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LAW OF THE LUNG AND LUNG FU NOW ON KINDLE AND NOOK ONLY $2.99

ENLARGE YOUR PERSPECTIVE ABOUT PULMONARY MEDICINE

The lung has 90 sq meters of surface area- enough to cover a tennis court. Dark, wet, & rich with nooks, here bacteria & foreign debris are inhaled, trapped & left to fester. A larger surface area exists in the mind of a clever respiratory therapist.

How would this therapist react if his twin’s murderer entered his sphere of medical practice in the very first chapter, this perpetrator a free man because of a legal technicality? What if for nine years the therapist had waited-idle in his suffering-visualizing all the ways to bring retribution should the moment arise?  Nick Fuller has always promised himself that if this perp were admitted to a bed on a floor to which he was assigned – it is fate that he should kill him. 

Nick’s fuse is lit when he sees his twin sister’s murderer in a wheelchair roll right past him. An unconsidered possibility exists in his blind rage. This spark of wrath could become a wildfire for nothing is more infectious than an idea without boundaries.

Touch the world of advanced practice medicine where one overvalued thought can morph into megalomania. Are we all just one idea from being pompous and two from insanity?

A smug clinician, Nick is an informal leader and self styled Moses with both vast talent and practical bedside apps to match the attitude. The zenith of clinical and didactic competence, he champions advanced practice. Woe to the person that cannot stand his pace.  To depart from the doctrine of Nick’s righteousness is to invite inquiry and scorn. 

He has devised a number of LAWS concerning the LUNG which serve as an undefeatable code of conduct, a framework for clinical excellence and an overall explanation for the absurdities of medicine. He uses these pithy and at times sarcastic sayings for teaching. Nearly as often, he throws these fireballs as insults.

Beyond this, some other evil phenomenon is growing in Cincinnati Sinai Hospital, the explanations for which few might accept-if they were looking. For over two centuries, someone has been watching over the site where this new hospital stands. What answers can be found in the metaphysical blowback built into the very foundation of the medical center where germs, genius and stupidity labor side by side?   

Discover the Cincinnati Sinai Hospital, where everyone has a secret. Witness murder most clinical and clever. Here you will see: Deceit. Humor. Betrayal. Professionalism. Character Assassination. Genius. Lung Sarcasm. Unleashed passion. Stupidity. Drama. Conceit. Here, Restrained Impulses and Paybacks are most cruel and full of glee.  

LAW OF THE LUNG is the first of a six part book series. Deliberately crafted as a fast plot, HBO series styled medical-insider, this suspense-thriller is sure to please. Here, fiction is dipped in philosophy with vivid characters for the reader to live vicariously through. All truths and beliefs shall be tested in the maelstrom coming in books 4, 5 and 6 as those who work in the medical professions must decide for themselves the meaning and impact of luck, time, cure, disease, suffering, fate and what may come after that. Books 1,2,3 are substantive, featuring character development, with riser plots and real discussion of the practice of the pulmonary sciences.

The Cincinnati Sinai Series. Highly visual, dialogue rich, it is as ribald as it is cynical. It explains the technicals and frontiers of pulmonary medicine.  It expands outward as the books go forward into the realms of nursing, physicians and a reimbursement system that is struggling to survive. All of this is set in a real world scenario, the year 2025 when Medicare cuts will arrive in full force.

Between then and now humanity has passed through a worldwide catastrophe. As said before two more catastrophes are brewing, their impacts coming in the later books in the series.

These witty and nimble thrillers are intended for three main reading groups: the medically trained clinician, avid medical genre reader and those who actually live the diseases described here, the COPDers and asthmatics who wonder what goes on in corridors just outside their politely shut hospital door.   

This series is written by a 38 year, highly experienced ICU based Respiratory Care Practitioner,  instructor and lecturer. He lectures at seminars and is sharing ONLY terms and analysis of his own making. Over the decades, some of his medical jargon and cynical terminology have made their way into common use at a national level. Far more than these, Frank has stored up lifetime of never shared descriptors and pulmonary slang sure to make you laugh and cringe while you learn the intricacies of the lung and the staff who work the ICUs.

Caution: Several episodes of disturbing imagery involve murder. Infrequent strong language. Several inferred sexual references, one graphic event.

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CLINICIANS: CONTINUE TO SCROLL DOWN TO READ PRACTICAL, SYNOPSIZED PULMONARY OP/ED s OFTEN WITH A SARCASTIC TWIST. ON SOME SCREEN FORMATS PRESS THE BLUE WORDING ABOVE THE HEADING “ENLARGE YOUR PERSPECTIVE OF PULMONARY MEDICINE” TO BACK TRACK ARTICLES

 

ERRORS CONCERNING NEBULIZATION WITH BIPAP AND MECHANICAL VENTILATION

LUNGLORD  REFUTATION:

INFLUENCE OF TYPE, POSITION AND BIAS FLOW ON AEROSOL DRUG DELIVERY IN SIMULATED PEDIATRIC AND ADULT LUNG MODELS DURING MECHANICAL VENTILATION

Aru Ari Phd RRT PT CPFT,   Orcin Telley Ataley Phd PT,   Robert Harwood MSA etal

Respir Care 2010;55(7):845-851

The above study should be scrutinized concerning several key assumptions regarding the use of bronchodilators on ventilators and Bipaps for the adult clientele.

