myths in icu: busted by team thomas

Thomas & ThomasNovember 2016

in ICU

Thomas & Thomas

ICUEDITION

2016

Myth #1

Myth #1

Giving O2 to a CO2 retaining COPD patient, knocks off their hypoxic

respiratory drive, leading to hypoventilation and further CO2

retention

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.

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.

So why dose pCO2 rise?

Theory 1: Loss of hypoxic vasoconstriction and therefore increased shunt and increased

alveolar dead space

Normal Conditions

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

With 100% Oxygen

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

Theory 2: The Haldane Effect

O2 therapy induces a rightward shift in the curve

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.

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.

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.

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

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

Myth #1

Giving O2 to a CO2 retaining COPD patient, knocks off their hypoxic

respiratory drive, leading to hypoventilation and further CO2

retention

Myth #1

Giving O2 to a CO2 retaining COPD patient, knocks off their hypoxic

respiratory drive, leading to hypoventilation and further CO2

retention

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/

Myth #2

•SIMV•VT 500ml•PEEP 0•FiO2 0.3

•SIMV•VT 500ml•PEEP 20•FiO2 0.5

•SIMV•VT 500ml•PEEP 8•FiO2 0.5

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

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

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

PEEP helps to overcome resistance…

PEEP helps to overcome resistance…

they lose their “physiologic” PEEP!

What the f*** is physiologic PEEP?

Collapse is due to a reduction in volume!!!

EELV 100%EELV 75%

EELV 66%

Loss in alveolar size caused by loss in FRC

Alveoli collapse due to…

• the loss in muscle tone (Sedation)• the underlying lung pathology

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

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

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

Myth #3

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

Coagulation factors produced by Liver

ADAMTS13 (vWBF cleaving enzyme)

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.

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.

Ok so we know INR does not reflect in vivo haemostasis in liver disease, but is there any evidence

of risk of VTE?

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

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

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

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): 5737-5745Ha 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

• 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): 5737-5745Ha 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

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

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

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

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

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

Myth #4

Myth #4:

Giving diuretics to patients with ongoing vasopressor needs to

achieve a restrictive fluid balance is harmful

Why would you want to diurese a critically ill patient?

Myth #4:

Giving diuretics to patients with ongoing vasopressor needs to

achieve a restrictive fluid balance is harmful

What do you believe?

My conclusion…

I am a believer!

Myth #4:Giving diuretics to patients with ongoing vasopressor needs to

achieve a restrictive fluid balance is harmful

Myth #4:Giving diuretics to patients with ongoing vasopressor needs to

achieve a restrictive fluid balance is harmful

Not yet…!

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

Myth #5

Myth #5

You can’t give noradrenaline through a

peripheral cannula

What are we afraid of?

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

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

• 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.

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

• 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

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

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

Cardenas-Garcia et al Conclusion

The delivery of vasopressors via PVC is safe and

feasibleJose 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

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

Myth #5

You can’t give noradrenaline through a

peripheral cannula

Myth #5

You can’t give noradrenaline through a

peripheral cannula

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