators
      • Vasospasm
        • Intracoronary Nitroglycerin, Adenosine, Nitroprusside, Nicardipine, or Verapamil
        • IV fluid bolus and/or atropine as needed
        • Remove all hardware and leave the guide wire in place to maintain position
        • Repeat prolonged PTCA for 2-5 minutes at low pressures (1-4 atmospheres)
      • Unknown etiology
        • Maintain wire position distally and pass a microcatheter distally to inject contrast
        • If flow distally, problem at site of vessel closure and needs to be investigated
        • If no flow distally, consider no reflow and give IC vasodilators


      1. de Feyter P.J., de Jaegere P.P.T., Murphy E.S., Serruys P.W. (1992) Abrupt coronary artery occlusion during percutaneous transluminal coronary angioplasty. Am Heart J 123:1633–1642.
      2. Francesco Giannini, Luciano Candilio, Satoru Mitomo, Neil Ruparelia, Alaide Chieffo, Luca Baldetti, Francesco Ponticelli, Azeem Latib, Antonio Colombo. Practical Approach to the Management of Complications During Percutaneous Coronary Intervention. J Am Coll Cardiol Intv. 2018 Sep, 11 (18) 1797-1810.
      3. Klein L. (2005) Coronary complications of percutaneous coronary interventions: a practical approach to the management of abrupt closure. Catheter Cardiovasc Interv 64:395–401.
      1. Huber MS, Mooney LF, Madison J, et al. Use of a morphologic classification to predict clinical outcome after dissection from coronary angioplasty. Am J Cardiol 1991;68:467–71.
      2. Rezkalla S.H., Kloner R.A. (2002) No-reflow phenomenon. Circulation 105:656–662.
      3. Piana R., Paik G., Moscucci M., et al. (1994) Incidence and treatment of “no-reflow” after percutaneous coronary intervention. Circulation 89:2514–8.

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