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Be a ZERO, Not a HERO

DISCLAIMER : This post is about how medics interact within the various tribes. It is NOT about primary care vs teaching hospital, ED vs medics, surgeons vs anaesthetists. I’ve had some people comment on twitter that this is ‘about being a GP undermined by colleagues’. It’s not. It’s about clinicians, of whatever ilk, either undermining each other OR failing to work effectively within a team as too busy showing off how good they are. It’s a piece inspired by astronaut Chris Hadfield’s book and the concept of new team members being either a’plus one’, a ‘zero’ or a ‘minus one’. Now read on…

Medicine attracts bright people. I am constantly amazed at the smartness of some of my colleagues…and the ongoing exposure to brilliance via the FOAMed community. Not that you have to be smart to be a medic. Before medicine I trained as a research scientist, with undergraduate, Masters and PhD in an arcane area of immunology. But a life at the bench wasn’t for me – I enjoy interacting with people too much – hence the drift into medicine as a mature-age graduate. At medical school it struck me that medics were NOT particularly smart – the ability to absorb, memorise and regurgitate several phone books worth of information seemed to be the prerequisite, rather than original thinking. But insistence on high grades and academic excellence are just a cut-off to limit intake into the over-subscribed medical schools…and this encourages competition at a very early stage.

“Doctors are ingrained to compete – there is competition to get into medical school, competition for intern posts, competition for residency programmes, competition in Fellowship exams, competition for the desired consultant post…plus the inevitable competition between specialties”

Don’t get me wrong. I am all in favour of clinicians who are high-achievers and keen to move themselves to the right of the Gaussian distribution curve (mindful of the fact that 50% of all doctors are, by definition, below average). FOAMed helps us achieve that goal and strive to be better. For guys like myself in rural practice, than means to aim to bring “quality care, out there”.

But there is an ugly side to this competition. We all have tales of colleagues who have fallen by the wayside – whether through alcohol or drug addiction, failure of relationships, mental illness (including suicide). I am pretty sure that most of us have engaged in badmouthing colleagues, whether in the same discipline or in other specialties. Some of this is good-natured banter (think anaesthetists vs surgeons)…but it can become ugly, particularly when detracts from patient care or is a result of stressors perceived as being outside our control (bed pressure, busy workload etc). Both Dr Gerry Considine and myself have blogged about this from the perspective of rural practitioners – but it works both ways – primary care vs tertiary & vice versa as well as between in-hospital disciplines.

It never ceases to amaze me that medical training fails to expose junior doctors to primary care, given that this is where most patient encounters occur. And of course the bullshit perception of ‘just a GP’ continues to be promulgated within the tertiary centres leading to the comment ‘just a GP, not a specialist‘. Dr Penny Wilson blogs nicely on this. From my perspective, the more savvy tertiary colleagues turn pale when I suggest they sit in my shoes – they understand the skills needed to spot illness in undifferentiated primary care patients and would rather the security of preselected narrow-focus work.

“before you criticize a man, walk a mile in his shoes…then you will be a mile away from them & have their shoes”

I have certainly been guilty of critiquing colleagues without understanding their work. Before making the move to rural medicine I was a dual-trainee in EM & ICU. It was VERY easy to sit back and criticise the perceived failings of other doctors, especially as EM & ICU generally see a narrow selection of cases that have not been caught in primary care – blissfully ignorant of the wonderful “saves” out there. Add to this a complete lack of awareness of what different specialties actually do, and the system creates perfect conditions for disharmony. One of my shorthands as an ED reg over 10 years ago was ‘GPFI’ – GP is a ****ing idiot. My how we laughed. Now I am older and wiser.

A recent article in the NY Times captures this problem well, describing a paper in the Journal of Internal Medicine “Physicians Criticising Physicians to Patients” which has been re-tweeted by myself and others. The NY Times article on doctors badmouthing other doctors is worth a read.

“doctors will throw each other under the bus”

As a more grownup clinician in rural practice, a salutary experience for me was managing a patient presenting with acute-on-chronic back pain. I admitted him for analgesia..then 24 hrs later his BP dropped suddenly and the underlying sepsis from his epidural abscess declared itself – the source from an infection picked up a week or so prior whilst gardening. His retrieval & intensive care stay was prolonged and complicated, with devastating sequelae.

