Venous Access for Fluid Resuscitation – You don’t need a central line!

Last week we asked, what venous access is the LEAST effective for fluid resuscitation? The options were:

A. 16G antecubital peripheral IV
B. 8.5F Cordis
C. Medial port of a triple lumen central line
D. Intraosseus line

Before we get into the answer with some numbers to back it up; take a second t go back to undergrad physics.. remember Poiseuille’s Law?


What it says is that the highest amount of flow is achieved when the conducting vessel is a) short, b)large, and d) has a high pressure gradient across it.

Now thinking about our options:
A) a 16G PIV has a relatively large lumen and is a short catheter
B) An 8.5F cordis has a huge lumen and is not very long
C) The medial port of a central line has a smaller lumen (18G) and can be upto 25cm long
D) An intraosseus needle is 16G and relatively short

So the answer is C.. a central line is NOT an effective way to provide massive fluid resuscitation.

Interestingly there are some numbers for those wondering just how fast fluids go through these vessels..
A) 16G PIV – 220ml/min
B) 8.5F cordis 126 ml/min, 333 ml/min under pressure bag at 300 mmHg
C) Medial port of triple lumen – 26 ml/min
D) IO – 80 ml/min, 150 ml/min under pressure *reference*

The take home message here is when you want to fluid resuscitate a patient, good peripheral IVs are your best option and if you can’t get them, consider an IO. While a triple lumen central venous catheter is an important line throughout an ICU stay; it is not a priority in initial resuscitation.

Thanks for participating!


Non-invasive ventilation – a primer

One of the questions for the last case is whether non-invasive ventilation (NIV) would be an appropriate intervention in a patient with severe hypoxemia. As a reminder, NIV employs a mask fitting over the nose and/or mouth and provides continuous positive airway pressure (CPAP) with or without positive inspiratory pressure (often referred to as BiPAP).

The most common diagnoses to use NIV in include CHF and COPD.

In CHF, the physiological rational for CPAP is that it reduces preload, decreases transmural ventricular pressure, and decreases afterload. Does it actually improve patient-centred outcomes? This 2013 Cochrane Review reviewed 32 studies with 2916 patients who received CPAP or BiPAP in addition to standard medical therapy compared to standard medical therapy alone found decreased mortality (RR 0.66) and need for intubation (RR 0.52) in the NIV group.

The COPD patient is another who may benefit from NIV where positive-pressure relieves the fatigued diaphragm and decreases work of breathing. This theoretical benefit has translated into improved outcomes in multiple RCTs and meta-analyses. This 2004 Cochrane Review showed decreased mortality (11% vs 21%) and need for intubation (16% vs 33%) when NIV was added to standard therapy.

The evidence base for the use of NIV is strongest in patients with CHF and COPD, but there is a body of evidence suggesting it may be beneficial in the following patient groups:
AsthmaThis small RCT of 30 patients showed improved FEV1 and decreased hospital admission (18 vs 62%) in the group receiving BiPAP.
Immunocompromised patients – The theoretical benefit in this population is avoiding intubation and its associated nosocomial infections. This 2001 RCT in NEJM showed decreased need for intubation and mortality. However, patients who fail NIV tend to have higher mortality. Risk factors for failure include higher APACHE II scores, need for vasopressors, and low P/F ratio.
Pneumonia – One of the most common reasons for intubation and ICU admission, but increased secretions are considered to be a relative contraindication to NIV. A Cohrane Review showed decreased need for intubation and mortality in patients with pneumonia who received NIV in addition to standard therapy. Care should be taken to only consider NIV in those patients who are able to clear their secretions on NIV.
ARDS – This is a generally sick patient population and there is limited data behind the use of NIV. A small RCT of 40 patients compared NIV vs supplemental oxygen in patients with ARDS, P/F ratio >200 and found decreased need for intubation in the NIV group along with a trend towards improved mortality.

