Transcript of Capnography: Why it is the anaesthetist's best friend! By Becky Robinson
Davies Veterinary Specialists
0:03so welcome to this webinar on0:06capnography and I've titled it the0:09webinar capnography and why it is the0:11anesthetist best friend and I'm hoping0:14to convince you that actually0:17capnography and capnography units are0:20one of the most informative pieces of0:24anesthetic monitoring equipments that we0:26have at our fingertips and can use if we0:29know how to use it and understand what0:31we're looking at so this is just a bit0:35of an outline of what I'm going to talk0:37to you about in this webinar so I'm0:40going to start about basic physiology0:43with particular relevance to capnography0:47so focusing primarily on the respiratory0:49system and this is because with any0:52piece of monitoring equipment I really0:55believe that a knowledge of the0:56underlying physiology is really0:58important in order for us to understand1:01what the monitoring equipment is1:03actually telling us and therefore for us1:06to be able to use it to its maximal1:08potential we're then going to move on to1:11the many possible uses of capnography1:14including what it can tell us with1:16regards to our patients and also the1:18equipment that we're using additionally1:21we're in a time when people are focusing1:23on how veteran professional1:24professionals can conserve oxygen and1:27inhalational agents this can be for a1:29multitude of reasons including for a1:32sustainability and environmental impact1:34for economic benefits and also for1:38potential availability issues therefore1:41we're going to briefly touch on why use1:42of a cap negraph can be beneficial in1:44this situation finally we'll discuss how1:47we can interpret our capnogram x' and1:50also make the most of them and i'm going1:51to go through a number of different1:53common exam pools so starting off with1:57the physiology the primary function of1:59the respiratory system is obviously the2:02exchange of oxygen and carbon dioxide2:03between the body and the environment the2:07respiratory system also has a number of2:09secondary functions including benefactor2:13being a filter for blood and airborne2:15substances it's a place of role in2:18immune defenses and also has some2:20endocrine and metabolic functions we're2:23not going to cover any of those2:24secondary functions today we're just2:25going to focus on its primary role in2:28terms of exchanging oxygen and carbon2:30dioxide2:31if the respiratory system is not2:34functioning optimally because of its2:36role in oxygen and carbon dioxide2:38exchange and the patient will suffer2:41from a reduced tissue oxygen delivery2:43with resultant hypoxia and also a2:46buildup of carbon dioxide with resultant2:48acidemia in terms of control of2:53ventilation the major physiological2:55driving force of ventilation is a2:57patient's arterial levels of carbon2:59dioxide not their arterial levels of3:02oxygen it should therefore come as no3:05great surprise that when we're measuring3:07carbon dioxide levels in a patient's3:08respiratory gases via capnography we3:11will be gaining some information on the3:13patient's ventilatory status the main3:19control of a patient's ventilation comes3:21about via central chemoreceptors as3:24opposed to peripheral chemoreceptors3:27these central chemoreceptors are highly3:30sensitive to changes in hydrogen ion3:32concentration and therefore are also3:34highly sensitive to partial pressure of3:37carbon dioxide3:38although the peripheral chemoreceptors3:40do respond to hydrogen ion concentration3:42they do so with the reduced sensitivity3:45compared to these central receptors3:47however the advantage of the peripheral3:50chemoreceptors is that they do respond3:51much more rapidly therefore allowing a3:55quicker response to change with regards3:57to the central chemoreceptors generally4:00speaking an increase in our partial4:02pressure of carbon dioxide in the4:04arterial system our PA co2 will cause an4:08increase in the patient's alveolar4:10ventilation although it's important to4:14note that this effect is lost with4:16extreme hypercarbia4:17which produces central depression and4:19narcosis and therefore reduces of4:21ventilatory response to carbon dioxide4:24on the flipside decreases in our paco24:28decrease our alveolar ventilation4:30although again this effect ceases at4:33less than 30 millimeters of mercury4:36there are various factors which can4:38influence the sensitivity of4:40chemoreceptors our importance for the4:43anesthetist is that an increased work of4:46breathing reduces the response to carbon4:48dioxide this is particularly relevant4:51for brachycephalic patients who usually4:54have an increased work of breathing due4:56to their anatomical features this means4:58that the level of PA co2 which acts as a5:02trigger point for these patients to5:04breathe will be higher therefore with5:07these patients we will commonly see i'm5:10hypoventilation under anesthesia because5:12their set point a trigger point to5:13breathe is higher anyway and we will5:16find that these brackets of Fallot5:18patients often have a higher paco25:20compared to what is usually considered5:22normal5:25while hypoxemia has virtually no effect5:28on our central chemoreceptors it is the5:31peripheral chemoreceptors which are5:33primarily responsible for detecting5:35decreases in PA co2 and blood flow as5:39these peripheral chemoreceptors are5:41positioned in the carotid and aortic5:43bodies they effectively act as oxygen5:46delivery sensors for the brain which is5:48obviously an organ which is particularly5:50vulnerable to hypoxemia Supra levels5:54Supra normal