Questioning Routine oxygen on PCA patients

#CageRattler
Should patients on Patient Controlled Analgesia (PCAs) be given oxygen routinely?

In this first of our dogma busting #dogmalysis posts, I wanted to review the evidence supporting the use of supplemental oxygen when a patient is attached to an intravenous PCA.   But couldn't find any.

Let's review the typical scenario.   Mavis has just undergone a total knee replacement surgery and returns from PACU (recovery) with a Patient Controlled Analgesia infusion.  She is receiving supplemental oxygen at 2lpm via nasal prongs.  It is estimated that she is getting 24-28% oxygen.

She is easily roused from dozing comfortably with a respiration rate of 14. A heart rate of 72 and is normotensive at 115/70.  she has good pink colour, her oximetry sats are 99% with a good reliable pleth wave.

Two questions come to light from this.

1.  Why is she getting oxygen?
2.  Does she need it?

The first question typically is answered : "because  policy states all patients on PCA must receive supplemental oxygen"
The second question's answer is No.

There is no evidence for supplemental oxygen in patients on PCA.  Oxygen use historically came from its use in patients in respiratory failure, where the treatment of desaturation was oxygen delivery.  It still is the cornerstone of managing respiratory failure.  Different jurisdictions have different thresholds for application of oxygen, but it is widely accepted by the AHA and Australian Resuscitation Council that oxygen should be used when sats drop below 94% (lower in COPD patients).

Here we have a well saturated post operative patient on a narcotic infusion.  She does not meet criteria for oxygen delivery until an assessment of her saturations on room air (21%) has taken place.

So why is she on oxygen (other than an outdated policy), what clinical indication is there for supplemental oxygen?   Respiratory depression risk?? Nope- let's look at this.

Narcotics (mostly) bind at the Mu , Kappa, and Delta receptors in the central nervous system.  All three receptors are like switches that, when flicked on, interpretation of pain is dulled.
The Mu receptor, when stimulated, also causes euphoria in low doses, and sedation in large doses; pinpoint pupils, slowed gastric motility and large (bigger than sedative doses, depresses the respiratory drive.

It's this respiratory depression that we fear, and rightfully so, because respiratory depression causes CO2 retention, and subsequently, as CO2 accumulates, respiratory acidosis.   We breathe (in part) to regulate our acidity of blood. This is where the post might get a bit sciencey.

Blood pH is kept in a tight range of 7.35-7.45.  A drop in pH below 7.35 is termed acidosis and the deeper the acidosis is, the less capable is the red blood cell's ability to carry oxygen.  In early acidosis, no desaturation occurs, but once a threshold is met, and acidosis reaches a critical stage, haemoglobin dumps oxygen, causing a desaturation event.   Slow shallow breathing reduces the "blowing off" of acidic CO2 gas which, when built up, drops pH into acidosis.   Because this is regulated by breathing rate and depth, this form of acidosis is called Respiratory Acidosis.

So your post op patient develops respiratory depression.  Her respiratory rate drops to 6. She is difficult to rouse, but isn't turning blue because she has been receiving supplemental oxygen via nasal prongs, yet her CO2 (if you'd measured it is sky high, and she has acidosis).  But sats are looking ok, because desaturation is a late sign of respiratory depression and it is delayed by unnecessary over oxygenation.

Now what?    Her acidosis worsens to the extent that her blood now can't carry oxygen. This sudden desaturation point has been met, and your patient decompensated into respiratory failure.

Now what do you do?  You hit the blue button on the wall!
In the crisis you see her sats hit 80% so it seems reasonable that you'd put high flow oxygen on, but the cause of this patients desaturation is not a lung disease (COPD, pneumonia, OE) it is acidosis, and acidotic blood won't carry oxygen.

Mavis needs stimulation, narcotic reversal (Naloxone), and to be bagged up to blows off CO2.   Her acidosis is what is killing her, and you must correct her acidotic blood before oxygen will have any effect.

Oxygen has no evidence based rationale as a supplement in post op patients on PCA.  You want to review sedation scores and respiratory rates, but saturation monitoring is of little use because by the time you see saturations that sink, your patient is too sick for its use to be of value without correcting acidosis first.

By all means have oxygen handy, but know this.  Oxygen does not prevent respiratory depression in PCA patients.

Look into your policies, see what they say. Challenge the dogma, generate a culture of practice from evidence.

If you find research that supports use, please let me know. I can't

#cagerattler

Therapeutic Hypotension- Trauma

Fluid resuscitation in Haemorrhage : Therapeutic Hypotension

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Caution : serious spoilers for Game of Thrones Fans

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Did Arya do The Hound a favour when she left him to die  from his wounds on that mountain?