A general principle to guide the use of NIV is consideration of a timed trial. It may be that CHF and COPD patients do so well with NIV because their underlying exacerbations show relatively rapid improvement with appropriate medical therapy. This is contrasted to pneumonia/ARDS where the natural history of resolution is over days-weeks even with appropriate therapy. Prolonged NIV comes with the cost of device-associated complications like pressure ulcers, but also importantly the possibility of delaying intubation. If your patient on NIV is not improving in the first 4-6 hours, you may have to first reconsider your diagnosis and second consider intubation and mechanical ventilation.

This post is a very brief superficial review of non-invasive ventilation. This CMAJ clinical practice guideline provides some more framework and references.

Case 2 concluded: Hypoxemia

Sincere apologies for the delay in this post. To summarize Case 2, we have a 50 year old woman with ovarian cancer who is extremely hypoxemic despite supplemental oxygen and positive pressure ventilation is being considered. I’d like to  use this post to introduce a couple of other great #FOAMed resources.

The questions to think about were..

1) What is your approach to undifferentiated hypoxemia?
A recent post found here by Mark Yoffe on his website does a great job reviewing a general approach to hypoxemia.
In this lady with an oncologic diagnosis, pulmonary embolus is high on the differential. However, shunting due to pneumonia and/or ARDS should also be considered.

2) Who would be a candidate for non-invasive ventilation?
Stay tuned for a comprehensive review on this topic!

3) How would you approach intubation in a severely hypoxemic patient?
Scott Weingart of EMCrit‘s article in the Annals of Emergency Medicine, found here, is a fantastic review on preoxygenation and prevention of desaturation during intubation.

I’m interested in whether people would consider non-invasive ventilation in this patient. Would you? Discuss with #icurounds on twitter.

Case 2: Approaching hypoxemia..


A 50 year old woman with a history of ovarian cancer presents with 3 days of worsening shortness of breath and a dry cough. You are called urgently to the emergency department for intubation and admission to the ICU. On arrival she is working hard to breath with a respiratory rate of 40, saturating 87% on a 100% non-rebreather. Her heart rate is 130 with a blood pressure of 170/90.

What is your approach to undifferentiated hypoxemia?

Who would you consider non-invasive ventilation for?

How would you approach an intubation in a severely hypoxic patient?

Engage in this case through comments here, on Facebook, or through Twitter #icurounds

#icurounds fundamentals – modes of ventilation


One of the most intimidating parts of being in the ICU is hearing something like “PCV, 15 on 10, FiO2 70%” What does that mean?!?! While this post is by no means going to go over the intricacies of ventilation, it should hopefully be enough of a primer to understand what’s being talked about on rounds.

The key to understanding modes of ventilation is knowing what you can control on a ventilator. The major variables are:

Trigger – time based (control) or patient initiated (spontaneous)
Delivery – Pressure OR Volume
Respiratory Rate – important in control modes
PEEP (positive end expiratory pressure)
FiO2 – From 21% to 100%

There are many others (flow rate, i:e ratio, cycle trigger, etc but I won’t get in to those for now)

Trigger/Respiratory Rate
In a spontaneously breathing patient, a ventilator breath is triggered by patient initiation (usually through a change of flow or pressure in the circuit when the patient breathes in). If a patient becomes apneic, a backup set rate kicks in.
In a controlled mode of ventilation, a breath is delivered periodically based on rate. If the respiratory rate is set at 20, a breath is triggered every 3 seconds.

Once a breath is triggered, the ventilator can either deliver a fixed volume of air (tidal volume) or a continuous flow until a pressure is reached (inspiratory pressure). Only one of the two can be set (since they are dependent on each other).

The positive end-expiratory pressure level is the pressure maintained in the airways between breaths. It is usually at least 5 cm H2O and may be set higher in certain conditions (i.e. ARDS). This pressure is meant to hold airways and alveoli open to prevent collapse

This is simply the percentage of inhaled air that is oxygen and can be room air (21%) to 100% oxygen. This should be titrated to the lowest level that gives you an acceptable arterial oxygen saturation.

