Interpretation of ABG

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Interpretation of ABG

22 Apr, 3:30 PM

[Music] and i welcome you for this session on interpretation of ape so basically abg as you all know it's arterial blood gases and it's a blood test which is used to give an indication of ventilation gas exchange and acid-base status it helps to know if the patient is in hypoxemia or hypercapnia it also gives us information about the activity in the respiratory as well as the metabolic system so to explain about it we have with us dr munira hiragani she is the co-convener at the nmc nodal center associate director jsmc primer regional institute and also the associate professor of physiology at the state gs medical college and kem hospital i am we welcome you on behalf of netflix and all our audience members with this man i will be just starting your ppt yeah so thank you the organizers and dr brushali for that intro and i am happy to be with all these audience who have joined us on a very warm friday evening so let's begin with the presentation so moving on to one topic which always is a bit difficult for beginners to understand that is interpreting arterial blood gases so i came across this quote earlier many years ago when i was first dealing with this topic that when we consider life life is a struggle but not against so many things that we think of like money power but against daily it's a daily struggle against maintaining the hi and balance before i begin my presentation i would like to acknowledge uh two main people who have advanced my knowledge in this topic one is dr hasset department of nephrology uh say gsmc and dr juhi kaware from department of medicine again from the same institute i have learned a lot from them by co-conducting sessions with dr juhi so the learning objectives for today's session is to diagnose simple as well as mixed acid-base disorders using arterial blood gas reports so uh when we see arterial blood gas reports what do we actually mean it is the analysis of the arterial sample of a blood mainly for the ph the pco2 po2 as well as the bicups of course we also have many other elements that is the base base excess which is a calculated value so uh the plan for today is since we have a mixed crowd i'll just be reviewing the basic physiology mechanisms for the first 15-20 minutes and then we'll move on to actually looking at case reports and doing a step wise approach to interpreting the gas reports so when do we do an abg you know when we want to diagnose dr bruchali already mentioned earlier we may want to diagnose the patient who is critically ill we might want to prepare the treatment plan we want we may want to manage the ventilator protocols we might want to improve the acid-base status and also the electrolyte levels which get affected by altered acid-base status so for those who have already collected bloods for abg you will know that it is collected mainly from the radial or the femoral artery and while collecting the blood though i am not going to go into the details of the procedure some aspects are important because they may affect your interpretation of abg they can be errors in the pre analytic phase so what you have to realize is when you are collecting the blood sample you have to collect it from the radial artery avoid and take care of the anatomical arrangement avoid taking a venous sample instead so we use a heparinized syringe to collect almost 2 ml of blood but before we collect the blood we need to do an allen's test to confirm the patency of the arterial arches so what is done basically in the islands test is the patient is asked to make a fist and simultaneously the radial as well as alnar artery there is a pressure applied and the arteries are occluded and then the finger or the hand is unclenched and at a time either the radial or the ulnar artery is released and we want to look at whether the pallor recedes so whether blood flow resumes or not in case there is any abnormality in this allen's test we will not use that artery for abg sampling in if there is any local infection thrombus a distorted anatomy in that area if there is a peripheral vascular disease if there is an active reynott syndrome you will not be using the artery for abg of course it's all done in the automated analyzer and that's how we go ahead and get our abg results so just this is a warm-up poll a very simple question to get you started i would request dr brushali to start this poll one the normal range of arterial blood ph is the values are displayed i request everyone to take a go and just try your hand out remember the ph values are different for the arterial blood for the venous sample and for the capillary blood yes when we have the final results yes yes so most of you have got it right the normal range for arterial blood ph is 7.35 to 7.45 ph is a doesn't have any units so let's like for those who have missed this question out let's recap and go back to physiology so when we say arterial ph it has a range from seven point three five to seven point four five we take the mid point seven point four to uh do all our interpretations uh pao2 normally is uh eighty two hundred millimeters of mercury uh paco2 is 35 to 45 millimeters of mercury we take standard as 40 bicarbs are 22 to 26 and again we take standard as 24 milli equivalents per liter oxygen saturation is between 95 to 98 percentage so we have certain terms like you know we use acidemia alkalinia so what is acidemia anytime the h iron concentration in the blood increases it is called as acidemia alkalemia is a reduction in the h iron concentration whereas when i use the term acidosis and alkalosis what we mean is that it is the pathological process the pathological process which leads to generation of acidemia or alkalemia and we call them as acidosis and alkalosis respectively though the survival range is very high as shown in the image there is lot of derangement produced whenever the ph shifts from the normal range in children many a times capillary blood gases are reported so instead of an arterial blood sample a sample from the heel is taken so there will be certain changes as we compare it with the arterial blood sample so the ph will be almost same or maybe slightly lower just remember the venous blood capillary blood will be more acidic as compared to the arterial blood the pco2 will be same or slightly higher the po2 will be slightly lower than the arterial blood oxygen saturation greater than 70 in capillary blood is considered to be acceptable so when we talk of capillary blood gases i told you it's usually done for pediatric patients who require when a repeated arterial blood gases is required so this becomes less traumatic now coming to the terms that we have that is metabolic acidosis metabolic alkalosis respiratory acidosis and respiratory alkalosis so if you look at the image it's all a balance in our body the acid-base status is a balance between the pco2 and the bicarbonate levels when they are in balance the ph is maintained at 7.4 so if you look at the image below what you can see is the changes that are seen when there is respiratory acidosis when i say respiratory acidosis what i mean is that pco2 you can see the weight increases means pco2 increases so the balance shifts to acidosis the uh carbon dioxide is an acidic substance whereas bicarb is an alkaline substance so in respiratory acidosis pco2 is more so it's a process