The premise of allowing someone to bleed to death is one that may be viewed as a barbaric act, but evolutionary biology would demonstrate to us that profound hypotension seen in hypovolaemia (from blood loss), facilitates both clotting and its spawn, coagulation.  Could it be a survival tool?

A caveman gored by some would be assailant had no fluid resuscitation.  He dropped, unconscious, and dies or wakes some time later, miraculously.  Perfusion has returned supporting consciousness. Slowly he returns to health to hunt mammoth with Ogg, Uhg and his other mates.

Here is the spoiler:  the Hound lives.

It begs to ask how? And it may even allow us to question the time old practice of prompt fluid replacement.

So What are we doing in fluid resuscitation ?

As a TNCC instructor some years ago, I always preached the doctrine of 

"If we don't water the veggies, they'll die".

Two large bore IV cannula and 2 litres of warm crystalloid straight in.  So important was this intervention, that it was a dogma that became indelibly etched into every emergency nurse's trauma primary survey.

We have come a long way since the mid 1990s, and in these 20 short years we have seen the removal of routine oxygen from chest pain protocols, removal of spinal boards and stiff collars from spinal protocols, the removal of routine antipyretics from febrile children management, and the introduction of countless new procedures and trauma techniques.

Included in the new wave, is therapeutic hypotension.  

The concept of permissive hypotension in trauma resuscitation is not new. What is more novel is the change in paradigm from "Permitting" hypotension as though it was previously considered to be naughty, to one where recognising that the bleeding patient's systolic blood pressure hovering at 70mmHg is actually desirable for 1-2 hours before intervention to fluid resus.  This shift from permitting it, to valuing it, as a therapeutic device is a cage rattler.

Therapeutic hypotension utilises the notion that hypovolaemia from haemorrhage leads eventually to hypotension so low, that the  bleeding patient's hydrostatic pressure allows small arterioles to adequately constrict, and a clot to form.

Even the ALOC that ensues with this drop in mean organ perfusion pressure (MAP), is beneficial as oxygen demand plummets, allowing what little perfusion and blood left to retain survival.

So how is this applied in the context of a modern emergency trauma setting.  Two words burn bright.... 

"Just Wait"!!

Clearing safely, assessing haemorrhage, Airway, breathing, circulation , level of consciousness; have long been and continue to be priorities.  As are interventions to stop haemorrhage, secure airway, augment oxygenation and ventilation, and of course intravenous access.  But hold off on that massive whole blood transfusion, or crystalloid bolus.   The suggested 60-90 minutes should pass before fluids in most circumstances.

Your one job in haemorrhage is to stop the bleeding.   It is not to immediately replace blood.  Stop the bleeding with digital compression on a bleeding point.  And if you can pack the hole, then you pack that hole.

Many companies manufacturing procoagulant impregnated gauze will try and convince you that they have some magic property but compression on the bleeder is by far the sovereign intervention. 

Where direct (and I mean direct pinpoint) pressure doesn't work, crank out that tourniquet for limbs, or a surgeon for the torso and neck.  But pressure is the boss, and this non-science love affair we have had with pouring in fluids when someone is still bleeding is just lunacy.  

When the time comes for blood or fluids (and it will), the patient should have had time for a clot to form, and reconstitution of what volume they have to adequately distribute.  We have an incredible ability to store clotting factors, water and red blood cells in reserve for those days that we get stabbed, or cut.  In fact, most adults can loose 20% (1000-1500) of blood and not skip a beat, because of this compensation.

Now think about all those times that we have taken a shocked Hypovolaemic patient, nearly drowned them with saline or Hartmann's in some inane quest to get elevation in their blood pressure (a poor indicator of perfusion).   Inevitably we have haemodiluted the life out of the blood.  Washed out the red cells to the point of anaemia, washed out platelets and coagulation factors to the point of coagulopathy, washed out white cells and immunoglobulins to the point of immunocompromise and finally filled their vascular highways with pressure exacerbating rebleeding.  

Now one thing has always rung true:  your first clot is your best clot. Say it out loud. Own it!  

Your first clot is your best clot!

So this is where therapeutic hypotension (permissive hypotension) is a game changer.   Holding off on aggressive fluid resus early, stopping bleeding, allowing natural clotting to occur, then introducing (ideally) blood, but if not small titrated aliquots of crystalloid in 100-200ml boluses to achieve a systolic pressure of just 80-90 is best practice.

