Plethysmography. That word! Quite possibly the hardest word to pronounce in the English language. Right up there with “thistle” and “chrysanthemum.” One of those dreadful words with legitimate “th’s” in them that thound like mithtakes and remind me that I therioulthy thuffered in thixth grade from a lithp.

Thuper. Theven years of thpeech therapy dithmantled in a thingle paragraph.

But beyond the manner in which it forces me to emotionally decompensate into a bullied preteen, plethysmography is like physics magic! And I’ve discovered that even those who use it daily as part of their PFTs often don’t really understand how mathematically awesome it is underneath.

From here on in I will refer to plethysmography as simply ‘pleth’ because it is just as annoying to type as it is to pronounce.

Pleth measures changes in volume. In respiratory therapy, we use it to calculate the FRC, Functional Residual Capacity, of the lungs. But it can also be used to calculate blood volume changes in the limbs, cerebral blood flow, and a more recent study, an exercise in “duh”, used penile pleth to measure changes in blood volume in the penis showing that, duh, the more homophobic men are, the more aroused they are by gay porn.

But that’s another story. Never mind. Anyway…. <–Sondheim Quote. Felt appropriate here.

To obtain lung volumes, we put the patient in a sealed box of a known volume that has a pressure transducer in it to measure changes in pressure. The patient is connected to an outside air source and another pressure transducer is placed at the opening of the mouth.

And if you believe in the physics – AND YOU SHOULD! – knowing the starting volume and the pressures of the box and the mouth opening gives you enough information to calculate the lung volume at end tidal expiration (not forced expiration), aka the FRC.

Our story begins with the Ideal Gas Law. It’s good to have ideals. And laws. Gas… not so much.

This law is expressed by the equation:  PV = nrT ,  where P,V and T are Pressure, Volume and Temperature respectively.

n = number of moles of gas. Neither a rodent nor a spy, a mole in chemistry is 6.02×10^23 p/mol.
r = Boltzmann constant = 1.38066×10^23 J/K

Both of these constants have rich, interesting science and history behind them but all you really need to know is that, in a closed system, they are both constant. And hey, if they are always constant why not just combine them into one and call it “k” for “constant” because “constant” starts with…. k? It must be a foreign language thing. I blame the Germans. But just roll with it. K? (It actually has to do with the standard conventions of proportionality mathematics.)

We’re left with: PV = kT

Well to make things even simpler, in our little body box closed system, T also is a constant. Or it becomes constant after a minute or so when the body heat of the person and the ambient temp in the box reaches an equilibrium. Until that happens you just make the patient sit there, trapped, on the edge of claustrophobic panic.

So with T constant, we can roll it right into k and reduce the equation to:

PV = k.

Pressure and Volume are inversely proportional. Meaning that as the pressure rises, the volume falls. And vice versa, if the volume rises, the pressure falls. It’s a simple, linear relationship. This was observed by scientist Robert Boyle’s in 1662 when he published his findings and labeled it ‘Boyle’s law’, stating that the volume of an ideal gas is inversely proportional to its absolute pressure at a constant temperature. They call these factoids of physics “laws” but they are more like “absolute truths”. You can break a law. You can’t break *this*.

So in a system where there is a change in volume

P1*V1 = P2*V2 <– This is everything. Know it. Live it. Love it. Become one with it.

Now back to our box:

The patient is asked to breathe normally from the mouthpiece for a while (because being trapped in a box breathing through a tube makes that so easy) until the end tidal baseline becomes steady and consistent. Just when they get comfortable, on exhale, you occlude the mouth piece. It’s probably best to warn them that this is going to happen to avoid unnecessary flailing and eye bulging.

When the patient tries to breathe against the occluded mouthpiece their thoracic cage expands and contracts and the pressure being measured at the oral opening rises and falls in proportion.

Also, the volume of the box falls and rises and its pressure also varies accordingly.

Here’s where it get’s fun! Or even *more* fun. Cuz, I’m already there.

Starting with the pressure and volume of the box during the occlusion maneuver: We know the initial Pressure – P1. We know the initial Volume – V1. And we measure the pressure after the thoracic volume change on an attempted inhale – P2.

And since P1*V1 = P2*V2, this allows us to solve for V2.

V2 – V1 = the change in volume of the box. Which is – TA DA!!! – the change in volume of the thoracic cage on attempted inhale.

Now to the patient! Like the box, we know the pressure before inhale – P1, and the pressure after inhale – P2. And we now know the change in the Volume of the lung – dV (d is for Delta. Normally a triangle but I don’t know how to make that character on here).