LIMITATION ONE

ALL TESTS IN THE STUDY WERE PERFORMED ON CLOSED CIRCUIT VENTILATOR CIRCUITS HEATED TO THIRTY FIVE DEGREES CENTIGRADE

DEVIATION FROM CLINICAL PRACTICE

NO INFORMATION IN THIS STUDY CAN BE APPLIED TO BIPAPS SINCE THEY ARE NEITHER TOTALLY CLOSED SYSTEMS,  HAVING BOTH ORAL LEAKS AND MECHANICAL CIRCUIT LEAKS, NOR ARE THEY USUALLY HEATED TO 35C  AT ANY TIME EXCEPT FOR TRACHEOSTOMY.            

RATIONALE FOR ARGUMENT

Bipaps are used dry at first in their administration. Some facilities deem that the first four hours of Bipap use is a temporary use and therefore the expense of humidification is unwarranted. Once a chronic need for ventilation is deemed appropriate, room air temperature passover humidification is used to partially bring the dry gas towards the moisture content of the room. In many institutions, such as at LUNGLORD’s facility, Bipaps are never heated regardless of length of patient stay, a point for discussion at another venue. What is gained in humidity is lost in patient compliance. Obtunded people reject our ventilatory lung sauna, though LUNGLORD  does try to sell the idea as a lung spa to those that are dioxide narcotic.

Reflect on this idea. Relative humidity in most hospitals is regulated to very low levels to retard bacteria growth. Therefore, it is a reasonable conclusion that, a mix of bone dry source oxygen and relatively dry entrained gas passing momentarily through a cold chamber will achieve only minimal amounts of humidity. 

A fair question concerning an RCP’s goal of highest possible reason and best practice should be asked here.

Consider. When we’ re giving a conventional nebulizer treatment, the mist disappears once it has traveled four to eight inches from the cup. Why? The very dry air robs the mist of moisture by evaporation, reducing particle size until the medicine is far below optimal size, in fact has an infinitesimal particle size. 

How much of this medication would be at optimal particle size after traveling seventy two inches through a corregated ( thus turbulent) BIPAP circuit or a ventilator circuit where it is well tumbled in dry gas?

Is any of the medicine at proper size for absorption?

LUNGLORD believes it is exceptionally imprudent and unreasonable that these questions weren’t asked by these Phds.

How much of the medicine gets past the pilot hole built into the circuit? 

How much is lost in the passover or heated humidifier?

We know that particle sizes that are too small are exhaled and not absorbed at all because they lack enough mass for inertial impaction.  

CONCLUSION:  NONE OF THIS INFORMATION AS PRESENTED BY THE AUTHORS  APPLIES TO THE EFFFICACY OF UNHEATED VENTILATORS AND BIPAPS.

LIMITATION TWO

THE FILTER USED TO COLLECT THE BRONCHODILATOR IS AN ABSOLUTE FILTER, THAT IS, 100% EFFICIENT AT CAPTURE OF ALL PARTICLES COMING TOWARDS IT.

LOGIC ERROR: STUDY DEVIATES FROM THE PHYSIOLOGICAL REALITY COMMON  TO ALL HUMAN ANATOMY

NO BIOLOGICAL SYSTEM OF THE BODY IS 100% EFFICIENT. ONLY PARTICLES LESS THAN A CERTAIN SIZE CAN GET INTO THE LUNG.  FURTHER, THE LUNG ONLY RETAINS PARTICLES IN A CERTAIN MICRON RANGE.  THIS STUDY IS OF LIMITED VALUE IN THAT IT DOES NOT SPECIFY WHICH SIZE PARTICLES AND THEIR PERCENT OF THE WHOLE ARE ARRIVING AT THE FILTER.

RATIONALE FOR ARGUMENT

Obviously, cigarette smokers exhale smoke, these particles too small and of insufficient mass to impact on the bronchial or alveolar walls.  Larger particles rain out in the upper airway resulting in stained teeth. Likewise with these aerosols, particle size must be right sized to impact and to prevent exhalation. The study used HCL to remove and sluice all albuterol from the filter. It was then weighed without regard to particle size. Only the crude amount was considered. 

This lack of specificity results in a lack of utility. 

Had the authors used absolute filters that would send the gas first through  a 5 micron,  then 4, then 3,  2, 1, .5,  .25, .15 and <.15 particle sizes in successive filter traps, the whole premise  of the study might have illuminated the elephant in the room.

The elephant here is that aerosol particles robbed of their liquid suspension have an unspecified mass and their particle size is far out of the specified range. 

True the meds are captured in the 100% filter, but this is sleight of hand.  This is a huge confidence distractor and reflects sloppiness on the part of the researchers who would have certainly known that the useable particle size would be an important consideration since is represents efficacy of retention of the lung in the lung, especially in any environment less than 37c.

An argument can be made that MDIs also aerosolize anhydrous albuterol, therefore what is the difference.  Simply, these MDI meds are formulated with HFAs and CFCs previously to a high degree of precision to achieve proper particle size.  No description of particle size is being offered by this study.

SUMMARY

Colleagues, is it not reasonable that the more proximal the HHN is to the patient, the more medication they will receive both in volume and in proper particle size, having avoided all these losses?   

