hello everyone Welcome to our live enclex RN review session for those of you who are just joining us for the first time we are currently on day 20 of our 90-day free en CLX review series and we are covering a wide range of uh nursing topics and we are going to tackle about 2,000 enlex questions with um detailed explanations so I want you to tell your friends who are preparing for the enlex about our classes they're completely free of charge now make sure to hit the Subscribe button and turn on notifications and uh make sure that you stay in the loop with our latest content now if you need more information kindly check out the description box below and we also value your feedback so feel free to drop your thoughts or questions in the comments and we'll be happy to provide further clarification on any topics now also guys we'd love for you to join our enlex review course course so if you can head over to our website at www Stan coand coaching.com for personaliz assistance our program is 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Strain on the uh right side e e e all right I apologize about that audio okay let me go back into the different causes of the core pulmonal or uh core pulmonal here so let's go back into the acute or chronic pulmonary vascular diseases so these are your factors they're actually going to cause that um hang on can you hear me right right now all right I hope that you can hear me all right now with that pulmonary vascular disease this is going to be a sudden flare up or it could be a long-term condition that could really mess up with those blood vessels now of course this is going to put strain into the right side of the heart the right ventricle all right now there is also that uh factor which is known as the idiopathic pulmonary hypertension now this is basically just a fancy uh name about the uh right-sided heart failure and this is again caused by the increasing pressure in the arteries of the lungs that will Skyrocket for no apparent reason and again it will also lead to the strain into the right side of the heart again guys when you're thinking about the core pulmonal think about the right side of the heart okay don't get confused here this is the easiest way to remember so that is the core pulmonal all right now as we are going to move into the different caes here especially COPD or let's say cystic fibrosis or or maybe interstitial lung disease all right so these are your lung disorders or diseases so these conditions that we have named are actually going to mess up with your lung function and this will make it harder for the oxygen to get into the blood and again this can cause overwork onto the heart for a long time now if you have heard about the polycythemia vera which is Po there's many cymia basically talking about the red blood cell so there is excessive production of the red blood cell and this is a disorder wherein the bone marrow will produce way too many red blood cells that's why it's called polycythemia vera and this will thicken the blood and this will now Force the heart to work harder to pump it around the body okay so again there is increasing viscosity in the bloodstream now again this will cause strain to the heart muscle to make sure that it can pump harder the viscous blood now we're also going to talk about the CLE cell disease so what is this this is another culprit guys where in those funky shaped red blood cells those Sickle cells they're not going to U maintain that uh biconcave type of form of the red blood cells this is its the own problem because it can really clug the blood vessels including the ones in the lungs and again this will cause extra strain into the heart all right don't forget about the CLE cell disease now there is also a condition called macroglobulinemia so what is this basically this is a type of a cancer which is rare but it can also contribute to the core pulmonal by thickening the blood and making it harder for the heart to pump okay that is the macroglobulinemia this is a rare type of blood cancer and there's also a condition maybe a severe kyoso use so when there is a structural issue especially with the spine this is going to mess up with the shape of your chest and it will make it harder for the lungs to function properly and then lastly in our que is the obstructive sleep apnea and I usually refer this as the Osa obstructive sleep apnea and so when the person who has this condition when they are snoozing their air we gets blocked intermittently okay so this will cause them to stop breathing for short bursts but over time though this can lead to high blood pressure in their lungs and guess what it will end up into core pulmonal okay so you see here the list is already long but there are way too many others that I just don't want to include uh but uh these are the primary causes of the core pulmonal and this is really going to set up this type of condition um but our Focus really is to uh put emphasis that all these caes will actually put extra strain onto the Heart by again messing with the lungs and also the blood vessels and again that problem onto the right side of the heart okay so basically this is what we have as the right sided heart failure rsh HF now we're going to move into the different clinical findings or the features that you will see in a patient with a core pulmonal all right so get ready here guys because there are so many of them and you might probably see these manifestations with the other uh problems in the pulmonary circulation or maybe with the um cardiac issues as well so I just want you to focus into those manifestations are really distinct into this disorder so one is the fatigue what is this well or actually the tachicardia itself or the tpia so when the person has at least some strain into the right ventricle this can really cause the person to compensate by elevating the respirations and this is because of the hypoxemia guys because of course there is poor exchange of the gases caused by the straining of the heart and also um in the pulmonary circulation the body will not be able to really accomplish the exchange of gases now there's also that exertional dnia okay so the person will definitely have that shortness of breathing and it will be more um harder for them to breathe when they are doing something else maybe a regular daily exercise or an activity they get really short of breath maybe a few distance of maybe just walking or maybe climbing up a a flight of stairs this would be really difficult for them to do because of that disia and they're also going to be fatigue well because of the poor exchange of gases and also the decrease in the cardiac output there is a decrease in the cardiac output because of the poor function on the right side of the heart the right ventricle itself so this can also decrease the oxygenation process and also the delivery of oxygen into the body tissues especially the brain and all the other major organs now take note guys that cough is also a manifestation in core pulmonal and sometimes they're going to end end up with hemoptisis okay and this is because of the increasing pulmonary pressure that can cause the small blood vessels to rupture okay so we'll add here heis all righty so cough with hemoptisis and then the patient will also have that anterior chest sprin why well because of the strain on the heart this can also lead into an angina okay remember that angina can be precipitated especially if it's going to be influenced by or it's caused by let's say an increasing need for oxygenation or maybe if there is a greater strain on the heart muscle so it will try to work harder so they're going to end up with that anterior chest pain now the person will also have that um jvd or positive jugular vinus distension why it is because the heart itself onto the right side okay let me uh just create another diagram here supposing this is the right atrium the right ventricle of course if there is now backf flowing or distension of the right side of the heart there is overfilling congestion it will now cause the backflow of the blood into the vinous system could be the inferior or the superior Vin a Cava and take note guys that we have our jugular vein right next to the vava so with this condition you will see that the person will have engorgement of the jugular veins especially the external one so even if they are sitting upright at 45 or maybe 90° angle it is ever it's even visible okay so you will see that jugular vein so engorged and this is not a common manifestation in a normal individual even if they are laying supine or 30° angle it should not be observed in a normal person however with the core pulmonal this is evident even when the person sits up okay all the more than when they are being placed in a 30° angle or let's say um semi's position okay now also we are going to expect the person to have um some peripheral edema and I'm talking about swelling of the feet the legs or maybe some swelling into the sacral area and this is again because of the backup of the blood coming from the right side okay so this will now increase the pressure into the veinous circulation and again it will be much more evident in the lower extremities into maybe the sacral area and over time this can also cause problem into the uh the portal circulation