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
During spontaneous inspiration; Pleural cavity ⬆️, Ppl ⬇️, RA pressure ⬇️ but still more than the Ppl, therefore, transmural pressure will increase which will increases the Vreturn to the RA and RV
The SVC (TEE) will distend. The IVC will collapse (Subcostal view TTE)
Why is that? the SVC is in the thoracic cavity the IVC in the abdomen. During inspiration Ppl ⬇️ the SVC will distend but the Abd pressure ⬆️ compared to thoracic Pr therefore the IVC will collapse
As we can see the IVC by subcostal view but we need TEE to visualize the SVC
During passive breathing the Ppl is always positive but more positive during inspiration compared to expiration.
During inspiration the Ppl ⬆️, the RA pressure ⬆️ but less the the Ppl. Therefore, the RA transmural pressure decreases (RA-Ppl) which that will decrease the venous return.
During passive inspiration the Ppl is high which tends to collapse the SVC (TEE) because it is in the thoracic cavity but the IVC will distend because the RA is ⬆️, thoracic cavity pressure ⬆️ will distend the Abdominal IVC
If the distensibility > 18% that indicate FR.
What’s about the RV afterload this is easier in both situation active inspiration or passive inspiration the transpulmonary pressure is higher therefor that will increase the RV afterload
This topic is very important, and controversial. Intermediate high risk PE is tough, as the mortality benefits evidence of CDT compared to AC alone its not strong, Therefore, I believe PERT is very helpful.
A large meta-analysis showed the mortality of Submassive (Intermediate high risk) PE is 2.8% and other study showed the mortality ranges from 1.8-10%.
We are dealing with Pts in the red circle 🔴 (before shock but more than low risk)
Evidence showed patients in intermediate high risk PE they might be in normotensive shock 20-40% of these patient can have low cardiac index < 1.8
How do you titrate your PEEP in moderate to severe ARDS Patients?
2004 alveoli trial
DOI: 10.1056/NEJMoa032193
549 Pts.
TV ~ 6 ml/kg
Pplat (24-27)
Low PEEP 8.3±3.2 cmh2o (death 24.9%)
High PEEP 13.2±3.5 cmh2o (death 27.5%)
Result= no significant difference between high or low PEEP
2008 ~ LOVS trial
JAMA. 2008;299(6):637-645
983 PTs
TV ~ 6 ml/kg
CG: Pplat<30, low PEEP mortality 40.4%
IG: Pplat <40, high PEEP ~ mortality 36.4%
The high PEEP group had lower rates of refractory hypoxemia (4.6% vs 10.2%)
COPD is a Heterogenous lung condition characterized by chronic resp symptoms due to abnormalities in the airway (bronchitis, bronchiolitis, emphysema) that cause persistent airflow obstruction
(2018 def in the pic)
65 yo/f with PMH of recently diagnosed SCLC s/p chemotherapy last session 1 month before presentation who was presented to the ER due to worsening SOA, Cough and after evaluation found to be tachypnic and tachycardiac
CXR showed mild enlargement of the cardiac shadow, obliteration of the right CP angle and bilateral central reticular pattern suggestive of pulmonary edema. Right mediport.
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