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Si, sono un operatore sanitario
Note: Ai sensi e per gli effetti dell’Art. 76 D.P.R. 445/2000 consapevole della responsabilità e delle conseguenze civili e penali previste in caso di dichiarazioni mendaci e/o formazione od uso di atti falsi, nonché in caso di esibizione atti contenenti dati non più corrispondenti a verità e consapevole altresì che qualora emerga la non veridicità del contenuto della presente decadranno i benefici per i quali la stessa è rilasciata confermo di essere un OPERATORE SANITARIO.
I contenuti presenti in questo sito contengono informazioni rivolte agli operatori sanitari, in quanto si riferiscono a prodotti rientranti nella categoria dei dispositivi medici che richiedono l’impiego o l’intervento da parte di professionisti del settore medico-sanitario.
Defoaming or anti-foaming agents are used to break up or reduce bubbles that form at the blood-air interface.
Polydimethylsiloxane (PDMS), the silicone agent used in many anti-foam agents, is "a hydrophobic or 'water fearing' liquid component that is insoluble in water and blood," explained Joseph Kalscheuer, Principal Scientist, Medtronic Coronary and Structural Heart Disease Management. "It disperses and spreads across the surface of the foam's lamellae — thin liquid films that separate the foam gas bubbles. The PDMS dispersion can create localized areas of extremely low surface tension which, when low enough, disrupt the stabilizing mechanism of the lamellae and cause the membrane to burst."
PDMS can also carry modified silica particles to assist in foam structure disruption. Silica particles are a naturally hydrophilic or "water loving" material made partially hydrophobic to allow its suspension in the PDMS oil. "The PDMS oil transports the suspended silica particles to the lamellae's surface. The lamellae's hydrophilic qualities allow the particles to bridge between the two layers, rupture the membrane, and ultimately disrupt the foam's structure," Kalscheuer noted. "It is through the mechanisms of local depression in surface tension and bubble rupturing particles that medical anti-foams disrupt foam generation."
Most entrained material exists at the blood-air interface due to the natural affinity of hydrophobic PDMS and the semi-hydrophobic silica particles for air — a similarly hydrophobic surface — and due to their mutual insolubility in blood.
Disc oxygenators, introduced in the 1950s, oxygenated blood by passing discs through the blood reservoir, where the turning discs would cause the blood to foam. To break up the bubbles, perfusionists had to lift the reservoir lid and spray the blood with an anti-foaming agent. For this and a variety of other clinical reasons, disc oxygenators were quickly replaced with bubble oxygenators.
In contrast, bubble oxygenators employed a diffuser, a simple piece of perforated plastic, which had a single-piece design upstream of the pump, including an oxygenating foaming column, a defoaming section, and an arterial reservoir that held the blood to be returned to the patient. During perfusion, blood was exposed over the top of the diffuser and oxygen ran underneath, forcing oxygen through the blood, which caused it to foam. This foam would then rise up a column, where it was oxygenated and CO2 was removed. The oxygenator's efficiency depended on the diffuser's design and the size of the bubbles it created: small bubbles were good for oxygenating, big bubbles were good for removing CO2. Thus, a balance was needed to provide adequate oxygenation and CO2removal.
Because bubble oxygenators purposely foamed blood, the blood had to be defoamed before being returned to the patient. Bubble oxygenator defoamers had to be large to ensure sufficient bubble break up to return blood to a liquid state. Blood passed through a defoamer — a black filter sponge saturated with a defoaming agent — then settled into the arterial reservoir.
As membrane technology became prevalent in oxygenator designs, blood had to be collected in a separate container. Initially, this container was a soft-shell or flexible venous reservoir and no defoamer was needed since there was no blood-air interface. The blood simply flowed into a bag already filled with blood.
Designs evolved to an open/hard shell reservoir configuration that merged the cardiotomy venous reservoir and defoamer into a single device that automatically removed air from the circuit. Smaller cannulae and smaller ID venous lines impacted venous return. For the increasing number of minimally invasive techniques requiring smaller cannulae, perfusionists needed the ability to use vacuum on the reservoir, possible only with hard shell systems. Consequently, hard shell systems became the go-to devices and today they are the most common configuration in use worldwide.
As with earlier reservoir designs, today's devices use a silicone anti-foam agent to disrupt foaming and return blood to a liquid phase. The difference is in how the cardiotomy/venous reservoir's (CVR) design features interact with blood and the anti-foam agent.
It is well known that air can be become entrained in blood. On the venous side, it may occur when there's a problem with the cannulation site. When this happens, blood flows into the bottom of the reservoir and foam rises to the top. Thus, the placement of the anti-foaming agent is critical. In the Affinity Fusion® CVR, the anti-foam agent is located high in the reservoir. Consequently, when venous blood flows normally, it does not touch the anti-foam agent. This design limits blood exposure to the anti-foam agent to instances when significant foaming occurs.
Blood is rich in proteins and other components that, when combined with air, produce significant structure, making blood defoaming essential. According to John Knoll, Senior Engineering Manager, Medtronic Coronary and Structural Heart Disease Management, "The Affinity Fusion's reservoir incorporates a fluid outlet that drains at the bottom while air escapes upward. If there's foam on the blood's surface inside the reservoir, it simply sits there and the anti-foam agent manages it."
On the cardiotomy side, foam is introduced in the CVR through the intermittent introduction of air and blood from the various chest cavity instruments that provide suction for a clear field of view. "In the Affinity Fusion CVR, blood flows over a cardiotomy cone and out through the cardiotomy filter," Knoll explained. "If the blood enters as foam, it contacts the anti-foam agent, which is strategically placed to defoam the cardiotomy blood as needed. Only liquid blood exits the cardiotomy inside the CVR. It's all about strategic location.
"Some anti-foam agent contact is inevitable on the cardiotomy side because the blood comes in as foam," Knoll noted. "The Affinity Fusion CVR design facilitates minimal contact between the blood and anti-foam agent."
The Affinity Fusion Oxygenator's design also minimizes gaseous micro emboli (GME) since they occur when air is entrained into blood. "Foam is visible, but GME cannot be seen," Knoll observed. "Our design ensures that GME are minimized, regardless of circumstance." The Affinity Fusion Oxygenator's design addresses GME in numerous ways:
Finally, the Affinity Fusion Oxygenator and CVR have features that ensure gentle blood passage through the device so that the device itself does not entrain air, including:
Modern day oxygenators and CVR's utilize many design and technological advances to manage air in the perfusion circuit, including smooth curves, the reduction of falling blood, and active air removal as seen in the Affinity Fusion System. While these design advances help reduce air entrainment in the oxygenator and CVR, anti-foaming agents are still required to facilitate air removal from the blood stream.
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