especially the liver um also there will be increasing carbon dioxide levels and again it's because of the impairment in the exchange of gases this will now cause a buildup of the CO2 in the bloodstream and you can see this um in the ABG results now because of that hypoxemia there's also going to be cyanosis which is evidently going to be seen through blue tinch coloration of the patient's skin all right you might see this uh purplish discoloration around their mouth or could be the fingertips will be purplish or bluish so guys have you seen those patients that have like hypoxemia or chronic low levels of oxygen have you seen those extremities there their fingertips are actually kind of bluish um yeah that's a sign that they're not getting enough oxygen now there's also going to be discomfort in the right upper quadrant of the abdomen and I'm talking about the liver here because of the buildup of that pressure and the congestion of the blood in the veinous circulation this can now push back into the liver especially the portal circulation so it will end up getting enlarged all right and it will also cause some pain and over time this will lead into jaundice okay now we're going to move into the next manifestation which is basically fainting with exertion so this is what we call as the Syncopy they're going to faint in our patient that could be an elderly person they're going to be at risk to developing those injuries it could be a soft tissue injury or it could be skeletal fracture and so we got to be paying attention to those patients that may have this kind of um nursing assessment or manifestation so another is the split second heart sound so what is this well because of the increasing pulmonary artery pressure this will now cause the delay in the closure of the pulmonary valve which is basically Ally right here let me enlarge this section so here we have our pulmonary artery and because again there is an increasing pressure in the pulmonary artery this will now delay the closure of the pulmonary valve or the pulmonic valve and that's why when you're osculating you will be hearing that split second heart sound okay now let's ex out here we are going to talk about the different diagnostic tests that the medical provider will be ordering and top of the list here would be the chess X-ray and what is expected in the chess x-ray is that there will be a right-sided heart enlargement right sided heart enlargement there will be dation into the right atrium and the right ventricle and again it is because of the increasing pressure that was produced by the pulmonary arteries right and so this side of the heart the right side will get much more dilated there will be increasing in its size okay now the 12 lead EKG please pay attention here guys we really want you to pay attention regarding the changes in the EKG especially in a case of core pulmonal so what's going to be seen here will be the following there will be tall R waves okay and this signify that there is now right ventricular hypertrophy there is now an increasing size of the right ventricle the muscle is hypertrophy now there's also that appearance of the peak p waves so this is very unusual and with that this is going to be seen in a patient with the right atrial enlargement so please pay attention the peak pay W waves will be seen when there is now enlargement of the right atrium whereas with the tall R waves is a scene when there is now right ventricular hypertrophy and moving forward we also have the inverted t- waves and this is going to be seen in the preoral leads V1 and the V4 okay so the leads V1 up until V4 now part of that will be the low voltage QRS complexes so when you are looking into the EKG there will be that reduced amplitude it's not really as going to be seen as the normal elevation of those uh of that complex and this is because of the low voltage now we're also G to be seeing some incomplete or maybe an incomplete uh incomplete or actually complete so let's get a r get rid of this I in so it's either incomplete or complete right bundled branch block and this is because of the widening the QRS complex you will see that and of course when you are going to look into the cardiogram this will give us some information about the ejection fraction guys please pay attention when we are talking about echocardiogram this is actually going to give us some idea of how the valves are working and how the pressures are being maintained inside those heart chambers now another thing that we need to pay attention here in the echo cardiogram is the ejection fraction so what is this this is basically the amount of the pressure in percentage and this will give us an idea of how well The ventricle is working okay and so normally the acceptable ejection fraction is somewhat somewhere between um in some books it says above 52% or in some books it says 55% and above okay so this is our expected ejection fraction now if there is a reduction in the ejection fraction it simply means that the ventricle or ventricles are not really able to pump the blood from the right or the left ventricles it's not able to really push the blood out into the lungs or into the systemic circulation and so here we really going to see that hey we are now seeing this patient with some form of a right-sided heart failure now another thing that we're going to have to look at is for the patient that may have the right-sided cardiac catheterization this will really confirm the diagnosis of the core pulmonal and it also will give us some idea of how bad the pulmonary hypertension is and the underlying uh Factor as well now what about the ABG the arterial blood gases well this is going to give us some information about uh the partial pressure of the oxygen and also the partial pressure of the carbon dioxide and again there will be hypoxemia and a reduction in the oxygen uh level and possibly a decrease in the blood pH which is going to signify there is some acidosis going on now for the pulmonary function test the pfts so this are going to be uh helpful in giving us an idea that it could the the core pulmonal itself has been caused by The Chronic uh illnesses or let's say chronic conditions in the lungs like COPD so um maybe a COPD in the form of the acute bronchitis or could be the empyema so if those values are going to reveal those poor pulmonary function tests then it could be caused by the acute bronchitis or the Mii SAA now I really want you to recall on the diagnostic test that I um lectured in the last few days um regarding the pulmon function test so um if you had forgotten about those I want you to go back and review those um testing because there are so many um uh values that will be involved in this uh diagnostic test now let's talk about the VQ scan so what is this basically this is going to give us an idea if the core pulmonal is caused by maybe a pulmonary embolism that could have lodged into one of the major arteries and again it will also rule out it will give us an idea if the high pressure in the pulmonary artery is caused by that blood clot okay remember about that uh uh massive pulmonary embolism that I mentioned in the past that it will now cause right sided heart failure remember about the detouring of the blood flow when there is that blood clut so mainly it will do that as well now let's talk about the hematocrit or the chest CT well this is going to also capture uh regarding the kind of causitive um uh or underlying disease which might uh reveal if there's maybe a pulmonary embolism or maybe an interstitial type of lung disease so that would be helpful as well and same thing with the hematocrite level so what is this this is really going to give us an information of how viscous the blood is and I'm talking about the viscosity of the red blood cell or the increasing concentration of the red blood cell so good luck with me here let me just write it down RBC elevation remember about the cative one of the causative um disease processes there when I said about the polycythemia varia yes that can increase the hematocrite count wherein it's going to tell us that the blood is so concentrated there is way much more of the cells the red blood cells compared to the plasma so your patient here will really have a viscous blood very thick blood that can cause some strain into the right ventricle now there's also that alpha1 antipin which I me mentioned way back when I was talking about the um empyema remember that this is a deficiency especially in that form of COPD and so if this is going to be uh of a significant value then this will pinpoint that the ca of the core pulmonal is the chronic obstructive lung disease which is the empa now let's talk about the anti-nuclear antibody level which is going to be elevated especially in the case of a collagen vascular disease and lastly we have the coagulation studies and this is to give us an idea uh how uh the blood is really uh rapidly going to cause some increase in the coagulation okay so it can easily probably clut and so we're going to be able to tell if there is some issue with the clotting mechanism or maybe there is just an abundance of those clotting factors or maybe a genetic disturbance that is causing that one now let's move on into the management the core pulmonale so pay attention here guys now the