A single comment from an ICU nurse “you should sue your doctor for missing this” drove a three-year wedge between myself, the patient and family – very difficult in a small rural community, but eventually healed once the time course and decision-making had been explained. Systems failings (no ‘early warning’ notification, failure to appreciate significance of raised respiratory rate and falling urinary output so deterioration not communicated to doctor) all had their part to play, as did cognitive bias ‘just a flare of usual back pain’. But that chance comment from an ICU nurse undermined the therapeutic relationship.

That’s one example. I am sure you will all have similar stories. The ‘barndoor’ appendicitis referred to the medics as gastro by an ‘idiot ED reg’. The flail chest mismanaged as an infective exacerbation of COPD on the Care of the Elderly ward after a patient has fallen against bed rails. Mistakes happen, diagnoses are revised. But we are often quick to hang our colleagues out to dry with the benefit of the retrospectoscope.

Beware critique of others - but NEVER be afraid to apologise for an error
Beware critique of others – but NEVER be afraid to apologise for an error

The more medicine I do, the less certain I am. As a senior doctor I have more appreciation of the myriad presentations of disease, the understanding that patients don’t always ‘follow the textbook’. Contrast this to the cocksure certainty of a relatively junior doctor. The old adage rings true – “How do I avoid making mistakes? By getting experience! How to get that experience? By making mistakes!

FOAMed helps broaden that experience, sharing experiences and clinical discussions with colleagues worldwide. “Doing the simple things, well” is the essence of not just critical care, but all branches of medicine – particulalry in resource-limited rural Australia. Meticulous attention to obs (especially RR), use of bedside testing such as point-of-care lactate, having a heightened sense of “what if?” all contribute to better outcomes.


To be a ‘plus one’ a ‘zero’ or a ‘minus one’? Your choice…

All of which brings us full circle and (finally) to the purpose of this post. As ultra-competitive clinicians, trained to be better than our colleagues in order to progress in a system that seeks to limit entry at every waypoint, it is all to easy to fall into the trap of self-aggrandisement and for want of a better word “pissing on perceived competitors”. But does this REALLY help anyone? Of course not. we are all players in the healthcare team, yet it is almost de rigeur to criticise the perceived failings in other specialties without any understanding of what they do.

How then does a team function well when all the members are highly competitive? I’ve just finished reading Chris Hadfield’s book “An Astronaut’s Guide to Life on Earth“. It’s not a bad read, although I suspect is a springboard for former International Space Station Commander Hadfield’s retirement from the space programme into motivational speaking.

Hadfield talks about initial assessment of team members as ‘plus ones’, ‘zeroes’ and ‘minus ones’

Astronauts are all ‘plus ones’ – highly competitive, incredibly skilled across disciplines (he describes a typical day as performing ocular & cardiac ultrasound on fellow astronauts, fixing a malfunctioning toilet, playing Bowie’s ‘Space Oddity’ on guitar and Commanding the ISS). ‘Plus ones’ add value to the situation – they are leaders. Everyone wants to be the ‘plus one’ in a situation, in order to demonstrate their value to the team. That’s only natural when you are used to competing.

It should go without saying that there is no room in space (or in healthcare teams) for ‘minus ones’ – people who detract from the team plan. They cause problems, whether through laziness, inefficiency or lack of awareness.

But Hadfield outlines the BEST astronauts as the ‘zeroes’ – people whose input is neutral and doesn’t tip the balance one way or the other. Typically they quietly get on with the business of ‘making things happen’ – helping colleagues not for personal gain but because it helps the team overall. Reflective before acting. Competent information sponges.

In medicine we all strive to be ‘plus ones’, often by being the first to answer in a small group session, the first to critique patient management until the patient came under your brilliant care, or to blame ‘the GP’ or ‘those clowns in ED’ for dumping a patient on the already busy acute medical take. But declaring yourself as a ‘plus one’ in a situation almost guarantees that you will be perceived as a ‘minus one’ regardless of the skills you have. we see this when selecting instructors for EMST – we don’t want the flashy know-it-all, we are looking for the quiet, reflective achiever (the ‘zero’) who helps others become ‘plus ones’.

The take home message? I paraphrase from Commander Hadfield’s book :

When you have some skills but don’t fully understand your environment, there is no way you can be a ‘plus one’. At best, your can be a ‘zero’. But being a ‘zero’ is not a bad thing to be. You are competent enough not to create problems or make more work for everyone else. And you have to be competent, and prove to others that you are….

