Abnormal Breathing Patterns

“Dysynchrony between inhalation and exhalation may lead to EXPIRATION….
What are the abnormal breathing patterns?”

CHEST COUNCIL OF INDIA Brings a Webinar on ABNORMAL BREATHING PATTERNS

The moderator is Dr Bharat Toshniwal, Nanded

There is a guest physiologist, Dr Kavana G Venkatappa

The panelists are
Dr Sushil Jain, Raipur
Dr Srikar Darisetty, Hyderabad
Dr Ambika Sharma, Jaipur

Kindly login this Thursday 21st March 8pm onwards by clicking on https://blueberry.webcastlive.co.in/c2047/

Dr Ashish Dubey
CCI President

Dr Anil Maske
CCI Secretary

E uh so good evening everyone I am Dr bat tnal pulmonologist from nanded Maharashtra uh I welcome you all to this uh wonderful initiative done by the CCI uh since like I think past two two and a half to three years uh the webinar series today’s webinar is about some

Physiological concept it’s like we have studied all of us from our physiology from our guidance it is about the abnormal respiratory patterns but what we have trying to do is uh 3.5 years for 3.5 years the webinars are going on so what we have tried to do is we are

Trying to make that physiological aspect into a clinical aspect and how we can help as clinicians diagnose our patient and treat our patients in a better way with this applied physiology I have very uh eminent p panelist with me today uh we have uh hod kaana Madam who is the hod of

Physiology uh from Karnataka Amba Madam she is a consultant chess physician assistant professor in SMS jaur we have shrier sir consultant pulmonologist from po poo Hyderabad and we all know sushil sir the imminent Interventional pulmonologist from rur I welcome you all uh for this webinar and

Uh the flow of the webinar is we have initially two talks so all of you can just brush up your knowledge uh what you have read and then we will follow it with uh the case discussions so uh the first talk I will uh call uh yeah kaana Madam uh for her talk

On Anatomy physiology and maintenance of respiration respected all good evening everyone thank you Dr Barat for that warm introduction I thank CCA for the opportunity given and I feel proud to be a part of CCI and this webinar too topic of today’s discussion is abnormal breathing pattern so before we move on

To the deviation from the normal phenomena let me highlight some of the few of the concepts in physiology towards the regulation of respiration the physiology of regulation of respiration the term Yia when we speak it depicts the normal respiratory Rhythm the normal rate and depth which is regulated by a complex integration of

The neural and the chemical control of respiratory mechanism as like we say the homeostasis which works in all over the body it is same with the ventilation too where in which any alteration in the ventilation as we are seeing here will be checked or taken up by The receptors or the sensors which

May be Cho receptors which may be pulmonary receptors the proprioceptors of The receptors in the Airways but the message will be passed down to the center of the controllers which we are going to discuss in the further slides this message again is transferred to the respiratory muscles which act accordingly and cause the

Change in the ventilation the way it is required regulation of respiration broadly we classify into neural and chemical regulation of respiration where neural mainly regulates the pattern of breathing and the chemical regulates the minute ventilation that is the rate and the depth ofation neural control is again divided

Into automatic control and the voluntary control voluntary control is mainly by the higher centers of the brain that is the cerebral cortex hypothalamus lyic system for example if I have to uh share the voluntary hyperventilation breath holding all these are the one which act where the caros spinal tract where it

Bypasses the medula so under automatic control it is the medular centers and the pontine centers again in the medary centers there are two group of neurons as you can see over here dorsal respiratory group drg and the vental respiratory group of neurons the dorsal respiratory group of neurons and Below

Which you can see inspiration that is drg contains the I neurons which can activate the inspiration stimulate the inspiration vental group of respiratory neurons they as they have both inspiration and expiration which where in which acts when the demand for ventilation is more so this shows the respiratory

Centers in the brain bra stem as we can see here in the upper pawns there is situation of the pneumotoxic center and in the lower pawns there is austic Center in the medula there are two respiratory groups that is the dorsal respiratory group and the vental respiratory group which are present in

The ventrolateral part of the medula apart from this we can also find the location of the central pattern generator cpg where in which there are PR bodinger complex cells which are nothing but the pacemaker cells as we say pacemaker it is a spontaneous generation of the of the rhythm of

Respiration so that cpg is the one which is present in between the nucleus ambigous and the lateral reticular nucleus so this was discussed let me move on the slides that is drg is the one which acts during the quiet breathing and the vrg when the demand for ventilation increases which contains

Both I and the E neurons so coming on to the Genesis of respiration here this uh flowchart shows how the inspiration expiration happens and how that rhythm of respiration is being maintained apneustic Center is the one which acts as stimulatory control over the inspiratory neurons and this inspiratory neuron passes on the

Impulses towards the respiratory motor neurons in the Spinal card which via the frenic nerve and the intercostal nerves stimulates moves towards the lungs which stretches the pulmonary stretch receptors the pulmonary stretch receptor why the vas carry the inhibitory influence to the austic center you can see over here Vegas has inhibitory

Influence over the austic center which keeps in check the inspiration should not happen for a longer time that is how the inspiration is Switched Off followed by expiration so expiration and inspiration they both have the reciprocal inovation apart from the inhibitory influence of vagus over the apneustic we can also see the influence

Of the pneumotoxic over the apneustic which shows the inhibitory influence again this image shows the effect of transaction at the of the brain stem at various level suppose if I consider the B level transaction where the transaction is happening between the pneumotoxic center and the agnostic Center here what is happening is because

Of this transaction when the Vega is intact you can see the rhythm of respiration or what we call the rate and depth of respiration is remaining the same there is regular uh breathing which is happening but when the Vega is cut what happens the negative influence of the vas is

Lost over the austic center because of which there is arrest in Inspiration what is called as apneusis so this image or the transaction at various levels of the brain stem explains us how uh the Rhythm the rate and the depth is well maintained by this neural respiratory centers so apart from the neural

Regulation there are again there is again proprioceptors there are some stretch receptors in the Airways there are G receptors there is something called as HB reflex that is hering bre inflation and deflation reflex which gets activated when the tidal volume is more than 1,000 ml uh so next coming on

To when there is apart from the non-chemical control mechanisms if there is any change in the uh chemical composition of the blood that is suppose if there is hypoxia or hypocapnea or acidosis what happens there is another set of receptors which gets activated that is what we classify it under

Chemical regulation of respiration where we can see the peripheral and the center peripheral koted bodies and the iotic bodies I’ll show you the where this exactly located you can see over here the koted bodies which are being located adj just at the bipoc of the common koted into external and the internal

Koted arteries and the iotic bodies are present you can see over the dots which are seen over the itic koted iotic bodies are the one which has got the more amount of blood flow that is 2,000 ml per 100 gram of tissue per minute which are made up of the glom cells

Which have being highlighted just by the side of these carotic and diotic bodies and the other part of the image you can see the Central and the medary chemo reipas which exactly lay over the lateral surface of the highlighted in different colors so when there is hypoxia when

There is acidosis it is the peripheral chemo receptors which get stimulated and there is hypocapnia it is the central chemo receptors which gets stimulated which incense the message to medary respiratory centers thereby increasing the ventilation this is one flow chart or the image which shows how exactly when there is

Hypoxia the ventil ation increases let me just brief you out how the hypoxia that is low po2 closes the potassium channels that is oxygen sensitive potassium channels because of which the cell depolarizes is the glomus cells depolarizes and the calcium enters we can see the entry influx of the calcium

In the picture which causes the synaptic vcle which are filled with the neurotransmitters dopamine to move towards the membrane where there is exocytosis and relas of the neurotransmitters which get combined with uh The receptors which are present with the glossop fenial neural ending which activates the action potential generation this signal is

