Thomas & Kass bust some common ICU Myths in a classic Podcast for Intensive Care Network (ICN). Here's the slide deck and references to go with it.

1. Thomas & Thomas
November 2016
in
ICU

2. Thomas & Thomas
ICU
EDITION
2016

3. Myth #1

5. Myth #1
Giving O2 to a CO2 retaining
COPD patient, knocks off their
hypoxic respiratory drive,
leading to hypoventilation and
further CO2 retention

7. Effect of minute ventilation during
oxygen-induced hypercapnia
Aubier M, Murciano D, Milic-Emili J, Touaty E, Daghfous J, Pariente R, Derenne JP: Effects of the administration of O2 on ventilation and blood gases in patients with chronic
obstructive pulmonary disease during acute respiratory failure. Am Rev Respir Dis 1980, 122:747-754.

8. Aubier et al Conclusion
The increase in arterial PaCO2 observed during
administration of O2 is not secondary to a
reduction in respiratory drive.
Aubier M, Murciano D, Fournier M, Milic-Emili J, Pariente R, Derenne JP: Central respiratory drive in acute respiratory failure of patients with chronic obstructive
pulmonary disease. Am Rev Respir Dis 1980, 122:191-199.

9. So why dose
pCO2 rise?

10. Theory 1: Loss of hypoxic
vasoconstriction and therefore
increased shunt and increased
alveolar dead space

11. Normal Conditions
https://dundeechest.wordpress.com/2009/08/12/why-do-copd-patients-retain-co2-when-given-too-much-oxygen/

12. With 100% Oxygen
https://dundeechest.wordpress.com/2009/08/12/why-do-copd-patients-retain-co2-when-given-too-much-oxygen/

13. Theory 2: The Haldane Effect
O2 therapy induces a rightward shift in the curve

14. Hanson’s computer model of multiple lung units
demonstrated plausibility that change in dead space
and the haldane effect could account for hypercapnia
Hanson CW, III, Marshall BE, Frasch HF, Marshall C: Causes of hypercarbia with oxygen therapy in patients with chronic obstructive
pulmonary disease. Crit Care Med 1996, 24:23-28.

16. Robinson TD, Freiberg DB, Regnis JA, Young IH: The role of hypoventilation and ventilation-perfusion redistribution in oxygen-induced hypercapnia during acute
exacerbations of chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2000, 161:1524-1529.

17. Robinson et al Results
• Minute ventilation decreased in the retainers
(20%), but not the non retainers
• Shunt increased in both the retainers and the
non retainers
• Dead space ventilation increased in the
retainers (24%), but not the non retainers
Robinson TD, Freiberg DB, Regnis JA, Young IH: The role of hypoventilation and ventilation-perfusion redistribution in oxygen-induced hypercapnia during acute
exacerbations of chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2000, 161:1524-1529.

18. Gemma Rialp, Joan M Raurich, Juan A Llompart-Pou and Ignacio Ayestarán. Role of Respiratory Drive in Hyperoxia-Induced Hypercapnia in Ready-to-Wean Subjects With
COPD. Respiratory Care March 2015, 60 (3) 328-333

20. My Conclusions
• The loss of hypoxic respiratory drive is an
oversimplification
• Hypoventilation may be a component,
however it is is likely due to a combination of
factors including increased V/Q mismatch or
alveolar dead space and the haldane effect

21. Myth #1
Giving O2 to a CO2 retaining
COPD patient, knocks off their
hypoxic respiratory drive,
leading to hypoventilation and
further CO2 retention

22. Myth #1
Giving O2 to a CO2 retaining
COPD patient, knocks off their
hypoxic respiratory drive,
leading to hypoventilation and
further CO2 retention

