ECMO Flow Sensor Coupling Paste

Resus Review

Knowledge of the blood flow in the ECMO circuit is critical for managing the patient safely. If the circuit is driven by a positive displacement pump, the blood flow rates are determined solely by the pump. However, with centrifugal flow pumps, the flow rate is dependent not only on the pump rotational speed, but also upstream and downstream pressures. In this case, ultrasonic flow transducers provide are able accurate measurements on circuit blood flow.

With the Maquet ROTAFLOW Centrifugal Pump, the flow sensor is located on the downstream side of the pump. It clamps over the circuit tubing going to the oxygenator.

ECMO Pump Ultrasonic Flow Sensor

The ECMO ultrasound flow sensors require a conductive interface between the sensor and the circuit. This is usually a gel or paste. Important properties for the include:

  • Highly conductive at frequencies used by the flow sensor
  • Non-marring
  • Does not dry out
  • Easy to remove
  • Non toxic

The most popular ultrasound gel found in emergency departments and intensive care units is Parker Labs Aquasonic. It is made of a combinations of propylene glycol, glycerine, perfume, dyes, phenoxyethanol or carbopol R 940 polymer along with lots of water. While it is useful to use for ultrasound exams, when exposed to air it dries out quickly which interferes with the flow sensor operation.

Aquasonic Ultrasound Gel

A better product to use is Em-tec Ultrasonic Coupling Paste. It is designed specifically for flow sensors. It remains pliable and does not dry out when exposed to air. This allows accurate performance of the flow sensor for weeks.

Ultrasonic Coupling Paste

ECMO Flow Sensor Coupling Paste

Dantrolene for Malignant Hyperthermia

Resus Review

Malignant hyperthermia is a life-threatening reaction to volatile anesthetics and the neuromuscular blocking agent succinylcholine. A genetic mutation in the ryanodine receptor causes sequestration of intracellular calcium and rigid muscle contractions, which requires large quantities of ATP which is is replenished by uncontrolled oxidative metabolism. The result is heat production and high body temperatures.

Dantrolene acts at the ryanodine receptor blocking the release of calcium from the sarcoplasmic reticulum, and reducing the intracellular calcium, thereby countering the effects of the malignant hyperthermia. Although, Dantrolene does not block neuromuscular transmission nor interfere with reversal of muscle relaxants, the mechanical response to nerve stimulation will be depressed.

Dantrolene Administration IV

The recommended starting dose is 2.5 mg/kg intravenously based upon the patient’s true weight rather than ideal weight, although no scientific study has addressed the difference in this dosing recommendation. Following the initial dose administration, if symptoms are not improving, continuing to administer up to 10 mg/kg is also recommended.

Dantrolene is provided as a powder and is prepared by mixing with sterile water. Sterile phlebitis may follow administration of dantrolene, and should be infused through the largest possible vein. When used with calcium channel blockers (verapamil or diltiazem), dantrolene may produce life-threatening hyperkalemia and myocardial depression. Once a patient has been successfully treated for 48 hours with intravenous dantrolene may be stopped.

Dantrolene for Malignant Hyperthermia

Post-Catheterization Hemoglobin Drop

Resus Review

Hemorrhage is a feared and potentially life-threatening complication following cardiac catheterization and coronary angiography. This may reflect retroperitoneal hemorrhage, pericardial bleeding including cardiac tamponade, gastrointestinal, intracranial, or hemolysis. It is important post-procedure to monitor for overt bleeding, hemodynamic changes, symptomatic anemia, and hemoglobin drops. However, a hemoglobin drop does not always reflect clinically significant hemorrhage, or possibly any hemorrhage at all.