Transferred to the medary centers which again increases the ventilation this is how hypoxia is going to increase or stimulate the ventilation so how about the increase in the carbon dioxide how carbon dioxide is going this are the same slide so I’m keeping skipping the slides uh Central chemo receptors how

The central chemo receptors gets activated it’s known that the carbon dioxide penetration to uh towards the blood brain barrier and the blood CSF barrier is very fast quick but h plus hc3 minus penetrates very slowly because of which the carbon dioxide when it gets into the CSF what happens it gets

Hydrated resulting in the formation of H2 CO3 which again splits up to form H+ and H3 minus this this is how increase in the carbon dioxide which might result in increase in the H+ concentration which stimulate the central chemo receptors there by the respiratory centers in the medula and brings about

The change in the ventilation or alteration in the ventilation this is again the summary which shows hypoxia acidosis stimulates peripheral and hypocapnea stimulates the central chemor so to summarize the ation of respiration apart from neural apart from Central there are even other receptors maybe pulmonary receptors chemoreceptors myocardial chemo receptors influence

From the higher centers of the brain all these are necessary which can bring about changes in ventilation why are these respiratory centers and the muscles of respiration so these are the references so thank you uh so I would like to uh conclude uh the discussion saying spontaneous respiration is

Produced by rhythmic discharge of motor neurons that’s going to innovate the respiratory muscles in turn regulated by neural and chemical control mechanisms accordingly the rate the depth of respiration gets altered depending on the requirements of the body so I have kept simple the discussion using the concept Maps flowcharts images to the

Maximum uh trying to avoid the theoretical explanation over the slides for making the complex uh Concepts to understand in a simple way hope the regulation of respiration was well understood and I once again thank CCI for giving me the opportunity thank you good evening everyone at the outset

I would like to thank Dr NH Krishna CCI chess Council of India and the office Bearer to giving made this opportunity to speak on the topic abnormal breathing pattern I would also like to thank Dr kwana to making the foundation for today’s webinar and for the excellent

Talk so why we are uh talking about this a abnormal breathing pattern because bedside observation of a patient breathing pattern can hint us to many of the pulmonary diseases so objective of my talk today is to understand various terms in respect to breathing identify various abnormal breathing patterns understanding certain differences

Between them and connecting each pattern with its cause so at the end we will be probably identifying unique feature to diagnose specific disorders so as Dr kaana mentioned in her presentation about what is normal breathing called it is called as eupnea it is the normal unlabored and regular

Breathing at rest and the respirative rate is usually between 12 to 20 per minute so it has a normal pattern depth and Rhythm as you can see here in the graph graphical representation where each waves looks very symmetrical very rhythmic and in the normal dep coming to the first abnormal breathing which is

Pipia where the breathing is abnormally at low rate it is as low as less than 12 breasts per minute and this can physiologically also happens in sleep but pathologically can be seen in hypothyroidism alkalosis narcotic drug poisoning and raise intracranial tension so if you remember EA you can carefully

See this these graph and these waves look little spaced out little slower in the speed opposed to bipa there is teip where there there’s a abnormally rapid breathing rates can be observed and in adults when the respiratory rate is more than 20 breasts perminate we call it technia so physiologically it can be

Observed in patients who are nervous on exertion fever and pathologically in all the cases associated with hypoxia various respiratory and cardiac conditions and metabolic acidosis so what we are observing in this graph is increase in rates of respiration which is more than 20 one now coming to the next abnormal

Uh breathing pattern which is apnea so here what we are seeing there is no breathing at all complete shutdown of respiratory system and we know two of this common variety of apnea which are the center and obstructive sleep apnea and this is what when we want to

Graphically present in apnea it is a straight line it is similar to a straight line as we see in cardiac arrest in this straight l what does it mean there is no respiratory movements hypopnea is decreasing depth of respiration and this will lead to decrease in tidal volume and minute

Ventilation if we talk in the language of sleep study it is more than 30% decrease in air flow but insufficient to meet the criteria of a flatline or an apnea so it is commonly seen in obstructive sleep apnea and if we want to observe in the graph we have a

Reference graph of annea on the uppermost figure and at the lowermost figure it is the normal breathing where the waves are very symmetrically at equid distance present can you see apnea which is a flat line and hypopnea looks like in between the two of them and it has a low

Amplitude hyperia opposite to the hypopnea has increased in depth predominantly and more or less many of time it is asso associated with rate increase in rate of respiration also but predominantly what does it mean is increase in depth of of breathing so because of the increase in depth there

Will be increase in tigher volume and increase in minute ventilation but this is consistent with the increase in metabolism as reflected by carbon dioxide production what does it mean is that P2 is normal in a patient with hyperpnea so whatever increased carbon dioxide is produced in response to that

The patient or person is hyper taking a deep breath and he is able to remove that carbon dioxide where can we see it the these condition and patients who are doing a moderate exercise they are probably taking a deeper breaths now we were talking about the amplitude of uh of respiration and then

We were also talking about the rate of respiration now here come the situation hyperventilation where there is both increase in depth and rate of breathing so whenever we are talking hyperventilation or hyperventilation probably we are dealing with the alular hyperventilation in this alular ventilation is increase out of the

Proportion to carbon dioxide production leading to decrease in P2 below than the normal range typically these patients complain of I Can’t Get Enough air or oxygen so here is a dag rtic representation of hyperventilation I have put a picture of teyia also here because as I mentioned teyia is just the

Increas in rate look at the ample of the graph each graph or each mountains here so they look smaller than the uh uh the graphic graphical representation of hyperventilation so this is a small Ro role play of a patient who is in a panic attack a fe young female and she is

Hyperventilating please look at her breathing pattern the chest movement and the shoulder movement and how and what she is speaking can you with me try to hold your can’t read all right about as we clearly saw she was taking rapid breathes and they were quite deep opposite to hyperventilation

Is hyperventilation where there is a insufficient ventilation and this insufficient ventilation is incapable of removing Advocate carbon dioxide from the blood this can commonly see in patients with chronic obstructive pulmonary disease sleep apnea obesity leading to obesity hyperventilation syndrome neuromuscular and CNS disorders and some of the drugs in intoxication

One of his causes onine curse where individual or patient with this disease forget to breathe during sleep but maintains relatively normal breathing pattern while they are awake coming to the next abnormal breathing pattern which is kmos respiration it is deep rapid and difficult breathing it is named after

Germal physician Adolf kmal and is caused by metabolic acidosis diabetic keto acidosis uremia cerebral tumor toxic indigestion and this is how it looks like deep red rapid and patient finds it very difficult to breathe and they are so rapid and deep that there’s hardly any pause between inspiration expiration or between the

Breaths so this is a video small video clip which is showing chmos breathing pattern in a 10 year-old male diabetic keto acidosis patient so deep breath and high reads so chain Stoke breathing is another uh important breathing pattern in which there is a cyclical breathing pattern characterized by apnea followed

By a gradual rise in respirative frequency and tidal volumes and this happens because there’s a swings in the cerebral blood flow so in other word what we can see it is a cyclic kendu dendu respiratory effort and air flow most commonly seen patients with heart failure and this is the graphical

Representation of the same what we can see here so started with Uka incre inreasing in the rate and depth of the respiration and then slowly it is decreasing and making going to the apnea and again the respiration is slowly gradually picking up so this is the ascending and descending or apneia and

Hyperpnea alternatively coming in patients with chain sto breathing so this is a small clip uh and it is taken from the chest movements of patients who is admitted in uh cardiac ICU a patient of heart failure with rejection infection of 25% what we can observe here the lower most graph

Started with apnea slowly gradually increasing braze and deeper braid increasing in Tidal volumes and what we can see again from the very beginning the amplitude of this graph is decreasing decreasing settling down and on and it will be followed with a complete session of breae which is apnea

