Blog

Most important item(s) to evaluate patient’s pulmonary status : pulmonary compliance

 

SHORT VERSION OF EXPLANATION :

Pulmonary compliance = how easy it is to move volumes tidally in and out of the lung.

Pulmonary compliance formula = dV / dP = 350 / 35 = 10 mls / cmH2O) in this image.

Relevance :  To move 300 mls of spontaneous tidal volume, a patient has to generate -10cmH2O of negative pressure while a normal person would generate -3cmH2O of negative pressure.  The patient spends 3x more energy than you trying to breathe the same sized breath.  That will translate to increased WOB and increased likelihood of respiratory failure and an increased need for proper caloric intake.

 

LONG WINDED VERSION OF EXPLANATION :

Evaluate your patient’s pulmonary compliance.

Some quick definitions :

PIP = peak inspiratory pressure.

PEEP = positive end expiratory pressure.

dP (delta P) = change in pressure, during tidal breathing.

dV (delta V) = change in volume during tidal breathing.

Compliance = ease of lung distensibility.

Compliance = change in volume (tidal volume) / change in pressure = delta V / delta P = dV / dP.

If you are in any Pressure mode (ex : PCV, PSV) , this is very simple :

delta Volume = 350 mls (see above image).

delta Pressure = 35 cmH2O (see above image :  PIP=49 ; PEEP=14 >> dP=35).

Compliance = 350 / 35 = 10 mls / cmH2O.

What is the value of  normal pulmonary compliance?

100 mls / cmH2O.

What is the average pulmonary compliance of a “normal”, intubated ICU patient ?

30 mls / cmH2O.

What exactly does pulmonary compliance mean in practical terms ?

This means for every 1 cmH2O, 100 mls of volume will be moved (the normal non-intubated patient).

This means for every 1cmH2O, 30 mls of volume will be moved (the average ICU patient).

This means the patient works 3x as hard as a non-intubate patient.

For better understanding, the statement can be rephrased as :

(With the caveat statement that we all move approximately 200-300 mls of spontaneous tidal volume).

How much pressure must be generated by a diaphragm to move 300 mls of spontaneous tidal volume in a normal patient?

If the pulmonary compliance = 100 mls / cmH2O, then only 3 cmH2O of negative inspiratory pressure has to be generated.

How much pressure must be generated by a diaphragm to move 300 mls of spontaneous tidal volume in an an average ICU patient?

If the pulmonary compliance = 30 mls / cmH2O, then 10 cmH2O of negative inspiratory pressure has to be generated.

This difference can translate into work of breathing (WOB) and if the patient is underfed, this can start to become a significant impediment to quick weaning and liberation from mechanical ventilatory support.

 

 

 

Most important item(s) to evaluate patient’s pulmonary status : P/F ratio

Evaluate your patient’s P/F ratio :

P/F ratio = PaO2 / FiO2 ratio.

It is a great way to index your patient’s oxygenation status.

It is cheap and not complicated but tells a lot about your lung in 30 seconds.

HOW  TO  CALCULATE  P/F  RATIO :

Divide PaO2 by FiO2 (in decimal format).

Normal P/F ratio value : 500-600 (on any FiO2).

Normal patient : (breathing room air)

PaO2 = 100 ,  FiO2 = 21%  >>  PaO2 / FiO2 ratio = 100 / 0.21 = 500.

Normal patient : (breathing 100% FiO2 via NRB (non-breather)).

PaO2 =  600,  FiO2 = 100%  >>  PaO2 / FiO2  ratio = 500 / 1.00 = 500.

WHAT  ARE  DIAGNOSTIC  VALUES :

P/F ratio > 500-600  =  Normal.

P/F ratio < 300  =  ALI.

P/F ratio < 200  =  ARDS.

P/F ratio < 150  =  AHRF (acute hypoxemic respiratory failure).

WHAT  IS  THE  AVERAGE  SURGICAL  PATIENT’S  P/F  VALUE :

P/F ratio on arrival from operating theatre / room :  PaO2 = 250,  FiO2 = 100%  >>  P/F ratio = 250s.

P/F ratio 4 hours after surgery :  PaO2 = 120,  FiO2 = 50% >> P/F ratio = 250s.

The Lung – What are 7 functions of the lung?

alveolus-7-functions

Joke (fun) answer :   1)  inhalation  2)  exhalation  3)  O2 exchange  4)  CO2 exchange  5)  phonation (voice)

6) buoyancy (while swimming)  7)  cushion (for the heart).

Real answer :

1)  Gas exchange.

2)  Vascular reservoir :   between right and left heart.

3)  Filter :  embolized material gets caught at the level of the capillary radius.

4)  Homestasis :  heat & fluid transfer.

5)  Defense barrier :  foreign organisms (bacteria) and particles (dust).

6)  Endocrine function :  angiotensinogen gets converted to angiotensin.

7)  Metabolic function :  surfactant synthesis & fibrinolytic systems.

The lung is a top shelf organ that is not given its due respect in the field of medicine.

Tons of research is done on the heart and the brain and the immune system.

However, the lung is simply seen as an oxygenation / ventilation tool and possible considered

as a gateway for foreign objects from entering  the inner milieu of the human body.

Great interest should also be given to the fact that the lung is a vascular reservoir.

When this pulmonary vascular reservoir is overwhelmed is when the pulmonary edema starts.

It is incredibly versatile and it should be followed by the research community as to

the result of the demise of the lung.

 

 

 

 

The Alveolus – understanding the many different visions / versions of the alveolus.

alveolus-many-views

The evolution of the understanding of the lung / alveolus in the last 30 years.

Old textbooks (circa 1970s) mostly offer hand drawings.

Since then, we have an improving understanding that has gone

from a view at the level of the microscope to the electron microscope

to the scanning electron microscope.

What is missing in the literature is giving the clinicians at bedside a

good understanding of the physics and physiology of the lung and the alveolus.

 

I’ll give one example :

One of the major functions of the lung is an endocrine function : that of

converting Angiotensinogen to Angiotensin.

The lung is the primary place where ACE (angiotensinogen converting enzyme is

located.  The kidney is the secondary place where ACE is found.

What happens to this pulmonary feature of conversion via enzymatic process in the

lung when the lung is significantly atelectatic or the lung is in serious crisis during

a pulmonary edematous event?

Angiotensin is the endogenous hormone that keeps vasculature constricted as the

body deems necessary.

Is it that we as a medical society do not know?

Is it that we do not understand this mechanism of action?

Is it that we have never entertained this notion?

 

 

eLibrary – high value pix – alveolus ARDS (normal vs. injured)

hi-value-pix-ards-nl-vs-injured-alveolus-nejm-2000

This picture printed in NEJM 2000 is a great picture to learn from.

I will expand on content at a later date.

Simply GOOGLE search for images with the following “nejm 2000 ards alveolus”.

Pick the image.

Then choose “view image” for a picture of moderate resolution.