As these are given the best measure of perfusion is not peripheral capillary refill, but etCO2 if your patient is ventilated.  If not, it's respiratory rate which is a barometer for acidosis.  It is complex and deserves a post all of its own, but to return CO2 to the lungs to be blown off, the patient needs to be perfusing tissues where CO2 is collected.  Hypoperfusion = reduced CO2 production = low etCO2 .

Anyhow we digress.

Stop bleeding- and don't be too keen to get that BP to normal.  Hypotension is a life saver in haemorrhage an the sooner we practice from what we have learned from cavemen the better off our bleeding trauma patients will be. 

You need to listen to this awesome podcast on the topic. https://itunes.apple.com/au/podcast/emergency-trauma-management/id634332324?mt=2&i=361877809

The Hound lives. 

Plasmids and antibiotic resistance

#KYJ -  Superbugs, Plasmids and Genetic mutation.

Make a note of " MCR-1 ".

It is a buzz term that you will hear more about.  We start our explanation of this, with a  a basic review of microbiology.... 

Hello.... Hello??  Are you still awake?  Stay with me.

Bacteria a living cells with cell walls made of carbohydrates (cellulose- a complex sugar).

Some have a fatty (lipid) membrane coating around the cell wall. 

Inside, are most of the goodies that other cells have, organelles like mitochondria, cytoplasm, lysosomes, and nucleus to name a small familiar sample.

Inside the nerve centre of the bacteria is genetic material (genes) arranged in to long protein strands called chromosomes.  This is where the bacteria gets its instruction to function and reproduce.  

Unlike animals and plants that must mate with a male/female combination to reproduce, bacteria are asexual; boring I know, but true none the less.  To divide into two identical copies of its self (producing offspring called Daughter cells), bacteria copies its chromosomes, then simply splits down the middle to form two new cells. 2 become 4 become 8 become 16 and so on ( look up you year 8 maths books , or have a chat to any Amway dealer to see how effective the power of duplication becomes.)

Anyhow I digress... 

Given that bacteria make absolute clones of them self, you would think they can't change.   But we know they do.   They become resilient, and adapt to new environments.  They mutate.

Enter the plasmid.

A plasmid is a rogue speck of genetic material that lives in the cytoplasm (watery juice) of the bacteria.  Plasmids are genetic coded proteins that can become altered when a bacteria is exposed to an antibiotic (that should have killed it) but survives.   Plasmids change, replicate on their own and translocate genetic information with genes inside the nucleus.

Now this surviving bacteria passes on this information to its daughter cells creating a bacteria that is now resistant to the antibiotic that previously would have killed its grand parents.

Are you still awake? 

Ok.  So plasmids don't just mutate and affect the host bacteria, but they can also share genetic information to other bacteria, even other species of bacteria.  A Strep can share its resistance recipe with a Staph, or an E.coli with an Enterococci, or a Bacillus with a diplococcus.

Frightened yet?

Recently, an E.coli strain was discovered in a urine sample of an American woman with a UTI.  This infection is resistant to every antibiotic.  EVERY ANTIBIOTIC.   

This drug resistant E.coli strain has a gene called MCR-1 which is harboured in the E.coli's plasmid.  

This E. coli bacteria with the mcr-1 gene could pass its plasmid and gene  to another superbug with other mutations-- creating a truly super-superbug that resists all known antibiotics.

The bio surveillance role that nurses and doctors have was always important, but this is going to have implications on infection control practices going forward.  

I'm off to wash my hands ... again! 

Adenosine

#KYJ.  Adenosine.
Have you ever given this IV drug to a patient?
It is used to cause a complete block through the AV node, in patients experiencing a Junctional Tachycardia (previously and more commonly called Supraventricular Tachycardia (SVT)).

Its use is common, and when given correctly it is very effective.  In the past you may have been taught to give it as a neat push IV.  But more recently it has become popular to dilute the required dose up to a 20ml volume and rapidly push in a largish (18g) IV cannula in the antecubital fossa, and quickly flush with a 10-20 ml saline

This drug has the effect of stopping the heart.  Thankfully it has a very short half life of 4-7 seconds (requiring the rapid push). Like a computer that is playing up, you get the sense that this drug is like a cardiac "Reset button", like someone said "have you tried turning it off, then on again?"

Vials come in 6 mg but it is very common (almost expected) that we start at 9mg.
A common regimen is
3 x 2 minutely doses starting at
9mg - 9mg - 12 mg.

If it works on dose 1, the other two are not needed.

Doses are expected to work in 5-10 seconds so as you give the push, the patient needs to be attached to the cardiac monitor.  You are watching for the SVT to deteriorate into a severe bradycardia or asystole (flat line).