23. Myth 1 References
• Aubier M, Murciano D, Milic-Emili J, Touaty E, Daghfous J, Pariente R, Derenne JP: Effects of the
administration of O2 on ventilation and blood gases in patients with chronic obstructive pulmonary
disease during acute respiratory failure. Am Rev Respir Dis 1980, 122:747-754.
• Aubier M, Murciano D, Fournier M, Milic-Emili J, Pariente R, Derenne JP: Central respiratory drive in acute
respiratory failure of patients with chronic obstructive pulmonary disease. Am Rev Respir Dis 1980,
122:191-199.
• Hanson CW, III, Marshall BE, Frasch HF, Marshall C: Causes of hypercarbia with oxygen therapy in patients
with chronic obstructive pulmonary disease. Crit Care Med 1996, 24:23-28.
• Robinson TD, Freiberg DB, Regnis JA, Young IH: The role of hypoventilation and ventilation-perfusion
redistribution in oxygen-induced hypercapnia during acute exacerbations of chronic obstructive
pulmonary disease. Am J Respir Crit Care Med 2000, 161:1524-1529.
• Gemma Rialp, Joan M Raurich, Juan A Llompart-Pou and Ignacio Ayestarán. Role of Respiratory Drive in
Hyperoxia-Induced Hypercapnia in Ready-to-Wean Subjects With COPD. Respiratory Care March
2015, 60 (3) 328-334
• Abdo WF, Heunks LMA., Oxygen-induced hypercapnia in COPD: myths and facts. Critical Care 2012, 16:323
• Stephen W Littleton. Hypercapnia From Hyperoxia in COPD: Another Piece of the Puzzle or Another Puzzle
Entirely? Respiratory Care March 2015, 60 (3) 473-475;
• https://dundeechest.wordpress.com/2009/08/12/why-do-copd-patients-retain-co2-when-given-too-
much-oxygen/

24. Myth #2

25. •SIMV
•VT 500ml
•PEEP 0
•FiO2 0.3

26. •SIMV
•VT 500ml
•PEEP 20
•FiO2 0.5

27. •SIMV
•VT 500ml
•PEEP 8
•FiO2 0.5

28. Myth #2
• Every intubated patient needs PEEP because…
– PEEP decreases the resistance caused by the tube
– they lose their “physiologic” PEEP
– we usually breathe with negative pressures and
the positive pressure ventilation causes alveolar
collapse
• The usually required PEEP is around 5cmH2O

29. PEEP decreases airway resistance caused
by the tube
• Resistance is the pressure drop needed to force a
certain volume in a certain time through a tube
nalogouslytoOhm's Law :
here:
Influiddynamics,theH agen–Poiseui
flow ingthroughalongcylindricalpip
andincompressibleandtheflow is th
diameter.Theequationis alsoknow n
W here:

30. But….
• PEEP can improve compliance
• External PEEP can help to reduce inspiratory work
of breathing in patients with intrinsic PEEP
• External PEEP can reduce hyperinflation in
chronic obstructive lung disease

31. PEEP helps to
overcome resistance…

32. PEEP helps to
overcome resistance…

33. they lose their “physiologic” PEEP!

34. What the f*** is physiologic PEEP?

37. Collapse is due to a reduction in
volume!!!

38. EELV 100%
EELV 75%
EELV 66%

39. Loss in alveolar size caused by loss in FRC

40. Alveoli collapse due to…
• the loss in muscle tone (Sedation)
• the underlying lung pathology

44. Myth #2
• Every intubated patient needs PEEP because…
– PEEP decreases the resistance caused by the tube
– they lose their “physiologic” PEEP
– we usually breathe with negative pressures and
the positive pressure ventilation causes alveolar
collapse
• The usually required PEEP is around 5cmH2O

45. Myth #2
• Every intubated patient needs PEEP because…
– PEEP decreases the resistance caused by the tube
– they lose their “physiologic” PEEP
– we usually breathe with negative pressures and
the positive pressure ventilation causes alveolar
collapse
• The usually required PEEP is around 5cmH2O

46. Myth #2 References
• Hedenstierna vs. Pelosi, Is optimal PEEP really “optimal”? Turk J Anaesthesiol Reanim 2016, 44
• Henderson W. Pulmonary mechanics during mechanical ventilation Respiratory Physiology and
Neurobiology 180 (2012)
• Tobin M, Extubation and the Myth of “Minimal Ventilator Settings. Am J Resp Crit Care Med 2012
• Pelosi M, The effects of body mass on lung volumes, respiratory mechanics and gas exchange during
general anesthesia. Anaesth Analg 1998
• Bikker I, End-expiratory lung volume during mechanical ventilation: a comparison with reference values
and the effect of positive end-expiratory pressure in intensive care unit patients with different lung
conditions. Critical Care 2008
• Olsen M, Positive expiratory pressure – common clinical applications and physiological effects. Respiratory
Medicine 2015

47. Myth #3

49. Myth #3
• Patients with liver cirrhosis who have an
increased INR are “auto-anticoagulated”
• These patients are protected against venous
thromboemoblism (VTE) and therefore we
don’t need to give them VTE prophylaxis

50. Coagulation factors produced by Liver
ADAMTS13 (vWBF
cleaving enzyme)

51. Coagulation is all about balance
Schaden E, Saner F, Goerlinger K. Coagulation pattern in critical liver dysfunction. Current Opinion in Critical Care. 2013 Apr;19(2):142-8.