levels of oxygen have5:57virtually no effect on ventilation but5:59once our pao2 drops below 60 millimeters6:02of mercury exponential increases in6:05ventilation occur with further pao26:07decreases the hypoxic ventilatory Drive6:12is particularly important for patients6:14with chronic lung disease who suffer6:16with chronic hypercarbia if these6:19patients compensate for hypercarbia by6:22retaining bicarbonate and therefore6:24producing a normal pH although it's a6:28relatively rare situation to be in and6:30such patients have their ventilation no6:33longer driven by a high pH co26:37I carbon dioxide as normal but it's6:39driven rather with a low PA o2 oxygen6:45supplementation in these rare cases of6:47chronic lung disease can therefore6:50suppress their ventilatory drive so in6:53these situations although clinically the6:56patient may need oxygen administration6:58caution is advised because we may reduce7:01their drive to breathe although this7:06talk focuses on our cat nog Rafi it is7:09important to remember that basic hands7:11on monitoring gives valuable information7:15occasionally anaesthetic monitoring7:17equipment will give artefactual7:18information and the basic monitoring is7:21critical to distinguish this from what7:23is really happening in terms of the7:26respiratory system there are a number of7:29things that we can do as part of our7:31basic hands-on monitoring firstly we can7:34have a visual assessment of the7:36patient's chest movements which allows7:38evaluation of the respiratory pattern7:40effort and rate we can perform a manual7:44inflation of the patient's lungs by7:46squeezing the reservoir bag with the APL7:49valve closed and this allows a crude7:51assessment of the pulmonary compliance7:53and inspiratory resistance this also7:56gives feedback regarding the presence of7:58upper respiratory tract obstructions and8:00in the case of anesthetized patients8:02that is primarily involving the8:05endotracheal tube and it can also give8:07us an idea of whether there's any plural8:09space disease finally we can perform8:12thoracic auscultation which allows8:14identification and location of abnormal8:17lung sounds indicating potentially8:20developing problems including pulmonary8:22edema or aspiration which can be8:24detected as crackles bronchoconstriction8:27which can be detected as expertly8:30wheezes or plural space disease which8:32can be detected as muffled lung sounds8:36however we're mainly today you're going8:38to be talking about capnography now8:41capnography is a what I call a real-time8:44it gives us information pretty much8:46straight away so it's a real-time8:48non-invasive measurement8:50and it provides a numerical display of8:53the carbon dioxide concentration in the8:55patient's respiratory gases during8:57normal breathing8:58it also can measure the patient's9:01respiratory rate while both inspired and9:04expired carbon dioxide concentrations9:07are measured and both do provide useful9:09information9:10it is the expired concentration with9:13which we are most interested in and the9:16peak expired carbon dioxide9:18concentration is referred to as the9:20end-tidal carbon dioxide or the et co29:23which we can see on this diagram here9:26and that's an important number to be9:29aware of and we'll come back to this9:30quite a lot through the talk so the peak9:35expired carbon dioxide concentration or9:37the end-tidal carbon dioxide is usually9:41displayed with the units of millimeters9:44of mercury and through the rest of the9:45talk that's what I'm going to be9:47referring to our end-tidal carbon9:49dioxide in is millimeters of mercury but9:52be aware that it can be measured in9:54other units as well and primarily9:57kiloPascals or percentage so some9:59monitors are set up to record in those10:03units10:04now our end-tidal carbon dioxide is10:07interesting because this is taken to10:09represent the alveolar partial pressure10:12of carbon dioxide so that is the amount10:14of carbon dioxide present within the10:16patient's lungs and in the healthy10:19patient this correlates well with the10:22arterial partial pressure of carbon10:24dioxide and in the healthy patient we10:27would expect the arterial partial10:29pressure of carbon dioxide to be only10:31about 2 to 5 millimeters of mercury10:33higher than the end-tidal carbon dioxide10:36and as we've just discussed it is the10:38paco210:39which is the main physiological driving10:42force of ventilation therefore10:45capnography is a really easy way to give10:47us a continuous relatively accurate10:50real-time measure of what is happening10:52with the patient's carbon dioxide levels10:54and it's certainly much easier than10:56taking repeated blood gas measurements10:58for example11:01carbon dioxide is produced in the body11:04cells as a result of metabolism and it11:07is then carried to the lungs by the11:09patient's circulation11:10it's then removed from the body and from11:13the lungs by alveolar ventilation so11:16therefore end tidal co2 is determined by11:19these three factors we have meta meta11:22metabolism circulation and alveolar11:25ventilation who of these three factors11:29are stable cap nama tree provides us11:32with information on the third factor so11:35for example this is the principle behind11:37using capnography during a CPR session11:40CPR we assume that in this short period11:43of time cellular metabolism is11:45continuing at a similar rate to11:47previously and that the alveolar11:49ventilation is constant because it's11:52being performed by a member of the11:53veterinary team therefore capnography11:56will be able to give us in on the11:58patient's circulation that is how12:01effective our