primary approach in the treatment of the core pulmonal is really to address the underlying issue and most often this is caused by The Chronic lung disease and we really want to make sure that we are going to uh manage the lung problem in order that there will be a reduction in the manifestations of core pulmonal now what would be that primary treatment well since there is a problem with the oxygenation we need to deal with the hypoxemia right and so the need for us to administer the oxygen is really critical here we want to make sure that we are improving the oxygen Del delivery in order for us to reduce the heart's workload and also to decrease the sympathetic Vaso constriction because if there is hypoxemia this will now also stimulate the sympathetic nervous system and it will now trigger vasel constriction and it can also can cause more of that problem and so we want to make sure that this is going to be controlled through the administration of the oxygen therapy and we are going to adjust the flow rates based on the levels the pao2 or the partial pressure of the oxygen or it could be based on the level of the pco2 as well the oxygen saturation and also of course we're going to have to look into the overall pulmonary uh function of the patient to see if they're improving if their shortness of breath is relieved then definitely we're going to have to at least maintain that oxygenation now also here we're going to talk about the targeted therapies this is very important guys so we're going to talk about the pharmacological management about the core pulmonal and here are the medications so one of those would be the prostacyclin analoges and so these are going to be vasodilator medications and we have our generic name it's the epoprostenol IV and there's also that trinil which is given intravenously and there is that uh inhalation form which is the iloprost okay so again these are Faso diors so it will actually going to act on into the pulmonary arteries it will cause Vaso dilation so when there is that change in the Lumen size especially in the pulmonary artery this will now cause relaxation and this will allow a decrease in the workload of the right ventricle okay so when that allows the um pulmonary arteries to vasodilate this will now uh decrease the workload of the right ventricle that's the simplest explanation about the Vaso dilators now talking about another medication classification is the endopin receptor antagonist and this is represented by the medication bosan and this is going to block the endothelin A and B all right so this is what we call as the Endy receptor antagonist so basically the medication will Target into the receptors and it will now cause Vaso dilation into that inner lining of the pulmonary blood vessels so when this happen this can also cause a an improvement of the capacity of the pulmonary arteries and of course this will also decrease the pulmonary hypertension again it will have a vasodilatory effect now let's move on into another classification here um including the pde5 inhibitor so what are these medications these are your s dinil and the tadil so remember these are actually one of those medications that are used in a person especially the male uh older old older population of male patients that may have um what do you call this Ed there is that uh dysfunction erectile dysfunction however though this is going to be a very useful uh classification of medications in a patient with a core pulmonal so it does really work okay for this patient no matter what about the gender so it doesn't work um for this patient to treat the Ed but here this medication will actually help out in relaxing the smooth muscles in the lungs okay so with these two medications in the pd5 Inhibitors classification again this will allow the relaxation of the smooth muscles and also the long blood vessels and again will decrease the pulmonary hypertension okay and this is really going to Target um the COPD type of pul pulmonary hypertension okay so please pay attention the sopy and the telop now let's talk about dexin so I hope that you still remember what this medication is well this is a cardiac glycosite and this is one of the medications that is used for a patient with congestive heart failure so the patient here will really get the benefit because the medication will actually strengthen the force of the contraction in the right ventricle right here remember about the dilation of the right side of the heart and because of that weakening it's not able to really pump the blood from the right side of the heart but when we are treating the patient with dexin this will now strengthen the heart muscle in order for it to be much more effective in pumping the blood and in order for it to deliver the blood into the pulmonary arteries and the pulmonary arteries will carry the blood into the cap iies in the lungs for oxygenation all right and this will now be transported into the left side of the heart via the pulmonary veins and then transported into the left atrium and the left ventricle so again think about the dexin as one of those medication that can cause an increase in muscle or ventricular contractility okay increase ventricular contractility so this is also what we refer as the positive inotropic effect contract the let me erase that okay contractility again this is what we call called as the positive enot Tropic effect hello everyone for those who just joined us we are talking about the core pulmonale and currently we are discussing about the treatment now part of the Care here is the administration of the anti- uh coagulants why well the anti-coagulants will actually work for the patient that may have the pulmonary embolism remember about the pulmonary embolism lecture especially when there is massive or submassive type of pulmonary embolism uh with a blood clot lodging into a huge portion of that U pulmonary artery in this medication the anti-coagulants will prevent the growth of that blood clut okay and so this is something that will really give some or it will really benefit the patient in order to control or it will lessen the development of the right side heart failure okay now another medication that we are going to expect in the treatment is the diuretic and I'm talking about Loop diuretic here fosite Loop diuretic let me try this one instead I hope this one will work for me is it working nope okay so let me try my pen again Loop diuretic which is a regular or actually this is a rapid acting um diuretic such as the Lasix or furosemide this is going to cause excretion of exess fluid in the bloodstream and will also uh assist the right side of the heart it will decrease the strain into the right ventricle so with that the patient will really have some improvement as soon as the medication Works within five minutes the patient will start urinating in large amounts so this will really allow a decrease in the strain decrease in the exertion of the right side of heart but again again you have to be careful guys when you are delivering the diuretic when you're injecting the furosemide you also need to be careful about the complication that might happen after you deliver the diuretic all right now we're going to have to focus into the uh core pulmonal for now now we'll also talk about the um other Vaso dilators or maybe yes the vasodilators first so this will include the calcium channel blockers or the CCB and we have here the names neopine and uh this is actually sustained release nephine sustained release or Sr and deltm so these are the known calcium channel blockers that will actually lower the pulmonary pressure this will decrease the pulmonary pressure it has that vasodilatory effect vasod dation so expect those two medications to be ordered now there's also probably an inclusion of the Bronco dilators if the underlying issue is COPD let's say empyema or bronchitis or let's say asthma the Bronco dilators can also ease the overload or the overworked um right ventricle all right so it will also improve the lung function and also diminishing the increasing workload of the um the right side of the heart okay now let's move on into the next classification here so what do we have okay we also have the mechanical ventilation here which is really going to help us out in uh treating the a uh hypoxemia especially if the patient is not able to maintain the level of oxygenation and so this is really going to be helpful for those patients that may have a severe form of hypoxia okay so here we are going to talk about uh maintaining the patient uh positive air we pressure and of course we really need to make sure that our settings are regulated and make sure that our patient is not uh getting way too much of that pressure as well now another is sodium restriction especially in the diet So the patient's diet will be limiting the intake of the sodium so we are expecting less than 2 gram of sodium in 24 hours less than 2 gram of sodium intake because of the increasing uh volume circulating within the bloodstream we don't want to cause some more fluid retained into the circulation now this time guys we're going to talk about the complications and these are your respiratory failure and because of the poor exchange of the gases we really have to keep a close eye into the patient and make sure