in which acidosis is generated because of increase in co2 when i talk of metabolic acidosis it's a process in which the bicarbs become less and that is a process which generates metabolic acidosis similarly for alkalosis respiratory alkalosis pco2 levels will be less and for metabolic alkalosis the bicarb levels will become more so the primary process or the change if it's in the bicarbs it is called as metabolic if it's in the respiratory or pco2 it's called as respiratory now what are the threats to ph normally what changes are ph the food that we eat uh many people are on special diets we have keto diets alkaline diets and what not normally also even if you're in a well-balanced diet of course you're going to be having some substances which will produce acids the cellular metabolism of the food stuff is going to produce atp as well as volatile acids we have non-volatile acids like amino acids etc they are all as generate acidic substances but it's not all acids alkalis are also generated and bicarbs are also generated on the other hand bicarbs are also lost in feces and a small amount in urine so what is the problem when the ph is altered why should the ph be maintained in such a small narrow range so there are a lot of clinical effects that we see when acidosis occurs or when alkalosis occurs so the main effects are seen on the heart on the central nervous system and the compensatory mechanisms uh including the kidneys and the lungs so in cns what happens is because of the fallen ph there is vasodilation the cerebral blood flow increases but the cerebral metabolism decreases and hence the patient may have altered sensorium patient may come to you in a drowsy state or a comatose state in the cardiovascular system the myocardial contractility reduces the cardiac output reduces the blood vessels will dilate the patient may be warm and the extremities might be flushed there is veno constriction with the centralization of the blood volume the patient because of the dilatation may have hypotension and many a times these patients the hypotension is quite refractory and requires aggressive management to bring the bp back to normal there is sympathetic over activity and all this might lead to cardiac arrhythmias and fibrillation if we talk off if you remember the o2 hemoglobin dissociation curve so because of the acidosis there is a right shift when you see a right shift of the o2 a dissociation curve it means there is impaired loading of oxygen metabolic effects remember that whenever the ph falls or the h ion increases the potassium levels in the blood also increase this is just to maintain the electro neutrality that whenever one ion is increased the other high is also increased because of shift in into the cell so trans cellular shift causes this apart from that acidosis there might be increased bone resorption whenever there is a chronic acidosis so from that bone resorption there could be hypercalcemia hyperphosphatemia and we will see later on that there could be a renal or a respiratory compensatory response and that would increase the merit ventilation and small's respiration may occur the person will have dyspnea and many a times these patients who have metabolic acidosis with respiratory compensation which i'll talk more about may have respiratory muscle fatigue later on and that is the time when we need to think of putting the patient on a ventilator if you look at alkalosis many of the symptoms are quite similar but here the blood flow is reduced there is one important aspect that is increased neuromuscular excitability uh because of alkalosis the ionized calcium levels become low and you might find the patient having carpal pedal spasm circumveral tingling and numbness in cardiovascular system we have arteriolar constriction the coronary blood flow might reduce and if there is the coronary blood flow is already compromised the patient may have a mi again this predisposes to arrhythmias there is a left shift of the oxygen hemoglobin dissociation curve with reduced availability to the tissues there is hypokalemia most of the cases of alkalosis especially the metabolic ones will always be accompanied by hypokalemia the serum ionized calcium is reduced anaerobic glycolysis is increased and organic acids are also produced for the rs if it's alkalosis there is compensatory hyperventilation provided it's a metabolic original bronchoconstriction will also occur hypoxia and hypercapnia will be seen so when we talk of regulation we have different mechanisms in our body to regulate the acid base balance first defense is always your buffers which work immediately and then it comes the respiratory system which takes a few minutes and almost in few hours the compensation is complete and the third defense mechanism is your kidneys which take some time maybe three days to note or the compensation to occur but the compensation is a better percentage so there are many buffer systems in our body which i have displayed here i will be focusing right now on the bicarbonate buffer system which is important in our blood and the bone buffer system for the chronic acidosis so when i talk of mica buffer system this equation should be in front of you it should be in your mind that is h ions plus pi carbs will form carbonic acid which dissociates into water and carbon dioxide so this is the equation which would already always come into your mind and what you have to realize is the bicarbs as well as the carbon dioxide both can be regulated by our body carbon dioxide by the respiratory system and bicups by the renal mechanisms written in colored font below h iron is equal to 24 into pco2 divided by bicarb this is the modified henderson hasselbach's equation instead of ph we are using the h ion concentration and 24 represents actually the figure which comes from the pk constant of that equation as well as the solubility of carbon dioxide because here we are using pco2 not the total co2 bone buffers the ionic exchange it is exchanged for sodium potassium or calcium it causes dissolution of bone crystals and that is also it causes osteoclastic resorption of bone chronic metabolic acidosis might lead to significant bone and mineral loss and this is also seen in patients of renal failure so just remember that buffering will hide from view the real change it's not going to alter anything apart from minimizing the immediate effects so let's move on to the respiratory regulation of acid-base balance which is quite simple to understand we know that normally the pulmonary expiration of co2 exactly matches or balances the metabolic formation so what is paco2 if you can see the box that i have made that is where you need to focus on the partial pressure of carbon dioxide is proportional to two things the vco2 that is the carbon dioxide production and va that is the alveolar ventilation so greater the alveolar ventilation lesser will be your paco2 lesser the alveolar ventilation greater will be your paco2 if you remember this you will understand the compensatory mechanisms so whenever the pa co2 increases the chemoreceptors are stimulated and the alveolar ventilation is stimulated so your rate and depth will increase and your paco2 will be brought back to normal for the other mechanism that is if there is a metabolic alkalosis so when the ph chemoreceptors will be affected by the co2 pco2 the po2 as well as the ph so whenever there is a respiratory compensation for the metabolic