chest compressions are12:02being it can therefore also fairly12:05reliably tell us when we have returned12:08to spontaneous circulation in our12:09patients because we will see an increase12:11in our end-tidal carbon dioxide of more12:15than 10 millimeters of mercury and this12:17is because the patient's heart is much12:19more effective at circulation than we12:21can ever be without chest compressions12:23so we get this improved and tidal carbon12:26dioxide with improved venous return and12:29circulation capnography can also give us12:34really valuable information regarding12:36our anaesthetic equipment with examples12:39including whether we have a correctly12:42positioned and paitent endotracheal tube12:44because if we place the endotracheal12:45tube in the patient's esophagus for12:47example we should not be getting any12:50carbon dioxide produced so we will get a12:52flat line on our capnography trace you12:55can also help us identify whether there12:57are any leaks in the anesthetic12:59breathing system whether our fresh gas13:02flow rate is in adequate or inadequate13:04if we're using a non rebreather13:06anesthetic system and we'll come back to13:09this in a little bit more detail later13:10and if we're using a rebreather13:13thing systems13:15such as a circle breathing system it can13:17tell us whether the carbon dioxide13:19absorber is exhausted or if we have a13:22malfunction in one of our one-way valves13:25and it can also give us some information13:27as to whether there is excessive dead13:29space within the anesthetic breathing13:30system so we can see from these last13:34couple of slides that actually we can13:35gain a whole host of information from13:38our camera graph not just about the13:40patient but our equipment as well so if13:43it's used in the right manner we can13:44gain loads and loads of information a13:48little bit about the different types of13:51capnograph that are available they can13:54either be known as mainstream analyzers13:57where the sensor is placed directly13:58between the endotracheal tube and the14:01breathing system all sidestream14:03analyzers and it's much more common to14:06have a side stream analyzer and so14:08therefore I'm going to concentrate14:09primarily on this type so side stream14:13analyzers require a gas sampling line to14:15be attached to connector near the14:17endotracheal tube samples are taken to14:21the anaesthetic monitor from this gas14:22sample line and water vapor is removed14:26prior to measurement through the use of14:29what's known as a water trap on the side14:31of the anesthetic monitor the gas14:34samples are taken away from the14:36endotracheal tube in the breathing14:37system at a rate somewhere between 50 to14:41200 mils per minute and that varies from14:44monitor to monitor which does mean that14:47there can be a delay from the patient14:49taking a breath and it appearing on the14:51Cata gram a higher sampling rate reduces14:55the response time of the monitor so you14:57get to see your response a lot quicker14:58with a higher sampling rate but it does15:01also mean that a larger part of the15:03fresh gas flow is lost each minute which15:06can become quite important or relevant15:09when we're thinking about using low flow15:13anesthesia particularly with our15:15rebreathing systems a useful thing to15:21think about with sidestream analyzers is15:24that they can actually be used in15:25consciousness or dated patients15:27and that's because ng shaquille to15:30endotracheal intubation is not actually15:32a prerequisite for sampling obviously15:35you get a better sample a more reliable15:38sample if you are taking your gas sample15:41from the end of an endo to kill you but15:43it's not essential the gas sample line15:48can be placed at the level of the15:50patient's Nerys and that can be for15:53example attached to an intranasal15:55catheter or you can use as you can see15:57in this picture here a normal16:00intravenous catheter with a stylet16:01removed attach that to the end of the16:04gas sample line and put it down inside16:07of a facemask next to non intubated16:10patients for people that are interested16:12in this picture the patient is actually16:15a beaver try appreciate is not our16:17normal species that we deal with but it16:19does illustrate the the point that I'm16:21trying to make quite well nasal16:24capnography has been shown to provide an16:26acceptable alternative to arterial blood16:29gas analysis in both sedated and16:31conscious critically ill dogs but we do16:35need to be aware that we need to try and16:37get the gas sample as close as possible16:41to the patient so as close as possible16:44to the daenerys or even better from a an16:48intranasal catheter in order to attempt16:51to measure an alveolar gas so just a16:57little word on how capnography can help17:00us be less wasteful and help us with our17:05drive to be more sustainable as a17:08veterinary profession now it will come17:11as no great news to to all that on a17:13global scale greenhouse gas emissions17:16are rising and it's reported that we're17:20likely going to be burning through the17:22rest of the 1.5 degrees centigrade17:24carbon budget within the next three to17:26ten years which I'm sure you're aware17:28could lead to some pretty scary17:31potential consequences from our17:34perspective as veterinary professionals17:36anesthetic agents are greenhouse gases17:39some of the agents are also17:40ozone-depleting therefore we have an17:43obligation to minimize the amount of17:45waste gases that we produce in our daily17:47work just as a couple of examples of how17:52significant anesthetic agents can be in17:54terms of their effect