So to solve for the volume of the lung at baseline tidal exhale, or FRC, (V1), we are left with this simple equation.

P1 * V1 = P2 * (V1 + dV)

Now just plug in the known values and, voila, you have the V1, or the FRC of the lungs. With the FRC, you can now extrapolate total lung volume, a critical measure to help diagnose pulmonary diseases!

Wasn’t that fun? I thought it was fun. Fun, fun, fun. Plethysmography is fun!

Now I have to call my speech therapist.



First Pretty, Then Fat

Despite the rather suspect title, and although my mirror is a daily reminder of the horrors of gravity and my ever-shortening telemeres, this isn’t a post about body shaming and the steady decline of beauty. Yes I may have gone from “Baby got Back!” to “Baby got Back Pain!” over the past few decades, but when it comes to my body, I have no choice but to dwell *in* it so I try not to dwell *on* it.

“First pretty, then fat” is a process I created for examining chest x-rays. I PRIMP and then I BLIMP. These two acronyms are, respectively, for assessing the quality of an x-ray and then studying the x-ray for anomalies.


PRIMP –  for assessing quality
Position – AP, PA. Lateral, Lordotic, Decubitus
Rotation – my favorite sentence “The spinous processes of the thoracic vertebrae should be equidistant from the medial ends of the clavicles.”
Inspiration –  The 5th to 7th anterior ribs should intersect with the diaphragm on the mid-clavicular line.
Margins – Can you see the entire lung field from the costaphrenic angles up to the apices of the lungs.
Penetration – The vertebrae should be just visible behind the heart


BLIMP – Just a mnemonic to remember the major areas to cover
ssues with tissues – It’s about the tissues. I needed a damn “I” to make it rhyme. 

One of my clinical rotation shifts I was asked to set up a vent for an incoming patient I knew nothing about so I asked for the details.

“Male, 6’1″, approximately 40, found down for an unknown time, requires lots of suctioning of thick purulent secretions… and oh… the xray they took for ET tube placement showed situs inversus!”

I was excited. I had never seen situs inversus before and I had read about its connection to primary ciliary dyskinesis recently. Again, read too much about zebras – one starts to see zebras.

“Thick purulent secretions? Situs inversus? Was it just dextrocardia or full situs inversus? Was the gastric bubble on the right? was the left hemidiaphragm raised to compensate for the liver? Is there a history of Kartagener syndrome – primary ciliary dyskinesis?”

I annoy people with questions. All of this was unknown. No history. She hadn’t personally seen the x-ray.

So we pulled it up. The computers were slow so I literally had time to primp before it was time to PRIMP. But there it was.

“Position: Portable AP. Rotation… No,” I said, “That is not situs inversus. The gastric bubble is appropriately on the left. And the heart looks odd because the patient is rotated about 30 degrees to the right on the saggital axis.”

“How can you tell?”

Here it was! My big moment. The one I had been rehearsing for! My chance to use my favorite sentence!

“The spinous vertebrae of the equidistant clavicles should be medial to the thoracic… GODDAMMIT!!”

My big moment. And I blew it.

“You mean the spinous processes of the thoracic vertebrae should be equidistant from the medial ends of the clavicles?”, said my understudy Shirley MacLaine, who laughed at my Carol Haney broken ankle and went on to win the Tony for The Pajama Game.

“Who is Carol Haney” you ask?




Mechanical Ventilation – The Basics!

Mechanical ventilation can be a daunting subject for people to tackle. The sheer volume of information about the subject can put a lot of pressure on a student.

See what I did there? Volume? Pressure? I am _that_ good.

But getting a basic grip on mechanical ventilation can be troubling. That’s trouble and that starts with “T” and that rhymes with “P” and that stands for Proprietary naming conventions.

While all ventilators do basically the same things and have the same set of features, there is no agreed upon industry naming conventions or taxonomies that have been standardized for simplification. Instead, the opposite has happened. Vendors, driven by sales quotas and stockholder greed, fancify their vents with special modal aliases so now we are far more likely to push the wrong button and make our patients explode.


We are left with this unnecessary translative layer of abstraction between the basics of mechanical ventilation and the novelty nomenclatures on the knobs causing pneumos.

So to start, ignore the vents themselves and learn the basic modes and functions of mechanical ventilation as a science rather than as a specific machine. Then, once comfortable with that, you can translate that to apply it to a variety of machines later.

Starting with a sedated, paralyzed patient who has no spontaneous breathing we generally have two choices: Volume control or Pressure Control.