alkalosis that will be limited so what happens in metabolic alkalosis you would want hyperventilation you want the va to reduce now this will cause hypoxia when the alveolar ventilation reduces there is hypoxia and hypoxia will stimulate the respiration so the respiratory compensation for metabolic alkalosis is limited renal regulation of acid-base balance so when you talk of renal regulation the reabsorption of bicarb ions there are three ways one is the reabsorption of bicarb ions then is generation of new bicarb ions with two mechanisms one is the excretion of titrative acid nothing but ah if you say simply excretion of h ions along with phosphate and synthesis of ammonia so ammonia genesis is one important thing and of course in certain conditions alkalotic conditions we can have bicarb can be secreted so if you look at the overview this is one image from guyton so those who have read this book earlier will identify this so from the 4320 this is the large amount which is filtered in one day so what happens is a majority chunk is reabsorbed where is it reabsorbed from it is reabsorbed from the proximal tubules it's reabsorbed from the distal parts also the collecting duct and only about one meal equivalence is lost normally now the mechanisms briefly i'll just review so what usually happens is if you look at this aspect the h ion in the proximal tubule is always excreted in exchange for sodium so sodium hydrogen exchanges are there so this hydrogen will combine with the filtered bicarbs and that will form carbonic acid carbon dioxide is taken back into the cell and absorbed into the blood the bicarbonate if you can see within the cell carbon dioxide again forms carbonic acid the h iron is pumped into the lumen on the right side and the bicarb is reabsorbed so in effect what you are doing is you are reclaiming the filtered bicarbonate this is not something new that we have generated now the same h iron which was pumped into the lumen can also combine with the phosphate buffers and be excreted similarly one bicarb will be reabsorbed but this is not the bicarb which was present in your lumen and hence you can say this is a new bicarbonate which has been generated if you move on to the collecting duct there are two type of cells in collecting duck if you recall there is the principal cells and there are these intercalated cells the intercollated cells there are two types one is the alpha and one is the beta intercalated cells the alpha interconnected cells deal with h iron excretion or secretion basically there are two types they could be a h iron pump and the other thing is there is a h potassium and hydrogen exchanger so in this way the collecting duct can actually pump out a chains and that is why the ph of the urine or the filtrate in the collecting duct can become as low as 4.5 which is not possible in the proximal term or the proximal tubule as you can see on the basal side you can see that bicarbonate and chloride they are exchanged and in effect bicarbonate is absorbed if you look at the lower image the beta intercalated cells what are these they have the reverse process we have the h and the hk plus pump on the basolateral side not on the lumen side on the lumen side they have a bicarb and chloride exchanger so in effect the same processes occur but this can lead to bicarb excretion so whenever the bicarbonate levels increase what will happen is you can excrete the vicar so by these beta intercalated cells now diuretics are known to affect these processes in the collecting duct and even in the loop or the thick ascending loop of henle so we have manitol furosemide thiazide diuretics which will increase the h ion secretion in the collecting duct and by increasing the high secretion they will they can lead to metabolic alkalosis on the other hand drugs like spironolactone which uh affect or alter the sodium potassium pump will reduce the air chance secretion and may cause metabolic acidosis so these drugs are given in many conditions so we need to be aware when taking the history about their consumption one other term that we need to be familiar is contraction alkalosis same thing once we have understood the mechanism by which bicarbs and h iron they are secreted or excreted or reabsorbed we should be unable to understand this contraction alkalosis so whenever there is vomiting loss of gastric hcl okay loss of fixed acids will occur so when there is loss of fixed acids as shown on the left side that will lead to metabolic alkalosis so vomiting leads to metabolic alkalosis similarly loss of fluids will cause ecf volume reduction the effective ecf volume so what will happen whenever there is an ecf volume reduction two things will happen there will be increase in aldosterone and increase in angiotensin when aldosterone is increased we have increased sodium reabsorption and increased potassium secretion when potassium secretion occurs there will be hypokalemia increased aldosterone will cause increased etch iron secretion and new bicup reabsorption sodium reabsorption and echin secretion that is the aspect which occurs here again leading to metabolic alkalosis what does angiotensin 2 do it is going to increase the activity of sodium hydrogen exchanger and again cause metabolic alkalosis we have to remember this because it helps us in the treatment the last aspect is ammonia genesis and acidification of urine in the nephron when i say amodia genesis it means that the proximal tubules are capable of generating from glutamine ammonium ions these ammonium ions from the proximal convoluted tubule they move along the tubule and then they are reabsorbed in the thick ascending loop of henle in replacement with sodium so we have that sodium potassium two chloride pump which on which the furosemide acts so there potassium is replaced by ammonium and ammonium is reabsorbed into the cell ammonium can break down into a lipid soluble nh3 and h iron since nh3 is lipid soluble it moves into the collecting duct and it is secreted into the collecting duct in the collecting duct it will combine with the h iron which is secreted we just saw intercalated cells and then as ammonium which cannot be reabsorbed it is excreted so in effect we are excreting ammonium and excreting h ions in this if you have understood this aspect you need to also look into urinary anion gap though it's not part of your arterial blood gas interpretation this is something separate but you have to understand how do you know that the kidney is excreting enough ammonium if you want to find out whether kidney is excreting enough ammonium you need not measure ammonia because that is not what is usually measured in the labs what we need to do is we can if you look at the image sodium potassium and ammonium these are the cations the major anion is chloride and of course we have the other unmeasured cations and anions the sodium potassium is what we measure along with chloride so if i take sodium add it to potassium and subtract chloride i am going to get a negative value if the kidney is secreting ammonium so to find out whether acidification process the kidney is generating ammonia ammonia genesis is occurring then we need to do a urinary anion gap remember compensation is just damage limitation it takes time and it follows the same direction rule so in case there is a metabolic acidosis and bicarbs are reducing the compensation is by the respiratory system and carbon dioxide or the pco2 