Now let’s go through some examples..

ACVC Vt400 PEEP10 FiO2 50% RR15
– In this mode, a tidal volume of 400 ml is delivered every 4 seconds. PEEP is maintained at 10 and FiO2 is 50%

PSV 10/8 FiO2 30%
– In this mode, breaths are triggered by patients and an inspiratory pressure of 10 is delivered with a PEEP of 8 and FiO2 30%
– Note that in some institutions this same mode may be described as 18/8 (where the nomenclature is Ppeak/PEEP instead of Pinsp/PEEP)

CPAP 5 FiO2 60%
– In this mode, all breaths are patient triggered and there is no additional ventilatory support of these breaths above the set PEEP of 5

To the veterans out there, look out for some more advanced ventilatory modes and discussion to come!

#icurounds fundamentals – indications for intubation


One of my favourite parts about having medical students in the ICU is that they remind us of some of the core questions in critical care. Today @mlipkus asked what clinical factors would push me to intubate a patient. Let’s review some of the indications for intubation..

1) Neurological status
– Airway protection is a commonly referred to indication for intubation. “GCS less than 8? Intubate!”
– The rational for this is that a patient who is not awake is a patient who is at risk for aspiration and subsequent worsening respiratory status
– When intubating for this indication, have a close look at the patient and how vulnerable their airway really is. Do they have a cough? A gag? Ever extubated a patient with GCS of 8 or below? (I have..)

2) Hypoxia
– My general threshold for hypoxia before I start considering intubation is ~ SaO2<90% on FiO2>60%
– It’s more than numbers – how hard are they working to breathe? How reversible is the underlying cause?

3) Hypercapnea
– Many patients are hypercapnic at baseline so important to look at pH as well
– Generally consider ventilation if pCO2>60 and pH<7.25
– Similar to hypoxia – think about the cause of the problem and how reversible it is.

Those are your basic 3 indications for intubation, but I’d like to offer two more indications that would push me to intubate..

4) Impending airway loss
– Think about this in your patient with facial/neck trauma, anaphylaxis, angioedema
– You may be better off protecting the airway early instead of dealing with an airway emergency later

5) Shock
– In normal conditions, about 10-15% of cardiac output is directed at respiratory muscles. In settings of shock and increased work of breathing, up to ~50% of cardiac output may be consumed by respiratory effort
– In this scenario, intubation and ventilation may help deliver precious oxygenated blood to the brain, kidney, liver, and gut instead of to the diaphragm

**Also remember scenarios where non-invasive ventilation may be indicated
– COPD exacerbation
– Decompensated CHF
– The immunocompromised patient with a reversible cause

Case 1 concluded – norepinephrine reigns supreme?

The poll results are in.. although a small sample size, 100% of respondents would use norepinephrine as their first pressor in septic shock. Let’s take a look at the evidence that may support this stance.

Before a full evidence review, it may be useful to review the basic physiology of pressors and inotropes. Chris Overgaard’s review in Circulation 2008, available open-access, is a great resource to review the basic science behind these medications.

Turning to the evidence, a number of trials have compared agents head-to-head including norepinephrine, dopamine, vasopressin, phenylephrine, and epinephrine. A 2011 Cochrane Review found that these trials have not found any significant differences in hard outcomes of mortality, ICU length of stay, or hospital length of stay, But a few nuances have been revealed..

When specifically comparing norepinephrine and dopamine, this meta-analysis in 2012 showed superiority of norepinephrine with regards to mortality (48 vs 53%) as well as being less arrythmia-inducing (RR 0.43). The bulk of patients in this analysis are from the SOAP II trial.

It’s this body of evidence that provides the background for the 2012 Surviving Sepsis Campaign Guidelines recommendation that norepinephrine be the first choice vasopressor.