that we are uh prevent them from developing into the this stage and then also the dismas that can happen because of the increasing uh strain into the right side of the heart this will lead into lifethreatening drimia as well now we're going to go talk into the different nursing actions um starting with the nursing assessment so what are we going to do here we definitely need to assess the patient for any kind of History all right so maybe the patient will have a long-standing history of lung disease and we have to get those information and also have to assess the severity of the patient's um what do you call this disia or the level of or the severity of their hypoxemia so how are we going to do that well we're going to have to measure the patients a uh ABG take a look into the values and also looking into the oxygen saturation continuously now we're also going to have to um check for the patient jugular veinous distension and peripheral edema yes the reason for that is because of the congestion of the blood especially into the right side of the heart and the veinous circulation we are going to see of how bad the back flow or the consolidation or the congestion is in the veinous system so again when you are doing this check you have to put your PTI paent in a 45° angle and to see if there is engorgement or distension of the external jugular vein okay so that would be uh the appropriate way of checking this jvd so we're also going to look for the peripheral edema so take a look into the ankles the legs which basically will give us an idea that there is now retention into the lower extremities because of the right-sided heart failure now we're also going to have to monitor the oxygen saturation the arterial blood gases so this will give us an idea of how bad the hypoxemia is affecting the patient okay and this will also help us adjust the oxygen therapy as needed okay guys we'll talk about the oxygen delivery here so we are going to administer the oxygen and this is really going to be helpful in reducing the pulmonary arery pressure and we want to make sure that we are keeping an adequate oxygen levels but again guys remember about the lecture about the COPD so you got to be careful if your patient has core pulmonal we really don't want to administer highly concentrated oxygen or we don't want to administer way too much of the oxygen because of its uh retaining um effect we don't want to cause a stop in their breathing and so the best way to deliver the oxygen to the patient with a COPD is to deliver it through the ventury mask okay now also here we are going to um avoid administering central nervous system depr presentence so if in case there will be some prescriptions that have been ordered in the past because the patient will need the these medications for a uh a condition that they have then probably this is the time that the doctor may have to order withholding some of these medications uh especially like opioids or let's say hypnotics uh because this can also lead into the respiratory it can also suppress the respiratory centers in the brain the medulla oblonga and because the medications are known to cause hypercapnea accumulation of carbon dioxide in the bloodstream so again we are going to avoid administering these medications all right the opioids and the hypnotics and if really it's unavoidable we really have to consult the medical provider about this if it's really needed for them to really survive then we have to be very cautious in admin ministering the medication because of the respiratory complications now we're also going to talk about monitoring the respiratory uh uh if there's any kind of infection because with this it can also cause retention of the CO2 and also hypoxemia so it's very important guys that you will detect any form of infection okay because this can exacerbate co23 attention any kind of infection especially in the lungs okay CO2 levels will be elevated if there will be infection so what are those signs again well recall about patient probably having uh fever or let's say increase in the speedum production or maybe a change in the sputum color so please pay attention into those changes when the patient has a concurrent respiratory infection and also guys we are going to monitor the patient for their fluid and electrolyte levels especially for the serum potassium because we really don't want to cause an imbalance here and make sure that we really keep an eye into the important electrolyte the serum potassium uh because if we are going to administer Lasix or let's say if there is an involvement about the administration of dejin it's going to make things more complicated so make sure guys that your patient is not hypokalemic at this time when you are administering Lasix or when you are administering the dexin so let me write this down here especially these three medications are involved you really have have to make sure that the potassium level is within the normal range okay remember guys about the fosite that this is going to cause excretion of the potassium and so if there is hypokalemia less than 3.5 and if they are taking dexin concurrently because the patient requires to take it in order for it to maintain uh ventricular function to increase the contractility of the heart well with that hypokalemia it can lead into digitalis toxicity not a good combination so please pay attention here guys this is very important digitalis toxicity can occur in the patient if there is hypokalemia and if they are given the Lasix or dexin make sure that the patient's potassium level is within the normal range make sure that you notify the medical provider right away hey doctor probably we need to replace the potassium first before um we're going to resume the administration of lasx and also the dejin because we don't want the digitalis to occur now guys if you have forgotten about the digitalis toxicity what are those manifestations well in the elderly population it can cause confusion what else it can lead into RAD cardia let me just put here arrow down HR Brady cardia even as low as let's say less than 50 beats per minute and we don't want any of that as well right um another thing is the envd anxia nausea in vomiting and also diarrhea a and VD those are your signs of the digitalis toxity and also when the person looks into the light source when they're looking into the um any kind of light source they're going to see Halo green coloration into um how can we have those note um Lindy filma can you please elaborate your question so we're talking about the um digitalis toxicity at this point and so we are going to have to focus into assessing those uh manifestation especially if there is dexin involved if there is faside or if there is potassium hypokalemia focusing on that one okay now aside from the hypokalemia basically the uh digitalis can also uh digitalis talk I it can also occur if there is low magnesium level let me just put that mg or there is elevation of the calcium so let me just put it here digitalis toxicity so these are the common electrolyte imbalances that can occur or that can result to dit tox toxicity let me erase that toxicity so one of those is decreased K level another is decreased magnesium but the exact opposite here is that when there is increased calcium level um the note I'm not quite sure what you're um talking about what note how can I find them what note I don't understand what the question is um are you talking about the notes that I'm writing on here here on the PowerPoint okay I'm not quite sure what's going on okay um if you could please clarify and I will answer the question so guys we are going to move forward here with the um other nursing actions especially in dealing with the core pulmonal and so there is also a need for us to make sure that our patient is monitored continuously especially looking into their cardiac function so make sure that we are going to capture those abnormal heart rhythms uh to capture those um let me see what's going on here and you still see my notes on the screen all right so I hope that you are able to see what I'm writing on the um the PowerPoint so continuous cardiac monitoring again is going to help us in capturing those lifethreatening disr IUS that we can at least um treat before the patient will go into a cardiac arrest now we're also going to have to limit the patient's physical activity during the acute phase because really the patient need to have a reduction in the workload of the heart especially the right ventricle and we want to make sure that we are only going to allow much more of the activity once the patient is stable okay now we are also going to have to talk about restricting the sodium intake I think I've already said that um again the limitation will be about two grams and uh less than two grams rather and this is to decrease the fluid retention and then we're going to have to go into educating the patient especially um their selfcare so we're going to have to really emphasize in smok cing cessation this is something that would really going to help them out especially if the core pulmonal is costed by a COPD okay um and also if with this if if they're going to be having that core pulmonale U because of the COPD we really want to make sure that they are going to get that uh education