levels will reduce similarly if it is a respiratory alkalosis and the co2 levels have reduced pco2 has reduced the compensation will be to reduce your bike ups by the metabolic processes remember this same direction rule and you'll be good to go for interpretation of abg reports okay so this is a question just look at it uh take some uh 15 20 seconds and then we can start the poll uh dr bruchali we can start the poll in 15 seconds for the audience yes so just diagnose whatever you know till now just diagnose with the arterial blood gases what would this report indicate dear doctors you can scroll down for the next option if you are unable to see it on the screen you can just scroll down for the fourth option so i am 63 for normal blood gas the a option got the maximum volts okay what about the b option just a second i might just tell you yeah the mixed metabolic acidosis and metabolic alkalosis b option got 12 yeah but 18 and d got five percent okay so i'm not going to be giving you the answer right now we'll be flashing this question later on and then we will look at the answer let's look at how to go about interpreting our abg report so now we come to the get down to the actual work so looking at the case i'll just read out the case it's a 57 year old female she's a known diabetic treated by oral anti-diabetic drugs she suffered from loose motions and now she's complaining of breathlessness her abg and serum electrolytes both were done and the results are displayed so i'll be displaying these values on each slide but the font might be less so if those who want to note it down you can but we'll be discussing this later on so now if you want to start interpreting there is there is a methodical way in which you can proceed so that you do not make errors in your interpretation so there is a six step method there are three step methods also but that is the basic now we are really looking into finding out all the different aspects so instead of jumping to conclusions and coming to diagnosis which may not be wrong we should try to look for hidden things also which you may miss out so let's look at the different steps so first thing is you analyze the clinical setting the second thing is you check the validity of the reports then you obtain a minimum diagnosis looking at the ph which most of you have done looking at the ph it seemed quite obvious that it is acidosis then you decide whether what type of acidosis it is and i can see in the chat function that many have said metabolic acidosis then we have to identify by the rule of the thumb that what is the compensation and is it what we expected if it's a metabolic acidosis or even if it's not you want to be sure there is no metabolic acidosis you may want to do the anion gap and then we may want to narrow down the cause of metabolic acidosis so the first step in this case what was the clinical setting the patient was an elderly diabetic she had already so the one of the things that can be going on could be a diabetic ketoacidosis she had loose motions there could be a diarrhea base loss there could be also lactic acidosis or a diabetic on an oral anti-diabetic drug there could be renal acidosis so many things could be going on we have to be sure of what's exactly happening so when i mean check the validity of the reports so we have two things we have the electrolytes and we also have the abg reports so we need to confirm by the electrolytes whether the ph that we can calculate from uh the the concentration of pco2 as well as the bicups from the electrolyte they are matching the ph value of your abg so we looked at bicarbs in abg and the electrolyte panel we calculate the h ions by using the hendersons hasselbach's equation so remember i had showed you this equation h i is equal to 24 into pco2 divided by by curves so if i do that calculation i get a h ion value of 158.9 if i look at ph which was given in my abg reports it was 6.828 below you can see there's a ph scale these are standard scales nowadays we have these apps and calculators available using that i get an h ion of 160. so using both the methods my h ion concentration is almost matching within a range of 10 percent errors are permissible so if it is matching i say yes my reports are valid there are no errors in the report in the way it is collected where it is analyzed and i can trust the reports and go ahead then we do what we started doing we look at the ph this is nowadays we do this first but do not forget the earlier two steps especially looking at the clinical setting remember the clinical setting becomes very important whatever the reports are have to be interpreted based on the clinical settings so one report may have multiple interpretations but the clinical setting if you analyze you do the proper history and physicals and of course the other supporting lab investigations then you will come to the correct conclusion so we look at the ph so ph in this scenario is less than three five it is six point eight two eight so it is definitely an acidotic condition so normally it is maintained as we consider it seven point four anything below seven point four definitely below seven point 7.35 is acidosis so we have come to step three okay now we need to identify whether it is metabolic or whether it is respiratory acidosis so how do you do that you look at eco2 and bicarb levels so many of you must be knowing this mnemonic that is rome respiratory opposite metabolic equal this is something which is very nice and this image illustration is something which you will remember so in respiratory conditions leading to ph alteration if the ph for example is less that is there is acidosis you will find changes in pco2 and bicarbonates which are in the opposite direction so if the ph falls bicarb and pco2 will be higher in metabolic conditions if ph is less bicarb will also be less and as a compensation pco2 will also reduce so if you look at this i'm just trying to yeah arterial ph so whenever the arterial ph is less it is acidosis when we look at bicarbs and pco2 if both are reduced it is metabolic acidosis if both are increased it is respiratory acidosis in respiratory acidosis remember primary change is in your pco2 bicarb changes your compensatory change so in this condition we are more towards metabolic acidosis am i right is it okay for everyone because if you see pco2 is also less and your bicarbs are also less okay though this condition is not often alkalosis but if you should realize that any time the ph is greater than 7.45 its alkalosis again we look at the bicarbs and pco2 in respiratory alkalosis the primary change is in the pco2 which falls the compensatory changes in your bicups in metabolic alkalosis the primary changes in your sorry its metabolic alkalosis the primary change is in your bicups which is raised and the respiratory change or the pco2 is your compensatory change okay now if you look at the various causes what i'm doing now is in the next four slides we are looking at not the details of each cause you have to understand that today's session is not not focusing on the different conditions in which metabolic acidosis alkalosis or these derangements will occur but more on understanding the broad causes so in metabolic acidosis what is the primary event primary event could be an increase in acid production and decrease in acid excretion or loss of base so if you look at the image there is acid production could be like diabetic