PF ratio and why we need it

#KYJ -  PF Ratio

In our respiratory seminar today we discussed PF ratio. I thought that is might be an interesting 'Knowing your jargon' topic.

PF ratio or P:F is a calculation to determine severity of lung injury.

The P stands for PaO2

The F stands for fiO2

So PaO2:fiO2

Normally on air, a persons PaO2 is 80-100 mmHg. Let's say 90.

The fiO2 on room air (21% oxygen) is 0.21

So a PF ratio of 90:0.21 is calculated as 90/0.21=428

Therefore a PF ratio of >400 is considered normal.  If a person develops an acute lung injury or acute Respiratory Distress Syndrome (ARDS), their PF Ratio is markedly diminished. 

The 100/50 rule is a diagnostic example. If a person's PaO2 is 100 while they are breathing 50% O2, then the PF is at the diagnostic point for ARDS.

(<200)

100mmHg / fiO2 of 0.5

100/0.5= 200

You would expect their PaO2 to be at least 200mmHg if breathing 50%. 

The PF ratio is a good way to determine if the ABG oxygen value is consistent with the concentration that the person is breathing.

Critical values

PF ratio >400 is normal

<300 = Acute lung Injury (ALI)

<200 = Acute Respiratory Distress Syndrome (ARDS).

Pathophysiology of Shock

#KYJ Pale, Cold 'n' Clammy

In this Knowing your jargon episode of #FOANed I look at arguably the most recognisable symptoms of shock and the Fight or flight response.

When many animals sense fear, threat or stress, they experience a neurohormonal response that aims at assisting the animal to stand and fight the threat (eg an attacking predator) or flee from it.  This is called fight n flight.  It manifests as tachycardia, adrenaline release, enhanced muscle strength, increased cardiac output/blood pressure, miscarriage, high blood sugar, pupil dilation, And our topic of the day "Pale, cold n clammy".  Let's look at these individually.

Pale

As the sympathetic nervous system is activated to cause increase in cardiac output, it achieves this in part, by constricting peripheral veins in arms, legs, feet, hands and skin. Given that our perfused skin takes on a pink tinge due to blood in the dermal vessels, vasoconstriction in skin leads to reduced blood, so reduced pink hues.  The skin looks pale to ashen in colour.  In dark skinned people, the palms and nail beds become pale.

Cold

For the same reason as pallor, reduced blood flow in skin causes the skin to feel cool to cold, to the touch. 

The vasoconstriction peripherally, redistributes blood away from tissues that ate not vital to immediate survival, and towards the core central circulation (heart,brain,lungs,kidneys).

Clammy

Perspiration or sweat is stimulated by the sympathetic nervous system activated during a stressful event or threat. This has its roots in evolutionary biology where at one time sweat contained many chemicals. Some were toxic to predators to ingest, some were foul tasting, dissuading the predator from eating you, and some, collectively called pheromones, are produced as a chemical attractant, or in the case of attack, as a repellant, offensive odour.  The Skunk is perhaps the most notable mammal that achieves this.   Clamminess it therefore an ancient symptom that serves little purpose in humans, but still seen as part of this fight n flight response of pale,cold n clammy.

Many intimate partners would attest to the fact that their partner's perspiration and scent is different when they are aroused, than when they are angry.  This is largely due to their being different sweat glands. Eccrine glands are the most abundant sweat glands that are all over our body, apocrine sweat glands are specialised and found around nipples, axilla, groin, genitalia and other areas. These produce scents usually associated with sexual arousal.

So there it is. Pale, cold and clammy =Shock (usually).  These symptoms represent a response to a physical or psychological threat.

Like, comment, tag  a nurse/paramedic, and I'd love you to share.  #FOANed is for you.

 

Methoxyflurane- The Green Whistle

#KYJ The Green Whistle.

In this short snipet we explore the drug Methoxyflurane marketed as Penthrox

This drug is a volatile anaesthetic analgesic, it was abandoned in general anaesthesia during the 1970s because of its association with hepatic and kidney failure, but in low doses is an effective safe analgesic.

Most nurses working in emergency departments will be familiar with the classic image of a patient sucking on what looks like a green whistle, being wheeled into a department by paramedics.  

The dose of 3ml of Penthrox is inserted into the "whistle" where it rapidly vaporises, is inhaled, and crosses the respiratory membrane diffusing into systemic circulation.  Being highly fat soluble, it crosses the Blood brain barrier and acts on the  

Pain relief begins after 6–8 breaths and continues for several minutes after stopping inhalation. Continuous use of methoxyflurane 3 mL provides analgesia for up to 25 minutes; a second 3 mL dose can be administered if required for up to 1 hour's analgesia. No more than 6 mL should be given in 1 day. 

It is a depressant which can cause euphoria, and drowsiness, and like most central nervous system analgesics, respiratory depression is likely.