as greenhouse17:56gases if we look at just one bottle of17:59ISO fluorine and when use that produces18:02equivalent emissions as driving from18:04Plymouth to John O'Groats and the18:07estimated annual global global impact of18:10anesthetic gases is equivalent to either18:13one coal powered station or around about18:161 million passenger cars so it is18:20important that we are conscious of what18:22we're doing and make an effort to try18:25and reduce our impact we can see from18:29this table here that also the different18:32anesthetic agents have a differing level18:34of impact with nitrous oxide and death18:36for rain being the the worst out of the18:40commonly available anesthetic agents in18:45terms of how capnography can help us18:48reduce our waste gases one example is if18:52we're using non rebreathing anesthetic18:55systems so that includes systems such as18:57our TPS or Bane or our parallel lag and19:01use of a cap nog capnography units and19:04can help us avoid using excessive fresh19:07gas flow rates while ensuring we're19:09maintaining safe rates for our patients19:12and this will help minimize the amount19:15of waste gases and that way that we're19:18producing it will also allow us to19:22conserve our resources or our oxygen and19:25volatile agents and it can help minimise19:28environmental and economic impacts that19:31we have so when we're using a non19:35rebreather anesthetic system it's19:36recommended that the fresh gas flow19:40rates for our patients are calculated in19:42the usual manner and that is taking the19:44patient's minute volume which is the19:46product of the tidal volume and the19:48respiratory rate and multiply that by19:50the circuit factor for the individual19:53a system that we're using however if we19:57then are using a Katla graph in addition19:59um from this calculated flow rate and we20:03can reduce a fresh gas flow to a rate20:06just above a point that a patient starts20:09to rebreathe and we can see an example20:11of rebreathing in the the schematic20:14diagram on this slide so rebreathing20:18basically means the patient is breathing20:20back in carbon dioxide from their20:23previous exhaled breath their exhaled20:27gas so they will have a trace which does20:31not reach baseline does not reach zero20:33and we want to avoid this and but with20:37using a cap negraph we can reduce our20:40fresh gas flow rate with our non20:42rebreathing systems down to the point20:44just above where this occurs so it20:47allows us to use the minimal safe flow20:50rate for that individual patient I'm if20:53you're interested in further information20:55on oxygen and volatile agent20:57conservation through particularly20:59through low flow anesthesia and21:01rebreathing systems this can be found21:03with previously recorded webinars21:05available from Davies Veterinary21:08Specialists in terms of any breathing21:13system so that's non rebreathing systems21:15that we've just discussed and also21:18rebreathing systems such as our circle21:20system camp nog raphy can aid with21:24detecting system leaks during anesthesia21:26and again if we can identify system21:29leaks we're going to help minimize waste21:32gases that we are producing so while all21:36breathing systems should undergo a leak21:38check before use it is possible for a21:41system leak to develop during anesthesia21:42and this is usually arising from an21:45inadequate seal around the endotracheal21:47tube cuff and if we have capnography we21:51can often detect this and this will give21:53us a trace similar to what we see here21:56on this slide which we'll cover in a21:57little bit more detail in the examples22:00later on but you can see that you end up22:02with a very different trace than the22:05last22:05two curves on this trace I'm very22:10different from the normal trace at the22:12start but as I say we'll come back to22:15this so in terms of how we can actually22:20interpret our capnogram most of the22:23capnography monitors don't just give us22:26a number for our end-tidal carbon22:28dioxide they also plot a capnogram which22:31is basically an illustrated version of22:34the changes in our carbon dioxide over22:38time and as I say we can gain quite a22:40lot of information by looking at the22:42shape of this katma gram as well as just22:44looking at the numbers that we can see22:48the capnogram can be split up into four22:50different parts we have phase zero22:53sorry starting with phase 1 phase 222:56phase 3 and we actually end on phase22:59zero so phase 1 that we can see23:03highlighted here represents the23:05inspiratory baseline now if we had our23:08graph axes on this picture we would see23:12that this baseline would be at zero23:15millimeters of mercury for concentration23:18of carbon dioxide and this makes sense23:21because when we breathe in we should not23:23be breathing in any carbon dioxide so we23:26would expect this to be zero phase two23:30represents the expiratory upstroke and23:33this is the beginning of expiration23:35which again it makes sense when we start23:37to breathe out we would expect there to23:39be carbon dioxide so we would expect23:41there to be a rise in the level of23:44carbon dioxide which is present and23:47phase two represents the expiration of23:51gases from the conducting Airways and23:54the alveoli and these two sets of gases23:57from the conducting Airways in alveoli23:59start to mix during this phase and they24:01generate a steep increase because there24:04is a very rapid rise in the amount of24:07carbon dioxide which is breathed out24:12phase 3 is the expiratory or the24:15alveolar plateau and this represents the24:18exhalation24:19pure alveolar gas this