ketoacidosis alcoholic ketoacidosis starvation acidosis patient could be in septic shock patient could be in any other cause of shock all these conditions will cause lactic acids a patient might have consumed salicylate so that is all going to increase your acid load whereas diarrhea there will be loss of base through the gi tracts renal failure the acid excretion is going to be less so these are broadly the conditions which will cause your will trigger the acid production or metabolic acidosis in response to this there will be a secondary event which is your compensation which will be increase in the alveolar ventilation so the rate and depth of ventilation will increase what will happen because of that acidosis h iron has increased ph has fallen bicarbs have fallen and pco2 will also fall because of increased ventilation moving on to metabolic alkalosis what is the primary event here addition of a base or loss of a chime when i say addition of a beige base if you look at the image on the right side what could be overuse of antacids or maybe if the patient is already in the hospital and there are some medications being given or corrections being done and there is an over correction uh there is vomiting which leads to loss of gastric juice or maybe diuretics are given which we already saw which might cause metabolic alkalosis remember there are three things normally the kidneys can handle bicarbonates very well they can excrete the bicarbs which are produced but there are three conditions in which the excretion of the bicarbs becomes limited so these three conditions are the volume depletion which can occur in vomiting or there could be a chloride depletion or any condition which causes increased aldosterone or increased glucocorticoids these three conditions are going to decrease the excretion of bicarbs by the kidney so these are the conditions which will maintain your metabolic alkalosis so once a metabolic alkalosis occurs there is a secondary event and that is decrease in your alveolar ventilation decrease in alveolar ventilation will increase the pco2 so when you see a picture like the one given in the table where ph is the h ion is low ph is high y curve high and pco high think of metabolic alkalosis what are the causes of respiratory acidosis the primary event is anywhere in the chain from the respiratory centers to the gas exchange which occurs in the lung so it could be a central nervous system depression like in a drug overdose it could be something to do with the phrenic nerve it could be something to do in the chest wall some limitations the chest wall there is flail chest there is something pneumothorax which prevents the chest from expanding there is some foreign body in the airways or it could be something pathology in the lungs per se there is pulmonary edema any neuromuscular defect anything which decreases your gas exchange all this is going to cause your respiratory acidosis so primary event is ultimately decrease in the alveolar ventilation which will raise your pco2 so as a response the kidneys are going to absorb the bicarbs and generate new bicups by the titratable acids and the ammonia genesis so the picture will be low ph there will be increased pco2 and increased bicarb as a response last condition uh primary event could be in the respiratory alkalosis something which is quite common nowadays anxiety which might lead to hyperventilation people going to high altitudes pregnancy progesterone is known to raise increase the ventilation in fever whenever there's fever ventilation increases uh initial steady stages of some lung disorders they could be like in pulmonary emboli there could be a ah increased alveolar ventilation and hence increased co2 removal as a response kidneys are going to excrete more bicarbs to bring the ph back to normal so if you can see the table below the ph is increased bicarbs and pco2 are reduced so coming back to our case so you have to decide what type of acid-base disorder it is so when you look at the pco2 and bicurves what we notice pco2 is less and bicarb is less so what is this condition it's our metabolic acidosis okay so our condition in this case is metabolic acid so we should feel happy that we have diagnosed but no this is not the end there can still be something more going on which we need to identify and now that's why we need to move on to step five and step six so what is step 5 step 5 we have to identify the presence of mixed acid-base disorders and how do we do that we look at the compensations or the thumb rule which are expected so this is an image from harrison and there are multiple formulas which will predict the change all the formulas are mentioned here let's look at one for each for metabolic acidosis if you pinch and zoom you can see the prediction of compensation for paco2 so in a metabolic acidosis the bicarbs are low so what will be the compensatory response of paco2 paco2 will also become low but what is the level of paco2 that we can come to know by this formula that is the winter's formula 1.5 into bicarbs plus 8 and there is a error margin of plus minus 2 this will predict your paco2 in metabolic alkalosis paco2 will rise 0.75 millimeters of mercury for every millimolar milli equivalent per liter rise of bicarbs for respiratory alkalosis and respiratory acidosis both you have to remember that compensation will take time so in acute the compensation formulas will be different chronic the compensation formulas will be different why because we know that respiratory disorders the compensation is metabolic metabolic means kidney kidney and bicarb that takes time it doesn't happen immediately respiratory compensation occurs within minutes so acute and chronic year will have different uh rules for compensation so displayed bicarbs will reduce by 0.2 in acute and in chronic by 0.4 for every millimeter fall in paco2 respiratory acidosis the acute and chronic the rules are rise by 0.1 millimoles per liter or 0.4 per millimeter of mercury of paco we keep this in mind and i will come back to this again and again when we discuss the cases so now metabolic acidosis you may want to know whether it's simple or whether it's fixed so we will find the predicted pco2 pco2 we will use that first formula winter's formula and then we will see whether full compensation as predicted has occurred in our reports or whether there is some over correction or over compensation or there is under compensation one thing i would like to tell you all even though here it is written as over compensation our feedback mechanisms our regulatory mechanisms they do not over compensate there is always under compensation there is some error so respiratory the compensation is only 50 to 75 percent effective so our mechanisms regulation mechanisms are not going to bring the ph back to the original level there is always going to be some margin of error and that margin of error is more in the metabolic conditions as compared to the respiratory uh conditions so when i say fully compensated means i will say okay yes what we expect has occurred it's a simple metabolic acidosis suppose i note that there is some over compensation in the pco2 so pco to fall is more than what i expected then along with metabolic acidosis i should think why the carbon dioxide has fallen more pco2 is more reduced as compared to the compensatory response so there could be in addition some respiratory alkalosis and if there is under