A hemoglobin drop without evidence of hemorrhage may reflect the preprocedural preparations or procedural techniques. Patients that have been NPO prior to the procedure may start out relatively hypovolemic and hemoconcentrated. Additionally, some institutions aggressively hydrate their catheterization patients prior to diagnostic and interventional procedures to counter the effects of sedative/vasodilatory medications and renal protection for contrast induced nephropathy. Nitrate medications used during the procedure can cause vasodilation, which expands the vascular space. These combined effects may lead to a post-procedural dilutional change in the hemoglobin that does not represent any true hemorrhage (BARC 0, see table below)

During the procedure itself, there are plenty of opportunities for blood loss. Blood draws for frequent ACT checks including the blood waste from the manifold (20 mL) prior to the ACT blood draw. There is also blood loss from the arteriotomy, catheter flushing/leakage. This is true blood loss which is often not tracked well, may or not but can exaggerate the post-procedural blood loss which complicates evaluating for hemorrhage complication.

Even if the hemoglobin drop does not represent a complication hemorrhage (BARC 1), it may still be clinically significant depending of the initial hemoglobin (BARC 2). Shortness of breath or ischemic chest pain from a dilutional anemia, may need to be treated with diuretics. Transfusion could be called for but may complication volume overload in patients with reduced ventricular function.

The Bleeding Academic Research Consortium (BARC) has defined a classification scheme for catheterization bleeding (see table below). It was originally used to standardize research reporting, but has been expanded its use for structured complications reporting.

BARC Bleeding Definitions
Type 0No bleeding
Type 1Bleeding that is not actionable and does not cause the patient to seek treatment
Type 2Any clinically overt sign of hemorrhage that “is actionable” and requires diagnostic studies, hospitalization, or treatment by a healthcare professional
Type 3a. Overt bleeding plus hemoglobin drop of 3 to < 5 g/dL (provided hemoglobin drop is related to bleed); transfusion with overt bleeding
b. Overt bleeding plus hemoglobin drop < 5 g/dL (provided hemoglobin drop is related to bleed); cardiac tamponade; bleeding requiring surgical intervention for control; bleeding requiring IV vasoactive agents
c. Intracranial hemorrhage confirmed by autopsy, imaging, or lumbar puncture; intraocular bleed compromising vision
Type 4CABG-related bleeding within 48 hours
Type 5a. Probable fatal bleeding
b. Definite fatal bleeding

Minimizing the procedural blood losses should be priority. This can include using radial artery access. Routine hydration is probably not indicated unless patient is clearing hypovolemic, especially if there is reduced ventricular function.

In all cases, a hemoglobin drop after PCI should prompt a thorough investigation for hemorrhage before calling it dilutional or insignificant, especially with femoral access.

Post-Catheterization Hemoglobin Drop

APRV Lung Demonstration

Resus Review

Airway pressure release ventilation (APRV) is a method of mechanical ventilation. Also known as inverse ratio or bilevel ventilation, the lung alveoli are opened with a high level pressure and ventilation is applied as the lung cycles between the high pressure and the set low pressure. In a previous post we discussed the details of setting up APRV settings and adjustments. I use this mode primarily for patients ARDS.

Unlike spontaneous breathing or conventional ventilation, the time spent at maximal inflation is typically much longer than time deflated. Time low is minimized to prevent collapse of alveoli and barotrauma. The video below shows shows treated pig lungs being ventilated with typical APRV settings.

APRV Lung Demonstration

vv-ECMO Gas Exchange

Resus Review

Patients with severe ARDS have significant impairment in their pulmonary gas exchange which impairs the ability to oxygenate and decarboxylate the blood. Lung compliance is very low which forces limits on the minute ventilation used to prevent barotrauma to the lungs (referred to as low tidal volume ventilation or lung protective ventilation). Without adequate minute ventilation the patient develops physiologically significant hypoxia and hypercapnia.

Using the Murray score as a guide we can assess whether a patient with ARDS would potentially benefit from venovenous extracorporeal oxygenation (vv-ECMO).

Once on vv-ECMO however, there are two factors that are most crucial in determining adequate blood gas exchange.

Percent ECMO blood flow / cardiac output

EBF/CO is the ratio of ECMO circuit blood flow rate as percent of cardiac output. Both are measured in L/min, and therefore you end up with a dimensionless percentage. Since the membrane lung is providing the oxygenation and CO2 removal, the larger portion of the total cardiac output that is passed through the oxygenator the more gas exchange that can occur.