phase may be24:22completely level completely horizontal24:24or it might have a slight upward stroke24:27which is is often seen because of uneven24:31emptying of the alveoli because they24:32don't all empty at the same rate and24:36then the alveolar plateau ends at the24:39highest point which is the end-tidal24:42carbon dioxide which as we've said is24:45it's usually the number that we're most24:47interested in and finally we have phase24:52zero which is the inspiratory downstroke24:54and that occurs at the start of24:56inspiration and if we think about what25:00happens when we're breathing when we25:02start to breathe in we expect there to25:04be no co2 in the gas that we're25:07breathing in so you would expect this25:09nice rapid drop in our capnography trace25:14in terms of what is normal for our25:18end-tidal carbon dioxide levels as we've25:21already said in most healthy dogs and25:23cats the end-tidal carbon dioxide is25:26very similar to the concentration of25:29carbon dioxide in the patient's arterial25:32blood and we can define our carbon25:37dioxide concentrations is either25:38hypercapnia where there is less than 3525:41millimeters of mercury of carbon dioxide25:44normal cap near where there is 35 to 4525:48millimeters of mercury or hypercapnia25:50where there is more than 45 millimeters25:53of mercury if we're looking at cats we25:56tend to find that cats have end-tidal25:59carbon dioxide readings which are more26:01towards the lower end of the normal26:03range but they equally they we still26:08tend to class26:09normal as the figures quoted here mild26:14hypercapnia is desirable in patients26:17with suspected intracranial disease and26:20this is because the hypercapnia can26:24result in cerebral vasospasm cranial26:32pressure26:32as a result of for example head trauma26:34or intracranial neoplasia then cerebral26:40mild amount of cerebral phase open26:42striction can be useful to help minimize26:45further increases in intracranial26:51pressure however in most patients26:54hypercapnia is not desirable as it can26:57result in cerebral ischemia it's27:02actually really hard to get a patient to27:04be hyper cat neck and it's rarely27:07achievable without mechanical or manual27:10ventilation most anesthetized patients27:13if they're breathing spontaneously will27:15not be hypocapnia27:17however its more common for anesthetized27:20patients especially if they're27:22spontaneously breathing to be27:24hypercapnia27:25mild hypercapnia is often not regarded27:30negatively and in most patients it can27:32actually have some beneficial side27:34effects mild levels of hypercapnia can27:37be sympathetic resulting in slight27:40increases in heart rates and slight27:42increases in blood pressure27:44however levels above 60 millimeters of27:47mercury should be addressed and this is27:50usually through a change in ventilation27:52whether that is instigating manual27:55ventilation or changing the ventilation27:57parameters that are already set up and28:00this is because excessive levels of28:02carbon dioxide can result in narcosis28:05reduced myocardial contractility phaser28:08dilation and metabolic acidosis28:12so when presented with a cat negraph28:15trace um sometimes it can be a little28:18bit confusing as to where best to start28:20and I think the the easiest place to28:23start is to decide whether the patient28:25is normal cap neck hypercapnia or28:28hypokinetic based upon the end-tidal28:30carbon dioxide from here once we've28:35decided whether the patient has an28:37increased or decreased carbon dioxide28:39level and we need to decide why for this28:42we can go back to our first principles28:45so remember that carbon dioxide is28:47produced in the body cells a result of28:49metabolism is carried to the lungs by28:51circulation and then removed by alveolar28:54ventilation we can then use these three29:00different aspects to try and determine29:03what may have changed in any of those29:05aspects to result in either an increased29:07or decreased entitle carbon dioxide so29:11we can see here the main reasons why a29:13patient may be suffering from29:14hypercapnia or that is an increased29:18end-tidal carbon dioxide this is most29:21commonly due to hypoventilation which29:24can occur due to a number of different29:26reasons including excessive anesthetic29:28depths underlying patient disease such29:30as cardio pulmonary musculoskeletal and29:33acid-base disorders or patient factors29:36including obesity pregnancy and patient29:39positioning however an increased29:42internal carbon dioxide level can also29:44occur due to an increased production of29:47carbon dioxide so that is an increased29:49metabolism for example a patient with29:53fever or who's shivering or it can also29:57occur as a result of an increase in the29:59inspired concentration of carbon dioxide30:01and that is with rebreathing as we've30:05already touched upon in terms of a30:10decreased end-tidal carbon dioxide or30:12hypocapnia and we tend to split the30:16reasons for this into those reason30:19through it can result in a gradual30:20decrease all those reasons which can30:23result in a sudden or complete decrease30:25when regarding a gradual decrease um30:29hyperventilation due to a light plane of30:31anesthesia or because of a noxious30:33stimuli is probably the most common30:35however other encountered scenarios30:39which are relatively common include a30:42reduced carbon dioxide production30:45usually because of hypothermia or as a30:49result of hypotension which can increase30:52the alveolar dead space less common30:56reasons can include30:57conditions such as a pulmonary embolism31:00but that would also result in