Myths in ICU: BUSTED by Team Thomas
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Thomas & ThomasNovember 2016
in ICU
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Thomas & Thomas
ICUEDITION
2016
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Myth #1
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Myth #1
Giving O2 to a CO2 retaining COPD patient, knocks off their hypoxic
respiratory drive, leading to hypoventilation and further CO2
retention
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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.
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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.
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So why dose pCO2 rise?
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Theory 1: Loss of hypoxic vasoconstriction and therefore increased shunt and increased
alveolar dead space
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Normal Conditions
https://dundeechest.wordpress.com/2009/08/12/why-do-copd-patients-retain-co2-when-given-too-much-oxygen/
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With 100% Oxygen
https://dundeechest.wordpress.com/2009/08/12/why-do-copd-patients-retain-co2-when-given-too-much-oxygen/
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Theory 2: The Haldane Effect
O2 therapy induces a rightward shift in the curve
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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.
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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.
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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.
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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
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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
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Myth #1
Giving O2 to a CO2 retaining COPD patient, knocks off their hypoxic
respiratory drive, leading to hypoventilation and further CO2
retention
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Myth #1
Giving O2 to a CO2 retaining COPD patient, knocks off their hypoxic
respiratory drive, leading to hypoventilation and further CO2
retention
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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/
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Myth #2
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•SIMV•VT 500ml•PEEP 0•FiO2 0.3
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•SIMV•VT 500ml•PEEP 20•FiO2 0.5
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•SIMV•VT 500ml•PEEP 8•FiO2 0.5
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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
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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
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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
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PEEP helps to overcome resistance…
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PEEP helps to overcome resistance…
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they lose their “physiologic” PEEP!
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What the f*** is physiologic PEEP?
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Collapse is due to a reduction in volume!!!
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EELV 100%EELV 75%
EELV 66%
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Loss in alveolar size caused by loss in FRC
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Alveoli collapse due to…
• the loss in muscle tone (Sedation)• the underlying lung pathology
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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
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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
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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
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Myth #3
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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
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Coagulation factors produced by Liver
ADAMTS13 (vWBF cleaving enzyme)
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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.
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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.
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Ok so we know INR does not reflect in vivo haemostasis in liver disease, but is there any evidence
of risk of VTE?
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Aggarwal A, Puri K, Liangpunsakul S. Deep vein thrombosis and pulmonary embolism in cirrhotic patients: Systemic review. 2014 May; 20 (19): 5737-5745
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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
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Ok, I accept that there is a risk of VTE in liver disease, but isn’t there also a risk of bleeding?
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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
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• 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
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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
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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
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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
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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
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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
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Myth #4
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Myth #4:
Giving diuretics to patients with ongoing vasopressor needs to
achieve a restrictive fluid balance is harmful
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Why would you want to diurese a critically ill patient?
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Myth #4:
Giving diuretics to patients with ongoing vasopressor needs to
achieve a restrictive fluid balance is harmful
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What do you believe?
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My conclusion…
I am a believer!
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Myth #4:Giving diuretics to patients with ongoing vasopressor needs to
achieve a restrictive fluid balance is harmful
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Myth #4:Giving diuretics to patients with ongoing vasopressor needs to
achieve a restrictive fluid balance is harmful
Not yet…!
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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
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Myth #5
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Myth #5
You can’t give noradrenaline through a
peripheral cannula
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What are we afraid of?
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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
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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
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• 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.
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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
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• 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
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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
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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
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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
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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
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Myth #5
You can’t give noradrenaline through a
peripheral cannula
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Myth #5
You can’t give noradrenaline through a
peripheral cannula
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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