Breath sounds part 1- crackles

#KYJ- knowing your jargon
Breath sounds, part 1.

Rattles, rales, crackles n creeps, Wheezes, and Rhonchi.

When I teach nurses about breath sounds, I always ask who does them, and who does them confident in the knowledge that they can name them.  In an average class of 25 nurses, 5-7 put up their hand indicating they auscultate chests, but only 1-2 of these (about 5-8% of all nurses) attending my nursing assessment classes, or respiratory nursing classes, agree they can identify different breath sounds.

Here is my simplified version of the terminology (our biggest hurdle).

Pitch (highs and lows)
Let's start with a beautiful pipe organ in a cathedral.  You know the ones I mean, huge gilded pipes arranged artistically around a dual layered keyboard and foot pedal system.  When a low note is struck, deep, chocolate vibrating sound emanates from the largest pipes.  When a high note is played, the tone bursts from the smallest pipes.

Lungs are similar.  As air rushes through them, the pipes (bronchi and bronchioles) vibrate producing noise audible with the diaphragm (flat surface) of the stethoscope.  Large airways towards the centre of the chest produce low pitch deep notes, and fine tubes on the outer periphery of the lung fields produce a higher pitch sound.... It's just like the pipe organ.

The first concept is this one of pitch. Low pitched sounds over the middle of a chest, high sounds in the outer reaches of the respiratory tree.

Next to master is the two major categories of abnormal sounds produced by diseased lungs.  Abnormal lung sounds are often called "Adventitious sounds".  They are lumped into two types.

Wet and squeezed.

1.  Wet sounds (crackles)
Wet sounds are produced as air moves through pipes filled with water and thin mucus. Typically heard in pulmonary oedema, wet sounds resemble that bubbly noise you made as a kid, sucking the last dregs of a milkshake through a straw.  Don't lie, I know you did.

Wet sounds are collectively called crackles, and depending on where in the lungs they are, they will produce a different pitch.

In smaller peripheral airways, the sounds are high pitched, so these crackles are called creps or fine crackles. Typical in pulmonary oedema, pneumonia, and chest infections.

In larger bronchioles and bronchi, the sound is lower pitch.  Still wet bubbling sounds, but lower in tone.  These crackles are commonly called Rales, or simply coarse crackles.  Typical of bronchitis.

If the wet sound is audible with no stethoscope, the gurgling sounds like comes from the back of the throat, it is fluid in the main bronchi, or trachea.  These sounds are called Rattles.  The gurgling death rattle common in an frail dying patient is a classic example.

Next episode we look at squeezy wheezes.
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#KYJ - Wound care series- Hydrogel dressings

Hydrocolloids. 

These dressings have been around for 30 years.  They are generally a thin film that has a thick rubbery adhesive which , when contacting a moist wound, creates a gel against the wound surface.

Some hydrocolloids  contain an alginate (seaweed base) to help with wound exudate absorption. Different hydrocolloids dressings come with many shapes for "difficult to attach" areas, and different thicknesses so the nurse can tailor the dressing to the amount of exudate.  The hydrocolloids dressings often stick to the wound's healthy skin margin with a water resistant film type adhesive.  

So how do they work?

Being water occlusive,  they provide a moist healing environment and heat insulation.  In episode one we discussed the need for a moist and warm wound bed.

These dressings also encourage a process called autolytic debridement.  This is where the gel from the hydrocolloids attract moisture from the wound like a sponge, and in doing so, promote the release of protein and debris dissolving enzymes from tissues.  These dressings clean the wound, not just cover it.

Pros

• Water resistant keeps bugs out.
• non stick to the moist painful wound surface, so gentle when being removed.

• Easy peel and stick application that can be used under compression stockings or lymphoedema bandages.

• Can and should stay on for days.  Many products report 3-7 days with the familiar mantra "leave it a week or till there's a leak"

Cons

• Never on infected wounds, and they are not great on heavily exuding wounds.  Venous ulcers and some diabetic ulcers are notoriously oozy.

• extreme caution on diabetic feet!!  Only safe if the wound is superficial with no signs of infection, there is low to moderate exudate, there are no signs or symptoms of ischemia, and dressings are changed frequently.  This last point negates the value of a dressing that is designed to stay on for days. 