So typical seen in patients with heart feeling and stroke coming to the first abnormal irregular breathing patter which is bias breathing it is named after French Physicians camel B uh who first time observed this breathing pattern so there is actually consistent de breast interspersed with apnea due to damage to

The PS from stroke trauma or anal Hy relation and with the worsening pawns insult the pattern becomes irregular eventually detering to another breathing time which is called the axic breathing the bias breathing can also be seen in opiate intoxication and this is how it looks like when we draw the graph of it

What we can see for sure it is not a regular breathing pattern it doesn’t have any set pattern so there is apnea there are deeper breast there are ynic breasts so it is a irregular abnormal breathing pattern now coming to another uh important breathing pattern which is gasping and

Many of us in our in our world have on kind of daily basis see this kind of breathing especially when we are working in ICU or or in other emergency department what it is actually is The Irregular quick Inspirations associated with extension of the neck and followed

By a long expiratory pause we can see these condition in several cerebral hypoxia shock and this is a critical sign of life threatening emergency which is can be cardiac arrest and this patient may be need CPR so this is again a rule uh display of agonal breathing please observe it carefully

Extension of net taking one gasp and there’s a pause again a gas and there’s a pause coming to the next breathing pattern which is ostic breathing so this is characterized by prolonged again gasping inhalations followed by extremely short and inadequate exhalations this also have a poor prognosis because the injury

Is at the Palms or stroke or trauma so temporary induction can occur by the administration of kitamin also for this kind of breeding and this is this is the graphical presentation how the breathe looks like another very interesting breathing pattern signing breathing pattern and I guess most of us have seen this quite

Frequently where the patients come with complaints of frequently interpers deeper breath in between normal breaths they say that there is a desire to take deep breath which no longer can be register and then they have to take a deep sign breathe to open up their lungs

And this can even seen at the rest it is not related to exertion and where can we see this can be can be seen in healthy subjects they are the habitual sign breathers patients with anxiety and depression disorder and again in the other word the patient have this illusion of restricted chest expansion

And insufficient breath so uh uh now I’m concluding my slides and presentations here is the diagrammatic representation of few of the abnormal breathing pattern which we have gone through uh today and but we will be learning about these abnormal breathing pattern or some of the one

Which I have not touched probably we all we will take all that abnormal breathing patterns in our panel discussion with this I thank you all these are my references so with this I end my talk here and we will be discussing more in detail about all this abnormal breathing

Pattern in our panel discussion thank you very much for patience listening uh over to you Dr bat thank you so uh we had excellent Talks by kaana Madam and Madam I think they more or less summed up what we are going to discuss today and uh this topic is bit tedious

Or bit difficult but they have simplified uh the talks and the concept I think very clearly the flow is we will have few questions we have to our panelist and then in the end we will have few cases so that all of you can take home very nicely what all these

Different types of breathing are my first question is for kavana Madam who is an imminent physiologist with us madam what is the role of J receptors in the breathing mechanism am I audible sir yeah yeah thank you sir for that question uh so when we consider J receptors actually uh they are gxtra

Pulmonary capillary receptors uh they are placed exactly in the interstitial space which lie between the alviola endothelial layer as well as the pulmonary capillaries they are nothing but unmarinated vagal nerve endings uh actually they are very sensitive to increase in the content of the interstitial fluid which gets stimulated

When there is pulmonary congestion maybe when there is pulmonary edema and when there is hyperinflation of the lungs suppose if we consider there is hyperinflation of the lungs what happens is this unmarinated wagal nerve endings they get stimulated that means this G receptors get stimulated when they get

Stimulated they are the one which are going to reinforce the action of the pneumotoxic center and as well as the centers in the bonds which produces the intermittency in Inspiration uh what we call as inspiratory neuronal discharge which results in maybe reflex apnea followed by techia there will be

Decrease in the heart rate as well as uh decrease in uh blood pressure and finally this can also result in the weakness of skeletal musles uh along with this if I have to explain the physiological role does it play any physiological role these G receptas exactly there is a physiological role if

We have to consider severe exercise what happens is when there is a severe exercise some excess fluid gets accumulated because of which the Gs are going to get stimulated which results in dis and J receptors are going to inhibit the spinal stretch reflex which decreases the skeletal muszle contraction that

Means uh during severe exercise uh the person get exercise because of this scal muszle weak and I at this point of time I would like to add one more important thing as we all remember the Bal gas tragedy which happened in 1984 2 or third December 9th uh where some around

40 to 50 tons of methy isocyanide escaped from the pesticidal plant the survivors of the Bal gas tragedy uh as painal who is the discoverer of JP has mentioned that uh the one who escaped from the Bal gas tragedy uh they had shortness of breath they had reflex

Apnea teia so and so and he has correlated that symptoms with the stimulation of J receptors so that is one point which we have to uh remember and remind of the tragic event of Bal gas wow we never this so this is a a good point I think everyone anyone wants

To add anything to this or or any other questions to Madam regarding any receptor if anyone wants please ping or we can have another question so the next question is for Amba Madam madam what is actually you have told about all the kinds of various kinds of breathing but uh my

Postgraduate students they ask me what actually is the clinical difference or how to differentiate between a bias breathing and a cluster breathing ma’am can you please elaborate on that so thank you very much for the question so yes it it’s a bit difficult especially when pulmonologist uh not that frequently come across with

This breathing pattern of bias or clusters breathing because this mostly is seen in the neurological disorders so both of them are abnormal breathing pattern and uh both of them are a serious neurological issue and what is the difference if you ask me so as I mentioned in my PP also that biased

Breathing is a irregular breathing pattern what happens there are deeper breeds or shallow breeds and in between them there is an apnea which can be of any duration so why we call this irregular because one cannot predict that deeper breath will come and then apnea will come or the shallow breze

Will come so it is a irregular pattern which cannot be guessed like the pattern will follow in this way so bias breathing is probably if we localize as Madam has mentioned about the central nervous system and respirat Center so it is the medula where the center can be

And the diseases or damage tumor or trauma or Uncle herniation of P of Pawns and medula both the places if they are involved we see this bias breathing patterns this can become more aggressive when uh this irregularity is increased and it is seen especially when there’s a pontine hemorrhage and paes involvment

Is also there and the breathing from bius become to the another breathing pattern which is a axic breathing pattern so this is the bias now coming to the another breeding pattern which is the cluster breeding pattern so unlike bias bias here what happens that breath comes in the Clusters and then there is

In between apnea breath will come in clusters there will be apnea then it will comes in the Clusters here if you say got where is the center Center is in the bonds again trauma tumor and infections of Pawns or brain stem can lead to the uh cluster breathing pattern

So both of them are neurological issues and mostly seen in neurological icus or in the neurological emergency area or in the trauma center one can see this building patterns fine fine great answer ma’am I think for all the postgraduates who are listening to this this is a good answer clinicians

Maybe but while you learning or uh for for you to write in your exams or to answer I think Madam has elaborated it very nicely my next question is for Dr shrier sir my very good friend from poloo Hyderabad sir what exactly do you mean by paradoxical

Breathing Sher sir can you hear us yeah yeah hello am I audible please yeah yeah please you mean by paradoxical breathing the question for you yeah so paradoxically breathing here we’ll refer to two concepts over here we’ll just discuss about them in detail uh one is we can be talking about the neurological

Diaphragmatic Paradox wherein when normally what happens is when we taking a deep breath the diaphragm is supposed to move downwards and that’s how the thoracic cavity expands and as a result of this the lungs increase in size the total lung capacity that’s how a person reaches total lung capacity only if the

Diaphrag moves down so if at all anything opposite happens that is if at all the diaphragm is moving upwards during inspiration and downwards during expiration this is known as the neurological diaphragmatic Paradox so in this what exactly happens is it could be either due to a weakness in the inspiratory muscles why could