how the smoking cigarette smoking can really affect the cardiac function and also those modifying behaviors that they can do in order for them to St um taking or using the cigarettes so let me just check real quick what's going on here um let me see all right so I hope that you can see this better this time now we're also going to treat or Rec recognize early uh signs of infection we want to make sure that we are also treating the infections because again with that it can lead to increasing CO2 and we want to make sure that our patient will have uh good quality of air especially in the home setting and we want to make sure that we are promoting good ventilation and also that if there is some uh issue with there um let say um air quality at home maybe there's a need for them to really have an air filter or maybe some air conditioning as well in order to um improve the quality of air in the home setting now oxygen supplement this is very important guys because they're really going to need to um require the use of the supplement at home and um they might need to get some assistance especially with setting up the device if this is the first time that they're using the oxygen now we're going to switch into another topic here about the pulmonary edema so what is this so basically um this is a problem that is caused by an excess of the fluid in the uh pulmonary circulation and this is really G to cause excess fluid in the alvioli okay or it could be the interstitial spaces as well now what is the cause here and what is the mechanism of the pulmonary edema well guys the fluid in the Alvi will basically impede the gas exchange and also the movement of the oxygen into the pulmonary arteries and so with that especially in a case of left-sided heart failure here well this is really going to make it harder for the patient to uh cost their breathing um it will make some them so dnic there are going to be some air hunger and also the accumulation of fluid into the uh Alvi as well so same thing with the Mi or let's say cardiogenic shock this can lead to that as well same thing with um aortic stenosis because of the increasing pressure into the aorta or it could be a mitro valve disease this can cause uh uh consolidation and also increasing blood into the pulmonary circulation high blood pressure can also lead to that and if in case guys you are probably treating a patient um an elderly person maybe they have been dehydrated for quite some time or let's say you are transfusing them with pack red blood cells and they really have that decreased adaptability um they also have some uh history of congestive heart failure the increasing amount of the fluid through IV and also the introduction of the blood product into the system could really overwhelm them as well so this might also cause that pulmonary edema so you got to be careful when you are treating an elderly person or for those who have a pre-existing congestive heart failure now same thing with the drug sensitivity this can also lead to uh pulmonary edema allergy poisoning also same thing with the pulmonary embolism like I've said because of its effect into the uh what do you call this the pulmonary circulation itself into the right side of the heart this can impede the uh regulation of the pressure and thus causing accumulation of fluid into the lung and if there's also infar or let's say history of stroke trauma um pneumonia as well postcard version or if the person probably just had some form of general anesthesia or an invasive procedure let's say a cardiopulmonary bypass this can predispose the patient to developing the pulmonary um uh what do you call this pulmonary edema now guys we're going to talk about the uh yeah there's more here high altitude renal disease especially for those patients that are not able to excrete the body fluids because of the impairment in the kidney function they're going to end up accumulating extra fluid into the circulation and will overwhelm the lungs as well so here we go our patient will become dnic they're not going to be able to maintain normal oxygen levels and this will really cause some respiratory compromise um and uh will lead to respiratory arrest if it's not dealt with accordingly and same thing the near drowning as well now we're going to talk about the different clinical SS that you should be watching for this patient with the pulmonary edema let me just check here are you able to see the the video clearly guys or not not quite sure what's going on let me just take a look real quick into my slide okay here we go so for the assessment findings take a look into the clinical signs here we are going to assess the patient for the most common findings such as the coughing um the restlessness during let's say sleep so these are the early manif ation okay so when the extra fluids start to um accumulate in the Alvi this is going to make their breathing so hard and especially when they are laying supine when they are um in a recumbent position this will cause them to do the cough and they will become breastless especially during sleep okay now guys let's also talk about the use of the accessory muscles so what is going on here well the person will be um having to use those special respiratory muscles because this is an attempt the uh in order for the body to get some more oxygen this will start using those accessory muscles to at least help with the breathing and this is really a sign that the breathing is much more difficult to achieve um and also when the patient will be having um that whitish or pink tinch sputum then this is really going to uh CA the mix the air and also the uh it will create that pink tinch pum because this is really going to allow the leaking of the blood from the capillary into the Alvi so when there is now mixing of the air it will now produce that frothy sputum and it will now indicate that there is some blood in the alvioli because of the buildup in the blood vessels and the alviola okay now talking about the severe anxiety here or Panic so what is this so basically um there is going to be that Panic or severe anxiety because of the Sensation that they are drowning in their own fluids and this is is going to cause them to have that intense fear and also will lead into that panic attack now moving into the uh noisy breathing here we're going to talk about the inspiratory and expiratory wheezing so this is causing the bubbling sounds the crackles or also the narrowing of the airway because of the fluid that's inside the bronchos so you will be listening or you will be able to hear those um air movement through the wet passages and this is going to indicate that there is significant fluid accumulation all right let me just pause this real quick I don't don't know what's going on here I hope that you're able to see the screen better and if not I am not quite sure what's going on okay all right there's also going to be that bluish tinge color of the patient's skin so this is basically the cyanosis right and that is occurring because of the poor oxygenation and this is caused by the filling of the fluid inside the lungs and of course with a cyanosis um this really signify that there is a lack of oxygen into the periphery now the patient will also have some profuse uh cold clamy sweating and again this is a response uh to the patient's lack of oxygen okay now there's also that jugular veinous distension which I've already talked several times again because of the heart failure this will cause the jugular vein to swell up and again um another sign that there is a pulmonary edema uh causing the back flowing of the the uh the blood into the vus circulation there's also going to be tachy cardia and this is because the heart is trying to compensate for the lack of oxygen and also um allowing the heart to compensate in order to circulate the blood more quickly but again this can worsen the fluid buildup inside the lungs now the patient here will also have the t uh tpia um the rapid breathing and again this is compensatory mechanism because of the poor oxygenation and hypoxemia is evident here um because of the poor exchange of gases and also the chest pain will occur especially if the patient had the acute MI then probably they're going to have a recurrence of the chest pain and here guys pay please pay attention here because only guria can be seen in this patient as we know that the kidneys receive about 20% of the total cardiac output so take note about the decreasing blood supply to the kidneys so what you're going to expect here is that the patient will end up with low urinary output that simply means that the glus is not able to receive or filter that enough blood coming from the system okay so again there will be Ola let's say less than 400 mls in 24 hours or let's say less than 20 MLS per hour this is what we call as olyria okay again the reason for that because of the decrease cardiac output and a decreased blood supply to the kidneys now let's talk about the different diagnostic test here so I hope that you're still there and so one of those diagnostic tests is the chess X-ray and this really can show fluid accumulation in the lungs and this will be seen as having cloudy uh there will be that uh whitish appearance into the lung Fields there will be also an ejection fraction of less than 