Diabetic wounds crash in hours when they crash, and you want to be there when that starts.  You don't want to pull off a dressing to find 2 weeks of healing undone overnight!

• unlike film dressings which are clear and transparent, hydrocolloids are opaque.  So you can't watch the wound.
• notorious for dislodgement if wound is too wet, and they curl or roll at the edges, potentially trapping bacteria.
• some patients (and nurses) complain that they are a bit on the nose.
• can cause wet maceration to healthy skin (all those trapped enzymes in the Slough )
• May cause trauma/injury to fragile skin upon removal... That prednisone abused nana skin is so paper thin!
• hypergranulation can be a problem leading to scaring

When to use

A hydrocolloid dressing is appropriate for these situations:
• necrotic or hard capped eschar covered wounds (lifts the dry nastiness)
• dry wounds
• partial- or full-thickness wound
• protection of intact skin ( but watch for maceration ) or a newly healed wound.

Frequency of dressing changes

• depending on the product specifications, dressings should be changed every 3 to 7 days.  This of course depends also on exudate.

How to apply a hydrocolloid dressing .

Gloves on and remove the soiled dressing (noting the date it was applied) - contaminated bin is wise, irrespective of colonisation.
Deglove, hand wash, reglove
Clean the wound with warm normal saline or warm tap water.
There is no evidence that chlorhexidine or other antiseptics are safe, or necessary or helpful.
Use gauze to pat dry the foot edges of the wound margin where the adhesive should stick.
Apply liquid barrier film or moisture barrier to the periwound area.
For deep wounds, apply wound filler or packing materials as indicated/ordered ( a whole other post).

Warm it by holding it between your hands to increase molding and adhesive ability.
Remove the paper backing from the dressing.
Bend the dressing (sticky side out) and apply it from the center of the wound, smoothing it outwardly like putting contact on the kids books.
Hold the dressing in place for a few seconds, warming it with your hands to improve molding and adhesion.
The dressing should be at least 2cm larger than the wound. 

Our next instalment will take a look at hydrogels.

Check out our Webpage for education opportunities.

Www.ect4health.com.au

#KYJ - Wound care series- Hydrocolloids dressings

Hydrocolloids. 

These dressings have been around for 30 years.  They are generally a thin film that has a thick rubbery adhesive which , when contacting a moist wound, creates a gel against the wound surface.

Some hydrocolloids  contain an alginate (seaweed base) to help with wound exudate absorption. Different hydrocolloids dressings come with many shapes for "difficult to attach" areas, and different thicknesses so the nurse can tailor the dressing to the amount of exudate.  The hydrocolloids dressings often stick to the wound's healthy skin margin with a water resistant film type adhesive.  

So how do they work?

Being water occlusive,  they provide a moist healing environment and heat insulation.  In episode one we discussed the need for a moist and warm wound bed.

These dressings also encourage a process called autolytic debridement.  This is where the gel from the hydrocolloids attract moisture from the wound like a sponge, and in doing so, promote the release of protein and debris dissolving enzymes from tissues.  These dressings clean the wound, not just cover it.

Pros

• Water resistant keeps bugs out.
• non stick to the moist painful wound surface, so gentle when being removed.

• Easy peel and stick application that can be used under compression stockings or lymphoedema bandages.

• Can and should stay on for days.  Many products report 3-7 days with the familiar mantra "leave it a week or till there's a leak"

Cons

• Never on infected wounds, and they are not great on heavily exuding wounds.  Venous ulcers and some diabetic ulcers are notoriously oozy.

• extreme caution on diabetic feet!!  Only safe if the wound is superficial with no signs of infection, there is low to moderate exudate, there are no signs or symptoms of ischemia, and dressings are changed frequently.  This last point negates the value of a dressing that is designed to stay on for days. 

Diabetic wounds crash in hours when they crash, and you want to be there when that starts.  You don't want to pull off a dressing to find 2 weeks of healing undone overnight!