This weakness occur either due to a neurological insult it could be a stroke or it could be some infection involving the frenic nerve for example a vasella herpes saer or it could be a potis or it could be a transverse mtis also causing frenic nerve injury or driving Direct

Fric nove injury it could be either during cardiac surgery as a complication of a cardiac surgery as a complication of CG or due to radiation induced injury or maybe direct trauma as in the case of road traffic accidents the other thing which we need to know about is flame

Chest it’s not exactly a form of a diaphragmatic Paradox but it is a form of paradox this occurs predominantly in trauma there are two different you know definitions for this one they say that two ribs have to be two continuous or contiguous ribs let’s say I talk about

Rib number two and three or rib number three and four this should be injured or broken or at least in two different places so one whole segment of the chest which is not in continuation with the rest of the chest we have a small piece of the side so this basically disobeys

The normal Inward and outward movement of the rest of the chest so in case of a fla segment we have a movement of the fra segment which is opposite to the movement of the chest wall so during inspiration the fla segment goes in and during the expiration uh sorry during

Yeah and during the expiration the fla segment moves out so this is what actually happens okay fine so this is what is paradoxical breathing anyone wants to add anything to this so uh sushil sir any more comment about paradoxical breathing you want to make I think he has very nicely

Explained it well I don’t think anything must to be added to it I think okay so we will go now to the clinical questions now I my next question is going to be you this is all Theory so now we will just go to some applications of this I

Feel just say I am very young into practice but Maxim there is no per se a problem it is just abnormal breathing like some of them hyperventilate some of them are anxious I don’t know this is my clinical experience for like four or five years

So my question to you sir is what is the most common type of abnormal breathing pattern which you see in your practice so that we can learn from you and how do you manage it now I think this you have already mentioned for a pulmonologist the most common uh abnormal breathing pattern is

Tpia that’s what we all see and I’m sorry this is nothing fancy but that’s what we all see I don’t think pulmonologist see anything else usually in routine clinical practice most of the time we see teia and whenever you see teia that is a patient is having a

Respiratory rate more than 20 even it there is a settle teia you should be cautious and you should start taking a detailed history a good clinical exam and and relevant investigation accordingly to figure out the cause of teyia now teyia can be various causes including anxiety or fever or various

Cardiac or respiratory illnesses and so we need to really try to figure out what is the cause of the teia and unfortunately in when the teia is relatively subtle sometimes in a busy practice you may miss it so we always I always believe that all of us should be

Doing a very good history an examination and look at the respiratory rate of the patient also as a part of your evaluation of a particular patient another important thing which I would like to add here is though we are ask you have asked for a common problem that

Is teia but what I say is that we should be able to know other relatively uncommon breathing pattern because sometime you will be able to pick them well if you brain and your eyes are trained to pick up those relatively uncommon or rare breathing patterns so I

Would put it this way that this the the whole exercise which we are doing today is to understand those subtle subtle simple things that by clinical examination or just by seeing the patient you are able to pick up those abnormal breathing patterns like biot breathing or chain stroke breathing so

Next time when you see a patient probably you’ll be able to see able to recognize them and believe me we are often overlooking these cases and for me for example we often go to neuro IUS and once you start seeing these cas start thinking about it you’re able to pick it

Up and for example if you have seen a bios breathing or chain stroke breathing you can actually narrow down your evaluation narrow down your history narrow down your focus your history your examination and also your relevant investigation according to the pattern of breathing you’re seeing for example

Just to say someone who is a diabetic and come with abnormal breathing you should start thinking that is it having AO acidosis that’s putting up the case like that so this is the way and for example a patient who is in a neuro IU having strok breathing or or biot

Breathing you should you should be able to focus your investigation and find out what is the cause of the problem you may having a neurological cause of problem and they called you for breathlessness which is not related to your system so what I’m trying to say is the the whole

Exercise is we should be able to exactly clinically figure out what is the particular type of breathing we are seeing and also narrow down the evaluation accordingly so I don’t think that these UNC commmon thing would not come to us all of us will see some of these abnormal breathing at some point

Of time and we should train our eyes and brain for them that’s what the whole issue is here yeah great great answer sir great uh my next question is for kaana Madam we’ll go now into more clinical questions and clinical applications Madam uh you being a physiologist what is the role of chest

Physiotherapy as such in the management of this all abnormal breathing patterns in a long long term um to answer your question uh regarding chest physiotherapy uh definitely a physiotherapy expert would be a a great regarding this uh answer but I I’ll try my best underlying the physiological

Basis uh for this actually when we say chest physiotherapy specifically we start with the objective of like to improve the ventilation to the areas of local lung area wherever there is obstruction uh as well as we also see towards with an objective of clearing the secretions as well as to improve the

Ventilation of the smaller Airways so that that increases the lung complience and so that the work of breathing as well as the oxygen consumption will decrease and that will definitely improve the gaseous so if I have to comment on few of the uh chest physiotherapy uh maners which usually

Followed uh uh I can talk about the diaphragmatic breathing wherein usually the diaphragm takes over the role during the quiet breathing but in case of the patients with respiratory illness what happens the patient might relay on the accessory uh uh musles of respiration where in which the patient complains of breathlessness or the

Shortness of breath so this diaphragmatic Brea manure uh might help uh in order in helping in clearing the secretions of the mucus from the respiratory passage so other than this uh there is one more manual what we call as incentive spirometry uh most of us are aware of that three colored balls

Which will be kept in the pipes where uh the different maners of inspiration will be done so this also helps in clearing of the airway decretion so other than this there is one more method called percussion where suppose if I consider this as the chest and usually we uh do

This cupping procedure where this axess gives a cushion effect and this hollow sound could be there so that this is the Manu which we do for the cupping for uh percussion where it also clears off the secretions it is said so other than this the vibration procedure where there is

Intermittent chest compression we do and as the person to uh take a uh normal briefing that this procedure is being done during expirations and other than this there are also few mans like other than a usual procedure like coughing which helps to remove the secretions and positive expiratory uh

Pressure manuals nowadays even uh just physiotherapy devices are also available that is prep continuous positive Airway CPAP uh procedures and on the chest wall oscillation where high frequency oscillation is being applied over the chest wall uh which helps in clearing their secretions and uh definitely uh each of the device or the manuals

Whatever we use is will be having uh the risk as well as the benefits and the main intention behind the chest physiotherapy is in order to improve the compliance decrease the work of breathing and in and to clear of the secretion so that the airway will be patent enough for the good better

Gases yes yes thank you thank you madam taking this question only or this discussion I my next question to Amika Madam is like Madam how do you really be differentiate I don’t know I I mean uh I might be wrong in this but this is what

Madam has spoken about is about our uh the cases which are diagnosed which are in the ICU or which are long-term diagnosed as COPD and I just want to give an example if there is some young male uh coming to your OPD especially after covid the perception of breathing

Has changed a lot among people this is what I feel so Amika Madam how do we really differentiate between tpia hyper apnea hyperventilation kusal breathing is okay but this tpia hyper apnea hyperventilation whether it is really clinically significant or what to do about it when a patient walks into your

OPD with such complaints Amika Madam thank you very much sir uh very interesting question no uh as sash s also mentioned you know the dnia is the most common uh abnormal breathing pattern which we see but unfortunately it is highly non-specific because tpia can be seen in cardiac problem metabolic

Problem respiratory problem or if there’s no problem is just because of the fever anxiety it can be seen in that way so it is nonspecific but one thing is that if this is an important viter sign and the patients respiratory rate is more than 20 per minute it means we

