User talk:BSCKI.Nhatduy

Case lâm sàng tim mạch
Welcome to ATCM the emergency medicine channel. A 60 year old male presented to the ER with complaints of generalized tiredness and headaches since two days of duration. Based on the SOAD criteria, the patient has been triaged on the basis of GCS BPA respiratory rate into the green area. On our initial 10 second assessment, patient was conscious, oriented and obeying commands. Coming to airway, airway was patent and no gurgling, no pooling of secretions. Coming to breathing, respiratory rate of 24 per minute, saturation of 95 % in room air. Coming to circulation, heart rate of 90 beats per minute with a BP of 200 by 110 mmHg. All peripheral pulses were equally palpable. At this point of time, we have took the upper limb and lower limb BP which was found to be normal. Coming to disability, GCS of 15 by 15, bilateral pupil equally reacting to light. Coming to exposure, GRBS of 190 mg per deciliter with a temperature that was found to be normal. The patient has a pain score of 4 by 10. Two large bore IV canals were inserted at this point of time and injection PCM 1 gram IV stent was given. Coming to adjanth of primary survey, ECG was taken showing a normal sinus rhythm with a heart rate of 85 beats per minute. No acute STD changes were noted. We have taken a VBG which showed a pH of 7 .42, PaCO2 of 43, bicarb of 23, potassium of 3 .8, creatine of 1 .2. No acute acid base disorders was also noted. Coming to sample history, a 60 year old male who was an alcoholic presented to the ER with complaints of generalized tiredness and headaches in students.

Disturbs his life and others' life. Then only he will become alcoholic. If somebody takes alcohol like 30 ml or 60 ml per day, he is not alcoholic. He takes alcohol that's all. What are the adverse effects of alcohol if it is more than 30 ml? After 30 ml, alcohol normally is not a problematic thing. More than that, it may create problems. What are the problems it can create acutely? What are the problems it can create long term? Acutely, binge drinking can lead to alcohol intoxication. Indoxication, encephalopathy. What happens to BP? BP can be raised. BP is one thing, like when you take alcohol transiently it can increase BP. That's why we advise patients not to take alcohol 24 hours prior to BP checkup. If they are taking alcohol, normally BP shoots up. What else? Tachycardia. Normally it produces tachycardia. Some chronic alcoholics, it can produce autonomic dysfunction.