• unlike film dressings which are clear and transparent, hydrocolloids are opaque.  So you can't watch the wound.
• notorious for dislodgement if wound is too wet, and they curl or roll at the edges, potentially trapping bacteria.
• some patients (and nurses) complain that they are a bit on the nose.
• can cause wet maceration to healthy skin (all those trapped enzymes in the Slough )
• May cause trauma/injury to fragile skin upon removal... That prednisone abused nana skin is so paper thin!
• hypergranulation can be a problem leading to scaring

When to use

A hydrocolloid dressing is appropriate for these situations:
• necrotic or hard capped eschar covered wounds (lifts the dry nastiness)
• dry wounds
• partial- or full-thickness wound
• protection of intact skin ( but watch for maceration ) or a newly healed wound.

Frequency of dressing changes

• depending on the product specifications, dressings should be changed every 3 to 7 days.  This of course depends also on exudate.

How to apply a hydrocolloid dressing .

Gloves on and remove the soiled dressing (noting the date it was applied) - contaminated bin is wise, irrespective of colonisation.
Deglove, hand wash, reglove
Clean the wound with warm normal saline or warm tap water.
There is no evidence that chlorhexidine or other antiseptics are safe, or necessary or helpful.
Use gauze to pat dry the foot edges of the wound margin where the adhesive should stick.
Apply liquid barrier film or moisture barrier to the periwound area.
For deep wounds, apply wound filler or packing materials as indicated/ordered ( a whole other post).

Warm it by holding it between your hands to increase molding and adhesive ability.
Remove the paper backing from the dressing.
Bend the dressing (sticky side out) and apply it from the center of the wound, smoothing it outwardly like putting contact on the kids books.
Hold the dressing in place for a few seconds, warming it with your hands to improve molding and adhesion.
The dressing should be at least 2cm larger than the wound. 

Our next instalment will take a look at hydrogels.

For ECT4Health information and courses
Www.ect4health.com.au

#KYJ -Wound healing Series. Part 1

What do I put on that wound?

Part 1

In this knowing your Jargon #KYJ series we look at the options for wound dressings.

Everywhere I nurse, treatment rooms and clinics have a poster helping nurses recognise different stages of wound healing and usually offering a suggestion of what dressing to use.  It's a confusing choice and often we come on shift to see that another nurse has changed to a different product.

So in this mini-series, we look at the different styles of dressing, and when they are indicated.

To get the ball rolling we must understand that wounds need 5 important things to heal.

*oxygen delivery

*nutrition (nutrients)

*moist wound bed

*warmth

*absence of infection

Oxygen / Nutrient

Oxygen and nutrients for cell growth need to be delivered to the wound systemically via the vascular network.  Arteries and arterioles deliver to the micro fine capillary beds to diffuse in to the wound.  This supports the proliferation of new tissue growth, and feeds hungry immune cells acting watch over the construction zone, preventing bacteria from colonising and initiating infection.  In diabetics and other people with poor vascular flow, there exists a chronic reduction in tissue oxygen delivery.  If the wound bed oxygen concentration should drop below an oxygen tension of 40mmHg, then wound stop healing.  They become indolent and dormant.

For oxygen to get into a wound, blood needs to be adequately drained from the wound.  In patients with heart failure (especially right heart), there is often venous engorgement/congestion.  This venous congestion (particularly in lower limbs) usually decreases the ability of blood the cycle through the wound.  Venous blood is notoriously hypoxic (without oxygen), so venous congested wounds will swell, hold and produce lots of exudate, and healing grinds to a halt.  These patients need compression bandaging or stockings to promote venous return. We have to get the oxygen right.

Moist wound bed.

Within 24-48 hours of tissue injury, fibroblast cells commence work to create a protein base to the wound bed.  It is called collagen and you could think of it as the frame or foundation of a deck verandah.  On top of the frame work, eventually the decking timber will be attached.  In wounds this construction is called granulation.

Granulation needs to take place in a moist/warm environment.  Ultimately the skin cells that form the decking need to slide (migrate) across the collagen frame to complete the surface of the wound bed (epithelialisation).  The process can take weeks, but in small wounds with close edges, the seal in just 48 hours.  The wound bed needs to be slippery.  This is where moisture comes into play. 

As nurses we need to choose a cover that maintains wound warmth (>30 deg), and traps moisture to maintain the slippery environment fibroblasts (builders) need.

