ECMO by Dr Mohamed

2. Complications
And Troubleshooting

6. Twelve studies were included (1763 patients), mostly reporting on venoarterial ECMO
After a median follow-up of 30 days (1st-3rd quartile, 30-68 days).
overall mortality was 54% (95% CI, 47%-61%), with 45% (95% CI, 42%-48%) of fatal events occurring
during ECMO and 13% (95% CI, 11%-15%) after it.
The most common complications associated with ECMO were: renal failure requiring continuous
venovenous haemofiltration (occurring in 52%), bacterial pneumonia (33%), any bleeding (33%),
oxygenator dysfunction requiring replacement (29%), sepsis (26%), haemolysis (18%), liver dysfunction
(16%), leg ischaemia (10%), venous thrombosis (10%), central nervous system complications (8%),
gastrointestinal bleeding (7%), aspiration pneumonia (5%), and disseminated intravascular coagulation
(5%).

7. Table 2: Common Complications of VA-ECMO (in Percent)
•Thrombosis: 1-22%
•Bleeding and coagulopathy, including hemolysis: 5-79%
•Limb ischemia: 13-25%
•Infection: 17-49%
•Neurologic events: 10-33%
Modified from Lafçı G, Budak AB, Yener AU, Cicek OF. Use of extracorporeal membrane oxygenation in adults. Heart Lung and
Circ 2014;23:10-23.

8. anticoagulation is a cornerstone, and potential pitfall of any ECMO circuit. Though an aPTT in
the 60-80 range is the starting target for anticoagulation, this can be adjusted, either higher or
lower, based on patients' individualized needs and risk profile.
In patients in whom the risk of bleeding may be higher, an aPTT goal of 40-60 seconds can be used. For
patients with lower anticoagulation targets, the flow through the circuit should be maximized to reduce
the chance of thrombosis.

10. Hematologic complications :
1. Anemia
In conjunction with bleeding, hemolysis associated with ECMO circuits will, over time, cause anemia that may
warrant blood product transfusion. Goals for transfusion, particularly of packed red blood cells, must be
weighed against the overall individualized treatment plan for each patient.
hematologic consequences of maintaining an ECMO circuit, other than hemolysis include acquired von Willebrand
factor deficiency, and thrombocytopenia, along with an increased risk of disseminated intravascular coagulation and
heparin-induced thrombocytopenia .

11. BLEEDING FROM CANNULA SITE
Management:
•Fully insert the cannula to the taper
•Thrombotic (Kaltostat) dressings
•Pressure (sand bag)
•Cessation of heparin and correct bleeding diathesis:
•platelets >80
•cryoprecipitate 5-10 ml/kg (1 bag ~ 20mL) -> fibrinogen >1.5
•FFP -> INR <1.5
•protamine 1mg/ 100 units of heparin in past 2 hours
•Vascular surgical review.
•Repair and re-cannulation (AS NEEDED).

12. After bleeding and thrombosis remains the most significant complication related to the
use of VA-ECMO. Sterile techniques and controlled implantation (operating room, cardiac
catheterization suite) portend greater success in comparison to emergent initiation.
Prolonged use of VA-ECMO also leads to a greater risk of infection. This is presumed to be from
a greater duration of indwelling catheters; additionally, patients who require prolonged support
with VA-ECMO also tend to suffer from critical illness and multi-organ dysfunction, putting them at
a greater risk for infection.18
Continued antibiotic prophylaxis after initiation of VA-ECMO (with an intravenous first generation
cephalosporin) remains an option to prevent catheter site-related infections, but its utility in the
prevention of systemic infections remains controversial.

13. Limb ischemia is also a known complication of VA-ECMO. Cannula size and positioning in relation to the
patient's vasculature plays a major role with this.
In addition to limb ischemia, compartment syndrome resulting in muscle necrosis, acidosis and lower
extremity amputation, can also occur.
The use of a reperfusion catheter to perfuse distal to the entry site of ECMO cannulas increases the
likelihood of limb preservation.