Points to remember. 

• Methoxyflurane provides rapid-onset short-term analgesia for:
  — initial management of acute trauma pain
  — brief painful procedures such as wound dressing.
• The disposable, single-use inhaler device allows patients (including children) to self-administer the drug, under supervision.
• Avoid use in children aged under 5 years and those unable to self-administer.
• Only use methoxyflurane in conscious, haemodynamically stable patients.
• Methoxyflurane is nephrotoxic at high doses:
  — do not exceed maximum doses — 6 mL per day or 15 mL per week
  — do not use on consecutive days.
• Do not use in patients with renal impairment.

More???...

Click the link

http://www.nps.org.au/publications/health-professional/nps-radar/2010/may-2010/methoxyflurane

Hypoxia vs Hypoxaemia

#KYJ- Hypoxaemia vs Hypoxia

Often we get things mixed up a bit saying or documenting one thing but meaning another. In this KYJ ( #knowingyourjargon )we look at two old favourites.

 Cells need oxygen to make energy (ATP) from Glucose.  It is called aerobic metabolism; but when cells find themselves with less oxygen than they need, the cell is said to be hypoxic.

Hypoxia therefore means- reduced (low) oxygen.  Ischaemia is slightly different, and implies causation.  Ischaemia of tissue is Hypoxia but caused through a narrowing (constricted or spasming) blood vessel leading to said tissue, or a physical blockage in that vessel (clot/thrombus, air/fat/amnionic fluid bubble)   Perfusion means blood flow.

So pulling this together, tissue hypoxia, is also called tissue ischaemia but only when the problem is due to poor perfusion.

Enter another important cause of hypoxia; that is, lack of oxygen being carried in the blood.  This is called Hypoxaemia. It can occur for two main reasons, but when blood oxygen concentrations are low, hypoxaemia, then delivery of oxygen to cells is impaired causing hypoxia.

Technically hypoxaemia is oxygen pressures in arterial blood below 80mmHg breathing air, OR, oxygen saturations less than 94%.

Causes 

Diffusion v anaemia v noxious atmosphere.

Respiratory diseases may reduce the ability of oxygen to diffuse into blood when there is fluid, inflammation or thickening(fibrosis) to the lungs, or if air flow is impeded.  Blood oxygen levels may also be low if the blood has less than the adequate numbers of Red Blood cells (bleeding) or less haemoglobin than optimum (anaemia).

Finally, where a person is not breathing in adequate oxygen, or where there exists poisonous gases (carbon monoxide, cyanide, smoke, my brother after cabbage). In these situations, oxygen in our air may be in such low quantity (norm 21%), or unable to bind and be carried in blood, then hypoxaemia is diagnosed. 

The take home here is Hypoxaemic blood always causes hypoxia, but hypoxia doesn't always mean that blood is hypoxaemic.

The classic example of this is seen in ischaemia like Strokes and MI (heart attacks).  Blood oxygen levels are fine, but cells are hypoxic.

Phew!! Big topic.

It's more interesting with pics, diagrams, and my white board images, so why not jump to our page and look at one of our Acute Deteriorating Patient seminars coming up, or our newest course. Basic Nursing Assessment skills (Resp/cardiac/neuro) in December. Last seminar for the year.

Www.ect4health.com.au/courses

#KYJ-Janeway Lesions

#KYJ-  Janeway Lesions

Many nurses I talk to agree that their assessment skills are up to scratch. Where do yours sit? Personally I know I never stop learning. I am preparing for another clinical sabbatical into the remote world of outer island nursing in the Torres.  Even with the local knowledge, and confidence of 25 years of emergency nursing under my belt, I'm a bit nervous. I was preparing for our newest course (Nursing assessment skills- booking for Toowoomba on 8 December).  In this I cover respiratory and cardiac assessment including lung and heart sounds. One of the exciting new sessions is a comprehensive physical cardiac assessment.

It starts looking at the hands and fingers of the patient.

One interesting assessment is to look for Janeway Lesions and Splinter nail haemorrhages.

Janeway lesions are Janeway lesions are painless reddened nodular lesions on the palm of hands and sometimes the soles of feet.  They are only 2-5 millimeters in diameter but may indicate an of infective endocarditis where the inside lining (think wallpaper) of the heart's ventricles are infected with a microbe. A common bacteria in indigenous Australians is the common Streptococcus (same one that causes school sores and Strep throat).  This classically inflames and damages the endocardium and attacks the valves leading to pump failure.

Interesting to note that looking at someone's hands can give nurses and paramedics a windo into a potential life threatening heart condition. 

If you found this interesting (like I do) and you want to tune up your assessment skills, then seriously look at this fantastic seminar we have running for nurses, paramedics and students in both disciplines.  Make that trek to Toowoomba and check me out.  You'll love this gig.