compensation then there is some condition which is preventing your carbon dioxide pco2 levels from falling and what would that be a respiratory acidosis so looking at the compensation you may find especially in critical patients some other disorder which might coexist so if you look at our case what was the predicted response using the winter's formula the range is 11 to 15 millimeters of mercury this is what should have been our pco2 but what are we noting the pco2 is 22 higher than expected or the compensation is less than expected so we then predict that it is there is some mixed disorder existing along with metabolic acidosis there is some respiratory acidosis also remember as i told you whenever there is increased ventilation there is a respiratory there is a fatigue so when the muscles get fatigued sometimes respiratory acidosis develops fine we have got metabolic acidosis but now we need to know what is the cause of metabolic acidosis so there are two broad categories of metabolic acidosis there are some causes which will raise the anion gap and in some causes in which the anion gap is normal what is an anion gap now this is not the urine and anger this is the anion gap in the blood so again as you can see in the table there are cations and there are anions blood and our body is electro neutral so i am not going to be measuring all the anions and all the cations the labs don't do that labs usually measure the sodium chlorides bicups the other ones we don't measure plus they are not in a very large quantity if you look at anions you can see the last second last row now you can see there are some phosphates sulfates lactates others anions also like ketones so all this will also contribute to the anions but we are not measuring them so if i take the sodium i'm measuring sodium and i subtract the chloride as well as the bicups what i will get is i will get some value some gap because i am not measuring the entire cations and the anions so this value is we call it as the anion gap and it is somewhere around a range of 12 milli valence per liter that is what we call as the normal cutoff from the for the anion gap so though i said 12 there is a range of 8 to 16 milli equivalents per liter the high anion gap acidosis so here what happens it is not the chloride or the bicarbs which are changing but the other anions which i had mentioned like lactates like ketones they are changing or some toxins are added and hence the gap is increasing so what i'm measuring is sodium chloride and bicarbonates and i found an anion gap but now my other anions have changed hence my gap is going to become higher so in high anion gap it could be keto acidosis remember there is a pneumonic for this also mud piles and cult so those who have gone through this that's a very nice way of remembering all the causes ketoacidosis uremia lactic acidosis and toxins acidosis because of normal anion gap diarrhea renal tubular acidosis and decreased anion gap could be because of decreased plasma albumin which binds the anions and the increased unmeasured cations so we determine the anion gap here sodium minus bicarbonate chloride and we find that it is high so this is a high anion gap of type of metabolic acidosis our case we have already spoken of the normal anion gap remember i want to know the normal anion gap there are two main reasons one is the renal reasons and one could be the extra renal causes like diarrhea so in those two causes you may want to find out what is the anion gap so you do a urinary net charge that is the utility anion gap so if the anion gap is negative it means the kidneys are excreting ammonium and the cause is extraordinary and if the urinary net charge or anion gap is positive it means there is some renal condition renal tubular acidosis may occur again this is something more that you have to look for apart from your abg analysis now you may want to know if there is in addition to metabolic acidosis metabolic alkalosis occurs or not so in that we do something called as a delta ratio so if your anion gap is raised then you will go ahead and check the delta ratio or sometimes it is also called as delta delta so what is this delta delta what are we doing we are looking at delta rise in an anion gap that is assuming that in this case the anion gap was 41.6 what is the normal anion gap 12 so this value comes to 29.6 so this is the change in the anion gap what are the change in the bicarbonates so normal value is 24 and the value in this case was 3.4 so the value is 20.6 normally if there is an added anion added acid it's going to be buffered by bicarb so the rise in that acid or anion is going to be balanced by a fall in the bicups so these changes should be equal so delta rise in anion gap should be equal to the delta fall in or change of fall in the bicups but in this condition can you see that there is a difference it means that there is some other condition which is causing metabolic alkalosis there is something which is causing a rise in the biker okay so in this condition if you can see we have already seen that there was metabolic acidosis sorry the conclusion is triple disorder what we have seen is my metabolic acidosis plus respiratory acidosis which we identified plus with the delta gap we can identify that there is a metabolic alkalosis component also okay so there is something which is going to cause metabolic alkalosis here so this is the delta ratio done in cases of whenever the anion gap is increased so in short how would you treat an acid those metabolic acidosis you will treat the cause there are protocols to infuse bicarbs we normally don't do it unless the ph is very low and again there are a lot of protocols and calculations for this and of course if required will give supplemental oxygen or mechanical ventilation i'm going to be skipping this davenport diagram and moving on to case two so that case one we have seen all the steps that is step one to step six and we'll just take a break and revise those steps first we look at the clinical setting which is very important then we look at the second thing that we look is at the validity of the reports then we go to step three we look at what is the primary disorder whether it is acidosis alkalosis make a tentative diagnosis then look at what is the type whether it's respiratory metabolic then you look at compensations what is the compensation predicted whether it's occurring that will tell you if there's a mixed disorder then we look at anion gap it is advisable to look at the anion gap even in other conditions sometimes it's a hidden high anion gap type of acidosis which you might miss out unless you calculate the anion gap and if the anion gap is raised you may want to do the delta ratio to find out if there is any metabolic alkalosis so let's move on to case 2. when you look at case 2 if you read it we have a 45 year old female was admitted with the attack of asthama so she is experiencing shortness of breath since admission three hours ago so it's an acute duration so this is the first thing we are doing astama what will happen what will be the condition when we predict there's going to be increased pco2 this is what we know so even without the abg we can think about what to expect and it's an acute condition so what do we notice in the ph so ph is 7.22 you are not given the electrolyte reports um assume that the reports have been validated so when we look at ph it's 7.22 that's the step 3 