Need to thoroughly see this patient this patient has come with a uh important finding of teyia let’s rule out the cause where it is lying whether it is a cardiac or the other one so here is one pattern the teyia is actually only the increase in respiratory rate and this

Can happen in more lot of clinical condition which I enumerated other than that is hyperpnea hypera is different from teia where teia is only in increase in rate hyperia is there is increase in depth of respiration the rates may or may stay same so the amplitude of the

Graph as as as I was mentioning in my uh PP so that is increased that means the tidal volume the patient is taking really deep tidal volumes and increasing the minute ventilation the good thing about hyperia is mostly it is seen in the physiological States like moderate

Exercise you know when there is more of the oxygen requirement a little more carbon dioxide is formed which is washed out with taking deep breaths like hyperia so these two are U this way and the similar looking thing is you know uh hyperventilation syndrome and in hyperventilation what happens it’s a

Mixture of both the rate is also fast and there is uh there is a depth of the respiration which is tighter volume and minute ventilation is also very high difference between uh hyperia and hyperventilation is very important when we do a ABG what we find hyperia

Patients have a Normal ABG and P2 levels are normal they never exceed to clear it out un uh opposite to this in hyperventilation what happen the P P2 is washed patient goes in respiratory alkalosis and as we know this can happen in many conditions the common one which

We show we saw in the video was a hypervent ulation syndrome and a panic attack in a female and in this such patients what we have to do we have to check for the clinical examination chest oscilations and all and if we find we do

A quick ABG and we find the patients in respiratory alkalosis so in that way it can hint to this and same similarly going when we are talking about teyia hyperpnea and uh hyper hyperventilation similar looking is the kusas breathing that is also fast and Rapid breathing in

Fact hyper when ventilation is is kusas is one kind of a hyperventilation but kusas is so fast it depends upon the level of acidosis in the blood so there is no pause between inspiration and expiration they are all coming touch to each other so this is a subtle

Difference between all the four patterns which we see in clinical practice and thank you ma’am I think Madam made a very good point here that a detailed ABG should be your goto or final investigation if you have any confusion uh about what kind of breathing pattern you are dealing with

Uh coming to our next question I think I want to ask Dr shrier which there is a very important subset in the abnormal breathing patterns which is the Sleep Disorder breathing so sir can you just I think this webinar will be short if we go into details of sdbs but in short can

You just answer what are the different types of sleep disorder breathing we see okay okay okay thank you bat so we’ll just as you said we’ll try to be as brief at possible because that is otherwise a Pandora’s box alog together and a separate webinar but just to

Highlight them we have just discussed about apnea Amika Madam has you know kind of shown us the graph and tried to explain so apnea is nothing but either a complete cessation or a near cessation of air flow to the tune of at least 90% decrease in the air flow compared to the

Preceding signal so as we all know during a polysomnography we measure the you know the the air flow as well as the change in rate of flow so for an apnea basically we differentiate it as an obstructive apnea or a central apnea or a mixed apnea based on whether the

Patient is having respiratory effort during the event so if at all the patient has stopped breathing that is the flow is 90% lesser along with continued respiratory effort as we can make out with the respiratory inducting SP graphy in that case we call it as an obstructive apnea which means there is

No breathing but the abdominal muscles do try to struggle and maintain some sort of an effort during the process of this apnea now Central apnea is absence of breathing and absence of a respiratory effort so the whole chest right from the sorry the whole uh chest

And the abdomen appear flat and it looks as if the patient is not is not trying to make an effort to breathe at all mixed apnea is a little different because initially there’ll be an absence of respiratory effort and the later part of the event is followed by the

Appearance of the abdominal movement this happens throughout without any air flow so initial part of a mix stpa there is no air flow and no respiratory effort and the later part of the mix stpa has a respiratory effort and hypopnea basically is there is a reduction in air

Flow to the tune of about 30% so we can make out a different if you are observing the video recording of a patient who is being subjected to a level one polography we can make out that the air flow does decrease to about

30 to 35% but not as much as an AA but of course in both the cases that is apne and hypopnea the diminish air flow should last for at least 10 seconds the only thing for an hypopnea we have an additional concept of a desaturation so

If at all there is a 3% desaturation from the Baseline let’s say started off with 94 close to 91 or there should be an arousal however because we have so much of inter observable variability if to make it simpler they mentioned that hypop should just have a 4% desaturation

Whatever be the initial value there should be a 4% drop from that initial value there is another interesting phenomena which is called as respiratory effort related Aros so this basically is a change in air flow that does not beet the category of an apnea or a hypopnea

But notice the ini initial part of the term that is respiratory effort so there’s a disproportionate increase in the amount of respiratory effort which is much more than what is observed for an apnea or a hypopnea so this is a thing which everyone should observe instead of relying on the machine

Related uh you know situation suppose the machine may you know interpret this as a hyp apnea or a hypopnea whereas a trained polyal graphit will interpret it as a respiratory effort related arousal chain Strokes breeding is already been uh described but as far as polygraphy is concerned we need at least three such

Events okay three such consecutive Central respiratory events in the cresendo and deep chendo State and we need to have a cycle length of at least 40 seconds so this is what differentiated especially if the person is asleep we want to label it as chain stroke respiration in our final report

These criteria have to be present and at least five such apneas and hypopneas of Central apneas and hypopneas should be present per hour okay so three consecutive Central events followed by at least five s apas and lastly hypoventilation hypoventilation M has already explained but as far as sleep is

Concerned we should be documenting a raise in the pco2 so it the absolute value of pco2 should be at least more than 55 mm of mercury for at least 10 minutes this we can document it with a transcutaneous pco2 monitoring transcutaneous CO2 monitor or or if at

All we are not able to get an absolute value we should document an elevation of at least 10 mm above the Baseline value for the same length of time this we have to see in a copia who is a habitual CO2 retainer say say started off with 55 mm

His value should go to at least 65 mm of mercury for a period of 10 minutes or more during sleep that’s when we call it as a hyperventilation perfect very nicely I think the last point is a very take-home point for all because an advanced COPD we might

Misinterpret uh the patient so my next question uh trying to summing up uh to sushil Sir who is the most experienced panelist we have sir uh what are the abnormal breathing patterns which you see in adults especially and uh does over Mobile use or anxiety stress due to exams does these all psychological

Issues have a predominant in manifest sttion of the same especially when you the outpatient Department patient with an abnormal breathing pattern sir uh yes uh psychological issues are important in pediatric patient and Adolescent patients I call I would divide the various abnormal breathing patterns in adolescents into three uh

Different uh categories one is psychological causes other is um the pathological cause and the third one is physical so to go into more details of it now if you look at the psych psychological causes anxiety depression and you as you rightly said over Mobile use and peer pressure all these things

Can lead to psychological pressure on the kids and they can have abnormal breathing patterns those psych psychological causes have an important role and that need to be looked at and should be hello yeah yeah sir I’m audible oh sorry so psychological causes need to be looked at and should be addressed if

There’s a psychological reason if there’s an anxiety or depression you are able to analyze and feel that then you may have to involve the psychiatrist to help you that is one thing second thing is um the as I said pathological causes um patients may have asthma which may be

Undiagnosed or their patient may be actually having something else and they have been diagnosed as Asma so need to be looked at the pathological causes a lot of times in kids the asthma may be misdiagnosed or maybe not diagnosed at all so then so that need to be thought

Of in case someone adolescent is having breathlessness on exertion along with other signs and symptoms of asthma third thing which comes to my mind is physical causes again that’s important because obesity is fairly common in adolescent nowadays and that also can cause abnormal breathing pattern so these are

The things we need to look at psychological pathological and and and physical causes so we need to look at all these possible causes in and as I already mentioned psychological causes and physical causes are now becoming more and more prominent and more and more visible once you start looking at