55% and like I have said earlier about the ejection fraction this is going to signify that there is now weakening and ineffective function of the ventricle to pump the blood from the ventricles okay now talking about another diagnostic test which is the the pulmonary artery W pressure with the use of the Swan Gans catheter so what is this so this is really going to give us some idea about the pressure in the left atrium okay so the swan Gans catheter so basically it is going to give us an idea it will differentiate the cost of the pulmonary edema and so the blood cultures will also be needed guys so for example if there is an ongoing uh infection we need to see if there is a pulmonary infection make sure that we are uh checking on that before we're going to initiate the antibiotics in order to um treat that and may also help in decreasing the pulmonary edema uh later on now for the cardiac markers so what are these markers we are talking about the tronin I or t uh the ckmb or the myoglobin so these are going to be elevated especially if the cause of the pulmonary edema is cardiogenic in nature so for example if it's caused by Mi then our tronin I and T will be elevated same thing with the ckmb and the myoglobin now another thing that we're going to have to pay attention are those Bu The Blood uran nitrogen the serum creatinin and the electrolytes and also the complete blood count because with those we will be able to see some imbalances in the electrolyte levels especially the sodium potassium and also if there is an elevation of the RBC okay or could be elevation of the white blood cell count which is associated to an infection or maybe an imbalance in the electrolyte as well now let's talk about the increased BNP what is the BP this is basically uh the beta natri urtic peptide again that is a beta Nutri uretic peptide so this is a hormone that is going to be released in the bloodstream if there is dilation or an increased volume in The ventricle so the reason why the beta natural uretic peptide is released is that this is now the body's compensation detecting that there is fluid volume overload the body wants to excrete the excess water and also the sodium so this is really just a triggering system it will just like hey I'm just going to sending you I'm just going to send you a message I'm going to elevate the BNP in order for you to work on decreasing the excess fluid however though the the function of the ventricle is already impaired and so the natri essis is not really going to occur at this point so it's not going to be effective anymore and so the patient will really benefit in um if we are administering them the lasx or the diuretic to get rid of the extra fluid and also with the use of the uh what do you call this the cardiac glycoside dexin now we'll talk about the arterial blood gases which is also going to be used in um determining if the patient has some form of respiratory failure we're going to see in uh the levels of the O2 the pac2 and we want to make sure that the patient is getting enough oxygen at this point okay now another procedure that we'll be expecting probably will be the thoracentesis and so if the cative um issue is probably a accumulation of fluid in the plural space causing compression Into the Heart then thoracentesis could probably uh help out while the procedure is removing the excess fluid from the plural space now guys we'll talk about here the long ultrasound so what is this basically the long ultrasound will detect the interstitial edema and this is going to reveal this what we call as a b lines or let's say the comet tall artifact so look at this one right here the tails that you are seeing in the um ultrasound right here so these are what we call as the comet tails and this signify that there is interstitial edema all right so that simply means that there is now a excess amount of fluid building up inside the lungs now we're going to talk about the management of the pulmonary edema we have to pay attention here guys because our goal of treatment for this patient is to improve the oxygenation and we want to make sure that we're also identifying and also correcting the precipitating factor and also we're going to have to reduce the lung congestion and the circulating fluid volume okay so that would be the goals of the therapy again improve the oxygenation we're also going to have to reduce the workload um of the heart and also the lungs by decreasing the congestion and also decreasing the circulating blood volume now we're also going to have to administer them the oxygen and the reason for that is to correct hypoxemia as easy as that um we're going to have to incorporate the use of the noninvasive ventilator or ventil or the use of the BiPAP and this is going to be one of the first line um interventions especially when your patient is really in that grave danger and they're going to be allowed to wear that mask um to maintain the ventilation and also oxygenation um mechanical ventilation will follow through if the patient is not going to respond to the BiPAP or the non-invasive ventilation then they're going to require intubation and managing the ventilator setting as well in order to uh reduce the amount of blood returning to the heart and also reducing the uh also the workload of the lungs now we're also going to talk about the morphine so what is the use of morphine in the treatment of pulmonary edema well the morphine itself can reduce the anxiety and it will also promote Venus pooling of blood in the vinous system so this will decrease the preload guys this will decrease the preload it will also decrease the anxiety so when the patient's anxiety level goes down this will also decrease the workload of the lungs and also the heart okay so that's why morphine can be important but guys please pay attention into the pulmonary function of a patient they're already dnic so if in case this medication might not be applicable so you really have to be cautious when you are administering this medication because it can cause retention of the CO2 so you really have to do your clinical judgment here make sure that you uh um think if this medication can really benefit the patient or not or maybe it can harm the patient so either or you have to be careful in administering the morphine now also the administration of the Vaso dilators especially nitroglycerin or the nitrite so maybe in a case of a pulmonary edema um the medical provider might order the application of the uh nitroid patch let's say the ointment type of nitroglycerin that can be applied with that U uh a li a little bit of a tube that you can apply on a piece of paper that is measured and this is going to be applied into the chest of the patient and again we know that the nitroglycerin is effective in causing the Vaso dilation and so when this happens this will now decrease the preload which is basically decreasing the end entry of blood into the heart and it will also decrease the vascular resistance which is basically the afterload and so the patient will really feel some relief as soon as the medication starts to take effect and I've seen this many times when I was a brand new meds surge RN um especially for those elderly people that may end up with um the fluid or volume overload if they have a pre-existing digestive heart failure I've seen the use of the Vaso dilator it's really effective guys they're really going to have the um some relief where the difficulty of breathing because of the vasod dilatory effect but again with that vasod dilation you have to watch for the patient's blood pressure when you are administering this medication because it can also cause some drop in their blood pressure so let's also talk about the diuretic which is the furosemide which I've mentioned several times already and so the reason for that is to decrease the intravascular volume we really want to make sure that the patient is not going to be overwhelmed with the increasing fluid volume okay so that's why we want to get rid of that uh fluid that is in excess and so we're going to give this medication most often IV form and the dur the the onset of action for this medication usually will start within five minutes okay so that is how rapid the medication can work for this patient five minutes and then you will see an increasing amount of urine that will be produced and also the amount of effort that you have seen in this patient will actually going to be decreased once the patient will urinate a whole amount of a big amount of urine now we're going to talk about the increased cardiac contractility what is this well of course this is pertaining to the use of the cardiac glycoside right we talked about that earlier uh strengthening the muscle force uh which we call as the inotropic effect so this is what we call as the positive enot Tropic effect meaning there is increased contractility of the heart muscle this will really improve the pulmonary edema um another is the use of the dobutamine which is an inotropic and this is a sympatic amen and this is also going to stimulate the beta adrenergic receptors which will help the increase contractility of the heart muscle okay and also improving the cardiac output okay so let's point out here the dexin will increase the cardiac output same thing with the debutant