Control Issues

‘Control’ comes in two forms: Controlled Mechanical Ventilation (CMV) and Assist-Control Ventilation (ACV). ACV allows patients assisted spontaneous breaths. CMV does not. The only cases I have seen where CMV was used were in high spine injuries where the phrenic nerve had been severed and there was no chance of spontaneous breath, and in late-stage neuromuscular diseases such as ALS or Muscular Dystrophy. In other cases ACV is commonly used, giving the patient a soupçon of respiratory autonomy should they wake from their sedation/paralysis.

In both pressure and volume control ventilation, assisted or not, you set an FiO2 (fraction of inspired oxygen), anywhere from room air (21%) to pure oxygen (100%) depending on the patients needs. You also set the Positive End  Expiratory Pressure (PEEP). This back pressure sets the delta between the alveolar pressure and atmospheric pressure and it helps prevent alveolar collapse, aka atelectasis, at the end of expiration. Generally, all mechanically ventilated patients start at 5 cm H2O. However, setting ‘optimal’ PEEP, the PEEP at which there is best oxygenation without any cardiovascular impediment, is a whole field of study in and of itself. I’ll write about that in later posts. Lastly, you set the breaths per minute (frequency), which again, depending on the patient and disease state, usually starts at anywhere from 10-16 breaths per minute.

Then, for volume control, you set the tidal volume: the volume of air per breath. Usually somewhere around 6-8 ml per kg of ideal body weight landing somewhere between 400-600 ml per breath. then, we titrate the volume down if the pressures are too high.

For pressure control, you set the peak pressure in cm of H2O, usually starting in a safe range, around 20 cm H2O and titrating from there to achieve a desired volume. Obviously the more pressure, the more volume.

So essentially ventilating with these two different control variables achieves the same result but in volume control we have to titrate to manage the pressures and in pressure control we titrate to manage the volumes.


The I:E ration in mechanical ventilation is the ration between the inspiratory and expiratory times. If you have a frequency set to 15 breaths per minute, then you have 4 seconds per breathing cycle. The percent of that cycle that is inspiratory and the percent that is expiratory is up to the technician. In general, again as always depending on the patient and disease state, we start with a 1:2 ratio. That means, with a 4 second total cycle, 1.33 seconds of inspiration and 2.67 seconds of expiration.

In volume control, on most ventilators, you also choose the I:E ratio directly. The shorter the inspiratory time, the higher the flow will be to achieve the set volume.

In pressure control you adjust the flow rate. The higher the flow, the faster the cycle pressure is reached, the shorter the inspiratory time. So here, flow is what determines the I:E ratio and this must be managed indirectly.

But Wait… There’s More

There’s always more. For patients who are spontaneously breathing there is Synchronized Intermittent MandatoryVentilation (SIMV) or Pressure Support (PS). Different vendors have different forms of ventilation that are closed loop dual-control and adjust the volume and frequency based on the pressures to achieve a constant minute ventilation. For the Hamilton G5 this is called Adaptive Support Ventilation (ASV) and Drager basically the same thing but with a different name because, I dunno, some CEO read Ayn Rand as a teenager and decided empathy was a character flaw.

Mechanical ventilation is a gigantic topic and it’s application varies from patient to patient and disease state to disease state. But to get started, you must understand the basics of pressure and volume controlled ventilation. Hope this helped.





DIC and DOC: Is not blood the wine of life?

Being an oenophile, at one point in my life I wanted to be a sommelier, so I set myself on a path of self study of wines..

I rampaged through Rieslings
Barreled through Bordeaux,
Rootled through Riojas
And muddled through Merlot

When I first wrote that it was a sentence. But due to the scan and rhyme I decided they were lyrics.

Now that I live in Oregon, my studies continue as I partake in pilgrimages to the pastoral periphery of Portland where I pleasure my palate with a potpourri of provocative, peppery, piquant and poignant Pinots.

That sentence was brought to you by the letter P.

Previous to Portland, don’t worry those two ‘p’s were coincidental, the country whose wine’s really resonated with my palate was Italy. Perhaps because I am, ancestrally, Italian, but more than likely because they just taste so damn good. Italian wines have their quality regulated by the DOC, Denominazione di Origine Controllata.

Being an iatrophile*, at one point in my life I wanted to be a doctor, so I set myself on a path of self study of diseases.

I rampaged through Rabies
Barreled through Bronchitis,
Rootled through Rubella
And muddled through Metritis

Oops I did it again. Lyrics. Special props for connecting Barreled to Bronchitis. ‘Barrel’ works with both wine and obstructive lung diseases. I think I have a musical in the works here…

Now that  live in Oregon, my studies continue as I read, review, and reflect on the rambling range of ruthless and rampant respiratory riddles.