LUNGLORD would humbly recommend that in the future all nebs be inserted in the circuit with a spring loaded T piece, that is, between the Bipap mask and the pressure sensor/pilot hole, as a matter of policy and practice. The spring loaded T piece is essential for safety, for should the neb disconnect, no pressure would be generated in the circuit.

Let us abandon the both convenient and highly inefficient practice of placing the HHN on the main flow filter where it comes out of the ventilator or Bipap, this some six feet from the patient.

The medicine our patient’s need to reduce their WOB should be placed as proximal and as close to an ideal particle size as possible.  This improvement in practice might well be the difference between intubating our COPD, CB, and asthmatic clients.  Consider the cost and morbidity such a change in your methodology might make to your clients and their LOS.

 What is factual and correct in the study is that the inspiratory limb can serve as a spacer, a plenum for the neb during exhalation, the mist building in volume and moving closer to the Y during this time, that is if the neb is backed away from the Y a foot or so and the circuit is heated. For this information, LUNGLORD is grateful to the researchers.

SCROLL DOWN FOR PREVIOUS POSTINGS SUCH AS PAV, LOW CO2 EFFECT ON THE BRAIN, VIAGRA VS HS CPAP, ALBUTEROL VS XOPENEX,

OPTIMIZING THE RESPIRATORY PUMP: HARNESSING INSPIRATORY RESISTANCE  TO TREAT SYSTEMIC HYPOTENSION

Victor A Convertino PhD, Kathy Ryan PhD, Caroline Rickards PhD, Steven Glorslky MD, Ahamed H Idris MD, Demetris Yannopoulus MD et al

Respiratory Care Magazine-June 2011 Volume 56 number 6  pg846-855

LUNGLORD SYNOPSIS

In times of acute hypotension, severe shock can develop as the heart loses its effective contractility because of low preload pressure.  As venous tone decreases, blood pools in the periphery. To reload the heart with blood, this study suggests that venous blood volume can be drawn from the periphery and back into the chest by strong Muller maneuvers, whereby the patient takes deep breaths against a valve which opens at seven cm below atmospheric. This in effect lowers thoracic CVP, milking the blood to the chest, creating a flow gradient from the periphery towards the heart.  As blood volume increases so does stroke volume and thus peripheral perfusion. Consider. If the blood that was once pooling in the periphery is now in transit back towards the chest it is not something the heart has to push again on systole. To say again, a decreased resistance to forward propulsion of blood creates less myocardial work.  Authors claim real effectiveness with Ambu bagging the hypotensive in the emergency arena. Patient is breath augmented at the very end of their inspiratory gasp with a breath prn when they fail to trigger the -7cm valve. In essence SVR is reduced in the head and extremities. The maneuver maintains sympathetic nervous system mechanisms in the face of the strong parasympathetic effects of shock. 

The researchers note average increases of systolic blood pressures of 10 mm, a formidable increase in stroke volume by fifteen ccs, and most importantly increases in cardiac output by 1.7 liters per minute.

To say it another way. SVR is the systemic vascular resistance to flow of any liquid through a conduit. SVR for our purposes  includes all blood vessels outside of the heart. The more conduit the more resistance. Or if that conduit is smaller in diameter-this also increases resistance to flow. Or if the conduit is full of fluid and not empty-this also increases resistance. How does this happen? The fluid from the last beat sits where the new wave should go. A heart that doesn’t have much blood to pump cant fill the coronary arteries well, a double whammy of more work and little pay for the myocardium.  The heart has a hard time of moving blood through the capillaries when they are already full of the last three heart beat’s blood flow. If we can get some of this blood out of the capillaries and flowing back towards the chest, this takes enormous burdens off of the heart to do work and feeds it at the same time. 

That is the goal of this temporary emergency regime.

This is not a substitute for hypotension management. This is for use in the emergent five minute window between the moment of realizing the patient’s situation and the ability to react with fluid and pressors. 

The study used a valve with an opening pressure of seven cm through which the patient has to open to get a breath, this administered via a tight mask. Google ResQUOD, ResGUARD, and CircQlator. All devices FDA approved.

LUNGLORD NOTE:  The idea is sound and well proven. But aren’t there simpler methods to accomplish as much? The raising of the legs and feet usually raises blood pressure esp for  LUNGLORD in certain situations. In the hospital, however, for the hypotensive patient,  leg lifts accomplishes much the same effect as inspiratory resistance pumping, However, pumping blood uphill is the same as increasing SVR.  What if we raised the legs and lowered them a foot every ten seconds, essentially dumping blood back into the chest? LUNGLORD says Hmmmm. Would there be any benefit to it?  This would require much less patient effort and cooperation. LUNGLORD declares this cogent trick nice to know and worthy of cranial space for those blanched patients discovered in chairs or on commodes where regaining blood pressure is critical before they can be safely placed with the legs and feet at a higher level than the heart. Further, requiring study, if decreased ICP were required, such a device would likely accomplish this objective as a means of control until surgery can be arranged. Avoid use in pulmonary edema and CHF, Pulmonary HTN, penetrating chest wound.

