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Case Discussion- Oxygenation Conundrums Dr. TH de Klerk.

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Presentation on theme: "Case Discussion- Oxygenation Conundrums Dr. TH de Klerk."— Presentation transcript:

1 Case Discussion- Oxygenation Conundrums Dr. TH de Klerk

2 Goals of Ventilation 1.Oxygenation: PaO2 >60mmHG, Sats >90%. 2.Lung protective ventilation: Tidal volume 15cm H2O, except when using PEEP set acc to transpulmonary expiratory pressure +2-3cm H2O. 3.Reverse cause for respiratory failure. 4.Patient comfort, decrease work of breathing. Avoid dyssynchrony (trigger, flow, cycling). 5.Acid- Base status: PCO2 7.20

3 Moving the goalposts

4 Case Study 1 Ms. MS, 33yr African female. Background HIV positive on HAART (TDF, 3TC, EFV) since 2009. CD4: 298 with undetectable viral load- Dec 2013. History of Pulmonary Tuberculosis 2010- treated for 6months. Secondary bronchiectasis with pulmonary hypertension. Currently 22wks pregnant. Now multi-lobar, community acquired pneumonia, CURB 65 score: 3, intubated and ventilated for a mixed Type 1 and 2 respiratory failure. Clinical features of right heart failure. CT Pulmonary angiogram couldn’t demonstrate pulmonary embolus, infiltrates suggestive of atypical pneumonia. Patient also treated for Pneumocystis pneumonia. Echocardiography demonstrated dilatation and systolic dysfunction of right ventricle.

5 Case study 1- cont. Patients clinical picture further complicated by acute pancreatitis, CT suggestive of pancreatic oedema, no necrosis. Intra- abdominal pressure 13mmHg (18cm H20). Oxygenation worsened: P/F ratio of 60, PEEP: 10cm H20, with Peak Pressure of 35cm H20. Plateau pressure 28cm H2O Unfortunately no oesophageal probes available at that time. PEEP was increased to 20cm H20, Peak Pressure at 40cm H20. Plateau pressure: 35cm H2O. Oxygenation indices immediately improved, P/F ratio went up to 150.

6 Case Study 1- Discussion What is the goals of ventilation in a pregnant patient with ARDS? What should we aim for in ventilating patients with pulmonary hypertension? What should we aim for in ventilating patients with intra-abdominal hypertension?

7 ARDS in Pregnancy 40% maternal mortality rate, 25% perinatal fetal mortality rate. Certain causes unique to pregnancy. Pregnancy altered physiology e.g.  respiratory drive,  FRC, etc. Definition: ARDS occurring during pregnancy, results from an obstetric cause or is otherwise modified by an obstetric- related factor.

8 ARDS in Pregnancy Commonest causes: Sepsis (most common): pyelonephritis, aspiration, chorio-amnionitis. Pre-eclampsia. Amniotic fluid embolism. Obstetric related hemorrhage: abruptio, etc. Tocolytic- induced pulmonary edema.

9 Ventilation in Pregnancy Goals of ventilation differ! PaO2> 70mmHg, Sats > 95%. PaCO2< 45mmHg. Needs a gradient between mother and baby. 7.45< pH< 7.30 Placental insufficiency- vasoconstriction placental bed.  intra- abdominal pressure with decreased chest wall compliance (  vascularity and edema)- tolerate higher inspiratory plateau pressure. Prone positioning- not feasible.

10 Ventilation in Pulmonary hypertension ARDS is most common cause for new onset pulmonary hypertension in ICU. The reason for decreased mortality in ARDS due to lung protective ventilation thought to be due to decreased incidence acute cor pulmonale. Prevent hypoxemia- esp. low mixed venous O2 saturation. Aim for PCO2< 55mmHg. Avoid pH< 7.25 Treat sepsis- causes pulmonary vasoconstriction. Lung protective ventilation- tidal volume <6ml/kg IBW, Pplat <27cm H2O, PEEP optimize to best dynamic compliance.  PEEP and Mean airway pressure- compress pulmonary capillaries. Treat intra-abdominal hypertension.