…even later, when you do understand the environment and can make an outstanding contribution, there’s considerable wisdom in practicing humility. If you really are a ‘plus one’, people will notice – and they’re more likely to give credit when you’re not trying to rub their noses in your greatness

Our environment as clinicians is the entire health care system. We occupy different ecological niches (with some amazing psychopathology between us) – primary care – emergency – surgery – medicine etc. yet we often have little understanding of what happens in other disciplines and are quick to critique. Even more so when all we see is other people’s mistakes (ED, ICU).

But unless you understand the nuances of another discipline, be slow to critique and quick to praise.

Be a ‘zero’ not a ‘hero’. Wise clinicians know this.

 

 

COMMENTS FROM TWITTER  – keep ’em coming or (better still) add a comment below :

@KangarooBeach Great stuff, spot on! The consultants I respect most: play zeroes, step up to heroes if need. Love the vid, @Cmdr_Hadfield !

Brilliant article from @KangarooBeach about badmouthing colleagues: Be a ZERO, Not a HERO

“Be a Zero, Not a Hero” Great stuff by the inimitable @KangarooBeach MT @emcrit: great read feedly.com/k/1euyYLb

Brilliant post from @KangarooBeach: Be a Zero, not a Hero. kidocs.org/2013/12/zero-h… #FOAMed

Such an excellent post Tim!!! Ironically a ‘plus one’ précis about some pervasive concepts 🙂 @KangarooBeach

Simon Carley @EMManchester

@AndyNeill @KangarooBeach Thanks for this piece – time to reset to 0

@KangarooBeach “Be a ZERO not a HERO” is a brilliantly written article, thank you. (def going to check out @Cmdr_Hadfield‘s book) #FOAMed

@KangarooBeach hey nice article on zero vs hero! maybe we can get @Cmdr_Hadfield to do a podcast about it?

@johnboy237: Follow this link ‘Be a ZERO not a HERO’ wonderful & truthful insight @KangarooBeach kidocs.org

@KangarooBeach @Cmdr_Hadfield Absolutely Tim! You enjoying the book too?

Andrew wrote: “Good one Tim, but would love to use GPFI on triage screen.”

So much hot gas – ETCO2 for non-anaesthetists

End-tidal CO2 is increasingly becoming used outside of the Operating Theatre and it is prudent for the rural doctor to have an appreciation of what it is, how to measure it, when to measure it and it’s utility in common scenarios.

“you get A, B & C in a single squiggly line” 

Casey Parker, BroomeDocs.com

It is my belief that ETCO2 should be used not just in intubated patients, but as a valuable adjunct for procedural sedation, for monitoring patients ‘at risk’ and to help guide resuscitation.

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What is end-tidal CO2?

Unlike plants, we breath in oxygen and exhale carbon dioxide – we can measure this as ‘end-tidal CO2’ (ETCO2). ETCO2 represents the partial pressure or maximal concentration of CO2 at the end of exhalation. The principle determinants of ETCO2 are:

(1) alveolar ventilation,

(2) pulmonary perfusion (cardiac output)

(3) CO2 production (and elimination)

How can I measure it?

We can measure ETCO2 in several ways

(i) colorimetric

Devices such as the Easy-Cap or Pedi-Cap are designed to confirm the presence or absence of expired CO2 – a pH detector (metacresol purple on filter paper) detects pH shifts and changes to the colour yellow in the presence of expired CO2.

Colorimetric ETCO2 device connect to endotracheal tube
Colorimetric ETCO2 device connect to endotracheal tube
GOLD IS GOOD
“GOLD IS GOOD”
colour change from purple to yellow indicates presence of CO2 > 2%

 

(ii) waveform capnography – during BMV or mechanical ventilation

A sample line is placed as a sidestream to the breathing circuit (usually via the HME filter at intersection of endotracheal tube and breathing circuit). Exhaled gas is sampled by a dedicated analyser (anaesthetic monitor or some defibrillators).

Typically such methods generate both a waveform (capnograph) and a number (ETCO2).