Emphysema Progression on CT Scan in Ex-Smokers Observed for 4 Years After Quitting

  1. Marina Miller, MD, PhD,
  2. Jae Youn Cho, MD, PhD,
  3. Alexa Pham, BS,
  4. Paul J. Friedman, MD,
  5. Joe Ramsdell, MD, FCCP and
  6. David H. Broide, MBChB

+ Author Affiliations


  1. From the Department of Medicine (Drs Miller, Cho, Ramsdell, and Broide, and Ms Pham), and Department of Radiology (Dr Friedman), University of California, San Diego, CA.
  1. Correspondence to:
    David Broide, MBChB, University of California San Diego, Biomedical Sciences Bldg, Room 5090, 9500 Gilman Dr, La Jolla, CA 92093-0635; e-mail: dbroide@ucsd.edu

Abstract

Background: Tobacco smoking is a principal cause of COPD-emphysema (COPD-E). Whether discontinuing smoking for at least 4 years halts airway inflammation and progression of COPD-E in prior smokers is unknown. In this study we investigated whether discontinuing smoking for approximately 4 years in ex-smokers with GOLD (Global Initiative for Chronic Lung Disease) stage IIb (moderately severe) COPD-E stopped airway inflammation (ie, sputum biomarkers) and halted the progression of COPD-E on chest CT scan.

Methods: Ten ex-smokers with COPD-E who had quit smoking underwent chest CT scans to document the extent of COPD-E, assessment of lung function (FEV1 and diffusing capacity of lung for carbon monoxide), sputum induction for biomarkers of inflammation (measured by enzyme-linked immunosorbent assay), and blood cotinine levels at baseline and approximately 4 years later. Normal healthy subjects (n = 7) and normal current smokers with no CT scan evidence of COPD-E (n = 8) served as sputum biomarker comparison groups.

Results: After approximately 4 years of not smoking (documented by cotinine levels), ex-smokers with COPD-E had persistent increased levels of mediators of inflammation in sputum (myeloperoxidase, leukotriene B4, IL-8, monocyte chemoattractant protein-1, matrix metalloprotease-9), which was associated with significant progression of COPD-E on chest CT scan.

Conclusions: Cessation of tobacco smoking in heavy smokers with moderately severe COPD-E is associated with evidence of persistent airway inflammation and progression of COPD-E on CT scan 4 years later. Discontinuing smoking may slow the rate of progression of moderate severity COPD-E, but it does not prevent persistent airway inflammation and significant progression of COPD-E on CT scan.

From CHEST Magazine

LUNGLORD NOTE: This does not refute the large data base which states that smoking cessation causes a reduction in mortality and morbidity. Their longitudinal study states that the ameliorative effects of cessation, though substantive, does not undo the underlying degradation of the structural integrity of the airways which continue at an accelerated rate.

That is to say, rust out enough metal wires on the Golden Gate Bridge and though it might stand, the corrosive stresses invoked are still multiplying, their force carried  on fewer and fewer competent strands, snapping those that are marginal, even after the bay area has been drained of all salt water.

 

 

 

ALBUTEROL VS LEVOALBUTEROL IN INTUBATED PATIENTS

Effects of Nebulized Bronchodilator Therapy on Heart Rate and Arrhythmias in Critically Ill Adult Patients.

1Pulmonary and Critical Care Medicine Department, Genesys Regional Medical Center, Grand Blanc, Michigan.
BACKGROUND:Tachycardia and tachyarrhythmias are associated with increased morbidity and mortality in adult intensive care unit patients. This study examines the effects of nebulized bronchodilator therapy (albuterol and ipratropium) on heart rate and arrhythmias in this population and tests the proposition that levalbuterol is safer than albuterol in that regard.

METHODS:

A randomized, single-blind, cross-over, prospective study with 70 critically ill adult patients treated with nebulized bronchodilators. Patients were randomized to nebulized albuterol alternating with levalbuterol every 4-6 hours. Group A received albuterol 2.5 mg alternating with levalbuterol 0.63 mg. Group B received albuterol 2.5 mg alternating with levalbuterol 1.25 mg. All patients received nebulized ipratropium bromide with each treatment. Heart rate (HR) was recorded before and after each treatment. Cardiac rhythm was continuously monitored using electronic telemetry units.

RESULTS:

In Group A, change in HR post-albuterol 2.5 mg (n=303) was 0.89± 4.5 (mean± SD) beats per minute (bpm), compared with 0.85± 5.3 post-levalbuterol 0.63 mg (n=301) (p=0.89). In Group B (n=114), HR decreased 0.16± 5.1 bpm post-albuterol 2.5 mg compared with an average increase in HR of 1.4± 5.4 bpm post-levalbuterol 1.25 mg (n=118) (p=0.03). Five events of arrhythmias (0.6%) occurred during the course of 836 treatments. Four consisted of occasional premature ventricular contractions. Only one patient stopped treatment due to five beat run of ventricular tachycardia (1 in 70 patients, 1.4%).

CONCLUSIONS:

In critically ill adult patients, nebulized albuterol and ipratropium does not cause significant tachycardia or tachyarrhythmias. Substitution of levalbuterol for albuterol to avoid tachycardia and tachyarrhythmias is unwarranted.