Note to self: Long form alliteration is much harder with ‘R’ than it is with ‘P’.

One of the rabbit holes I went down during my studies was identifying different forms of coagulopathy: Idiopathic Thromocytopenic Purpura (ITP), Thrombotic Thrombocytopenic Purpura (TTP), Hemolytic Uremic Syndrome (HUS), and notably Disseminated Intravascular Coagulopathy (DIC) which can be secondary to both liver failure and sepsis.

During my clinical rotations, while assisting a doctor putting in a central line in a patient with a multitude of comorbities including CHF, liver failure, renal failure and an acute infection that had led to sepsis, I noted purpura around the blood pressure cuff on the patient and the incision made for the line began to bleed more profusely than expected.

I exclaimed proudly, “Disseminated Intravascular Coagulopathy! DOC!”

“D *O* C”? questioned the Doc.

“Is not blood the wine of life?” I deflected pseudo-philosophically confusing everyone in the room including myself. “I’m pretty sure that’s from MacBeth” I explained.

They seemed satisfied with that justification. I’ve found you can resolve any tangent with a Shakespearean quote and people will nod like you’re smart.

*Iatrophile – A neologism I invented using Greek roots for “person who loves medicine”


I suggest reading this brilliant article from the NEJM by Dr. Beverly J. Hunt:

Bleeding and Coagulopathies in Critical Care

This publication is a great primer in the differentiation and management of the most common coagulopathies one might come across in the ICU.

Also I just searched MacBeth for the quote “Is not blood the wine of life?”.

Nope. I totally made it up.


That’s so Hawt!

In a random medical discussion with a surgeon friend over a bottle of Oregon Pinot as we Portlandiputians are wont to do, she brought up a condition she had come across in surgery that piqued my interest.

Malignant Hyperthermia.

Despite never having heard of it (being relatively new to this field this happens a lot) it has it’s own association! – The Malignant Hyperthermia Association of the United States.

We’ll just ignore that this is an American institution and yet the acronym they chose, “haus”, is German. I’m certain to lose sleep over that inconsistency later, but for now let’s just merrily roll along. Yesterday is done… see the pretty country side. <–You might find I quote Sondheim a lot. I encourage you to do your research in that specific field as I do mine in this one. 🙂

So… Malignant Hyperthermia, ‘MH’ from here on in because typing, is a medical crisis that is triggered by commonly used surgical anesthetics and the particular neuromuscular blocking paralytic succinylcholine. An MH crisis comes with the rapid onset of increased metabolism, muscle rigidity, tachypnea, and body temperatures that may exceed 110F.

Yes you read that right: 110F. Or 43.3C if you’re German and live in a ‘haus’. I will never let that go.

This condition is obviously, extremely deadly.

It’s also genetic and passed through a dominant gene meaning the children of an MH patient are 50% likely to also have it.

Physiologically, this gene mutation results in an abnormal protein in the muscle cells that, when exposed to certain agents, commonly anesthetics for surgery, causes a rapid deploy of calcium from the sarcoplastic reticulum, triggering hypermetabolism that depletes the muscles of their ATP leading to muscle death leading to a a potassium storm (hyperkalemia) which causes arrhythmias and on to cardiac arrest and multiorgan failure / injury.

It may be hot, but it ain’t pretty.

The drugs that trigger this are the general anesthetics in the “ane” class, Halothane, Isoflurane, Enflurane, etc. But the most serious culprit is the depolarizing muscle relaxant succinylcholine.

List of safe and unsafe drugs for MH patients can be found here. You know, just in case you were about to perform surgery and needed my guidance.

MH has one antidote: Dantroline. So again, if you’re about to perform surgery  you might wanna keep it handy. In fact, in most hospitals, having Dantroline at hand for surgery is… wait for it… wait for it..

Haus rules.

Because being hot is not always a good thing.


Always Breathe

The Hering-Breuer reflex, eponymously monikered by Viennese scientists Ewald Hering and Josef Breuer in 1868, prevents over-inflation of the lungs.

The ‘Hering-Breuer reflex’ is often confused with the ‘Herring Brewer reflex’ which causes one to throw up when eating fermented fish, a common problem with tourists visiting Iceland. I’ve been to Iceland and I can say from experience, my Herring Brewer reflex is functioning at full capacity.