 

wave-2
The ETCO2 capnograph – consider the baseline, height, shape, frequency, rhythm

 

The normal capnograph trace can be divided into distinct phases

I – the end of inspiration & the beginning of expiration, when the Co2-free gas occupying dead space in airway is exhaled. Hence in theis phase the ETCO2 = 0 mmHg

II – there is a rapid rise in measured CO2 as alveolar gas appears

III – expiration continues but CO2 doesn’t rise much further – a plateau in normal lungs. ETCO2 total is derived from the maximum on this plateau

IV – a sharp drop in CO2 to zero, representing inspiration

 

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Propellor heads can get excited about different phases. Be aware of them.

 

 

The capnograph gives us lots of information in addition to the absolute number of ETCO2 (aim 35-45 mmHg). It is easiest to consider the waveform baseline, height, frequency, rhythm & shape.

You can correlate changes in patient or equipment as being reflected in the ETCO2 trace eg:

baseline – non-return to zero caused by re-breathing

height – increasing ETCO2 due to excess production eg: malignant hyperthermia

frequency – decrease or increase in ETCO2 peaks in hypo- and hyperventilation respectively

rhythm – patient breathing vs mechanical ventilation as neuromuscular blockade wears off

shape – obstructive ventilation pattern causes a slow phase II upstroke

 

There are some must know waveforms in the ‘rogues gallery’ later below. The ones I worry about most are the absent or rapidly disappearing ETCO2 rtace seen in inadvertent oesophageal intubation…and the falling ETCO2 waveform with loss of cardiac output.

 

(iii) waveform capnography – during spontaneous ventilation

As an alternative to sampling expired gas directly from the anaesthetic circuit or HME filter attached to an endotracheal tube, it may be useful to monitor ETCO2 for spontaneously ventilating patients, whether on room air, nasal specs or oxygen mask.

I use this routinely during endoscopy, colonoscopy in the operating theatre, as well as when performing procedural sedation in the ED. I am increasingly using ETCO2 monitoring to confirm ventilation in other situations – particularly to confirm ongoing ventilation of the agitated psychiatric patient who has been effectively sedated with agents such as benzodiazepines, haloperidol or ketamine – mindful that hypoventilation or apnoea may be missed.

Remember that relying on SpO2 to confirm ventilation is inadequate – measured oxygen saturation may remain elevated for some time after cessation of breathing-  and once a fall in SpO2 has been detected, your patient is already hurtling down the oxy-haemo-coaster.

Beware the falsely reassuring statement “He must be breathing – the sats are OK” – use ETCO2 to gauge ventilation

In ED ot theatre, there are different gizmos. Most ETCO2 sampling equipment is dedicated to sit in-line as either an adaptor between ETT and circuit, or as a filter line to attach to HME filter. There are also sampling devices designed to sit under nares like nasal specs.

I tend to just take the sampling line from the HME filter, attach to a microfilter and then attach to either blunt cannula or plastic tube of an IV – this can be pushed through the holes in a Hudson mask to detect ETCo2 for patients receiving sedation NB: the ETCo2 will be LOW as diluted by oxygen.

Ubiquitous Dr Minh le Cong offers some hints on MacGyvering ETCO2 setups below :

Prehospitalmed.com “Capnography with LifePak 15” – Dr Minh le Cong

Noninvasive Capnography Setup (PK talk) – Dr Minh le Cong

as do the mob from the EM resource ‘Standing on the corner minding own business’ (SOCMOB)

how to make your own end-tidal CO2 detector

When should I measure ETCO2?

End-tidal CO2 is classically considered as the standard of care when performing intubation. Either colorimetric or waveform capnography can be used to confirm the presence of exhaled CO2 and hence confirm desired tracheal vs inadvertent oesophageal intubation.

The waveform also gives clues to alveolar ventilation (hypo- or hyperventilation), airway resistance, cardiac output, CO2 production & elimination, as well as the obvious confirmation of tube placement within the trachea – both initial & ongoing.

Other uses include :

  • confirmation of tube placement & efficiency of compressions during CPR
  • sudden increase in ETCO2 during CPR may indicate ROSC
  • during sedation to confirm ventilation when direct observation of the patient may be difficult (eg: under drapes/blankets/on side)
  • in psychiatric sedation to achieve effective sedation & avoid apnoea
  • during transfer to confirm presence of cardiac output & adequate ventilation
  • as a numeric target to aim for eg: in treating the head-injured patient where normocarbia, normotension and avoidance of hypoxia are key goals to avoiding rises in ICP.