so it's acidosis the ph is less pco2 is increased bicarbs are increased so if you remember the mnemonic rom what is this this looks like respiratory acidosis moving to step 5 what is the compensation since it's an acute condition the compensation is a change in the bicarb level and it's a change of 0.1 milli valence per liter for every one millimeter of mercury rise of carbon dioxide so roughly we predict that there would be a change of 1.5 milli valence per liter of bicups and if you note vycab was 20 normally is 24 now it's 25 so there is some compensation which has begun uh we do not have anything to check the anion gap right now so we leave that step six so if you diagnose this what is the diagnosis it's a partially compensated respiratory acidosis how will you treat give or bronchodilate improve the ventilation give oxygen therapy if required you might have to move in for mechanical ventilation that's the case too okay moving on to case three so this is a 55 year old person admitted with bowel obstruction and has currently intractable vomiting for last several hours his abg is as below so now again if you go through the step one clinical setting something which is causing vomiting loss of h ions so what we expect ph should be raised and that's what we see i have told you reports here also have been validated ph is raised then what do we see in the paco2 paco2 is also raised bicarb is also raised so what is this condition it is metabolic alkalosis again remember rome now we have to do step 5 look at the compensation bicarb is high okay that's 14. so compensation what we expect is uh it the it should be raised by 0.7 so your bicarb should be now 9.8 milli ah equivalence per liter that should be what is expected so here what we notice 24 and 38 so it's almost same so it is a fully compensated metabolic alkalosis so our rise in bicarb is what is predicted what was our respiratory alkalosis so we had metabolic alkalosis and we had a rise of 0.7 for every 1 millimeter of mercury rise of paco2 so paco2 rise by 9 so we get a compensation which is complete when we look at metabolic alkalosis that is in this condition we might want to do a further investigation by testing the presence of chloride in the urine if it's lesser than 10 okay it's a chloride responsive kind of condition and it will respond to volume expanders and sodium chloride whereas if the chloride is greater than 10 milli valence liter means the causes are like excess of hype aldosterone that is corn syndrome or pushing syndrome or maybe someone is given an exogenous steroid or there is some genetic abnormality of barter syndrome so knowing a urine chloride might give you help you manage the case better so these were the three cases there's one more case which i will do later before we do that let's take a break for this poll and let's see uh this this is the poll sorry this is the poll that we have already done where you had given the responses that it was a normal blood gas but now i am giving you the scenario okay if you look at the scenario you may want to change your option so if the scenario is that the person is normal not having any symptoms conscious cooperative etc then your option a would be right but if it's a man who is slightly intoxicated following a two-day binge of intense drinking and heavy vomiting then we are having two conditions one is vomiting so metabolic alkalosis and intoxication that is alcoholic ketoacidosis so it is it could be a mixed metabolic acidosis and metabolic alkalosis which is maintaining both the pco2 and bicarbs within the normal range and ph within the normal range so remember always look at the clinical setting i just wanted this important point to be thrust out here okay so since we are done with all the three cases even without reading this case i'm sure many of us would assume that this is a case of respiratory alkalosis because that's the only one which is remaining but still let's go through the case so it's a 22 year old male who's staying in calcutta and has gone to a high altitude for pilgrimage so on the night of arrival at this altitude he had some complaints of tightness in the chest breathlessness tiredness exhaustion altered sensorium in form of irrelevant talking improper behavior so if you look at the abg which was done what do you expect yes there has to be some respiratory alkalosis high altitude there is decreased partial pressure of oxygen and that is going to stimulate your chemoreceptors the person is going to increase the ventilation hyperventilation is going to occur and carbon dioxide is going to be blown off when carbon dioxide is blown off ph is high paco2 is low you can see the pao2 is also low which is significant here and the bicups are 22 which is slightly on the lower side so if you look at the case 4 what you will notice is that the pco2 bicups both are low so this is a case of respiratory alkalosis and now if you want to look at the compensation the compensation would be the fall in the pco2 is by 12 right so 40 minus 28 acute compensation the bicarb is going to fall by 2 milli valence per liter for every 10 millimeters of mercury fall of pco2 so in this case the bicup should fall by 2.4 so you have to look at the time gap also it takes some time for complete compensation to occur you can say that it is partially compensated and compensation is ongoing but if there are some history you should also think of is there some other cause where the compensation is not completely occurring is there some other cause of alkalosis going on is there some metabolic alkalosis so you could think of that the treatment here is descent to a lower level gradually without effort give supplementary oxygen you give hyperbaric chambers are there and treatment with dexamethasone acetazolamide symptomatic treatment antimatics and nacids so remember this six step method to interpret any abg however normal or however abnormal and confusing they can appear if you use this method you are sure to come to some conclusion which will help you so remember response will bring the ph towards the normal but variables will still be away from the normal so compensation will occur and as i mentioned if the compensation is complete sometimes the ph may also be within the normal range but not equal to the original with that i leave you to practice this case and of course i'll be discussing the answers but we can take a minute here for you to look into this case and then we will start a poll after a minute i request you all or urge you all to use that six step approach to find out the solution to this patient here i have not validated the results you have to validate the results so there is a patient who is hospitalized has nasogastric drainage he develops fever respiratory rate and depth has increased bp has fallen the abg is given along with the serum electrolytes now you try to find out the answer of course this is an multiple choice and the responses are given meanwhile someone had asked what is this validation which i could see flashing the question validation basically means you are using your abg results that is the ph which is given and trying to calculate the ph from your serum electrolytes using the hendersons equation hasselbach's equation that is h ion is equal to 24 into pco2 divided by by curves so trying to match both these values if both these values are almost equal it means your results are correct because sometimes they could be