other31:02concurrent signs such as a reduced blood31:05pressure and desaturation we can also31:09detect equipment problems with a31:12decrease in tidal carbon dioxide we've31:14already discussed detection of breathing31:17systems leaks or leaks in the breathing31:20system and that's a key example of some31:23of the equipment problems we can find31:25and then when we're thinking about31:28sudden or complete decreases event idle31:31carbon dioxide which includes traces it31:33can give us a flatline we have to31:36consider conditions such as equipment31:39disconnection so disconnection of the31:42endotracheal tube from the breathing31:43system esophageal intubation as we've31:46already mentioned or it could be31:49something much more severe on the31:52spectrum including ventilation or31:55circulation failure so we do have to31:58have that on our radar when we see a32:00reduction idle carbon dioxide so we've32:06already discussed what the normal32:07capnogram looks like here we've got an32:09example of a slightly more prolonged32:13trace we've got three breaths here on32:16this example but what we're expecting is32:19that each breath should look square or32:22rectangular we should see that all of32:25the traces reach baseline which is zero32:28millimeters of mercury during32:30inspiration we should have that nice32:32rapid upstroke and down stroke and32:35alveolar plateau may have a slight32:39upward gradient that is normal that32:42we've already covered our next example32:46is cardiac or cardiogenic oscillations32:48and this is a variant of normal it's it32:52seemed relatively commonly but if we do32:56see it it's nothing really to worry32:58about so basically what we see with33:01cardiac oscillations is that our down33:04stroke has a number of undulations and33:08if we had the patients in front of us we33:10would see that the undulations would33:13match the patient's heart rate and the33:15theory behind this is that as the heart33:17is beating it's compressing the33:19pulmonary tissue and moving some of the33:22gas out of there the lungs we generally33:26see this in barrel-chested patients and33:30in particularly when they have a low33:32respiratory rate and when we're using33:35low oxygen flows so we can see here and33:39the real-life example and the culprit33:43that was responsible for this trace you33:46can see he's quite barrel-chested and33:49you can see we have these nice33:51undulations on the down I'm stroked and33:54as I say this is just a variant of33:56normal nothing to worry about if we see33:58this we've already talked quite a lot34:02about hypercapnia and obviously we all34:06know now the definition of hypercapnia34:08is more than 45 millimeters of mercury34:11and usually when we have a hypercapnia34:14trace the trace appears normal34:17simply there is the elevated end-tidal34:20carbon dioxide we've already talked in a34:24reasonable amount of detail about the34:26likely causes of hypercapnia the most34:29common reason is is usually34:30hypoventilation34:32which can occur for the reasons already34:35discussed including patient positioning34:39patient factors such as obesity or34:41pregnancy or increased anesthetic debt34:45but it can another likely cause of34:48hypercapnia is also increased carbon34:51dioxide production for example if the34:55patient is feverish I'm again just34:59another real-life example here as we35:03discussed previously35:04mild levels of hypercapnia are often not35:09negative for the patient's so levels of35:12up to sort of 50 to 55 millimeters of35:15mercury are usually reasonably well35:19tolerated35:20unless35:21patient has intracranial disease and can35:24actually have some benefits but when35:27you're starting to get to levels such as35:29that we can see in this picture here35:31sort of above 55 to 60 millimeters of35:35mercury and tidal carbon dioxide we35:38probably need to be thinking about what35:40we can do to alter that and that is35:42usually instigating a change in the35:45patient's ventilation hypocapnia again35:50we've we've discussed some of the35:53reasons why we might have a patient who35:55is experiencing hypocapnia usually we35:59have a normal-looking trace but simply36:02the end-tidal carbon dioxide is below36:05the normal level of 35 millimeters of36:08mercury and again this may occur due to36:11reasons such as hyperventilation36:14decreased carbon dioxide production due36:17to for example hypothermia or due to36:20increased alveolar dead space due to36:22hypotension36:25having said that we often have a normal36:29looking trace with hypercapnia sometimes36:32and particularly with a patient who is36:36hyperventilating we can see traces that36:39are not or don't have the very typical36:44square wave form like we can see in this36:46example here so here we have a patient36:49who is hyperventilating and we seem to36:52have lost some degree of the alveolar36:54plateau this patients is hypocapnia with36:59an end tidal co2 of 28 millimeters of37:02mercury but this was due to37:05hyperventilation37:06and we can see this combined with the37:09patient's heart rate of a hundred and37:11ninety would seem to indicate that37:13they're responding to some sort of37:15noxious stimulus during anesthesia we've37:20already touched a little bit on37:22rebreathing so we've already said that37:25re breathing is basically when the37:28patient is breathing back in some of37:30their37:31previously expired gas that contains37:34carbon dioxide what we usually see with37:38rebreathing is that we have a relatively37:40normal looking trace apart from the fact37:43that it is not reaching zero millimeters37:46of mercury it doesn't reach baseline37:48we've