Anyhoo, this reflex, the non-fish version, one would assume is simply a function of physical mechanics. The more you inhale, the less compliant the lung, the more pressure is placed on the thoracic cage, there’s pain, you stop.  But no. Biology, as always, is far more complicated than that. Our lungs are colonized by mechanorecptors, biological manometers sensitive to pressure, known as pulmonary stretch receptors. These mechanoreceptors exist in many places in the body, but in the lungs they are primarily found in the pleura and the smooth muscle surrounding the bronchi and bronchioles.

Hering and Breuer also came up with name for the reflex that causes us to inhale when the lungs deflate. They named it, not surprisingly, The Hering-Breuer Deflation Reflex.

I’m not sure if back in the late 1800’s neurology had progressed to a point where we knew about mechanoreceptors and chemoreceptors. More than likely, they just stuck a flag in something they observed and called it their own. A form of physiological colonialism. “I don’t know what this is exactly but I’ll name it after me and y’all can figure out the details later…”

The respiratory centers of our brain are located in the medulla oblongata and pons sections of the brain stem. These pulmonic manometers send a signal via the vagus nerve to  the medulla. The ventral and dorsal sections of the medulla control expiratory and inspiratory movements respectively.

The pons has the apneustic and pneumotaxic respiratory centers. The apneustic sends signals to increase tidal volume, inhibited by the Hering-Breuer inflation reflex and also by the pneumotaxic respiratory center which decreases tidal volume.

The apneustic and pneumotaxic centers work in parallel to control the rate and volume of breathing. the involuntary aspects of breathing are mainly controlled by chemoreceptors that monitor the PaCO2 (partial pressure of carbon dioxide) in the blood. By managing the PaCO2 level through respiration, we control the pH level of our body.

Christopher Durang, in his play Laughing Wild, offered up this one important piece of advice that, until recently, was a mantra I lived by.

“Always Breathe”

Like I have a choice.



Post-viral cough

A friend with a lingering dry cough started asking me questions about it. I, of course, because no one ever really does, had no definitive answers. I had recently been reading a chapter in Egan’s about interstitial lung disease and on taking down his history I learned he runs his own farm. So Portlandy!

“Hypersensitivity Pneumonitis – Farmer’s Lung!”

When you’re reading about zebras, everything looks like a zebra.

Hypersensitivity Pneumonitis is a general category of  parenchymal inflammation as a response to inhaled organics and it can be caused by a multitude of biological compounds. There’s Coffee Worker’s Lung, Humidifier Lung, Hot tub lung, Cheese Washer’s lung, and my favorite Bird Fancier’s Lung because it’s fancy and involves birds. Each has its own pathogen at its root but the result is the same: Pneumonitis – swelling of the lung tissue. It is differentiated from pneumonia by the lack of an infectious agent.

Symptoms of pneumonitis include fever, chills. malaise. chest tightness, dyspnea, rash, headache and, of course, *drum roll* cough.

Radiographic features tend to show a diffuse micronodular interstitial pattern. Which is a technical term to “giant ugly mess”.

Farmer’s lung is a form of hypersensitivity pneumonitis that is most commonly caused by moldy hay, specifically the aspergillis that thrives there.

So I see a farmer, I see him cough, I just read about zebras, I see a zebra.

However, he had had a chest x-ray. It was clear.

No stripes. No zebra.

He had however, weeks ago. recovered from a chest cold. And this lingering, nagging, dry cough just would not subside.

And here’s where I came across something I hadn’t heard of. Possibly because it is recognized as an officially recognized condition in Europe but not the USA. Those sassy Europeans. They’re always ahead of us.

Post-viral cough.

“a lingering cough that follows a viral respiratory tract infection, such as a common cold or flu and lasting up to eight weeks. ”

There doesn’t seem to be any hard evidence as to it’s cause but there is suggestion that the infection leaves behind something that upregulates the receptors that stimulate cough. Or it’s a continued immune response upregulating the cough receptors that lingers even after the virus is defeated.

It seems American’s are hopping on board with the term “postinfectious cough” and like typical cavalier Americans willy nilly inventing words because a hyphen is really hard to find on a keyboard, they went with “postinfectious” instead of “post-infectious”. This kind of portmanteau neologism is downright Shakespearean.

You can read about it here.

In the end, the answer, like always, is steroids. Inhaled if it’s not too bad. Oral prednisone if it’s so paroxysmal the patient can’t function.

Until I decided to go back to school for respiratory therapy, I thought love was the answer.

I was wrong. It’s steroids.

He’ll live. He’ll go back to his farm and tend to his zebras. I mean… horses.