Too wet and the healthy tissues in the wound swell and cease to function. Too dry and the migration, and epithelialisation can't happen.

In our next part of the series, we will look at the dressings that do this task.

Absence of infection

If a wound is colonised by pathogenic (disease causing) bacteria, it won't start repairing.  In infections, the immune system is activated to search and destroy bacteria, and using many signalling chemicals (cytokines) to aid communication between white blood cells (chemotaxis), the process of tissue repatriation ceases while active infection fighting occurs.  Infection is the enemy of wound healing.

When assessing wounds, especially chronic wounds like leg ulcers, and decubitus ulcers, get into the practice of taking a baseline bacterial culture swab.  If colonisation is present then the patient should be started on antibiotics for reduction in bacterial numbers.  A colonised wound is not an infected wound, but given moisture, time and warmth (all things a healing wound needs), that little bacterial colony becomes a rampant infection.  When wound bacteria do the dirty, they secrete toxins into the wound bed that destroys the fresh new growth, causes Vasoconstriction which reduces oxygen to the wound, and fills up the wound with excessive toxic exudate.

Wound cleaning

Warm water/saline irrigation under pressure of a 20ml syringe, and a blunt 18g needle is needed to irrigate /clean the wound.  An uninflected wound often needs very little cleaning if it is healing well (every 3-7 days).  But in infected wounds, healing is not our goal, cleaning is.  Refrain from swabbing with gauze.  This cleaning of the wound bed 1-2 times daily during active infection inhibits pus, exudate, and aids in reducing bacterial numbers.

Ok that is it for the first instalment.  A primer as it were.

Next episode we will look at the start of our wound dressing list starting with

Hydrogels, and gel based dressings.

For ECT4Health information and courses
Www.ect4health.com.au

Hypertensive Crisis

Hypertensive Crisis

This clinical presentation is characterised by an uncontrolled high blood pressure (BP) of systolic >180mmHg leads to progressive or impending end-organ dysfunction. 

The treatment focuses on  lowering BP aggressively over minutes to hours.

Neurologic end-organ damage due to uncontrolled BP may include hypertensive encephalopathy, cerebral vascular accident/cerebral infarction, cerebral haemorrhage.

Cardiovascular end-organ damage may include myocardial ischemia/infarction, acute left ventricular dysfunction, acute pulmonary edema, and/or aortic dissection. 

Renal injury, retinopathy and even Microangiopathic Haemoliyic Anaemia can also occur. 

For those being treated for essential hypertension, antihypertensives, have offered tremendous value.  The advent of crisis sits at about 1% of patients with hypertension.

Before 1950, hypertension leading to crisis demonstrated a Proor prognosis with 1-year survival rate at 20%.  Today with monitoring and a medicine cupboard full of innovative anti hypertensives, stats report  a survival rate of more than 90%.

The most common clinical presentations of hypertensive emergencies are stroke (24.5%) and pulmonary Oedema (22.5%), but CCF and cerebral encephalopathy are in high numbers.

In pregnant patients, acute hypertensive crisis usually results from severe pregnancy induced hypertension (preeclampsia).

In assessing the presentation of hypertensive crisis, the severity of the patient’s preexisting hypertension , and the duration of their HTN needs to be factored into treatment strategy.  A drug history of antihypertensives, patient compliance, use of over-the-counter (OTC) and recreational preparations such as caffeine, red bull, decongestants, Salbutamol, and , illicit drugs such as MDMA, methamphetamine and cocaine are all important, as these preps exacerbate hypertension.

The physical examination should assess whether end-organ dysfunction is present. BP should not only be measured in both the supine position and the standing position (assess volume depletion), but it should also be measured in both arms (a significant difference may suggest aortic dissection).

The presence of new retinal hemorrhages, exudates, or papilledema suggests a hypertensive emergency. Evaluate for the presence of heart failure, which may be indicated jugular venous distention, crackles on auscultation, and peripheral edema. Central nervous system (CNS) findings may include changes in the patient's level of consciousness and visual fields, and/or the presence of focal neurologic signs. Abdominal masses or bruits may be noted.