11 Ventilation Intra-abdominal hypertension. 25-80% of IAP transmitted to intrathoracic compartment- not predictable. Mechanical ventilation  intra-abdominal pressure 1-2mmHg. Increasing PEEP add additional 1- 2mmHg intra- abdominal pressure.  chest wall elastance,  intra-pleural pressure=  transpulmonary pressure. Recommend using esophageal pressure. Prone position compression of abdomen. Elevating head 45°-  IAP 5-15mmHg. Reverse Trendelenburg position- improve lung mechanics, but  splachnic perfusion. Setting PEEP in cmH2O= IAP in mmHg. Or setting PEEP @ ½ IAP in cmH20. Only rough guide.

12 Case Study 2 Mr. JDB, 38yr Caucasian male. Background VSD repair at age 20 (not palliative),morbid obesity (BMI:68), proportional short stature (5ft, 3inch), poorly controlled hypertension, dyslipidemia and impaired glucose tolerance. Presented acute pulmonary edema with mixed type 1and 2 respiratory failure requiring intubation and ventilation. Collateral history from wife suggestive of obstructive sleep apnea- excessive day time somnolence, nocturnal apneic episodes.

13 Case Study 2- cont Patients optimal PEEP determined with trans- pulmonary pressure measurement: 16cm H20. Echocardiogram limited: LVEF:40%, no significant residual VSD and possible pulmonary hypertension. Oxygenation indices improved over next few days, but PCO2 remained 55-70mmHg. Patient awake and calm, no increased respiratory rate or increased work of breathing. Possible central sleep apnea. Patient subsequently weaned and extubated.

14 Case Study 2- Discussion How to determine the optimal PEEP for patient with morbid obesity? During the weaning phase, what is the optimal level of PEEP?

15 Ventilation in Obesity  BMI ∞  inflammatory mediators- esp. bronchospasm. ARDS H1N1 mortality  - X 5-15.  TLC,  FRC,  VC,  pleural pressure,  upper and lower airway resistance,  intra-abdominal pressure. Hypoxemia- Atelectasis and V/Q mismatch due to airway narrowing. Pplat <30cm H2O not adequate- due to  pleural pressure. Pplat poor surrogate for transpulmonary pressure in this setting. Use esophageal pressure measurements to set PEEP and transpulmonary pressure. Some studies recommend ‘empiric’ PEEP of 10-14. Ventilate in sitting position. NB cause dynamic hyperinflation- set PEEP to 80% of Auto-PEEP. Counter act collapsed airway.

16 Ventilation in CNS injury Neurogenic pulmonary edema- sympathetic storm with myocardial stunning. Hyperventilation  global brain oxygenation-not good idea ischaemic stroke, cardiac arrest. Hypoventilation  cerebral blood flow-  hemorrhage in patient with intracranial bleeding. Diffuse cerebral edema- hyperventilation to PCO2= 30-35mmHg used if imminent herniation- temporary effect.  PEEP+  MAP=  ICP, not linear effect. Due to decreased venous return. Avoid bronchoscopy in patients with  ICP. Don’t extubate high spinal cord injuries within first 72hrs- cord edema, extending injury.

17 References Hibbert K, Rice M, Malhotra A. Obesity and ARDS. Chest 2012 Sep; 142(3): 785-790. Cole DE, Taylor TL, McCullough DM, Shoff CT, Derdak S. Acute Respiratory Distress Syndrome in pregnancy. Crit Care Med 2005 Oct; 33 (10 Suppl): S269-278. Esquinas AM, Petroianni A. Pulmonary hypertension in critically ill patients with mechanical ventilation: still a greatest challenge for intensivists. J Crit Care 2014 Feb: 29(1): 166. Stevens RD, Lazaridis C, Chaleta JA. The role of mechanical ventilation in acute brain injury. Neurol Clin 2008 May; 26(2):543-563. Malbrain M, De Waele J. Intra- abdominal Hypertension. Core Critical Care Series 2013.

18 Thank you!

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