Their heart stops.... Then in 3-5 seconds it automatically restarts, hopefully into a normal sinus rhythm .... It's a reset button.

Patients often experience fear, and altered consciousness as their brain oxygenation ceases for that few seconds.  Many describe a sense of doom, or near death phenomenon like a Tunnel of light, out of body experiences or a peaceful place of comfort and warmth.  Some report an experience of meeting their deity or previously deceased loved ones.  Rarely this experience is one of terror, and there are documented case reports of Post traumatic stress disorder.  This drug is excellent but has some issues.

Nurses should comfort the patient and prepare them for a sensation of "passing out". Tell them that you will stay with them and keep them safe.  Hold their hand.  They are often very frightened.

Have you had a patient on this drug?  Tell us your story.

#KYJ - HbA1c in Brief

Understanding HbA1c (#knowingyourjargon)

Smooth RBCs  are kind to your blood vessels, but sugary sticky ones damage the walls stimulating the inflammatory system that initiates cholesterol to be sent out from the liver to repair the damaged walls.

Red blood cells live 120 days.  During that time they slowly accumulate glucose and the haemoglobin protein (most famous for transporting oxygen) becomes glycated.

This glycated haemoglobin is measured as a percentage (old measurements) or in mmol/mol

The test for this stickiness of red blood cells is called HbA1c

As a percentage less than 6% is normal.
More modern tests measure in mmol/mol where less than 42 is considered normal.

Diabetes is commonly diagnosed with HbA1c levels above 6.5% or 48 mmol

Unlike a random BSL, the A1c test looks at glucose control over a period of 3 months, and is accurate as a control monitoring test for diabetics.

ACE inhibitors- why they cause cough

#KYJ - #KnowingYourJargon

ACE inhibitors and that nasty Cough.

With many classes of blood pressure drugs on the market, it can be a mind storm navigating them all as nurses.

A common first line antihypertensive is the humble ACE inhibitor.  It's main side effect is cough and it drives patients and their partners crazy.

... But why? 

How does it cause cough?

Well let's understand ACE.

Angiotensin Converting Enzyme.

ACE is created in lungs and there, it has a role in destroying inflammatory chemicals called Bradykinin and Substance P.   These pro-inflammation proteins cause lung tissue irritation- notably cough (tussis).

ACE also notably converts Angiotensin into a vasoconstrictor that raises Blood Pressure.  It stands to reason if I inhibit ACE then I can't convert Angiotensin.

Hence its valuable role as a blood pressure lowering drug.

BUT....

If you give an ACE inhibitor, and prevent the breakdown of bradykinin and substance P (Inflammatory chemicals), there is an accumulation of these protussive mediators (coughing stimulants) in the respiratory tract. 

This side effect is not dose-dependent and often precludes the use of all agents within the drug class.

Common offenders are Lisinopril, Perindopril, and a new one released after March and before May called April😆😆😆.

No seriously.  ACE inhibitors cause cough and often this means that the patient needs a new approach to BP control.

 

Polypharmacy and drug interactions

#KYJ - Polypharmacy
www.ect4health.com.au/rustypills/
Interesting term, but one we need to know more about.   Polypharmacy is defined as 4 or more concurrent medications.  The issue is drug to drug interactions that occur when a person takes two or more drugs that are metabolised by the same enzyme systems in the liver and other tissues.
Many medications use a system called Cytochrome 450 enzymes(P450).
If drug A and drug B are both metabolised at the P450, then metabolism of both drugs can be impaired or delayed, rendering both inactive or toxic.  These interaction can make one or both medicines overly potent.

The issue compounds with every extra medication a person takes. In fact if your patient takes 5 medications, there is a 50-80% chance of an adverse effect.  What's worse, is that the risk increases 12-15% for each extra drug in that little dosette box.

Take Lipitor (Atorvastatin) the worlds most prescribed drug.  It has over 250 drugs that interact with it to cause adverse effects.
Common medications  causing issues in combination with Lipitor include:
amlodipine
aspirin
atenolol
Cymbalta (duloxetine)
Fish Oil
gabapentin
hydrochlorothiazide (Enduron)
Lasix (frusemide)
levothyroxine
lisinopril
metformin
metoprolol
Nexium & omeprazole
Plavix (clopidogrel)
Synthroid (levothyroxine)
Vitamin D3 (cholecalciferol)

These drugs are hard to get our head around, but the issue of polypharmacy being linked to dementia, falls and muscle atrophy in elderly is one that is on the rise, and needs clinicians to be wary and hyper vigilant.

Our latest Rusty Pills seminar discusses this issue and many others.
Check out http://www.ect4health.com.au/rustypills/