errors in sampling errors in analysis so you do not want to base your treatment or your diagnosis on incorrect abg in that scenario you would repeat an abg many a times a venous sample is taken i can see a question from sagar uh venus sample if it is taken venus sample the values will be different so if you really want to take repeated samples then sometimes only the serum electrolytes are taken even the ph is not measured and the total co2 is measured in that case and interpretations are made based on that but maybe initially once an abg is taken and later on to understand the changes a serum electrolyte would be sufficient to continue the treatment so for those who have looked at the question just a few seconds more and then we'll start the poll thank you dr bhushali most welcome man okay okay so let's look at if we do it step wise so the same scenario so first we analyze the clinical setting so hospitalized patient mesogastric drainage so loss of etch ions develops fever so respiratory rate will be increased and bp is falling okay so with this scenario we expect some changes to occur so we can see that the ph is raised which would match our nasogastric drainage so there is some alkalosis there going on so if you check the validity of the reports using hnh equation the ph comes to 7.58 which is almost equal to the ph measured by the abg reports and we now take these reports as valid then we obtain a minimum diagnosis looking at ph it's alkalosis then decide which is the acid-base disorder sometimes there might be multiple changes going on then you have to look at the change which is a greater percentage change so in this condition if you are looking at pco2 and h bicups it seems to be a respiratory alkalosis and by the history it looks to be an acute scenario but if you look at the ph bc to pco2 and vicar the pco2 is reduced but the bicaps is slightly raised so it doesn't seem any compensation is now doesn't seem to be working here so if you look at step 5 so you have to identify the presence of mixed disorders so if you look at the rule of compensation we are actually seeing that instead of a low bike up we are noting that the bike up is actually greater there could be multiple reasons for this one could be that his earlier bike was already raised for some reason and second is there is some other condition which is raising the bicups like a metabolic condition so then we have to determine even though it is a respiratory alkalosis i would still look at the anion gap here i am noting that the anion gap if i calculate its 26 so there could be fever infection sepsis some lactic acidosis could be there so coming to the question why is the bicarb not low so there is a nasogastric drainage hence there is a situation where there is some metabolic alkalosis so knowing the clinical history we can come to this conclusion so this is actually respiratory alkalosis plus metabolic acidosis plus metabolic alkalosis so it is a triple again a triple disorder so i know it's not very easy but if you take step by step and given time and practice i am sure each one of you will be able to come to the almost correct interpretation of the abg so can we read out what was the actual poll results for this question and the d option that's metabolic acidosis plus respiratory alkalosis plus metabolic alkalosis got the maximum votes that's 36 percent okay so but uh the boats were almost divided amongst the other options so we need to think yes respiratory yes so we need to look beyond the obvious that is the take home message from here and of course your questions we will be having we have a short time to take your questions and uh this is my email id you all are welcome to communicate with me ask your queries on this email id so over to dr grushali thank you all for this patient listening so if you have questions uh thank you so much ma'am it was very educative informative uh yes yes ma'am i'll take and uh i must say i'm sure our audience members have loved it the emojis are just flowing in it's non-stop they've loved it we also saw a few they are looking for replays they want to see the slides again and again although if there are any questions you can just put up i'll just take up any more questions if they have this topic is so exhaustive that the more you start thinking about it the more you will find smaller things and my topic whatever i have discussed is not complete once you will start working on it you yourself will find more uh nuances finer things and different aspects you will come across in patients true very true uh so now i think uh most of the questions you took about the compensation equation and all uh if there's uh like dr sagar asked if you could explain validation again like summarize it a bit yeah so i did i looked at his question and i did mention answer his question so if he still has the question then we could go ahead okay in the end i had answered this question about the validation i guess uh which cases uh which case in high highlight so whenever there is a decrease perfusion of the tissues that time the lactic acid will increase so that could be because of sepsis because of cardiac conditions has up to what level of ph and co3 bicarbonate infusion can be started i i'm very sorry but that is not the objective and i am not an expert in uh management of people i am not an md medicine i am an md physiologist so i would leave that to the experts and avoid answering your question sorry yes no problem other than that we have some very good comments thank you ma'am for an elaborative session it was an excellent they have learnt a lot from you so i must say thank you dr mahadev sir is asking as i understood only a combination not possible is respiratory acidosis and respiratory alkalosis yes these two combinations cannot occur rest all combinations are possible [Music] that is why we are doing both we are doing abg as well as electrolytes so we are comparing uh both so that's one way of looking at it plus we take all the precautions while collecting the abg sample see that it is kept over eyes when you are collecting don't do multiple breaks so because that also changes your carbon dioxide level when the patient starts hyperventilating because of pain so if you take precautions and do the process correctly maybe at least the pre-analytic phase the errors will reduce and of course clinical setting is always important true that's true so i would like to thank you so much ma'am thank you for such an amazing session thank you for taking out the time and i know it's quite late so thank you from all my heart and from all the team of netflix also thank you to all our audience members all the doctors you


Arterial blood gas (ABG) analysis is an essential part of diagnosing and managing a patient’s oxygenation status and acid–base balance. In order to analyse blood gases, it is important to understand the associated physiology including the nature of acids and bases, and pH levels. Acid–base imbalances can cause complications in a variety of diseases, and the deviation can sometimes be so extreme that it becomes a life-threatening risk factor. The proper collection, management, and analysis of an ABG specimen are all critical to accurate results. Join us LIVE on Medflix as we comprehend the fundamentals of ABG Interpretation with Dr. Munira Hirkani, Associate Professor at Seth GSMC & KEM Hospital, Mumbai.


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