PMID:
21960699
[PubMed – as supplied by publisher]
LUNGLORD COMMENT: Many factors contribute to tachycardia in the ICU including anxiety, alarms, altered sleep patterns, inability to find a position of comfort, IV access, restrains, medications of every sort, as well as weepy and creepy family members.  LUNGLORD was reading this article with skepticism from the outset, thinking that there could be no smoking (had to get that in there) gun of proof without controlling for these data deflecting gorillas also.
In clinical practice LUNGLORD has seen only a small benefit derived from this drug. For routine use, the cost of levoalbuterol, which is approximately 8x albuterol has little benefit to cost ratio unless therapies are spaced so that fewer treatments are needed and staffing is thus right sized.
In the ER setting, levoalbuterol should be reserved for adult patients who present with HR greater than 100 or have a history of SVT or A fib. The best care is not always the most expensive care. This is not a new conclusion unless you are trying to get a 2,500 page health care bill through Congress without reading it first ala N. Pelosi. If the  patient has pre medicated before coming to the ER with many albuterol doses, the beta sites are 50/50 full of R and S isomers of albuterol. If tachycardic, further treatment may be contraindicated since the S side of the molecule has far more negative effects and is slower to metabolize. Repeat dosing proportionately layers up their S isomer load. Therapeutic space in the B2 site may not be available. The third great bronchodilator ( a very old LUNG LAW circa 1980)  Ativan should be employed, along with Atrovent and steroids to manage the patient unless their condition warrants immediate dosing or their ability to give an accurate history is in question. As far as remembering R and S isomers-which is which?  R is the RESPONSIVE side chain. S is the SIDE EFFECT CHAIN. Mnemonics often substitute for intelligence at a certain point in the late adult development process. LUNGLORD requires a mnemonic to recall the spelling of the word itself without consulting the dictionary. Please advise.

PROPORTIONAL ASSIST VENTILATION

FOR INTENSIVE CARE CLINICIANS: Over decades, many methods for ventilator weaning have been devised.   At one time, the national standard for weaning from a ventilator was to decrease the number of effort free, large tidal volume, cleansing, SIMV breaths, thus allowing the patient to flex their diaphragm in between these synchronized, free breaths. They could pull as many breaths as they were capable, at a depth they were able. As the number of free breaths decreased they were required to make up the difference increasing their effort both in number and strength.  These natural inspiratory efforts placed a demand on the patient to perform the work, between the mechanical breaths, slowly toning their muscles. Once they were down to only 2 or 4/min mechanical breaths they were then considered to be good candidates for extubation and breathing on their own.

With the advent of PSV, Pressure Support Ventilation, the therapist was able to give a preset inspiratory nudge at the start of each spontaneous breath.  This would take the inertia out of the start of the breath and the source of greatest work and inspiratory demand. Our goal was to allow them to do the mid inspiratory work and as they improved, allow them to slowly resume the more difficult leading edge early inspiratory phase work- work that, if loaded on early in the wean caused them to fail more often than not. Bigger tidal volumes resulted. A refinement of SIMV, PSV soon became a stand alone weaning technique with no rate behind it at all, just alarms in case the patient fell off the edge.

But what is PAV?

PAV is a software program. Imagine that we had multiple math coprocessors that looked at numerous factors at the same time.  Suppose that every few hundred milliseconds the program could update the inspiratory flow through a tube, the amount of volume that moves in sections of that time frame, the inspiratory time, the starting pressure and the finishing pressure for the breath.   Through all these numbers, Warren Sanborn, was able to calculate the amount of “draw” on the endotracheal tube throughout the breathing cycle, since we know it’s length and diameter.  He factored in Poiseulle and voila we can now calculate resistance to flow on per breath basis, hence our term RPAV.  The determination of work of breathing is an extension of this number.

PAV uses a split second calculation to determine compliance also.  We call this CPAV. This is the ease of distensability of the lung. It is the reciprocal of elastance.  Compliance is “the change in pressure  given a change in volume.” To determine compliance, a known volume must be given and the airway closed so that the distribution of ventilation equilibrates inside the lung.  Pressure will also equilibrate. In a clever manuever, on random unpredicted breaths, so the brain cannot anticipate the test, the PAV program makes the patient hold their breath 300 milliseconds. a third of a second. The normal brain cannot prepare or predict the timing of this maneuver.

For time immemorial, we, and all who came before us have been taught that we need a time constant of inspiratoiry hold of 1 to 1.5 seconds for the flow and pressure wave to equilibrate in the most distal portions of the lung. This has been proved over and over in anesthetized patients. However, none of our patients are likewise medicated. In fact we have turned down their sedation to encourage good breathing effort. The breath hold time constant of 1-1.5 seconds is especially required for accuracy in measuring the diseased lung, with its blebs, bronchospasms, mucus blockages, atelectatic areas, with endless top to bottom V/Q mismatches etc. Some think a true measurement, with accuracy might require 2 seconds.

But, do we need this accuracy? No.  We are following a trend of CPAV and for our purposes the numbers obtained are accurate enough for usage. If we were to use 2 seconds for our inspiratory hold, most people would push against the closed valve and do a ValSalva manever, raising their pressure, giving faulty readings. Doing this twice a minute would cause anxiety and restlessness  In my questions to Mr Sanborn in an email, he stated that a 300 millisecond hold, is only “80%” accurate.  He said that it isn’t as true a number, but the accuracy doesn’t matter in that we are charting a trend- the real value is the relative index-not the actual number.

Though this sounds much like Washington budget accounting, simply said, we are sacrificing accuracy for measureability and reproducability of a useful trend.  If the trend is off by 20%, we correct for this in our software. The same ventilator alarms are in play as with PSV so there is no danger to the patient.  However, these alarms should not be set loose, since the entire idea behind it is to see the lactic surge coming before we would with PSV, so we can increase support or decrease it, if they are strengthening.  Our goal?  To keep the load level on the muscles consistent with their ability to do work. This is done through a graphic on the screen shows the patient’s amount of work in joules. Work is reduced or increased based upon patient effort to maintain a stable weaning ramp towards extubation.

