Optimal dosing of corticosteroids in septic shock

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Case DiscussionOxygenation Conundrums
Dr. TH de Klerk
Goals of Ventilation
1. Oxygenation: PaO2 >60mmHG, Sats >90%.
2. Lung protective ventilation: Tidal volume< 6ml/kg
IBW (male height in cm- 100, female height in cm110). Plateau pressure < 30cm H2O.
Transpulmonary plateau pressure<25cm H20.
PEEP set acc to best dynamic compliance- not
>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 < 120mmHg, pH >7.20
Moving the goalposts
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.
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.
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?
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 obstetricrelated factor.
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.
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.
Ventilation in Pulmonary
hypertension
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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 pressurecompress pulmonary capillaries.
Treat intra-abdominal hypertension.
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 12mmHg 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.
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.
Case Study 2- cont
• Patients optimal PEEP determined with transpulmonary 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.
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?
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.
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.
References
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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.
Thank you!
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