52. So why then is the INR elevated?
INR only measures pro-coagulant factors, not
anti-coagulant factors.
Therefore, INR does not reflect the balance
between pro and anticoagulant factors.

54. Ok so we know INR does not
reflect in vivo haemostasis in liver
disease, but is there any evidence
of risk of VTE?

56. Aggarwal A, Puri K, Liangpunsakul S. Deep vein thrombosis and pulmonary embolism in cirrhotic patients: Systemic review. 2014 May; 20 (19): 5737-5745

57. What about VTE risk?
• There is a growing body of evidence that demonstrates that
cirrhotic patients have significant risk of VTE
– May actually be higher risk than in non cirrhotic patients
• No difference in the risk with increasing INR or low platelets
– May be an increased risk with worsening liver function
Aggarwal A, Puri K, Liangpunsakul S. Deep vein thrombosis and pulmonary embolism in cirrhotic patients: Systemic review. 2014 May; 20 (19): 5737-5745

58. Ok, I accept that there is a risk of VTE in liver
disease, but isn’t there also a risk of bleeding?

59. Risk of bleeding with VTE prophylaxis
• No RCTs
• The current body of literature has not found
an increased risk of bleeding in cirrhotic
patients with pharmacological VTE prophylaxis
Aggarwal A, Puri K, Liangpunsakul S. Deep vein thrombosis and pulmonary embolism in cirrhotic patients: Systemic review. 2014 May; 20 (19): 5737-5745
Ha NB, Regal RE. Anticoagulation in Patients With Cirrhosis: caught between a Rock-Liver and a Hard Place. Annals of Pharmacotherapy 2016 50(5) 402-409

60. • Hypercoagulation may
lead to progression of
liver fibrosis, possible
due to hepatic
microthrombi
• There is some evidence
that prophylactic
enoxaparin decreases
the risk of
decompensation in liver
cirrhosis
Aggarwal A, Puri K, Liangpunsakul S. Deep vein thrombosis and pulmonary embolism in cirrhotic patients: Systemic review. 2014 May; 20 (19): 5737-5745
Ha NB, Regal RE. Anticoagulation in Patients With Cirrhosis: caught between a Rock-Liver and a Hard Place. Annals of Pharmacotherapy 2016 50(5) 402-409

61. So should we give VTE prophylaxis to
our liver patients in ICU?
At least consider it… in patients exposed to high
risk conditions for thrombotic complications

62. My Conclusions
• We can’t judge a liver patient’s haemostasis
based on their INR.
• There is no such thing as auto-anticoagulation
in liver failure
• Liver patients are not protected from VTE

63. Myth #3
• Patients with liver cirrhosis who have an
increased INR are “auto-anticoagulated”
• These patients are protected against venous
thromboemoblism (VTE) and therefore we
don’t need to give them VTE prophylaxis

64. Myth #3
• Patients with liver cirrhosis who have an
increased INR are “auto-anticoagulated”
• These patients are protected against venous
thromboemoblism (VTE) and therefore we
don’t need to give them VTE prophylaxis

65. Myth 3 References
• Schaden E, Saner F, Goerlinger K. Coagulation pattern in critical liver
dysfunction. Current Opinion in Critical Care. 2013 Apr;19(2):142-8
• Stravitz RT, Lisman T, Luketic VA, Sterling RK, Puri P, Fuchs M, Ibrahim A,
Lee WM, Sanval AJ. Minimal effects of acute liver injury/acute liver failure
on hemostasis as assessed by thromboelastography. Journal of hepatology.
2012 56 (1): 129-136
• Aggarwal A, Puri K, Liangpunsakul S. Deep vein thrombosis and pulmonary
embolism in cirrhotic patients: Systemic review. 2014 May; 20 (19): 5737-
5745
• Ha NB, Regal RE. Anticoagulation in Patients With Cirrhosis: caught
between a Rock-Liver and a Hard Place. Annals of Pharmacotherapy 2016
50(5) 402-409

66. Myth #4

68. Myth #4:
Giving diuretics to patients with
ongoing vasopressor needs to
achieve a restrictive fluid
balance is harmful