Who is PAV not for?  Those patients under 25 kg and those without an inspiratory drive.  Neither is it proper for the neurologically hyperpnic.

According to Sanborn, “Patients with neurologically-related asynchronous breathing will not be good candidates for PAV. A patient who actively exhales during the pause will cause the maneuver to fail due to corruption of the raw data. Or if the patient forcibly exhales during exhalation, the RPAV value will be corrupted. If you observe a patient breathing as you described, he/she should be changed to another mode/breath type.

“The PA algorithm has built-in safety pressure and volume limits should the patient become over-supported; but the clinician would be expected to recognize the incompatibility between the selection of the PA algorithm and the wrong patient.”

LUNGLORD COMMENT:

The defect in PSV is that it is crude in the sense that one size fits all.  It does not quantify the patient’s individual work of breathing and unique parameters that could monitor this work. This is the difference between automobile carbueration and full computerized fuel injection that accounts for temperature and altitude. 

Until now, the patient information as to the sustainability of the wean was gathered by physical assessment. 

We monitored heart rate, blood pressure, flowloops, the nurse’s level of anxiety as well as the patient’s. Again this is the difference between an experienced mechanic listening to an engine run with a diagnostic ear, as opposed to putting it on a computerized display that lists problem codes.

In this, PAV definitely will help lesser experienced therapists make good clinical judgements. It will help all therapists to right size spontaneous support levels. After all, if we are looking at their WOB and seeing that their work is very low, this could give a early weaning signal as to readiness for extubation.  Readiness is less obvious to see than unreadiness. We may observe that they look worse than they are and have more reserves available for breathing on their own than we thought.

Ventilator weaning is much cussed and discussed in our realm, with armies aligned with each position, even those who still believe in T-Piece trials, all with good effect. Can PAV definitively prove itself superior to any and all comers? There is a limitation to all technology, because weaning lengths have not drastically changed.  There is art and science to it.  What is agreed is this. Weaning is a dependant function. We cannot bend the laws of the lung or trick pathophysiology, nor can we bait and switch the aging process.  None of the curves for homeostasis are in the right place. Determining patient readiness is the most intuitive aspect of starting a wean, since breathing costs are so high, as are their metabolic demands given their infections.  

PAV does provide, in LUNGLORD’S opinion, a capability to foretell where the patient will be soon, whether they will crump or not. By dialing up PAV support early, to a point they can meet their glycogen support, we can edge them away from a lactic build into anerobic metabolism and a wean fail.  If we are lucky, we may well keep these 1929 model lungers chugging along, breathing ugly, but ultimately prolonging their weans and getting them to the front door.

COLLEAGUES: PLEASE ASK SPECIFIC QUESTIONS OR BLOG YOUR BEDSIDE INSIGHTS BELOW FOR FURTHER DISCUSSION.  LUNGLORD WILL BE DELIGHTED TO RESEARCH FURTHER INTO THIS MATTER TO PROVIDE MORE INFORMATION FOR YOUR ALREADY ADVANCED CLINICAL PRACTICE.  WE MAY WELL LEARN THE NUANCES OF THIS SOFTWARE MODALITY TOGETHER AS ITS USE WIDENS.

LOW CARBON DIOXIDE’S EFFECT ON BRAIN INJURY

HYPOCAPNIA  AND THE INJURED BRAIN: MORE HARM THAN BENEFIT

Curley J, Cavanaugh BP, Laffey JG Crit Care Med 2010;38(5):1348-1359

This is a retrospective data extraction analysis, not an actual study. Their goal: to chart the effects of lowering carbon dioxide in the circulating blood. Their conclusions are that beyond the immediate concern for the acute management of herniation of the brain, carbon dioxide levels should be normalized as quickly as possible. They claim that outcomes are, in fact, lowered due by keeping a client’s Pco2 in sub normal ranges. The very mechanism that prevents swelling, that lowers blood flow through vasoconstriction also lowers oxygen delivery – especially to those areas of the brain which are already disrupted and have localized edema and bruising.  Further, since the body will buffer this lower Pco2 with less bicarb ions over several days anyway, then, when the the ventilator is set for a normal Pco2, a transient hypercpania may well occur causing vasodilitation in the head and causing swelling.

ERECTILE DYSFUNCTION: VIAGRA VERSUS NOCTURNAL CPAP

SILDENAFIL VERSUS CONTINUOUS POSITIVE PRESSURE FOR ERECTILE DYSFUNCTION IN MEN WITH OBSTRUCTIVE SLEEP APNEA: A META-ANALYSIS

Li X Dong, Wan Y, Wang Z.  Aging Male 2010;13(2):82-86

Obstructive Sleep Apnea prevents the brain from cycling through its subconcious modes at night. One of these modes is the resetting of the sexual clock, a source of Erectile Dysfunction. This study compared the efficacy of Viagra to CPAP, (which is a tight fitting nasal mask which turbocharges the throat with pressure, pushing flappy and fat tissue aside so that ventilatory efforts are unimpeded, thus preventing snoring and obstruction which leads to waking.)  Seventy patients were included in two randomized and controlled studes. The study sought to determine if medication was more factorial than normal rest in improving outcomes. After twelve weeks of comparison it found that both provided improvements in outcome as measured by successful and satisfactory sexual experiences.  Viagra’s effect on outcome was “significantly” better.