14. •HIGH FREE HAEMOGLOBIN LEVEL
•Look for intravascular haemolysis:
— dark/red urine or CRRT effluent with high K+
• Circuit should be assessed for signs of malfunction:
— “noisy” pump head (pump head thrombosis), or high transmembrane
pressure gradient (oxygenator thrombosis),or visible access insufficiency.
• If neither present -> repeat free Hb level
•if >0.10 g/dL -> likely low level haemolysis
— access insufficiency without visible kicking (may require echocardiography to detect
venous “suck-down” with a multistage cannulae)
— vessel- cannula impingement due to pericardial collection or retroperitoneal haematoma

15. ACCESS INSUFFICIENCY.
shaking of the circuit tubing draining to the pump. It indicates access insufficiency.
Access insufficiency occurs when the suction pressure at the access cannula can
draw in blood flow greater than venous return.
When this occurs inflow is interrupted due to partial or complete occlusion of the
inlet ports of the access cannula by the walls of the collapsible vein.
After a few seconds, ongoing venous return fills up the vein again and the cannula
ports reopen to function once more.
This cycle repeats itself resulting in unstable, fluctuating ECMO flows (shown in
L/min on the ECMO console) despite a stable pump speed (rpm).

16. Hypovolaemia/ haemorrhage
Poorly sited access cannula (too low)
Excessive pump speed (rpm setting) relative to the Cannula size
Patient coughing or straining
Positional (e.g. after turning the patient)
Acute vasodilatation (e.g. sedation bolus)
Increased intra-abdominal pressure
High output cardiac failure (e.g. septic shock)..relative hypovolemia
Cardiac tamponade /tension pneumothorax
Thrombosis /kink at cannula access site/circuit
Worsening cardiac function (e.g. cardiac arrest or acute heart failure while on VV ECMO)

19. Reduce the pump speed (rpm) until evidence of access insufficiency resolves, while still
attempting to maintaining adequate oxygenation.
The rpm can be decreased by 500 rpm every 10 seconds until kicking resolves.
Ensure that the patient is adequately sedated and consider neuromuscular paralysis if
appropriate (this will prevent coughing and straining from causing access insufficiency).
A fluid bolus can be given as a temporising measure if pump speed settings cannot be
re-established. However, recurrent fluid boluses should be avoided if possible as they
will lead to fluid overload and oedema.

20. Ongoing access insufficiency requires a systematic approach that includes:
•Exclusion of ongoing haemorrhage and/or hypovolaemia
•Confirmation of adequate cannula position
•Optimise cannula positioning (remember that ECMO cannula are not usually pushed
in further once they have been inserted, although arterial cannulae may be re-
advanced by a consultant if it is the site of bleeding)
•Optimise patient position
•Avoid vasodilators
•Check intra-abdominal pressure, seek and treat underlying cause if increased.
•Exclude causes of obstructive shock (e.g. perform echocardiography)
If these measures are unsuccessful an additional access cannula may need to be
inserted (high flow configuration).

21. PUMP FAILURE
Causes
Pump head/centrifugal pump disengagement
Electrical motor failure – either console or pump head
Battery failure (no AC power connected)
Rotaflow Power Isolation Switch “OFF”
Flow sensor problem
Management(if nothing simple)
Clamp circuit
Call for help.
Examine for a cause :
— Console (front): Power (On/Off Switch)
— Console (front): AC Power Supply Indicator lights
— Console (rear): Power Isolation Switch
— External Drive: Pump head position

22. Address Cause and re-establish pump function or obtain new console (IF THE PROBLEM IS NOT SIMPLE
FAILURE OF THE PUMP OR THE CONSOLE)
Engage Emergency Drive Unit (“Hand-crank”)
— Transfer Pump Head to Emergency Drive Unit
— Rotate hand crank to 1000 rpm and remove circuit clamp
— Gradually increase revs to previous speed
Transfer to new console
— Ensure power to new console
— Clamp circuit
— Transfer Pump Head to new console
— Establish pump speed to 1000 rpm and remove circuit clamp over 3-5 seconds while increasing pump
speed to obtain full flow

23. UNINTENDED EMCO DECANNULATION
Effects:
•bleeding from the cannula insertion site.
•ECMO support will stop -> same as pump failure
•Access cannula decannulation: air will rapidly enter and extensively de-prime the ECMO circuit and may reach
the patient ( air embolism)
•Return cannula decannulation: Patient’s blood volume will rapidly be lost from the circuit( AND FROM THE
VESSEL) until the circuit is clamped.