okay and the next medication that we will be expecting here to be included in the therapy will be the nerti so what is the nerti this is a Faso dilator and a synthetic form of the beta natri urtic peptide so what is the mechanism of action for this nerti well it actually will mimic the effect of the endogenous BNP and so this will now cause the Vaso dilation and it will also cause a reduction in the preload it willed reduce the preload and also decrease the after load okay now the necessary tide will also promote diuresis so it has so many effects guys it will cause excretion of urine so you're basically going to expect that the patients breathing will be improved once they start taking this medication so think about Faso dilation causing the pre-load to decrease and also a decrease in the afterload now there's also another medication here we call U the mil Renown so what is the mil Renown the mil Renown is one of those phosphodiesterase uh three or the pde3 inhibitor and the effect of that medication is also to also inhibit the phosphodiesterase and it will now cause increase in the ventricular contractility increase ventricular contractility and again strengthening the force of the muscle contraction by the heart again the patient with the CHF will benefit from this medication contractility so that is again the M renew all right so basically these medications will have similar effects into the heart muscle it will improve the contraction and again we'll just use the term positive inotropic effect all right so please pay attention those medications will improve the heart muscle pumping ability and so this will really help out the patient with a pulmonary edema now this time guys we'll talk about the use of the intra aortic balloon pump so what is this this is another modality of treatment that will be helpful in a case of a severe pulmonary edema and so the main goal of the use of this uh instrumentation is to decrease the after Lo so we are talking about decreasing the systemic vascular resistance okay decreasing the systemic vascular resistance so let me explain to you first what is that systemic vascular resistance supposing this is the heart and we are focusing now into the left side of the heart the left ventricle and remember guys that when the blood gets pumped into the systemic circulation we are going to see that the blood is expelled via uh wait the aorta right so this is the left ventricle here this is the left atrium and so the systemic vascular resistance really is going to cause some strain into the left side of the heart so what is the systemic vascular resistance this is the amount of pressure that the left side of the heart is actually going to overcome okay so for instance let's say there is let's say a a hypertension or maybe aortic stenosis there is a problem in the structure in the aorta itself well the exit of the blood coming from the left ventricle will cause a whole lot of intense pressure into the left side of the heart especially the The ventricle so so if the pressure goes up if the svr goes up because of the hypertension well what do you expect that increasing pressure will now cause The ventricle to work harder it will cause The ventricle to push harder make it uh exhausted at some point it will no longer be able to um pump effectively the blood so this will now lead into that left-sided heart failure okay now talking about the use of intorc balloon pump let me erase this the intra oric balloon pump actually is a uh device that is going to um include the placement of the balloon into the descending aorta so let me uh increase the size here so the balloon is actually inserted via the uh either the femoral artery or it could be entered into the axillary artery okay so it will be introduced there and the balloon will be lodged into the iorta since it's called intra aortic balloon pump so the device will really help the heart to pump the blood more efficiently and it will improve the blood flow to the heart muscle which can be helpful in treating the pulmonary edema so what is the mechanism of the iabp the intra aortic balloon pump so basically guys when this happens when the balloon pump is inserted it will be regulated by the external machine right so it will be connected to a certain tubing that will be regulated by the machine so with this the setting of the balloon is actually going going to be um synchronized with the cardiac cycle so the balloon pump or the balloon itself will inflate it will also deflate and this is going to be synchronized according to the cardiac cycle so for example during the diast this is going to allow the balloon to inflate so this will cause the balloon to grow bigger in size so when we are taking a look here into the the balloon inflating into this area okay let me just uh exit here we have a better picture when the diaso occur occurs so take a look here the balloon will get inflated when this happen this will now increase the aortic pressure when this happens the blood will be able to peruse into the the coronary arteries okay so it will not be able to profuse enough oxygen into the coronary arteries and also during the Cy this will cause the balloon to deflate so right here the size of the balloon will grow small or it will become smaller and it will now decrease the aortic pressure and so when that happens this will now decrease the after load so basically the workload of the left ventricle around this time will be much lesser so the heart will pump less harder around this time and this is really going to benefit them because with that the heart's cardiac output of course will be increased it will also decrease the pulmonary congestion and there will be also a reduction of the manifestation especially the difficulty of breathing those are the things that you're going to expect again there will be a decrease in the pulmonary congestion there will also be an increase in the cardiac output and finally there is also symptom relief okay so think about the iabp as one of those means to decrease the systemic vascular resistance or known as the afterload okay now let's move right along with the other complications here so the complications namely will include the dysmas so if we are not able to control the pulmonary EMA of our patient we are going to end up with a much more problematic scenario here the patient will go into irregular heart rhythm that will become lifethreatening and we want to make sure that we are preventing these because with that com comis in the cardiac function this can overall worsen the patient's condition and also another complication is a respiratory failure because the pulmonary edema itself can impair the gas exchange and also the lungs will not be able to provide sufficient oxygen into the blood and will also be causing a buildup of the CO2 and definitely we're going to end up with placing the patient into the Medical vator in order for them to breathe effectively now the right sided heart failure is going to occur as a result of the pulmonary edema we are going to uh make sure that the patients manifestations are well controlled we're going to have to decrease the circulating fluid volume um because of that malfunction now let's move towards the nursing uh assessment find findings here or the U nursing interventions that we can do we're going to have to monitor the patient's breath sounds um take note of those adventitious sounds such as the crackles the wheezes or the ronai these are indicating that there is now fluid accumulation inside the lungs we don't want this we really want to reduce the excess fluid in the lungs so we can get rid of that with the use of the diuretic we're also going to have to assess the patients level of Consciousness so if you're going to notice any changes in the loc then that is actually signifying that the patient is not getting enough oxygen to the brain and our goal here is to maintain oxygenation now for the other assessment we are going to have to assess if there is decreased cardiac output so what are those signs the patient will have increased heart rate there will be diminishing pulses in the lower extremities or the distal pulses the patient skin will be clammmy it will be cold and they will be having that PO and also a reduced urinary output so these are science that you need to pay attention guys now for the assessment um we are going to need to continuously check the patient's cardiac function and look for those lifethreatening arthas so make sure if you're seeing any of those deadly Arias notify the medical provider right away or if there is any standing order if we have medications to administer if their patient goes into arhythmia or premature ventricular uh premature ventricular contractions or let's say uh vac then definitely we need to carry out those orders now if there is um a HAPO smia of course there is going to be um we're going to have to administer the oxygen uh through the different routes could be the nasal canula could be the MK could be the ventur or the simple mask or the non-rebreather mask or maybe with the use of the BiPAP as well now we're also going to have to uh monitor the patients's arterial blood gases and also the pulse up Symmetry and um we'll make sure that we are going to adjust the amount of oxygen that we are delivering um