69. Why would you want to diurese
a critically ill patient?

72. CONTEXT:
OBJECTIVE:
DESIGN:
PATIENTS AND SETTING:
MAIN OUTCOME MEASURES:
See 1 citation found using an alternative search:
JAMA. 2002 Nov 27;288(20):2547-53.
Diuretics, mortality, and nonrecovery of renal function in acute renal
failure.
Mehta RL , Pascual MT, Soroko S, Chertow GM; PICARD Study Group.
Abstract
Acute renal failure is associated with high mortality and morbidity. Diuretic agents
continue to be used in this setting despite a lack of evidence supporting their benefit.
To determine whether the use of diuretics is associated with adverse or favorable
outcomes in critically ill patients with acute renal failure.
Cohort study conducted from October 1989 to September 1995.
A total of 552 patients with acute renal failure in intensive care units
at 4 academic medical centers affiliated with the University of California. Patients were
categorized by the use of diuretics on the day of nephrology consultation and, in companion
analyses, by diuretic use at any time during the first week following consultation.
All-cause hospital mortality, nonrecovery of renal function, and
the combined outcome of death or nonrecovery.
1
Author information
Page 1 of 2https://www.ncbi.nlm.nih.gov/pubmed/?term=Mehta+RL++P ICARD…tion+in+acute+r enal+failure.+JAMA+288% 3A+2547–2553% 2C+2002
RESULTS:
CONCLUSIONS:
Diuretics were used in 326 patients (59%) at the time of nephrology consultation.
Patients treated with diuretics on or before the day of consultation were older and more likely to
have a history of congestive heart failure, nephrotoxic (rather than ischemic or multifactorial)
origin of acute renal failure, acute respiratory failure, and lower serum urea nitrogen
concentrations. With adjustment for relevant covariates and propensity scores, diuretic use was
associated with a significant increase in the risk of death or nonrecovery of renal function (odds
ratio, 1.77; 95% confidence interval, 1.14-2.76). The risk was magnified (odds ratio, 3.12; 95%
confidence interval, 1.73-5.62) when patients who died within the first week following
consultation were excluded. The increased risk was borne largely by patients who were relatively
unresponsive to diuretics.
The use of diuretics in critically ill patients with acute renal failure was
17.11.16 12:43Diuretics, mortality, and nonrecovery of renal function in acute renal failure. - Pub Med - NCBI
associated with an increased risk of death and nonrecovery of renal function. Although
observational data prohibit causal inference, it is unlikely that diuretics afford any material benefit
in this clinical setting. In the absence of compelling contradictory data from a randomized,
blinded clinical trial, the widespread use of diuretics in critically ill patients with acute renal failure
should be discouraged.
Comment in
Loop diuretics for patients with acute renal failure: helpful or harmful? [JAMA. 2002]
Diuretics in critically ill patients with acute renal failure. [JAMA. 2003]
Diuretics in critically ill patients with acute renal failure. [JAMA. 2003]
Diuretics in critically ill patients with acute renal failure. [JAMA. 2003]
Diuretics in critically ill patients with acute renal failure. [JAMA. 2003]
Diuretics in critically ill patients with acute renal failure. [JAMA. 2003]

75. Myth #4:
Giving diuretics to patients with
ongoing vasopressor needs to
achieve a restrictive fluid
balance is harmful

76. What do you believe?

79. My conclusion…
I am a believer!

80. Myth #4:
Giving diuretics to patients with
ongoing vasopressor needs to
achieve a restrictive fluid
balance is harmful

81. Myth #4:
Giving diuretics to patients with
ongoing vasopressor needs to
achieve a restrictive fluid
balance is harmful

82. Myth #4 References
• Eisenberg P, A Prospective Study of Lung Water Measurements during Patient Management in an Intensive
Care Unit. Am Rev Resoir Dis 1987
• Mitchell J, Improved Outcome Based on Fluid Management in Critically Ill Patients Requiring Pulmonary
Artery Catheterization. Am Rev Resoir Dis 1992
• Grams M, Fluid Balance, Diuretic Use, and Mortality in Acute Kidney Injury. Clin J Am Soc Nephrol 2011
• Labib M, Volume Management in the Critically Ill Patient with Acute Kidney Injury. Hindawi Critical Care
Research and Practice 2013
• Goldstein S, Pharmacological management of fluid overload. BJA 2014
• Malbrain M, Fluid overload, de-resuscitation, and outcomes in critically ill or injured patients: a systematic
review with suggestions for clinical practice. Anaesthesiology Intensive Therapy 2014
• Ogbu O, How to avoid fluid overload. Curr Op Crit Care 2015