already discussed some of the37:50reasons why we can have a patient who is37:53rebreathing37:54so with our non rebreathing systems such37:57as TPS37:59a Bane or parallel luck then this is38:03indicative of having too low of a fresh38:05gas flow rate whereas if we're using a38:08rebreathing system then we may have38:11depleted soda-lime or faulty one-way38:14valves so we no longer have the38:18unidirectional flow of gas and we can38:21see that in this picture here so the38:25rather fuzzy capnograph trace apologies38:28for the photo quality I was trying to do38:31about three different things at once at38:33this point but we can see that this38:36patient is not only hypercapnia with an38:39end-tidal carbon dioxide of 5938:42millimeters of mercury we can see that38:44the baseline is not reached so we have38:48an inspired carbon dioxide concentration38:51of 10 millimeters of mercury and the38:53reason for this was that we had a38:55malfunctioning inspiratory valve on our38:58circle breathing system and that was39:00because somehow some of the soda-lime or39:04carbon dioxide absorber had got caught39:06between the valve so it could no longer39:09close so we no longer had the39:11unidirectional flow of gas through the39:13system and it ended up with the patient39:16rebreathing significantly we can also39:22use our cat no graph trace to determine39:25whether we have a patient who is either39:28fighting the ventilator sometimes known39:31as bucking the ventilator or the more39:33correct term is patient ventilator39:34asynchrony and what we can see here is39:38that we will have periods of normal39:41looking waveforms with occasional narrow39:44or smaller breaths sometimes we can see39:48small clefts in the plateau the alveolar39:51plateau of the trace and what this means39:54is that the patient is breathing either39:55against or in between the ventilator39:58breaths now we can see in this example40:01here on the the picture on the Left we40:05have some relatively normal-looking40:07capnograph traces which are relatively40:10square giving an end-tidal carbon40:12dioxide of 44 millimeters of mercury and40:16then we have the much smaller waveforms40:19coming pretty much after every single40:22ventilator breath and this is the40:23patient trying to breathe spontaneously40:26in between the ventilator now we can see40:30the ventilator settings at the bottom of40:32the screen in the brown boxes the the40:35number that says 200 is the patient's40:37tidal volume in mils so with a tidal40:40volume of 200 mils we can assume this40:43patient was around about 20 kilos if40:46we're using the caveat of 10 to 15 mils40:50per kilo for a tidal volume the next40:54number along is the risk patients40:56respira true rate so this patient has a40:59respiratory rate set to 12 breaths per41:03minute and this clearly this combination41:05of the the tidal volume and the41:07respiratory rate is not adequate for41:09this patient to try and stop them from41:12fighting the ventilator so the picture41:14on the right is was taken five minutes41:16later and illustrates what has happened41:18after I've made some changes to this41:20patient's ventilation so we can see the41:23time now increase the tidal volume to41:25230 mils so I have given the patient a41:29bigger breath and I've increased the41:32respiratory rate to 16 and the41:35combination of increasing each breath41:38and increasing the patient's respiratory41:41rate that's overall increase in minute41:45ventilation has stopped the patient's41:48drive to breathe they no longer are41:51trying to fight the ventilator and we41:53can see this in our cap negraph trace41:55because we now have a nice41:57normal even square waveforms but also42:02interestingly we can see that the42:05end-tidal carbon dioxide has not changed42:07in either of these so it's still reading42:10at forty four millimeters of mercury42:14this example of what's often called a42:19shark fin appearance to the trace42:22indicates an increased expiratory42:25resistance and this is because if we42:28look at the expiration so the upstroke42:32it's taking an increased time for42:34expiration now this increased expert's42:40your resistance means it's harder for42:42the patient to breathe out and this42:44often occurs in situations such as42:46bronchospasm examples being patients42:50with asthma or who are undergoing an42:52anaphylactic reaction it can occur with42:56a partial obstruction or kinking of the42:58endotracheal tube but it can also be an43:01artifact in patients who have a low43:03tidal volume when we're using a side43:05stream analyzer that has a long response43:07time we can see here I had an example of43:14a cat who was showing that very43:16stereotypical shark's fin type43:19appearance to the cat negraph trace so43:22this is taking a long time for the43:25patient to expire they're finding it43:27quite hard there's a lot of resistance43:29for them to expire and this was because43:32they had a mucous plug in the end of the43:34endotracheal tube that we can see here43:36this is also resulting in the patient's43:39hypoventilating slightly with an43:41end-tidal carbon dioxide of 4743:43millimeters of mercury and they also had43:46D saturated slightly with a pulse43:49oximeter reading of 89% so this is an43:54important trace to appreciate and if we43:58see this trace and we need to do a bit44:00of troubleshooting to try and find out44:01what's going on because it could44:03indicate that I'd say in this instance44:06we had a partial obstruction of the tube44:08but it could also indicate44:10the patient is suffering some degree44:12from crow constriction in this case44:15thankfully once we excavated