Inverkan av behandling med konstdjord lunga (extrakorporal membranoxygenering) på kärlmotståndet i lungkretsloppet och höger hjärtkammarens funtkion hos grisar.

Bakgrund: During severe hypoxaemic respiratory failure, e.g. severe ARDS, increased pulmonary vascular resistance (PVR) may partially be caused by hypoxic pulmonary vasoconstriction (HPV). HPV is influenced by oxygen tension in the alveoli (PAO2),the pulmonary artery (PvO2) and bronchial arteries. PAO2 is the strongest stimulus.

The sensing site for HPV is located precapillary. Increased PVR may cause right ventricular dysfunction or failure. Veno-venous extracorporeal membrane oxygenation (v-v ECMO)for treatment of severe ARDS is indicated when conventional intensive care treatment fails.

Before the start of v-v ECMO and during ECMO treatment patients may develop right ventricular failure due to HPV. It has been suggested that increasing the PvO2 by

v-v ECMO would attenuate HPV and stabilize the circulation in severe ARDS with right heart failure. According to earlier studies a decreased PAO2 has to be compensated by an increase of PvO2 > 100 mmHg (> 13.3 kPa) to effectively reduce PVR. This is difficult due to the admixture of venous blood to the oxygenated blood coming from the extracorporeal device and recirculation of ECMO oxygenated blood, i.e. the drainage of blood coming from the extracorporeal device into the ECMO system without passing the native circulation.

According to the clinical experience and published singel centre data v-v ECMO does usually not attenuate HPV in the most severe forms of ARDS.

Målsättning: Whether increased PvO2 by v-v ECMO will decrease PVR and stabilize right ventricular function in an experimental model of severe ARDS.

Arbetsplan: 36 pigs (male and female, 45-55 kg) will be randomly assigned to control or intervention. Animals will be sufficiently anesthetized according to our laboratory standards and standardized mechanically ventilated. Severe ARDS will be induced in all animals by lung lavage and in the intervention group we increase PvO2 with v-v ECMO.

Betydelse: It has been suggested that increasing PvO2 by v-v ECMO attenuates HPV and stabilize circulation. This hypothesis has not been investigated in a controlled experimental setting. According to our experience right ventricular function is dependent on lung function during severe ARDS. When v-v ECMO fails to stabilize circulation, changing the circuit from v-v to veno–arterial (v-a) ECMO to bypass the heart until lung function has recovered is the appropriate therapeutical option.