according to the values and part of the Care here very simple we are going to elevate the head of the bed in order to allow maximum lung expansion um in order to facilitate much more uh effective uh exchange of the gases and also maintain the bed rest during the acute phase because this will lessen the workload of the heart and we will be administering the medication patients like I've said in the treatment slide keep in mind about the diuretics we are going to get rid of the excess fluid the Vaso dilators will be used in order to decrease the preload decrease the afterload same thing with the morphine this is going to decrease the anxiety of our patient when when the anxiety is decreased this will also decrease the oxygen demand and with the use of those different inotropes the cardiac glycoside dexin the dobutamine the melrone and so much more so think about the positive inotropic effect which will enhance the ventricular uh contractility um which will be enhanced by these medications now guys we're going to talk about the patient education what will be included here well we are going to emphasize here that they need to be compliant in adhering to the medications um especially to make sure that they take the duration of the therapy and also that they need to start modifying their lifestyle which is really going to U result to um some massive changes in their lung function and also we're going to emphasize that they need to show up for their follow-up appointments and make sure that they are going to really make that call that they need to be there um in order for them to have that um conversation with a medical provider if they're still not responding to therapy um maybe there are some more modifications that can help this patient to really achieve a better um uh or let's say an improvement in their uh cardiopulmonary function now we're also going to talk about the different signs of the worsening condition and this is very important especially when we are going to discharge them to their home setting and to let them know what signs that they need to recognize in order for them to seek help that they can call their medical provider in order to address these emergent issues and also there will be a need to change their diet especially redu in the amount of sodium intake in order to prevent the accumulation of fluid or excess accumulation of fluid in their lungs now guys before we I'm going to end here I really want you to uh point out which part of the discussion that you were not able to understand and I think that somebody complained about the notes um can you please point out which side of those uh which part of the lecture wasn't really clear enough for you to um see the notes can you please point out please so I can address that right away okay so right now I just want to hear your feedback um if you want me to go over with those sections that you were not able to understand okay all right so I'm still checking the comment right now um and so we're gonna have a short recap here regarding the um the two disorders that we just talk about okay now I really want to emphasize regarding the care um about the pulmonary Emon also the core pulmonal um again the mechanisms are quite different however the manifestations are actually quite similar and I really want to emphasize about the patience education is very important between the two disorders here we want to make sure that we are emphasizing the adherence to medication regimen also the lifestyle modification and also making sure sure that they are going to show up for their regular follow-up appointments and also to make sure that they're able to recognize those manifestations that will signal them that there is an ongoing problem or any complications that might arise so make sure that they're able to identify these so they can notify their medical provider and I hope guys that you're able to gain some valuable insights from this lecture um I really want to know your feedback and also we can um give you some clarification if you have any questions about the complexities of the nursing care um I hope that I will see you again tomorrow and we are going to be talking about the tuberculosis and we'll focus on the nursing care so till then I'll see you tomorrow you have a great day and uh you take care bye-bye oh okay so I wasn't able to exit right here so the EKG part so this is mar FL Jean okay thank you for that so let me go back I hope that you're still guys are you still there okay let me go back to that section real quick EKG and I think you are pertaining about uh let me go to the next slide pulmonary edema okay I think we are talking about the um let me go back into the car uh cor pulmonal I think that's where it was that you're pertaining let me just go back to that real quick guys let me just catch up treatment okay EKG all right so this is the section I believe that you were able to um okay let me erase all those okay so back to the core pulmonal I think this is a section that probably you had a problem looking into the notes so we're back in the core pulmonal diagnostic evaluation and focusing on the EKG part so this is where that um you need to pay attention into the different um waveforms especially with the r waves this is signifying that there is right atrium hypertrophy okay so there is enlargement of that chamber and the p p waves okay this is going to symbolize that there is right um also right ventricular again right ventricular hypertrophy for the right uh for the tall R waves however if there is right atrial enlargement then there will be Peak p waves now there's also inversion of the t-wave which is really going to be evident in the preoral leads V1 up to V4 and with the Qs complexes there will be low voltage there and so you will see a a shortened height of the Qs complexus this is what we call as low amplitude and the patient will also have that either incomplete or complete uh right bundle branch okay so what you're going to see here is that there will be widening of the QRS complex and also an rsr pattern in lead V1 so again this is complete and incomplete right bundle branch and so going into the echo cardiogram this is going to give us an idea that the patient is not able to properly pump the blood from The ventricle there is weakening of the right side of the heart and so the right side will also start to dilate okay and the ejection fraction will be decreased as well the percentage will be decreased less than 55% okay and then there's also that right-sided cardic catheterization which will reveal the diagnosis of course that there is really a core pulmonal um also will be able to assist the medical provider in uh diagnosing the pulmonary hypertension and the abgs will also give us idea about the different imbalances in the partial pressures of the oxygen and the carbon dioxide and also the pH so this will help us in uh treating the patient's hypoxemia so we can adjust the oxygen therapy okay or let's say if they're using the BiPAP or maybe the ventur mask we will be able to adjust the levels of oxygen accordingly now for the pulmonary function test this will give us more information if the underlying cost is caused by the COPD right so if in case if there is empyema or the acute bronchitis then definitely this can affect those um vital capacity and also the tital volume and everything as well now the VQ skin what is this this is a test that will be useful in determining if the patient has some pulmonary embolism and of course this is going to give us an idea if the patient probably has an allergy to the CT skin if they can't really uh if they're not going to qualify for that testing because of their allergy or adverse reaction from the Dy then the VQ scan will be uh used for them in order that the medical provider will see the perfusion function and also the ventilatory function of the lungs okay now the chest CT is also another tool that will be helpful in diagnosing the interstitial lung disease to to check if there is pulmonary edema and for the hematocrite levels this is going to reveal if there is hemo concentration increased RB C such as in the case of poly cymia Vera and it's going to make the blood so viscous so thick that it will cause strain to the right side of the heart okay so this is the significance why we are going to look into the hematic rate levels now the Alpha One antirion this is another testing which is going to give us an idea the person has a problem in creating that lung recoil or promoting that lung recoil so this is something that will be seen in a patient with empyema a form of COPD okay so if they're going to figure out hey this is a patient that has a deficiency of the alpha 1 antipin so we are going to have to deal with the COPD of the patient and hopefully this can improve the patient's lung function and also will lead into an improvement in the cardiac function and lastly we have the anti-nuclear antibody level which is going to detect if a person will have a collagen vascular disease and so guys I hope that you were able to capture those items that you were not able to get earlier and please throw in your comments so I can address those tomorrow um again I'll see you again in the next session we'll be talking about the uh tuberculosis so thank you and have a great day bye-bye