24. Air embolism
Air embolism into the circuit
This tends to happen with circuit rupture (wheels on tubes ,Fabric problem) or accidental access
decannulation or loose connections.
The circuit will rapidly de-prime (i.e. fill with air and froth)
The pump will become filled with foam, and pumping will not occur
The good news is, the loss of output will hopefully prevent air embolism
The bad news is, there will be loss of output.
Again, either hemodynamic instability, arrest (VA) or profound hypoxia (VV) will be the
overall result.
Additionally, air embolism into the patient's circulation may still occur.
.

25. Rescuing the circuit
Unless the whole circuit is clotted up due to the blood-air interface, one might be able to de-air
and reprime it. The arterial part of the circuit is clamped, and air is aspirated from the lines
using a 60ml Luer lock syringe (the air can be guided to the three-way tap by manipulating the
tubing, allowing to bubbles to percolate to the site of aspiration). The clamp can be taken off
and pump restarted when the circuit is again full of blood
Air in the oxygenator is aspirated from the oxygenator
In venous side direct it to the oxygenator then aspirate the air
(circuit contains stopcocks).
Small air foci in the oxygenator can be aspirated without clamping the circuit and stopping the
pump.

26. Air embolism into the arterial circulation via the VA circuit
Management strategy:
Clamp the circuit
Start CPR and/or manual bag oxygenation /support the hemodynamics as needed.
The arterial air emboli are likely to travel to the uppermost parts of the patient; thus, the brain and
upper limbs are most at risk.
Thus, neuroprotective measures should be considered.
There is little literature to guide one in this matter.

27. Air embolism into the patient's venous circulation
Management strategy:
Clamp the circuit
Start CPR and/or manual bag oxygenation
Tilt the patient head down (so the air collects in the apex of the right ventrile, and the base fills with blood- this
way, hopefully something other than air will get pumped into the pulmonary circulation)
The only way to get that air out is by aspirating it with a PA catheter /or central line advanced to the RV

28. PULMONARY EDEMA.
The problem is ongoing blood return to the left heart especially in the absence of any left
ventricular ejection causing greatly raised left atrial pressure.
The problem is exacerbated by even mild degrees of aortic and mitral regurgitation.
The diagnosis can be confirmed by demonstrating a distended left ventricle with
echocardiography.

29. What Can Be Done to Improve the Situation?
A modest reduction in left atrial pressure may be obtained by ??? increasing ECMO circuit flow (to
reduce pulmonary blood flow) and restarting inotropic support (to facilitate left ventricular
ejection),diuretics .
However, decompression of the left heart via an atrial septostomy (which may be performed
surgically or percutaneously) should be urgently performed, as, untreated, severe left ventricular
distension causes permanent cardiac and severe pulmonary injury.
Other types Of LV decompression …..IABP ,Empella ,drainage pipe to the left ventricle and
connected to ECMO

30. Harlequin syndrome
NORTH SOUTH SYNDROME

31. Hypoxemia 2ry to recovery of cardiac function in the presence of impaired pulmonary function in the setting of
peripheral VA ECMO.
In this circumstance, blood ejected from the right ventricle passes through the non-functioning lungs.
This deoxygenated blood preferentially supplies the coronary arteries, cerebral circulation, and upper limbs (the
usual site of a pulse oximeter probe or sampling of arterial blood gases). By contrast, oxygenated blood from the
femoral arterial cannula preferentially supplies the lower body.(North-South or Harlequin syndrome).
The diagnosis can be confirmed by demonstrating a lower SaO2 in the right arm compared to the lower limbs.
Note that this problem does not occur to the same extent with central VA ECMO, as the upper body is supplied by a mixture blood from the ECMO circuit and the left ventricle (LV).(when the mixing point is in the arch )

32. MANAGEMENT
.

33. 1-Increasing circuit flow(..higher afterload and proximal mixing blood site,reduce pulmonary
flow with more blood drained from the right side) and stopping any inotropic support /b blockers will
reduce LV ejection respectively.
2-Improving lung condition and increasing the vent setting .