LUNGLORD COMMENT: Viagra, the little blue pill proves itself again.  Therefore, the term “blue bloater” has a new, secondary definition. The combined use of both modalities would likely have an additive effect since they treat the problem from different modes of action. LUNGLORD regrets using the term outcome in this synopsis and trusts it was not distracting to his readers.  Equally distracting are the bona fide names of the Asian physicians who wrote this study. OOops. These are, in fact, their actual names.   If LUNGLORD had been the editor at Aging Male Magazine, he would have thought long and hard about whether this was some sort of Korean practical joke. 

If the reader likes this content/format/perspective/style they may be well entertained by LUNGLORD’s first of six novels available on this site starting February 19th, 2012.  The reading is less concentrated than this–made for both the clinician and for the non medical reader. But, these ideas are examples of the small moons circling planets that travel in orbit around the central plot.

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THE NEWEST PULMONARY DRUGS

Forest Laboratories (NYSE: FRX) is introducing a new, twice a day, DPI format anticholinergic drug.  Named aclidinium bromide, (Genuair, Eklira – trade name) this medication is purported  to have a sustained effect for up to 24 hours.  It may be offered in three strengths.

According to the manufacturer, it is faster arriving at the target M3 site than tiotropium and so, therefore, is supposed to have fewer side effects because it does not remain in solution in the plasma for as long a period of time.  The inhaler mechanism itself is quite advanced, displaying a warning when ten doses remain, has a faint taste to confirm dosing and also has a visual color change when the dispenser detects enough flow that adequate dosage has been achieved.

In 2010, the FDA received their application to test this drug with formoterol fumarate.

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Daliresp (rolfumilast) is a new medication also made by Forest Laboratories.  Released in the spring of 2011, the therapeutic action of the drug is not well understood.  It increases c-AMP, but is not a bronchodilator.  According to the company press release, “It is the first and only selective phosphodiesterase-4 (PDE4) inhibitor approved by the FDA.”  The once daily tablet is offered at 500mcq and is now widely availiable.   Daliresp claims to have decreased “moderate and severe exacerbations by 15-18% in clinical trials.”

Be advised. 5.9% of patients taking the drug during clinical trials had “adverse psychiatric reactions” compared to 3.3% treated with placebo. Three suicide attempts were attempted during the trials and one of these was completed. These three attempts occurred inside a test population of 3100 participants. Weight loss is common, up to 10% of pre trial weight.  This drug significantly boosts liver P450.  Use with liver impairment is not recommended.  10% of trial participants had diarrhea vs 3% of placebo users.

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Novartis announced that the FDA has approved their new, once daily, DPI format, long acting broncholdilator named indacaterol maleate. (Arcarpta) The company professes that the drug has a measurable effect on lung function within five minutes and is only for stable COPD.  Based on the product literature that is to be offered, Arcapta is “not indicated for asthma.”  It has not been studied “in patients with acutely deteriorating COPD.  Use in this setting is inappropriate.”

Further, the corporation has plans for release of a new drug which they claim will produce revenues of “4 billion USD” currently named QVA149. The combination preparation is a mixture of indacaterol (above mentioned) and glycopyrronium bromide.  This is a LABA/LAMA combo like Combivent or Duodose, but with much longer effects.  The implication for tomorrow’s combination drug would be Spiriva together with Serevent or Foradil.

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Dulera, made by Merck, is a combination preparation of two drugs – a long acting bronchodilator named formoterol fumarate, ( the active ingredient in Foradil) and a steroid mometasone furoate,  (the active ingredient in Asmanex)  Meant to compete with Advair and Symbicort, Merck released this drug summer 2010. These drugs are well studied and are just being packaged for ease of use and for marketing purposes.

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LUNGLORD COMMENT: 

The Reece cup approach to medications, “Hey, you got chocolate in my peanut butter. No, you got peanut butter in my chocolate” is a rapidly growing mode for comprehensive treatment.  These multitargeting agents reduce the symptoms of lung disease, the way that simultaneously getting a cat, using mousetraps and baiting with De-Con all work together to reduce a rodent population.  Expect combinations of LABAS LAMAS with various strengths of steroids within two to three years and attempts to put leukotriene inhibitors in after that.  

Though these might be cheaper purchased as stand alones, their combined convenience outweighs the number one reason medications do not work: patient noncompliance with the drug regime.  One giant breath, once a day, is the ultimate goal for achieving a stable, daily, therapeutic level. Absolute key to symptom control is marriage of this routine to another. 

Therefore, LUNGLORD recommends all such drug combos should be kept on the shelf by the toilet, since this location is the most urgent and predictable of all A.M. routines.  Such multitasking drug combos as part of natural life rhythms will produce the best outcomes.

SYNOPSIS: OBSCURE FACTOIDS ABOUT INHALED MEDICATIONS

FORADIL  (formoterol) The FDA ruled against this drug and others which are similarly advertised as stand alone, long acting bronchodilators.  The FDA says they will have to amend labeling to reflect the unsafe nature of this regime.  All patients requiring LABA also require inhaled steroid coverage.  More combo drugs will follow this ruling.