It and with today’s lifestyle these two are important cause apart from the various pathological conditions like Asma or other chronic respiratory diseases so we need to look at in all Pediatric and Adolescent cases also I think sir has put it up very nicely divided it into three types and I think

All of us right from day one of our practice we see or we are likely to see such patients uh there is one more question from Dr harendra Tucker from Gujarat uh how to differentiate with between various types of acidotic breathings I think Dr shiker sir I would like you to answer

This yeah so as far as acid IC breathing is concerned uh there is a very variable presentation though we associate kusal breathing more commonly to acidosis we may have a slight difference between or an overlap between pipia pmal breathing and also simple hyperopia as far as the acidosis is concerned and the

Rate of or sorry the depth of acidosis also kind of differentiates between so in very severe acidosis once we have a uh you know once it goes beyond the peripheral chemoreceptors to pick up estasis we do see because the the the activation of the peripheral chemo receptors or the glomus body rather is

Going to increase the depth and the rate of respiration but once the aerosis becom so severe That central nervous system is affected once the CSF bicarbonate levels are affected then we can have a classic deviation from this pattern of breathing we may actually have sometimes you have variable

Presentations like maybe a bradia in some individuals you may actually have irregular breathing patterns in some individuals so uh the the level of acidosis and the extent of uh you know the change in b or the bognet shift in the CSF is what you know decides the

Pattern of breathing in a patient with acidosis very nicely uh explained so I just got a message that uh this webinar is being watch by approximately 1,155 people are watching it live so we thought it is an abnormal topic but many people are definitely interested in this uh hearty congratulations to the entire

Team of CCI the core committee uh NH Krishna sir especially who is the brainchild behind this topic and obviously Sia for this great academic initiative uh if there are no more questions I think we can go to few cases to sum up our discussion for everyone uh

So that people can understand what we have all discussed up until right now is it okay if I share my screen yeah please just a so we have four cases here uh for us to discuss and uh I’ll take them one by one uh the first case I think I will ask uh

Most senior panelist of us uh to answer this case scenario one a 27y old student was admitted to the ICU with decreased level of Consciousness GCS 9 his lab investigations with a very high sugar Ura of 282 High creatinin the ABG shows the pH is 7.24 pco2 15.6

P214 the bicarbonate is 6.7 his breathing pattern was observed to be deep labored and Rapid type sir what are we dealing with this uh as you have already mentioned this is a young male coming with altered sens sodium and very high blood sugar and with Aki so and with the acidosis so

This is a metabolic acidosis so this patient is having a diabetic keto acidosis with Aki and that’s the diagnosis I would make now important things to see look at it here is that this patient is also having something which is kumal breathing so patient of diabetes coming with an abnormal

Breathing you should always keep this in mind that this can be possibly a case of diabetic keto acidosis so if you see an abnormal breathing like that and with a high blood sugar then definitely that need to be think thought about so a diabetic patient when he comes to you in

Your clinical practice with abnormal breathing I would like to do of kumas breathing if you are able to figure out that this is a kumas breathing you do three things one is do your the blood sugar second is look for the ketones uh either blood or you can you at the if it

Is not available you can see the urinary Ketone and the third is the blood gas so once you have done these things you should be able to diagnose a case of diabetic keto acidosis on the basis of it and once you have diagnosed it as a case of diabetic keto acidosis we I

Would suggest to do three more things one is look at the serum electrolytes get the renal function test done and the CVC so these are the tests we should do so that we can further manage this patient better so now this patient is a case of diabetic keto acidosis with AI

And in this patient the management as all of us know we should treat this patient with fluids this patient will need fluids we’ll need IV insulin therapy to get the sugars down and to manage the serum electrolyt these are the core things we need to look at treat

It and then once we do that we should be able to manage this patient properly so that would I would uh suggest uh uh that’s way I man this patient yeah so as Sir had already told all of you that once you look at these breathing patterns probably you can diagnose the

Patient better and you can manage the patient also better what investigations to send and how to manage you can get an idea with this so uh my second case uh this is for Sher sir a 54y old female known case of type 2 diabetes hypertension presented to emergency

Department with complaints of new onset whato and left-sided weakness of 5 hours duration she also presented with left-sided hemisensory loss with decreased pain and temperature perception facial asymmetry was noted the MRI brain revealed the presence of large infact in the right paramedian pontine region his breathing pattern was

Assessed which revealed a series of normal tidal volume breaths alternating a prolonged respiratory pause followed by a similar breath patterns there were varying apnea intervals between each such respiratory cycle so what are we dealing with this sir yeah b s so this is a classical case

Of a pontine stroke and we can notice in the right p in you know in the paramedian region so the problem with the ponds is unfortunately it’s a pretty big area so here we have got so many you know vessels which are supplying it you have parts of the anterior inferior

Cerebr artery Superior cerebral artery you know you have you know the the whole posterior circulation and as far as this particular area is concerned you have the paramedian Perforating AR which are basically basil artery origin so as you can notice once the Bas arter is involved you can see the other

Symptoms which you’re seeing here you know as they are having vertigo here and they also having you know this thing this contralateral weakness and along with uh the spinothalamic and the corticospinal tract involvement as you can make out the Spain and P temperature perception so once the pawns is involved

Depending on the level even though it’s mentioned in literature that you know the lower pawns and higher medul involvement you can have cluster breathing and but in you know in reality if you read the case reports there’s no particular clear differentiation as to which area of the pawns can cause which

Type of breathing of course we have got biot breathing and Madam had very beautifully explained the difference between biots and you know uh cluster breathing and axic breathing but it is to be noticed here once you have got certain changes after this in fact if at all you’ve got Uncle herniation what

Started off as a biot breathing can progress further it may move on to axic breathing ultimately and may go on to agonal breathing too so having a diagnosis here of a biion breathing of course this case is something which we won’t really encounter on a day-to-day

Basis it may go to the neurologist but we may be called in uh you know as so that we assess what exactly is going on here you know they may get a doubt because the patient is immobile do we need to Ru out a palmary embolism so

What our you know primary aim is is to try and identify this pattern here so after identifying the pattern and discussion with the neurologist it is important for us to thereafter prognosticate the patient as biots can lead away to some other pattern of breathing depending on the ongoing

Insult let’s say there is a bleed into the left paramed region so the the the inal pressure may increase and we may switch over to another pattern of breathing so the mere identification is a sign of emergency our role is to make sure that we reveal the seriousness of

The situation ABG may help us or may not help us as far as a biots pattern is concerned but it is to you know inform the neurosurgeon and probably a Neurosurgical team to tell us that something more ominous is going to take place the patient is by no means

Clinically stable and we may have to prepare for the work first or rather take action so that we try to reverse this pattern of breathing with effective treatment very very nicely told I think for everyone listening this should be a take-home point in nowadays where uh even in all places wherever you practice

Medical legal scenarios are increasing so this especially when you’re dealing with a neuro case the type of breathing pattern may help you to prognosticate a patient may help you tell the seriousness of the patient and probably you can counsel the patient’s relatives accordingly I think this is a very

Practical Point made by shrier Sir which everyone of us should follow henceforth uh coming to my third case this is yeah anyone important thing what I would like to add to what in the second case is that now lot of times we are as a pulmonologist are called for cross

Consultation into neuro and neuro IUS and whenever there is abnormal breathing pattern is thought that it is because of the respiratory cause so please don’t forget that they can be a lot of neurological causes which can cause abnormal breathing pattern so that need to be thought of and should be managed

Accordingly yes yes perfectly said sir so we may get a call from the ICU from a neuro IU where we diagnose a breathing pattern and as both of them said we involve the the neurophysician or neurosurgeon and then we talk about it and it’s a joint management