83. Myth #5

85. Myth #5
You can’t give
noradrenaline through a
peripheral cannula

86. What are we afraid of?

88. The vast majority of events occurred when
vasopressors infused > 12 hours through cannulas distal
to the antecubital and popliteal fossa
Loubani OM & Green RS. A systematic review of extravasation and local tissue injury form administration of vasopressors through peripheral IV catheters and central venous
catheters. Journal of Crit Care. 2015 653.e9–653.e17

89. Ricard JD, Salomon L, Boyer A, Thiery G, Meybeck A, Roy C, Pasquet B, Le Mière E, Dreyfuss D. Central or peripheral catheters for initial venous access of ICU patients: A
randomized controlled trial. Crit Care Med 2013; 41:2108–2115

91. • Grade 1: minimal symptoms, invasive intervention not indicated
• Grade 2: minimally invasive intervention indicated
• Grade 3: interventional or operative intervention indicated
• Grade 4: life-threatening consequences, major urgent intervention indicated
Verbal report from the authors, all extravasation events were managed conservatively
and nil required intervention.

92. Ricard et al Conclusion
• CVC have less complications compared to PVC,
however the majority of these complications
were minor with no real clinical adversity.
• Both PVC and CVC seem safe and certainly
starting with a PVC may allow appreciable gain
of time in some critically ill patients needing
urgent treatment.
Ricard JD, Salomon L, Boyer A, Thiery G, Meybeck A, Roy C, Pasquet B, Le Mière E, Dreyfuss D. Central or peripheral catheters for initial venous access of ICU
patients: A randomized controlled trial. Crit Care Med 2013; 41:2108–2115

94. • 953 patients received vasopressors
• 783 (82%) via PVC, 170 (18%) through CVC
Jose Cardenas-Garcia, Karen F. Schaub, Yuly G. Belchikov, Mangala Narasimhan, Seth J. Koenig, Paul H. Mayo. Safety of Peripheral Intravenous Administration of Vasoactive
Medication. Journal of Hospital Medicine. 2015

95. Jose Cardenas-Garcia, Karen F. Schaub, Yuly G. Belchikov, Mangala Narasimhan, Seth J. Koenig, Paul H. Mayo. Safety of Peripheral Intravenous
Administration of Vasoactive Medication. Journal of Hospital Medicine. 2015

96. 19/783 (2%) had extravasation
• 16/19 were on noradrenaline
• No tissue injuries at the site of extravasation
• No infections
Jose Cardenas-Garcia, Karen F. Schaub, Yuly G. Belchikov, Mangala Narasimhan, Seth J. Koenig, Paul H. Mayo. Safety of Peripheral Intravenous Administration of Vasoactive
Medication. Journal of Hospital Medicine. 2015

97. Cardenas-Garcia et al Conclusion
The delivery of
vasopressors via
PVC is safe and
feasible
Jose Cardenas-Garcia, Karen F. Schaub, Yuly G. Belchikov, Mangala Narasimhan, Seth J. Koenig, Paul H. Mayo. Safety of Peripheral Intravenous Administration of Vasoactive
Medication. Journal of Hospital Medicine. 2015

98. My Conclusions
• Yes, you can indeed give
noradrenaline peripherally.
• If you are going to do it, you
should use a decent sized, well
placed cannula as proximal as
possible, which is diligently
checked for any signs of
extravasation.
• This should be considered in
situations where it is not
possible or there will be a delay
to putting in a CVC

99. Myth #5
You can’t give
noradrenaline through a
peripheral cannula

100. Myth #5
You can’t give
noradrenaline through a
peripheral cannula

101. Myth #5 References
• Loubani OM & Green RS. A systematic review of extravasation and local
tissue injury form administration of vasopressors through peripheral IV
catheters and central venous catheters. Journal of Crit Care. 2015 653.e9–
653.e17
• Ricard JD, Salomon L, Boyer A, Thiery G, Meybeck A, Roy C, Pasquet B, Le
Mière E, Dreyfuss D. Central or peripheral catheters for initial venous
access of ICU patients: A randomized controlled trial. Crit Care Med 2013;
41:2108–2115
• Jose Cardenas-Garcia, Karen F. Schaub, Yuly G. Belchikov, Mangala
Narasimhan, Seth J. Koenig, Paul H. Mayo. Safety of Peripheral Intravenous
Administration of Vasoactive Medication. Journal of Hospital Medicine.
2015