SALMETEROL (Serevent)  Approved by the FDA in 1994. No tachyphylaxis after years of use (Larsson,1991) (Booth, 1993)

PIRBUTEROL  (Maxair) has a small additional benefit in improving cardiac ejection (Awan, 1981) (SHARMA, 1981) (Dawson, 1981) (Clolucci, 1981) However, if the patient is taking MAO inhibitors extreme headaches are not uncommon. Hypertensive crisis is improbable, but not unheard of.  For these reasons, this drug is not administered frequently.

FLUTICASONE (Flowvent)  Twice the affinity for targeted sites over beclomethasone. Significantly less effect on long bone growth over beclomethasone.

TILADE (nedocromyl) 25% improvement over Intal but the taste is so horrible and long lasting that it has fallen out of favor.

THEODUR (theophylline) a xanthine with similar effects to coffee.  In slow release formulas it is better tolerated, improving diaphragmic muscular ability from 15 – 20% (Hendles, 1995) Further, a blood level range of 5-15 instead of 20 has a majority effect with minority side effects.  Be advised. Levels can be increased with calcium channel blockers, steroids, and E-mycin.

MUCOMYST (acetylcystine)  Used for Tylenol OD, of course, but it also has cellular protective mechanisms.  A POWERFUL free radical scavenger, it improves the production of human glutathione which slows aging. (Henderson-Hayes, 1994)  (Bakker, 1994) (Dinarello, 1993) (Greech,1993) (Ferrari, 1990)  Also, there is evidence that it can prevent renal damage due to cardiac cath dyes. Further, this med is often given pre and post op in heart surgeries.

AURANOFIN a gold preparation lessens steroid dependance-interferening with leaukotriene mediation.  (Nierop, 1992) found 6mg a day reduced somewhat steroid requirments in 32 patients.

ISUPREL (isoproterenol) catacholamine.  Sledge hammer bronchodilator. Instant. Its cardiac effects have similar prowess.  Interest for clinicians to note, it causes a shunt.  Increases pulmonary flow flow far more than it increases bronchodilitation. This effect is not marginal.

LUNGLORD COMMENT: 

These factoids are of moderate practical clinical use in and of themselves, though LUNGLORD has carrried them for decades with only rare places to use them in the ICU or ER.

Tilade use in the youngster is waste of money. In LUNGLORD’S view, it is more likely to get a child to put several old pennies in their mouth and suck on them for twenty minutes daily than to get a compliant use of Tilade. Product should be dispensed with a Binaca co-spray, like that two part, foaming action Drano.  Maybe Drano’s brand name could be used on a new mucolytic?

As for chugging a forty cc oral dose of Mucomyst for cellular protection–this is the rough equivalent of drinking a glass of raw, rotten eggs with a big splash of vodka stirred in.

Isuprel (isoproterenol) is an old drug.   In the 1960’s, the Ben Casey outcomes were two: extreme tachycarida and SVT if you did treat their asthma and vaporlock if you didn’t.  The big “I” was replaced by a much safer little “i” isoetharine. Marketed by Breon as Bronkosol, it was already in therapeutic dose decay by the time one started charting at the end of the therapy. It was the first dual drug combo with 1% phenylephrine in it, a vasopressor, which combated asthma mediatated airway edema. In this regard it was very effective.  Lunglord rues the day this drug approach was discarded for acute treatment and still uses it, with MD approval, for status asthmaticus, provided their heart rate is not already excessive. Bronkosol was replaced by Alupent, which lasted 3 hours, woohoo, but was not the answer and was replaced by even longer lasting albuterol giving 4-6 hours of duration- in the mid 1980’s. It is now undergoing obsolescence because of levoalbuterol, an eight hour duration drug.

LUNGLORD regrets to inform his dear readers, he is this old.

With Isuprel, heart rates had to be monitored more closely than a top fuel dragster’s rpms, with similar rates of acceleration. Some people however, liked the buzz with a Valium chaser.  The “synovial shakes” coined by LUNGLORD in his youth was evidence of the presence of an adequate dose, akin to blue gingiva (pre CPO) giving clinical evidence of hypoxia. LUNGLORD actually took a 1.0cc dose with 3.0cc NS (a double dose) via IPPB PR-2 full nebulizer spray.  This cowboy action was to self medicate a severe bout of bronchitis in 1975.

LUNGLORD could actually feel his aortic arch flex and deform its shape with each beat at peak, riding in fright the pulsatile wave, this while amphetamine like panic rushes overwhelmed and vibrated his world for twenty minutes. Muscular twitches. HR increased from 72  to 120 in perhaps three minutes. Think ten cups of coffee. This drug is the equivalent of starter fluid sprayed in the carburetor. It may work, but sooner or later some vital portion of the valvetrain— probably a bicuspid—is going to be ejected through the chest wall.. er… hood of the vehicle.  This is LUNGLORD’s last experience with this drug and when he sees it hanging at a patient’s bedside he always discusses its shunt effect with the nurse.  However, this is now rarely used.

If the reader likes this content/format/perspective/style they may be well entertained by LUNGLORD’s first of six novels available on this site starting NOVEMBER 1st, 2011.  The reading is less concentrated than this–made for both the clinician and for the non medical reader. But, these ideas are examples of the small moons circling planets that travel in orbit around the central plot.