The last point I want to briefly touch upon is the role of vasopressin as an adjunct to norepinephrine in septic shock. The VASST trial (NEJM 2008) compared patients with septic shock already on norepineprhine to either higher doses of norepinephrine or adding vasopressin. No difference was found in mortality or adverse events. When looking at the predefined subgroup of less severe sepsis (on 5-14 mcg/min of norepinephrine), mortality was lower in the vasopressin group (26 vs 36%). The approach of adding vasopressin to norepinephrine is supported in the 2012 Surviving Sepsis Campaign.

Thanks again for following, and stay tuned for more cases and pearls!

Case 1.. back to the pressor.

Thank you and welcome to all the followers through WordPress, Twitter, and Facebook over the past week.

The #icurounds discussion on fluid choice had some great contributions (@petrosoniak, @brambo43, @canibagthat, @RB_cavalcanti, @joshualandy, @ACSmaggus, @rjggoldberg). Seems as though the consensus is initial fluid resuscitation with a crystalloid – normal saline or Ringer’s Lactate. 

So let’s go back to our patient, a 75 year old with community acquired pneumonia admitted earlier in the day. Upon reviewing the chart, you find that he’s been resuscitated with 4L of NS to this point.

His pressure is 86/52 with a heart rate of 120, on dopamine 10 mcg/kg/min.

What would you do at this point for pharmacological support of his blood pressure?

Case 1 continued… the fluid debate

Thanks @RB_Cavalcanti, @canibagthat, and @rjggoldberg for being the first contributors in the #icurounds discussion.

Great points were raised – shouldn’t we address fluids before talking about pressors? What type of fluid?

Let’s take a look at some of the evidence behind fluid choice in resuscitation…

The SAFE trial looked at 4% albumin vs normal saline for intravascular fluid resuscitation in critically ill patients over the first 28 days of hospitalization. There was no difference in any endpoint, including mortality. When looking at the subset of patients with septic shock, there was also no difference in mortality.

The 2008 VISEP trial  was a two-by-two factorial trial looking at glycemic control and fluid resuscitation in patients with septic shock. 10% Pentastarch and modified Ringer’s lactate were used for fluid resuscitation. The trial was stopped early because of a trend towards increased 90 day mortality in patients receiving pentastarch.

Finally, in 2012 the 6S trial  resuscitated patients with septic shock with either hydroxyethyl starch or ringers acetate up to 33 ml/kg/day. At 28 days, mortality (51 vs 43%) and use of renal replacement therapy (22 vs 16%) was higher in the hydroxyethyl starch group.

That’s a fair amount of evidence suggesting that crystalloids are the best choice for fluid resuscitation. But which type? Normal saline? Ringer’s lactate?

The CHLORIDE trial looked at the use of high chloride solutions (0.9%  saline, 4% succinylated gelatin solution, or 4% albumin solution) vs “low” chloride solutions (Hartmann solution, Plasma-Lyte 148, or chloride poor 20% albumin). There was no difference in mortality, ICU length of stay, or need for long term renal replacement therapy. There was however a trend to higher rates of acute kidney injury and use of in-hospital renal replacement therapy in the high chloride group.

With all of that considered – should we consider a buffered, low-chloride, crystalloid solution (i.e. Ringer’s Lactate or Hartmann’s Solution) to be the ideal initial fluid for resuscitation in septic shock?

Please contribute your thoughts below, on twitter with the hashtag #icurounds, or on our Facebook page.

Case 1: A pressing issue…

A 75 year old patient is brought to the ICU from the general medicine ward with hypotension. He was admitted a few hours earlier with community acquired pneumonia but had progressive hypotension. He was started on dopamine at 10 mcg/kg/min and currently has a blood pressure of 86/52 with a heart rate 120 on the floor and on arrival to the unit, you’re asked whether you are happy with dopamine or if you would like to switch to another “pressor”?

What are your thoughts on choice of pharmacological support in this patient with septic shock?