Accordingly my third case is for Amba Madam uh we as pulmonologists are more likely to see such case I feel a 65y old male patient known case of diabetes hypertension CAD post ptc2 lad with a ejection fraction 35% and there is some ISD components still present who has

Presented for a routine checkup his Baseline symptoms showed no acute worsening usual symptoms included breathlessness on exertion n gr to mild pedal edema orthopnea occasional episodic we and nocturnal cuff his spouse had not noticed off late that he would progressively increase his depth of breathing to a point of gasping

Followed by a decrease which would ultimately end in Long breathing pause this pattern was observed during sleep as well as during wakefulness State while he was reclining on an armchair madam what are we dealing with so the breathing pattern described in this case scenarios is consistent with chain Strokes breathing so if

Somebody has to learn the definition of chain this question has been designed so very beautifully it it takes all the important Point what is seen in the patients with chain St breeding one Elderly with CAD ection infection 35% patients have dnia petal edema orthopnea and nocturnal cough these are

All goes with the congestive card cardiac failure and the what the wife has noticed for his husband’s her husband sleep pattern is that she’s noting that he’s slowly gradually taking breathe and sometimes he’s not taking bre breath and that is the probably the concern the wife has because many times

It looks like the patient is not breathing at all or is it or something like that the apneas can go really long for the even it has been reported that can go up to the 40 seconds also so the patients goes in the Gasping pattern and uh interestingly the other very

Important point which has been mentioned in this question also that these patient can have this breathing pattern both when they are in sleep or they are awake so this pattern of ascending descending breathing pattern and apnea goes very consistent with the chain stroke breathing I also want to bring a very uh

Important pathophysiology which is postulated for this condition you know uh because if we see all the graph this graph looks most interesting you know it is very good to draw slowly gradually picking up and then a flatline then so what is the reason behind this pathophysiology so patients with uh

Chain sto breathing and patient with the central sleep apnea especially with the patients of heart failure so they have a BAS Bine decrease paco2 level as Dr kaana Ma has mentioned about the chemo receptors the neural inputs so the chemo receptors in the blood they can sense

This hypo uh hypocapnia and what they will do they will ask uh they will ask uh the uh brain the the signals will go to the brain and the Brain will ask the respirative muscles to slow down to slow down to maintain the P2 level as we all

Know that balancing is the nature of our body the pH need to be balanced the P2 and po2 need to come in the compensations so the compensation starts and what will happen the PS2 will start because there’s an apnea it will start building up it will come to the normal

So in ideal situation when it comes to the normal the brain should and the chemo receptors should make the uh the brain know that the pH is normal but what happens in patients with heart failure their heart are really pumping slow so there is a delay from the

Pumping to reaching the uh cerebral circulations so by the time the brain Rees again that the apnea uh is over the PS2 normalize the patient stays in apnea for longer and then he eventually goes in uh hypercapnia the P2 Rises so what brain will get another signals is about

That carbon dioxide has Rose and it will give the brain uh the brain will direct to the respirative muscle that you have to take half fast breed hyperpnea so that carbon dioxide goes off and wash off and when it is washing off again the same U because of the delay in the

Circulation it will wash up too much and there will be decrease in P2 and this keep on going this cycle keep on going in patients with congestive heart failure and uh um surprisingly it is quite common in patients with heart failure it can be seen as common as in

50% of these cases and if the acne episodes last longer and this are very consistent finding in the patients sometimes it it it suggest that it is not a good prognostic uh finding what we are seeing in patients with heart failures so all these patients uh maybe probably can be treated with oxygen

Inhalation and CPAC therapy works very magical so sleep study has become very popular in these patients and we are picking a lot of central sleep apnea and chain stroke breathing pattern in patients with heart failure I think very nice Point made by Madam that especially when you’re are dealing

With a heart failure patient in all parts of India now sleep study is picking up and then uh we we have a mixed sleep disorder breathing maybe a chin stroke breathing and accordingly you can uh manage this patient my last case uh uh is uh to kaana Madam this

Question is an 87y old man presented to OPD with shortness of breath of one month duration along with loss of weight and appetite examination revealed a cic male with mild confusional State routine blood investigations were Normal ABG showed a pH of 7.6 pc24 p2115 H3 bicarbonate was 11 CT chest was

Normal MRI brain revealed a T2 prolongation of the right frontal lobe and right dorsal midbrain it was a biopsy proven CNS lymphoma his breathing pattern was assessed which showed a tpia without respiratory for pauses and showed no response to uh deep SED madam what are we dealing with hello kaana

Ma’am so uh it’s a case of 87 year old man who presenting to the OPD as we see here the ABG analysis pH is pco2 value is low uh where the ABG analysis Point towards the respiratory alkalosis uh so Amika Madam has excellently explained already the

Scenario behind this uh it’s a case of central neurogenic hyperventilation uh from the physiological point of view uh if I have to explain this uh actually when there is a supram medular inhibitory Pathways damage what happens exactly is the medary central chemo receptors they become more sensitive to the action of

The carbon dioxide that is where we see this hyperventilation once there is hyperventilation uh the phenomenon of increase in the rate and depth P pattern of breathing happens so along with this year we are also uh noting uh the mild confusional state where Dr suil s has already explained even the psychological

Issues that happens with the uh breathing patterns so the technia the low levels of PC2 usually what does it do is it decreases the formation of H+ and H3 minus in the blood which is going to cause the increase in the pH to about 7.6 what has happened here so along with

This there are even other explanation with the physiological basis if I have to explain uh what happens exactly here in the central neurogenic hyperventilation is there is uninhibited stimulation of both the inspirated as well as the expiratory group of neurons in the medula uh right from the lateral

Reticular formation and as well as from the laterally located descending Pathways so because of this uh the hyperventilation is being seen here which is the breathing pattern abnormal breathing pattern explained in this scenario hope I think Dr suil sir can help me out in connection with the uh clinical symptoms along with the

Physiological basis is I think you have already described it nothing more to add in this particular case um anyone else from the panelist want to add something to it I think this is uh all what we have discussed is enough for this particular case I feel uh because uh these cases

Are generally seen or what we see as a pallative medicine kind of uh thing is there this breathing pattern as shrier Sir had pointed out we may be able to prognosticate patients on basis of this breathing pattern especially when a neurological case you’re dealing with a neurological case uh there is one

Question from our very own triip sir from Mumbai um I will keep it open but I will put up it to saana Madam because it is how actually useful are these oscillation devices are positive pressure devices like the aerobica which is marketed by a company they uh are

They supposed to have some uh good action in clearing secretions when especially you’re dealing with any abnormal breathing pattern patient Madam please what are your views on it ma’am can you hear me H so you were talking about those percussion therapies and all so are what are your views on any particular device

Like this aerobica device which the is being spoken about or any other device which a physiotherapist uses for clearing of secretions how useful is that uh so as I said sir uh like actually each device has its own risk has its own uh benefits and actually when we speak of this oscillation uh

High frequency chest wall oscillation devices uh what usually it involves like there’ll be a inflatable West which will be covered over the chest which will be attached to a mission and uh usually it’s like a physical chest therapy where high frequency vibration is being given

Off and it is uh said that the West which covers the chest wall uh which vibrates at a high frequency is going to uh loosen and uh loosen the secretions as well as it is going to thin out the mucus secretion so every person every five minutes what

Happens is the person stops the machine coughs and takes off the secretions this is what happens in usual oscillation devices which we use uh these have been I guess being used in uh the chest therapy department physiotherapy department where definitely it’s going to loosen the secretions at the end of

The procedure the person is made to cough out and throw out the secretions I would you like to add any clinical aspect for this like how we I put it this way now we are talking about abnormal breathing patterns and we are talking about cuff cuff releasing devices and those devices which could

