Another Pt with HFrEF < 20%, and AKI on GDMT and 40 mg Lasix BID on PE he has Bil LE 2+ edema, no respiratory distress. Would you just increase his Lasix or work on improving his LV contractility, afterload with keeping the same preload control?
🤯🤯 The plan was written (stop Lasix for 2 days and then re-evaluate) their rational is the patient is clinically dry and his creatinine is up?!!!!!!!!😓 these images was taken while Pt on Debutamin
Transmular pressure is the pressure difference between the inside & the outside of the cavity i.e the RA transmural pressure = RA-Ppl(We are assuming the pericardium is normal)
Then venous return depends on volume, pleural pr (Ppl), RA pr, transmural pr, elasticity & compliance
During spontaneous breathing 😮💨 Ppl always negative, but during inspiration it is more negative than expiration. Due to the increase in the thoracic cavity size
The Pr changes can affect the Vr and the effect will be more pronounced if the Pt is dry & fluid responsiveness
This thread for people who are interested in CRRT and critical care 😓🤦🏽♂️
Basics about RRT;
Convection: It depends on Hydrostatic pressure (HP)
Diffusion: it depends on solutes gradients
Filtration (Convection): blood from the Pt goes through the filter, In the filter with the effect of HP plasma, small, and medium size molecules get filtered by the HP effect, then the blood goes back to the patient and the filtered fluid and molecules goes to the effluent bag
What’s the main mechanism behind hypoxia in pulmonary embolism?
As @ParijatSen11 Redistribution of the blood flow secondary to pulmonary embolism increases in flow to areas with normal ventilation which leads to hypoxia
The reduction in the flow where the PE is leads to high ventilation to perfusion mismatch, however, this is not the cause of hypoxia