1. Non invasive ventilation and LV dysfunction Fekri Abroug ICU. CHU F.Bourguiba Monastir. Tunisia

2. How can cardiogenic pulmonary edema-induced respiratory dysfunction aggravate cardiac dysfunction and circulatory failure ?

3. Cardiogenic Pulmonary edema Hypoxemia Hypoxemia WOB WOB Exaggerated decrease Exaggerated decrease in pleural pressure at inspiration

4. Cardiogenic Pulmonary edema Hypoxemia Hypoxemia WOB WOB risks of myocardial myocardialischemia risks of critical organs critical organshypoperfusion

5. Viires et a. J Clin Invest 1983

6. Cardiogenic Pulmonary edema Hypoxemia Hypoxemia WOB WOB Exaggerated decrease Exaggerated decrease in pleural pressure at inspiration Increase in LV afterload Increase in LV afterload

7. Cardiogenic Pulmonary edema Hypoxemia Hypoxemia WOB WOB Exaggerated decrease Exaggerated decrease in pleural pressure at inspiration risks of myocardial myocardialischemia Increase in LV afterload Increase in LV afterload risks of decrease in Stroke Volume Stroke Volume

8. Cardiogenic Pulmonary edema Hypoxemia Hypoxemia WOB WOB Exaggerated decrease Exaggerated decrease in pleural pressure at inspiration risks of myocardial myocardialischemia decrease decrease in CaO 2 risks of critical organs critical organshypoperfusion Increase in LV afterload risks of decrease in Stroke Volume Stroke Volume Risks of aggravation of cardiac dysfunction (vicious circle) Risks of aggravation of cardiac dysfunction (vicious circle) and of circulatory failure

9. How can positive pressure ventilation improve cardiac dysfunction and circulatory failure in patients with cardiogenic pulmonary edema?

10. Positive pressure ventilation in cardiogenic pulmonary edema Positive pressure ventilation in cardiogenic pulmonary edema Hypoxemia Hypoxemia WOB WOB Exaggerated decrease Exaggerated decrease in pleural pressure at inspiration risks of myocardial myocardialischemia decrease decrease in CaO 2 risks of critical organs critical organshypoperfusion risks of decrease in Stroke Volume Stroke Volume Postive pressure ventilation by breaking the vicious circle prevents aggravation of cardiac dysfunction prevents aggravation of cardiac dysfunction and of circulatory failure

11. NIV and Cardiogenic Pulmonary edema (CPE)  NIV: important tool in ARF Reduces the need for invasive ventilation Reduces IMV complications Reduces ICU complications, stay, mortality  CPE common medical emergency NIV increases cardiac output Improves gaz exchange Decreases endotracheal intubation Trends towards decrease in mortality

12. Clinical goals in CPE  Improve systemic oxygen saturation  Reduction in LV preload  Reduction in LV afterload Oxygen through high flow facemask Morphine Diuretics nitrates

13. CPAP is effective in CPE unresponsive to medical Rx Poulton Lancet 1936  Increase in inspiratory and expiratory flow and pressure Increases Vt Unloads inspiratory muscles Improves alveolar ventilation Reexpands flooded alveoli Counteracts intrinsic PEEP  Prevents micro-atelectasis  Improves the P-V curve relation  Increases in intrathoracic pressure reduces the left ventricular preload and afterload  Increases cardiac output in CHF

14. Both CPAP and bilevel non- invasive ventilation proved effective in treating CPE Better than conventional oxygen therapy

15. Resolution time: p=0.002 N=19 N=18 Intubation rate: 5% vs 33% (p=0.037)

16.  130 patients attending the ED for CPE  Randomized to O2: n=65 NIPSV: n=65  Primary endpoint: need for intubation  Secondary endpoints: mortality, physiological variables

17.  Intubation rate: 25% vs 20% (p=0.5)  Mortality: 14% vs 8% (p=0.4)  Subgroup analysis: no difference P=0.01

19. CPAP vs Conventional medical treatment: intubation rates NNT=7

20. CPAP vs Conventional medical treatment: death rates NNT=8

21. BiPAP vs Conventional medical treatment: intubation rates

22. BiPAP vs Conventional medical treatment: death rates

23. How does CPAP compare with Bi- PAP?

24. CPAP vs BiPAP: intubation

25. CPAP vs BiPAP: mortality

26.  36 patients with CPE and hypercapnia (in the ED)  Randomization to CPAP (n=18) or NIPSV (n=18)  Endpoints: Endotracheal intubation Death rate Resolution time (SpO2>96%, BR<30)

28. Role of NIV in CPE due to LV diastolic dysfunction

30.  In all types of CPE, CPAP improves oxygenation  In LV diastolic dysfunction, this occurs through a decrease of LV diastolic volume (preload) and in MAP  In LV systolic dysfunction, CPAP both decreases preload and increases LVEF

31. Greetings from Monastir