Webpage and enrolment

http://www.ect4health.com.au/nursing-assessment/

More info -- admin@ect4health.com.au

KYJ- Antihistamines

#KYJ- Antihistamine drugs

In #KnowingYourJargon we explore common terms to improve nurses confidence,

Today I look at Antihistamine drugs.

We have had antihistamine drugs now for 4 generations. So common are these drugs that most in this category are sold over the counter in pharmacies, and even in some supermarkets.

You know them as Zantac, phenergan, Zyrtec, Loratadine, painstop nighttime, polaramine and Allergeze to name just a few.

To understand these drugs we need to understand a few terms.

Histamine is a protein secreted by specialised white blood cells called Mast cells and Basophils when stimulated.  They are mostly associated with an allergic trigger.  Histamine attaches to 4 receptors in different tissues in the body, stimulating and chemically instructing target tissues to behave or respond in certain ways.  Histamine 1 (H1) receptors are found in the CNS causing pain and drowsiness. They are also found in smooth muscles of the bronchioles of lungs, and vascular smooth muscle. Here they exert classic allergy symptoms like vasodilation and bronchoconstriction in lungs (Asthma).

As vessels in local tissues dilate, capillaries become engorged and leak into interstitial spaces.  This swelling is called oedema, and can be life threatening as seen in the swollen airway and lips of someone with angioneurotic oedema.  It can be minor and simply manifest in skin as hives (urticaria).

H2 receptors in the gut lining are stimulated to secrete digestive juices and hydrochloric acid in the stomach.  Ranitidine (Zantac) is an example of an antihistamine that selectively blocks these H2 receptors.

H3 receptors in the nervous system respond by producing neurotransmitters like acetylcholine and dopamine

H4 receptors on while blood cells and other immune organs are stimulated into action by histamine which causes chemotaxis ( cell attraction ).

So now that stuff is out of the way and we know what histamine does, it stands to reason that antihistamine drugs selectively block one or more of the four Histamine receptors.  The vast majority of antihistamines we use are for allergic symptoms of itchiness, hives, rash, and swelling.  These are certainly H1 blockers, but the use of H2 blockers has been well established for gastritis and ulcer symptom relief. 

In the 70s and 80s, allergy targeting antihistamines were indiscriminate, and having strong CNS effects, drugs like Promethazine (Phenergan, and dexchlorphenaramine (Polaramine) were common antihistamine choices.  These lost out in popularity to the newer drugs like Loratidine (Clarytine), and Zyrtec, because the new generation Antihistamines can't cross the blood brain barrier (BBB) so don't cause drowsiness.

That said, few nurses or parents would contest the inherent value of Promethazine as an added "angel" in the PainStop preparation, or as a nightcap during the allergy season's restless night routine.

Years ago the antihistamine was a very common treatment option for Asthma flare ups, but modern evidence has given us faster acting smooth muscle relaxants like the SABA Salbutamol.  Notwithstanding, there may still be an adjunctive role for antihistamines in asthma management plans, particularly for well known seasonal allergic asthma. 

Share this post, comment, dot or ask questions, our KYJs are your bite size #meducation and my contribution to #FOANed

My respiratory and Acute deterioration seminars delve into this meaty stuff in more depth. 

Would you like to book one of our ECT4health one or two day seminars in your neck of the woods?  Just grab 10 colleagues and we will be there. Email us for more details admin@ect4health.com.au or www.ECT4health.com.au

LDLs, HDLs and Cholesterol

#KYJ- LDLs and HDLs and Cholesterol.

Cholesterol is fat (lipid) that your liver makes at a genetically predetermined rate. Your cholesterol level is what it is mostly because of your genes, and marginally influenced by diet. In fact nothing you eat raises it, but some foods can lower it.

Being fat, it can't be transported in blood (water), so special proteins are made to carry it in plasma. These proteins or lipoproteins package the cholesterol. Depending on their molecular weight, they are called Very Low & Low Density Lipoproteins(LDLs), to High Density Lipoproteins (HDLs).

HDLs transport cholesterol deposits from your artery walls back to the liver for reprocessing, they therefore shrink fatty plaques called Atheromas inside arteries. 

How do Atheromas grow?  That is where LDLs come in. LDLs or "bad cholesterol" are responsible for laying down fatty (cholesterol) deposits inside arteries. 

So sugar in your diet enhances the formation of LDLs

And good fat in the diet (fish oils, nuts, fruit oils, eggs) enhances production of HDLs. 

Recently it has been discovered that a diet rich in polyunsaturated fats (canola oil, sunflower oil, and other seed oils) actually contributes to the very vessel injuries that sugar is also implicated in, stimulating more LDLs and thus Atheromas and its vessel hardening atherosclerosis.