34. .
3-However,if these measures are unsuccessful:
A* If cardiac function has largely recovered the patient can be converted to veno-venous (VV) ECMO by
removing the arterial cannula and placing an additional venous cannula for return blood.
B* If cardiac function is inadequate for VV ECMO (but still enough to cause upper body hypoxemia) veno-arterio-
venous (VAV) ECMO may be used. With VAV ECMO the patient is maintained on VA ECMO but a second return
cannula (containing oxygenated blood) is placed in the superior vena cava (usually via the right internal jugular
vein).
In this way oxygenated blood passes through the lungs.
*******VAV ECMO requires higher flows than standard VA or VV ECMO.
Additionally, an adjustable occluder may need to be placed on one of the return cannula to optimize flow: too much
flow through the arterial return cannula can cause upper body hypoxemia; too much flow through the venous return
cannula can result in inadequate hemodynamic support.
C* Central Cannulation ?

35. A 33-year-old male, 70 kg, was commenced on VV ECMO for pneumonia. Prior to initiating VV ECMO his
FiO2/PaO2 ratio was 55 mmHg and his SaO2 was 82%, despite maximal mechanical ventilation.
A 19 French (Fr) return cannula was inserted into the right internal jugular vein and advanced to the right atrium. A
24 Fr drainage cannula was inserted into the femoral vein and advanced to the inferior vena cava.
Thirty minutes following initiation of ECMO he has persisting hypoxemia (SaO2 82%), despite a circuit flow of 5.5
L/min and a post-oxygenator SO2 of 100%.
Pump speed is 3500 rpm and SDO2 is 78%. Increasing the circuit flow to 6.5 L/min does not improve the SaO2.

36. The most likely cause of the arterial hypoxemia is recirculation of blood
between the return and drainage cannulas.
The goal with VV ECMO is for the (oxygenated) return blood to pass through
the tricuspid valve and into the lungs. Thus, the tip of the return cannula
should be in the right atrium.
Deoxygenated blood typically drains to the ECMO circuit from a cannula
positioned in the inferior vena cava. Three common cannula arrangements
for VV ECMO are shown in Figure 1.

37. Ideally, no oxygenated blood from the return cannula passes directly to the drainage cannula, although in
practice a degree of recirculation always occurs. The cardinal sign of recirculation is a low SaO2 in association
with a high SDO2.
In this case, the difference between the SaO2 and the SDO2 of 4% strongly suggests recirculation as the cause
of the hypoxemia. With recirculation, little improvement in SaO2 occurs with increasing circuit blood flow.
The problem can be further investigated by examining the position of the cannulas with chest radiography
and by interrogating the flow pattern of the return cannula with TEE.

38. Adjusting the position of the cannulas under TEE guidance can reduce recirculation. The return cannula should be
adjusted so that the tip is positioned in the right atrium and, ideally, the blood flow directed towards the tricuspid valve.
The position of the drainage cannula in the inferior vena cava can usually be assessed with transthoracic
echocardiography from a subcostal window.

39. SaO2 is influenced by
(1) the degree of recirculation
(2) pulmonary function and the extent to which the lungs are ventilated, and
(3) the relative contributions to pulmonary blood flow of ECMO blood
(oxygenated) and systemic venous return (deoxygenated blood)…low in
sepsis.
(4) Oxygenator function
Assuming that pulmonary function has not changed, recirculation is
insignificant, and the oxygenator is working normally, SaO2 is mainly
determined by ECMO circuit flow relative to the patient’s systemic venous
return (i.e., the patient’s cardiac output).

40. Early aggressive treatment of sepsis is essential. Empiric broad-spectrum antibiotics should
be administered. If sepsis is strongly suspected,
intravascular catheters should be changed (central venous, intra-arterial, dialysis). It is not
usually appropriate (or possible) to change the ECMO cannulas.
Fluids and vasoactive drugs (norepinephrine) should be administered as appropriate.
However, aggressive fluid therapy may further increase cardiac output, potentially reducing
SaO2.
Metabolic rate and cardiac output can be reduced by sedating and paralyzing the patient and,
if necessary, by active cooling (e.g., to 34–35°C).
Increasing circuit flow will improve SaO2. The main factor limiting circuit flow is usually
venous drainage.
Thus, it may be necessary to insert a second venous drainage cannula to increase flow (in
this scenario the second drainage cannula can be placed in the contralateral femoral vein and
advanced to the iliac vein). Even with two drainage cannulas, it is rare to be able to achieve
flows above 7 L/min.

41. Thank You…