If EBF/CO can be consistently maintained >60%, then oxygenation saturation (SaO2) is almost always >90%.

vv-ECMO circuits can usually support blood flows up to about 5 Lpm before cavitation/chatter limit further increases. So for typical patients, EBF/CO is not usually a problem unless the patient has a very high cardiac output as seen in liver failure, septic shock, hyperthyroidism, or severe anemia.

Maintaining a patient’s hemoglobin level above 10 g/dL with red blood cell transfusions can improve O2 delivery and achieve adequate SaO2, while allowing for lower EBF/CO ratios and lower total circuit blood flow rates.

Recirculation Blood Flow

Recirculation in ECMO circuits occur when oxygenated blood is returned to the ECMO circuit without passing through the peripheral vasculature. This represents wasted ECMO blood flow, and in can be thought of as reducing the effective EBF/CO.

Recirculation blood flow (RBF measured in Lpm) can be assessed by comparing pre-oxygenator pO2 with a peripheral pO2 (not ScvO2 from the pulmonary artery catheter which should be the same as post-pump pO2). Measuring a true mixed peripheral pO2 is difficult in vv-ECMO because pulmonary artery catheter has received oxygenated blood from the ECMO circuit. A venous sample from the internal/external jugular vein or other peripheral vein can be used as a substitute, but reflect local circulation that may not be reflective of the overall system. A theoretical, but often not practical method is to turn off the sweep gas and measure the gas sample from the pre-oxygenator.

Recirculation occurs because of the inherent geometry of using vv-ECMO cannulas that are both drawing and returning blood to the sample venous blood pool. Cannulas can also be misplaced or misdirected, which is critically important in the double lumen venovenous (DLVV) cannulas (eg Avalon) where recirculation can range from 20-50%.

Once an adequate effective ECMO blood flow has been established, (EBF-RBF)/CO, by ensuring that there is that ECMO flow is >60% of the cardiac output, and that recirculation is minimal, we can optimize the oxygen and CO2 gas exchange. Fortunately, these can generally be set independently on the vv-ECMO circuit using the air/oxygen mixer (blender) and sweep gas flow regulator.

Sweep gas flow rate

Carbon dioxide elimination depends on sweep gas flow rate (set on the the sweep gas regular). The rate of sweep gas flow through the membrane lung determines blood decarboxylation. Carbon dioxide tension (pCO2) is mostly unaffected by FDO2 or ECMO blood flow once it is adequate.

Fraction Delivered O2 Gas

The fraction of delivered O2 gas (FDO2) is set on the blender, and directly affects oxygenation of the blood. The sweep gas flow rate has little effect on blood pO2/SO2.


1. Intensive Care Med 2013. Blood oxygenation and decarboxylation determinants during venovenous ECMO for respiratory failure in adults.

vv-ECMO Gas Exchange

Perc Trach difficulty caused by deformed Shiley edge

Resus Review

In the last step of a percutaneous tracheostomy, there are cases where it has been very difficult to cannulate the tracheostomytube into the trachea.

In these cases, it is important to first verify that the tracheotomy has been adequately dilated. If they has been done, I have found that the problem is with the Shiley tube and trocar. Even if you are meticulously careful aligning the bevel of the tracheostomy tube with the trocar, the edge of the Shiley tracheostomy tube can catch of tracheal rings. It then becomes very difficult to cannulate it into the trachea because any additional pressure or manipulation simply compresses the trachea rather and forcing the Shiley into the trachea.

In these circumstances, what I have found is that the edge of the Shiley tube has been distorted by catching on the tracheal rings. If this has occurred, I have replaced the Shiley tube with a new one and the procedure has proceeded smoothly from there.


Have you ever seen this or had this problem during your perc trachs? Share your experience below.

Perc Trach difficulty caused by deformed Shiley edge