 

Thus we can summarise ETCO2 measurement as :

  • to confirm tube placement
  • to confirm ventilation & perfusion of patients during mechanical ventilation
  • to confirm ventilation of patients who SHOULD be self-ventilating (but at risk of hypopnoea or apnoea)

 

The clinical bottomline?

End-tidal CO2 monitoring is mandatory not just for the intubated patient, but should be used whenever using a neurolept eg: sedation in ED, monitoring of psychiatric patient etc.

Even if you are not performing anaesthesia, know how to hook up ETCO2 monitoring for your spontaneously ventilating patients at risk of hypopnoea or apnoea.

Dedicated ETCO2 monitors exist, but most capnographs will hook up to existing monitors in OT, ED and ward defibs.

Insist on the use of ETCO2 monitoring in your shop.

 

ETCO2 waveform capnography is now available in handheld monitors - along with SpO2, HR, RR etc
ETCO2 waveform capnography is now available in handheld monitors – along with SpO2, HR, RR etc

 

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ETCO2 monitoring is available for the Phillips Heartstart MRX used in most rural EDs and with SA Ambulance

M3536A-2T

Where can I find out more?

Life in the Fast Lane posts on capnography and interpreting waveforms

Check out Prof Kodali’s website capnography.com & read his excellent paper entitled “Capnography outside operating rooms” (download here)

You may also be interested to read those Norse Gods of resus (ScanCrit) on capnography in cardiac arrest & Cliff Reid’s post on ‘even the dead exhale CO2’ – explaining why you MUST use waveform capnography in resus

 

 

ROGUES GALLERY OF ‘MUST KNOW’ ETCO2 WAVEFORMS

 

NB: these images downloaded from Google. I haven’t been able to find the author to attribute, so apologies if unattributed. I reckon an American source (who else omits the diphthong in oesophagus?)

 

OESOPHAGEAL INTUBATION

HYPOVENTILATION

HYPERVENTILATION

 

REBREATHINGONSTRUCTION CUFF LEAK

FAULTY VALVE

INADEQUATE NEUROMUSCULAR BLOCK

 

SUMMARY OF CAUSES & ETCO2 CHANGES

 

FLAT ETCO2 TRACE

  • Capnograph not connected
  • Oesophageal intubation
  • Airway (ETT) misplaced
  • Respiratory or cardiac arrest
  • Capnograph sampling tube kinked or blocked
  • No ventilation – either forgot to bag the patient or there is a ventilator malfunction

SUDDEN DROP IN ETCO2 TO ZERO

  • Kinked ET tube
  • CO2 analyzer defective
  • Total disconnection
  • Ventilator defective

SUDDEN CHANGE IN BASELINE (NOT TO ZERO)

  • Calibration error
  • CO2 absorber saturated (check capnograph with room air)
  • Water drops in analyser or condensation in airway adapter

SUDDEN INCREASE IN ETCO2

  • ROSC during cardiac arrest
  • Correction of ET tube obstruction

ELEVATED INSPIRATORY BASELINE

  • CO2 rebreathing (e.g. soda lime exhaustion)
  • Contamination of CO2 monitor (sudden elevation of base line and top line)
  • Inspiratory valve malfunction

INCREASED ETCO2

CO2 production

  • Fever
  • Sodium bicarbonate
  • Tourniquet release
  • Venous CO2 embolism
  • Overfeeding

Pulmonary perfusion

  • Increased cardiac output
  • Increased blood pressure

Alveolar ventilation

  • Hypoventilation
  • Bronchial intubation
  • Partial airway obstruction
  • Rebreathing

Apparatus malfunction

  • Exhausted CO2 absorber
  • Inadequate fresh gas flows
  • Leaks in ventilator tubing
  • Ventilator malfunctioning

DECREASED ETCO2

CO2 production

  • Hypothermia

Pulmonary perfusion

  • Hypotension
  • Hypovolemia
  • Pulmonary embolism
  • Reduced cardiac output
  • Cardiac arrest

Alveolar ventilation

  • Hyperventilation
  • Apnea
  • Total airway obstruction (high airway pressures)
  • Extubation

Apparatus malfunction

  • Circuit disconnection (low airway pressures)
  • Leaks in sampling tube
  • Ventilator malfunctioning