Help to bring out the C there are two I think there are two different aspects of the problem uh I what I would say is that yes these devices are there in the market for a long time lot of devices I’ve seen in last two decades which have

Come and gone none of them have really become very popular yes theoretically there are paper theoretically I would say even there are papers which have suggested that these devices are useful to bring out the secretions and the thick mucus plugs which are in the Airways they help uh but those

Commercially available devices for the patient directly have not taken off very well in real world practice that’s what I would say yes the physiotherapist whatever they are doing for Physiotherapy and exercise training and other things they doing in the department that has well proven that is but those devices which are commercially

Available for direct use to the patient have not really taken off very well that’s what I’ve seen there are a lot of devices which came the flute came and then there other devices came which didn’t really took off very well at least from the clinical perspective

Anyone would add to it I have seen so many devices which came and gone none of them has really stayed with a test of time in clinical practice uh sir please correct if I’m wrong so what I also wanted to uh you know kind to understand is whether these

Devices have a role only if used correctly like let’s say the person has to use hyponic saline first to moisten or humidify the airway Then followed by the use of oscillating pep device and at the same time probably add on a chest physiotherapy to ultimately loosen the

Cations and cough it up at the same time using additional techniques like maybe an active cycle of breathing technique or a diaphragmatic breathing exercise I think if all are used in synchrony and in a correct fashion probably then it would have I think opep has no individual role by itself if a person

Doesn’t humidify the airway there’s no meaning in using aerobica to Lings practically none of them has really really stayed the test of time I remember there was a device for lung flute which came in it was FDA approved and they never asked for all these prerequisites for using it and uh we

Were very excited about it and really it didn’t stood the test of time and it just gotone we no longer having it in the market anymore so all those devices which are been given to the patient for use at home have somehow doesn’t stayed well in real world that’s what I’m

Trying to say they may have some role but somehow practically they have never stood the test of time in real world as far as the physiotherapist who are using them devices various devices in the physiotherapy department they have really gone well for example the percussion device and other things that

Have been there but these are all and we are talking about devices like aerobica or lung flute which is not really I would say in clinical practice it has not done much though they have some proof that they may help to bring out the secretions or mucus flux from the

Airways and help them to breathe better but really in practice has not taken off well that’s what I would say what is your comment I don’t know any other panelist would add to it Amika Madam any comments you want to make you know I think sir has elaborated

Very nicely but uh uh when uh I had a question when sir was mentioning about a common uh respiratory or abnormal respiratory pattern what he see in his practice so uh I think this is it’s not very serious problem but we see quite frequently and I want to know s’s

Experience also on this Dr shash s if he can take this question about the sign breathing many patients come sit on the OPD chair and you just display and serious problem yeah they find Madam I have to take this way the breathing and uh over the years of

Practice now we become very confident initially we used to evaluate like they need psychologic but sir I want your uh you know uh comments on this uh this situation how do you handle this and what works for the habitual sign breathers you know when when we not finding anything especially I’ve seen

That patients who has nasal blockage they also do lots of sign breathing and I I was I lost my connection in between can you just brief it in one or two lines yes so about the sign breathing taking deep Brea between normal breathe you know they have everything normal and

Their complaint will be just that taking from the mouth a deep breathe and feeling relaxed kind of and they have this irresistable feeling of taking this and and there are some habitual sign breathers also so uh what what maybe a psychiatric consultation may help a psychiatrist consultation may help in

These patient I have seen patients who have everything normal and they have a problem and with good counseling and a psychiatric consultation has helps sometimes not in every patient but some patients that’s why once because you have done every possible test still the patient keeps on coming every few month

Saying that I’m a problem and somehow psychiatric consultation and a good counseling may help in some subset of patient I don’t know what other panelists have the viewpoint on that uh so sir I basically practice neural linguistic programming and administer CBT myself due to having a degree in

Cognitive psychology so what I noticed about side breathing is as you rightly said sir they do have an underlying psychiatric issue but to be more specific they are not psychotic because they have insight into the problem they’re definitely a neurotic subtype most probably it could be generalized

Anxiety disorder so if at all we have got time it’s better to call these patients towards the end and try to go to the root cause since how many years did they start saying and or rather when usually most of the time as Madam sushil s has mentioned they won’t say they just

Complain of breathlessness and then on subtle questioning they mentioned that yeah I have to force air deep into my lungs sometimes or in the night also I have to force air deep into my lungs then I feel satisfied and then go off to sleep so there are different variations to each person’s

Expression so if at all we need to make them comfortable and they are generally in a denial mode they feel there’s something wrong with their lungs and they’re not ready to accept the fact that there is a problem a a mild neurotic problem so we give them the

Example saying that try to imagine yourself if they’re a well educated person we say that give them an example either 10 minutes before obtaining a important exam result or maybe four five minutes before getting an interview result so we can try to tell them that

This is is this how you would have felt at that time and probably even if I give you your favorite food you would not touch it but you would definitely appreciate eating or interacting with people after you get your result irrespective of what the result is whether it’s positive or negative so

Then they try to picture themselves in that situation and PSY problem is if they all they start them on ssris SSRS would only try to change this side pattern but it’ll do nothing to correct the anxiety cause so the minute they stop using SSRI and a benzoin combination after which they again

Resume sign so the best is along with the psychiatric consultation we go and start them on usually cognitive behavior therapy for a generalized anxiety disorder we start them on CBT then within about the third or fourth session once we have managed to try to diagnose the root cause of it whether it’s a

Financial cause or whether sometimes it can happen postmenopause also they feel like talking a lot and they are having hot flushes the people around them their own children who are already probably in a very busy phase of Life they’ll be in their 20s by the time the woman is in

Menopause stage then they stop listening to them so they say that I’m not able to speak to anyone if I try to talk I get scolded very frequently during this time they will come to our OPD with s side breathing so it’s like trying to get to

The root cause and then trying to slowly you know help them so it’ll take a good 2 to three months of intensive Counseling and Family Counseling also the patient alone being counseled will not help we need the family members to be present along with them and uh trying

To get them out of denial is the first step before treating them this is what I had experienced in like the last like seven or eight years very nicely elaborated very nice basically yeah we need patient we need to counsel ourself we may need a counselor and maybe we

Need a psychiatrist I think this is a team work and then we sit with the family along with the patient and then once everything is comes together then maybe we are able to help these patient to some extent and this is a long process this is not a one day job and

It’s a teamwork probably yes so with that teamwork I think I had a very very fantastic team today we were discussing but now I think we are P our time we had a very good discussion I would like to thank all my panelists sushil sir shikar sir Amika Madam kaana Madam for making

This discussion so interactive and wonderful so that everyone could understand it from Basics right up to the top obviously uh I want to thank my elder brother uh Vijay sir he is the backbone of all these CCI webinars for making me a part of it and uh arranging

This webinar such smoothly that uh we don’t feel all the stress about it and definitely all the CCI core committee and NH Krishna sir for this wonderful uh topic of his which got us to the basics and keep us thinking that how can we manage patients on depending on their

Breathing patterns I think thank you everyone any more comments from anyone and so that we can end just one thing I would like to add now once we decided this topic in last few days I picked up two abnormal breathings in my clinical practice in my ICU one was a shain’s

Breathing and one was kumal breathing I picked up just because I was thinking about it and there was able to pick up so as you once we think about it we will catch it last four four days or five days I picked up two abnormal breathing and we were able

To say that okay this is the type of breathing we recorded it and then we showed it to my resident that okay this is the abnormal breathing we seeing here so that’s what I’m saying once you start thinking about it you able to pick it up and that’s what is clinical medicine all

About yes yes perfect perfect so thank you everyone once again and uh uh wish you everyone a very good night and we will see you with some other CCI webinar soon all of us okay thank you thank you thank for