Renal impairment is a likely consequence of hypertensive crisis as increasing renal vessel pressure bombards the glomerulus with more molecules of protein, causing injury.  Blood testing UECs to assess renal function is common.  A dipstick urinalysis to detect haematuria or proteinuria and microscopic urinalysis to detect red blood cells (RBCs) is an intervention we should perform at the bedside.

A full blood cell (FBC)  obtained to exclude microangiopathic anemia, and pregnancy test, and endocrine testing may be obtained.

ECG is needed if only for a baseline, and if any headache, or CNS signs are apparent , a head CT scan is considered.

One presentation is malignant hypertension.

This hypertensive emergency, always has retinal papilloedema as well as flame-shaped haemorrhages. Often there is features of LVF manifesting as pulmonary oedema which masks the initial cause.

Treatment of hypertensive crisis involves reduction of BP.

You've probably noticed that many patients have big BPs and some we treat aggressively, whereas others we tend to no be so reactive. The reality is that only a small proportion of patients will require emergency treatment. As always an important point to remember in the management of the patient with any degree of BP elevation is to "treat the patient and not the number."

We aim to identify which patients with acute hypertension have symptoms of end-organ damage.  It is these that require immediate mitigation of their hypertension. Usually IV therapy is initiated with agents like sodium nitroprusside, glyceryl trinitrate or a short acting alpha and beta-blocker, or calcium channel blockers.

The aim is to increase vessel diameter to decrease vessel pressure. Reducing afterload is the target.

With patients presenting with acutely elevated BP (systolic BP [SBP] >200 mm Hg or diastolic BP [DBP] >120 mm Hg) without symptoms and whose BP stays significantly elevated should have initiation of medical therapy and close follow-up in the outpatient or GP setting.

So crisis management is really about symptoms. 

#KYJ - Hold breath while pulling CV lines

#kYJ -  Valsalva during removal of tubes

I was sent this question:

Rob can you please explain the rationale of holding breath for 10 seconds during removal of CVC!

I understand this action minimizes risk or air embolus .... But how?

...

You may know that this is a common instruction given to patients when we remove CV lines and chest tubes.  We do it to minimise the risk of air entering the thoracic cavity when pulling out the tubes.

Ok so here is the physics.

To understand the rationale you must understand 4 concepts. 

1 Atmospheric pressure 

2 intrathoracic pressure

3 intrapulmonary pressure

4 Pascale's principle

But First, a refresher on the pressures.

All pressure (air pressure, blood pressure, intracranial pressure etc) can be measured using different pressure units.

In medicine we use 

Centimetres of water(cmH2O) or millimetres of mercury (MmHg) also called "torr" but only nerds say Torr.  Eg blood pressure might be 120/80 MmHg.

Car tyres use pounds per square inch (PSI) or kilo pascals (KPa). Eg  a full tyre may be pumped up to 36 psi or 250kpa.

Atmosphere and weather reports use Bars or pascals.

1 bar = 1000 millibars=100000 pascals.

(100 KPa or 1000hectopascals)

Thus a millibar is also a hectopascal.

It's confusing and looks like a horrible highschool maths nightmare but just know that all units of pressure can be converted into each other.

1 Atmospheric pressure is the pressure of air that we breathe.  At sea level it is 760mmHg.  If you saw it on the evening weather forecast map they would say 1013 hPa.

This atmospheric pressure is all around us and fluctuates slightly.  A tropical low might be reported at 1004hPa and a cyclone reported as 890hPa.

1013 hPa converts into 760MmHg

I will use MmHg because we are speaking in the medical context.

Just know that seal level pressure is 760. 

2.  Intrathoracic pressure is the total pressure inside your thorax.  Predominantly influenced by the changing pressure in your lungs as you breathe. This brings us to intrapulmonary pressure.

3.  Intrapulmonary pressure is the pressure inside your lungs.  As you go to breathe in, your diaphragm contracts, drops, and creates a vacuum or negative pressure change inside you lungs.  The pressure in your lungs is less than atmosphere so considered to be a relative negative pressure when compared with the atmosphere.  The change is small, only 6-8 MmHg, but enough to allow the atmosphere to rush into your lungs to equalise pressure inside.  We call this breathing in, or negative pressure ventilation. 