and44:17reintegrated with a new tube everything44:20returned to normal44:24now this is an example of a gradual44:27decrease in the amplitude of the trace44:31and this can represent a sliding scale44:34of things from relatively minor to some44:38quite severe scenarios so on the44:41relatively minor side of things a44:44gradual decrease over time can increase44:47or can't can represent an increase44:49minute ventilation of the patient but44:53obviously if this is the cause of this44:56decrease in amplitude of the trace over44:58time then there must have been a change45:01in the patient's respiratory rate or45:03effort or a change in the manual or45:05mechanical ventilation in order to see45:09this change in minute ventilation this45:13trace might also indicate a leak of gas45:15from the the system again this could be45:19a leak in your under keel tube cuff so45:23that's something that would need to be45:24investigated but at the more severe end45:28of the scale this sort of trace might45:31represent a decreased delivery of venous45:34blood back to the heart and therefore it45:36might be an impending cardiac arrest so45:40if we see something like this the key is45:42not to panic to troubleshoot things that45:45are that might be happening but also45:47have in the back of our minds that it45:49might be the first indicator that45:51something more serious is going on now45:55in this video this is a video of a horse45:58so don't be alarmed at the low heart46:00rate that is normal for this horse but46:03this horse is about to be euthanized we46:05can see here that the patient's the46:08horse has gone into ventricular46:09fibrillation it's a very good example of46:11what happens on an ECG with ventricular46:14fibrillation but watch what happens with46:17the patient's capnograph trace this46:19patient is being mechanically ventilated46:23throughout the euthanasia the euthanasia46:26of this horse is obviously under46:27anesthesia but we can see that the46:31capnograph trace is decreasing over time46:33because as there is decreased46:37circulation that the patient has gone46:38into a cardiac arrest there is a46:43decrease in the the amplitude of the46:45trace of our camera graph now in this46:48particular instance the ventricular46:50fibrillation occurred very quickly and46:52that was our first indication that46:54something was not altogether normal but46:57occasionally it can be that the changes47:00that we're seeing on the capnograph47:01trace happen first and they are our47:04first indicator that something is going47:06wrong we do some sometimes come across47:12traces where we have a sudden flatline47:15on the Cata graph now if we've had a47:18normal-looking trace prior to the47:21flatline the most likely cause is that47:23the patient's has become disconnected47:24from the breathing system and therefore47:26disconnected from the camera graphs47:28sensor it's also possible that the47:31machine is calibrating and therefore47:32just needs a minute to re-evaluate47:35things and then it will start giving you47:38a normal trace again if you're in the47:42situation that there's never been a cat47:44no gram trace from the start of47:46anesthesia then it's highly likely that47:48the endotracheal tube has been placed in47:50the esophagus rather than the chipiya47:53however such a trace could also indicate47:55other patient factors for example apnea47:59or respiratory arrest or it could also48:02indicate a sudden cardiac arrest so48:04again it's just something if we see a48:06sudden flatline on our cat negraph trace48:08we need to just start troubleshooting48:10and evaluating the patient and trying to48:13figure out what's going on and then48:17finally we've already briefly touched on48:20this is what we might see if we have a48:23system leak and this this example is48:26almost perfect mnemonic for a system48:28leak what we tend to see is a shallow48:31expiratory upstroke a48:34low end tidal carbon dioxide and a short48:37alveolar plateau and personally I tend48:39to call these short and peaky waves and48:42this is most commonly occurs as a result48:45of an inadequate seal due to usually a48:47poorly inflated or a damaged48:49endotracheal tube cuff or if we have an48:53entity or two which is too small always48:55simply using an uncuffed endotracheal48:57tube or a nun cough tracheostomy tube49:00but this if we see that we have normal49:03capnogram traces at the start of49:06anaesthesia and then over time we end up49:08with the shape this change in morphology49:10it's worthwhile checking the49:12endotracheal tube cuff so to conclude as49:18with any piece of monitoring equipment49:20knowledge of the basic physiological49:23principles will hopefully allow us49:25easier interpretation of our capnography49:28capnography is a very useful piece of49:31monitoring equipment in clinical49:32practice and it can provide us with49:35information on both the patients and the49:37equipment that we're using and then also49:40capnography can contribute to oxygen and49:43volatile agent conservation which can be49:47important in order to help us minimize49:50our economic impacts our environmental49:54impacts and also help us conserve our49:57resources we should be hosting a50:03question-and-answer session with one of50:07the members of the anesthesia team50:08particularly on capnography but also on50:11any aspect of of anesthesia on Thursday50:14the 16th of April so if you have an50:18interest in joining in with this50:20question-and-answer session then please50:22don't hesitate to email Devi CPD and we50:26can get you registered up for this thank50:29you for listening
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