The Lung – What are 7 functions of the lung?


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.


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?



The dynamic renal system – the “poor man’s Swan”


In a nutshell : urine is formed in proportion to the cardiac output exerted on the nephron.

If the clinician is improving cardiac output, the urine output should improve.

Ex :

give Epinephrine  >> cardiac output increases >> urine output increases !

give 500cc NSS in a dehydrated patient >> cardiac output increases >> urine output increases !

apply Alveolar Recruitment Techniques (ART)  >> cardiac output increases >> urine output increases !

decrease PEEP (in a stellar pulmonary status patient)  >>  cardiac output increases >> urine output increases !


The “long winded story” :

The renal system in all of its dynamic glory is a beautiful passive organ system.

The dynamic renal system is referred to as the “poor man’s Swan”.

It’s state of flux demonstrates the strength of the cardiodynamic system.

When cardiac output is strong, urine is formed quickly and flows to the urimeter quickly.

When cardiac output is weak, urine is formed slowly and flows to the urimeter slowly.

For doctors / hospitals / states / countries that cannot afford the luxury of a Swan-Ganz catheter, the urine collection system is thus referred to as the “poor mans Swan”.

As long as there is integrity in the system from the nephron (beginning)  to the end (the urimeter), it is a great way to tell of the cardiodynamic status.

This attached movie clip (p1090771 – activate the “replay” feature on your PC’s movie player app) will allow you to envision the urine formation.

The process :   cardiodynamics will bring blood from  :    LV  >> LVOT >> Ao  >> descend Ao >> renal artery >> nephron  >> renal collecting tubules >> bladder >> urimeter.

In this movie clip, the patient had excellent cardiodyanmics and was given Lasix (forced diuresis) so the patient was literally “pouring out” urine.

Traumatic brain injury (TBI) / nueuro-injury may result in sequelae to include SIADH (syndrome of inappropriate anti-diuretic hormone) which allows urine to “pour out” as well.

The beauty of this movie clip is to envision for “x” amount of heart beats, a drop of urine is formed.  When you see urine forming at the rate you see in this movie clip, one has to stand in awe of a passive physiologic process.


2 min Evaluation – Urimeter – darker yellow – 10 seconds to reach a conclusion


2 min Evaluation – Urimeter = darker yellow – 10 seconds to reach a conclusion

The quick explanation :

Situation :    urine = darker yellow.

Background :    dehydrated / intravascularly depleted.

Action :    cautious intravascular volume repletion.

Recommendation :     Alveolar recruitment technique (ART).



The “long winded” explanation :

S-B-A-R format reporting – quick reporting format for handoff from one healthcare professional to another.

A lot of this presentation is conjecture … but time and experience has proven correct 99 out of 100 times.

Darker yellow urine is a likely indicator that your patient is intravascularly depleted to some extent.

A “passive leg raise” maneuver (MORE TO FOLLOW AT A LATER DATE) will provide additional information as to the value of  intravascular volume repletion.

If the patient’s systemic blood pressure / cardiac output improve significantly, a 500ml NSS repletion regimen is
likely going to improve outcomes.

Whenever fluid is repleted, alveolar should be protected via ART (alveolar recruitment technique) to avoid unintended
migration of NSS into the pulmonary interstitium and unintended alveolar compression (= compressive atelectasis).


2 min Evaluation – Urimeter – translucent green – 10 seconds to reach a conclusion

The quick explanation :

Situation :    urine = (translucent) green.

Background :    hypotension.

Action :    methylene blue intravenous injection.

Recommendation :     Alveolar recruitment technique (ART).



The “long winded” explanation :

S-B-A-R format reporting – quick reporting format for handoff from one healthcare professional to another.

A lot of this presentation is conjecture … but time and experience has proven correct 99 out of 100 times.

Translucent green urine – refractory systemic vascular hypotension (from excessive nitric oxide in general systemic circulation) >  methylene blue dye irreversibly binds nitric oxide (NO) molecules – systemic blood pressure should increase status post  random scavenging.

The patient’s vascular system is producing excessive amounts of nitric oxide in endovascular epithelial tissue.
Last resort to refractory hypotension is to offer a free floating agent in the cardiovascular system to be reduced by nitric oxide
and thereby decrease the systemic vascular dilation (increased SVR) by “free range” nitric oxide.

Last resort because methylene blue is nephrotoxic.


The ICU patient – evaluating the patient in 2 minutes



Why would you want to evaluate a patient in 2 minutes?

>> To be able to answer anyone who asks : “How’s my patient doing?”

> answer quick and BE READY to defend your stance!

>> Why you think the patient is faring well vs. why you think the patient is decompensating.

>> if they like your answer over the course of 1 to 2 patients (and you were correct),

they will trust you for the rest of your life with anything respiratory related and

patient related as well.

How do you evaluate the patient in 2 minutes?

>> 7 zones to focus on :  2 min = 120 seconds

>> patient.  10 sec

>> patient monitor.  10 sec

>> IV pumps.  30 sec

>> ventilator.  10 sec

>> chest tube.  10 sec

>> urine collection bag.  10 sec

>> any other unusual device in room.  10 sec

>> conclusion and defense thesis.  30 sec

PATIENT :  10 seconds

cyanosis / pale / normal

MONITOR :  10 seconds

HR :  hi  /  lo  / normal
BP :  hi  /  lo  / normal

PA :  hi  /  lo  / normal

CVP :  hi  /  lo  / normal

SpO2 :  hi  /  lo  / normal

IV PUMPS :   30 seconds

Vasoactives :  constrictors  vs.  dilators

Cardiotonics :  inotropes  vs.  chronotropes

Sedation :

Analgesics :

Paralytics :

Epi  /  Levo  /  Neo  /  Vaso  /  Milrinone

Diprivan  /  Ativan  /  Versed  /  Fentanyl

VENTILATOR :   10 seconds

Type & Mode of Ventilation :   VCV  vs.  PCV  ;  AC  vs.  SIMV  vs. PSV

PEEP :    hi  /  lo  / normal

FiO2 :    hi  /  lo  / normal

P/F ratio :  hi  /  lo  / normal

Lung compliance :   hi  /  lo  / normal

CHEST TUBE :   10 seconds

Qualitative analysis :

Quantitative analysis :  hi  /  lo  / normal


Qualitative analysis :  clear  /  yellow  /  pink  /  red  / green  /  blue

Quantitaive analysis :    hi  /  lo  / normal

UNUSUAL DEVICES  :  10 seconds

EEG  /  Hypothermia Induction Device  / IAB / VAD / ECMO, CVVH, hemodialysis, wound VAC, compression stockings, external pacing device, cardio-defibrillator, video monitor, patient escape alert device.

CONCLUSION :  immediate

Rationale :  30 seconds

(MORE TO FOLLOW next week)