On inspiration

Atmospheric pressure 760

Intrapulmonary pressure 752

A relative vacuum.

Now breathing out is the opposite. I must push air pressure inside my lungs to blow air out to the world.  Diaphragm relaxes, rises and puts the lungs under higher pressure than the world.

On expiration

Atmospheric pressure 760

Intrapulmonary pressure 765+

Air rushes out.

Stay with me we have nearly answered the question.

Inside the chest wall, the pressure emulates the fluctuation of the inside of the lungs.  Thus intrathoracic pressure rises on inspiration and falls on expiration. This close relationship is described by Pascal's principle which suggests that a pressure increase in one area of a confined space (thorax) is equally transmitted across the whole confined space. I know... Boring!!! 

Back to holding your breath.

Take a big breath in now and hold it. Hold it!  Hold it!

Feels full hey?  Ok breathe normally.  

When you held your big breath (valsalva manoeuvre) you held pulmonary (and thoracic pressure) at its highest point relative to the atmosphere.

Your thoracic pressure while breath holding was perhaps 770mmHg, and thus higher than the word. It would be impossible for air to enter your lungs or chest cavity through surgical holes, because the pressure inside you was higher than atmospheric pressure.

Asking the patient to hold their breath during tube removal then makes it impossible for air to invade the hole before you seal it with an opsite or other occlusive dressing.

The pressure inside was too high.

Now the consequence of air getting in through the CVC site is an air embolism.  A very small risk, and even if air did get in it enters the venous network and bubbles flow into the right atrium.  Bubbly blood is then pumped to the lungs, where most bubbles are filtered out. 

In the context of a chest drain tube; well they are sitting in the pleural cavity not a central vein.  The tiny bit of air that can get in while pulling out a tube is insignificant and reabsorbs in a hour or so... But safe practice implores you as a nurse to take steps to avoid this introduction of air into a chest when pulling out tubes, drains and CV lines.

Just get them to hold their breath.

Pressure 

Should we reduce fever?

Fever

So I found myself banging on about kids and fever again last week in a trauma course of all platforms.

The message is slowly getting the through, but where literature focuses on efficacy of paracetamol and ibuprofen, it conclusively agrees on two key points:

1.  that these drugs should be reserved for pain and discomfort .

2.  There is no evidence that they will prevent a febrile convulsion. 

In 2010 the RACGP (college of GPs ) in Australia released a paper redefining what a fever was. Previously a patient was considered to have a fever when there core temperature rose above 37.5 degrees of Celsius. Now it is 38.0.

This was also coupled with the notion that fever should not be treated until at least 39.0. 

A common ignorance in health care providers is that at the slightest hint of a fever, some over the counter antipyretic would be given. The medical world is calling for this nonsense to cease. But it is so hard to sell this message to "out of date" parents, doctors and nurses.

Here it is - as blunt as I can put it. Stop treating fever like it is a bad thing!!

Recognise that fever is the body's normal natural response to fighting an infection.

After invasion by a virus or bacteria, phagocytes coming into contact with pathogens release signalling chemicals called pyrogens which stimulate prostaglandin release. These prostaglandins alter the body thermostat in the hypothalamus. As long as phagocytes are active in killing pathogens, they will release these chemicals to keep the temperature high. It aids in proliferation of immunity compounds and cells to the site of invasion. Fever cures infection .

Now paracetamol, and ibuprofen acting as antipyretic medicines, inhibit these prostaglandins, thereby inhibiting the natural immune response. By reducing the fever, they can mask sinister symptoms and prolong an infection

Reserve these drugs for pain and discomfort associated with illness. They don't prevent febrile convulsions, and there is NO evidence that they improve the illness. 

Just Stop treating fever!!! Fever is your friend!

Share this with your parents, colleagues and anyone you know sucked in by advertising that tries to sell a message that "Brand N" or "Brand P" is for pain and fever. 

FEVER IS YOUR FRIEND!!

This 2011 article is just another paediatric journal that refreshes the notion that antipyretics are to be reserved for discomfort.

http://pediatrics.aappublications.org/content/pediatrics/127/3/580.full.pdf

For ECT4Health information and courses
Www.ect4health.com.au