The patient complains of generalized tiredness and on and off headaches in students. Due to which he went to a clinic and checked the routine BP, which was around 200 mg of mercury and was referred to here. On arrival, the patient complained of headache which was on and off. The patient expressed the headache as fullness or tightness over the frontal region, mainly during the morning hours, which decreases on analgesics. The patient also gives history of snoring and daytime somnolence. He also gives history of choking episodes during sleep. There was associated personality and mood changes as per the history from the bystander. What it indicates? Daytime sleepiness, night time choking sensation, high BP, all these things indicate what disease? Obstructive sleep apnea syndrome. No history of any photophobia, vomiting, fever, no changes with any bending or lifting or coughing, no local pain, no weakness and no signs of any dangerous headache. No history of any weakness, deviation of angle of mouth, seizures, involuntary movements, blurring of vision and altered behavior. Throughout CV and hypertension encephalopathy. No history of any chest pain, breathlessness, orthopnea, PND. Thus, symptoms were not suggestive of any MI, aortic dissection or pulmonary edema. No history of any decreased urinary output or pedial edema or drug intake. Thus, ruling out renal symptoms. No history of any palpitations, sweating, giddiness on standing, abdominal pain, no features of any pheochromocytoma. No history of any muscle weakness, stria, bruising over the body. Thus, no suggestive of any Cushy syndrome. No history of any hyperactivity, irritation, loss of weight, cold or heat intolerance, constipation. Thus, ruling out thyrotoxicosis and hypothyroidism. The patient has similar complaints in the past 3 months back, following which he went to outside hospital and found to have elevated BP and the patient was started on Ayurvedic medications. No history of any allergies in the past. The last meal was taken at 6 am. Coming to general examination, the patient was conscious and cooperative, well built and nourished. BMI was 32. According to the latest Asian population guidelines, 32 corresponds to Grade 2 obesity. No pallor, ictherus, cyanosis, clubbing, generalized lymphadenopathy or pedial edema. Coming to systemic examination, CNS wise, GCS 15 by 15, bilateral BP was 200, 110. Was standing BP checked or not? Yes, there was a post hypotension and both upper and lower limb BP was also checked. Same and there was no post hypotension. No post hypotension. What is the importance of post hypotension in the early phase of the hypotension? What is the importance of post hypotension in late or after starting the treatment? How do it differ? Early itself we are getting post hypotension. What it indicates? One disease which can point to post hypotension is fear chronocytosis. Post hypotension initially always indicates a secondary hypotension. Whereas after starting your treatment, there are lot of conditions, there are lot of drugs which can produce post hypotension. Like Acin, ARBs, Hydralazine, so many drugs can produce post hypotension. Early if you are getting a post hypotension, you have to always be careful about fear chronocytoma. What is the typical feature of fear chronocytoma? The triad of fear chronocytoma is episodic hypertension, palpitation and profuse sweating. Tachycardia, sweating and hypertension. Most of the time they are episodic. Some patients will have persistent hypertension. They also can have post hypotension. Come to systemic examination. GCS was 15 by 15. Bilateral pupil equilary reacting to light. The patient was moving all four limbs. Power 5 by 5. Come to respiratory system. Normal vesicular breath sounds, no added sounds. CVS examination, S1, S2 present, no murmurs. GAT examination, the abdomen was soft, no under and bowel sounds were present, no brewy was noted. So, professional diagnosis was asymptomatic markedly elevated blood pressure, which was formerly called hypertensive urgency. According to the endocrine society of India, we can approach hypertension in two ways. One, one patient present with emergency or urgency. In the case of urgency, we can either go ahead with 24 hour ambulatory BP monitoring. So that we don't miss out white coat hypertension, nocturnal dipping or episodic hypertension. Other is triaging into hypertensive emergency and urgency. According to the endocrine society guidelines, we can classify a patient as diagnosed as hypertension. If the first visit, the patient comes with hypertensive emergency. Or in the second visit, patient comes with a BP of more than 180 bar, 110 or 140 bar 90 with a target organ damage or CKD or diabetes mellitus. Or a third visit with a BP of more than 160 bar, 100 millimeters of mercury. In this case, the patient had multiple episodes of elevated BP and went to outside hospital and started on ayurvedic medications. So this patient can be a case of, diagnosed case of hypertension but not on regular medications. First of all, you tell me how to manage this condition in emergency room and we will discuss. If patient has come to you, what do you do? First we need to classify whether it is a hypertensive emergency or a hypertensive urgency. In case of hypertensive emergency, the systolic BP has to be more than 180 milligram per mercury or diastolic BP has to be more than 120 with target organ damage should be present. That is AHM only should be present. Acute hypertension mediated organ damage to the brain, retina, heart, renal or the larger arteries. If it is hypertensive emergency, then the BP should be normally more than or equal to 160 to 180 systolic or diastolic around the range of 100 to 120 without target organ damage. In this case, the patient was not having any symptoms of any target organ damage. This patient is having high BP but there is no symptom. How do you manage this case and another patient who is having high BP with permanent redema? How do you manage that case? Both are different. This patient has come with high BP but he is not having any symptoms. In hypertensive emergency, in this case... How do you know that this patient is having long term hypertension? First time he is coming to a modern surgery. How do you know that? She never tells I have hypertension. Now she has told that she is on some treatment. Otherwise she never tells because hypertension is known as a silent illness. Most of the time you don't get any history. How do you manage that? The degree of hypertension should be proportional to the... Do you know that this patient is having hypertension? We can take ECG. ECG is the most important thing. What we can do in emergency room, ECG or ECHO. ECHO will tell you LVH. ECG also will tell LVH. That both things, if it is there, then it is a long term hypertension. If you can see the retina and find out changes, that also will help you. If urine examination shows protein, that also will help you. Otherwise it will be difficult for us to diagnose whether the patient is having long term hypertension or... It is only a recently increased hypertension or a transiently elevated BP because of pheochromocytoma. How do you manage a patient who is having high BP with no symptoms like this? We will start the patient on oral antihypertensive. What oral antihypertensive you would like to start in this patient? We can start either patient on basically three lines of drugs. ACE inhibitors or calcium channel blockers or diuretics. Usually we will... ACE inhibitors or ARBs. ARB, calcium channel blockers or diuretics. So now, how you select the drug? Usually the first line we go ahead with ACE inhibitors or ARBs. Before starting ACE inhibitors, what... The renal status has to be assessed. Reactin has to be ruled out. Second thing? History of any hereditary angioneurotic edema has to be... What are the contraindications for ACE inhibitors in a patient with hypertension? One is you told renal failure, reactin more than three, better to avoid this drug. ACE or ARB. Other contraindications for ACE or ARB? Contraindication, pregnancy, contraindication... Pregnancy is a contraindication. Then? Hereditary angioneurotic edema in a patient... Only if there is ACE inhibitors can produce this one, that is not a contraindication. After starting the drug only you will come to know that. If you already know that, you avoid it. Not a common condition also. You have to check for something before starting ACE inhibitors. What is that? Pop is a side effect of ACE inhibitors. You have to look for carotid stenosis, you have to look for renal artery stenosis. That two things also you have to rule out. So basically creatinine should be normal. Second thing? What you told? One more thing, pregnancy. Third one is stenosis of renal artery, especially renal artery or carotid stenosis. All these things, if that is not there you can safely start ACE inhibitor or ARB. How do you reduce that BP? Immediately or slowly? Slowly, for urgency we need to slowly reduce the BP. If you take more than 24 hours, you can slowly reduce the BP. You can take more than 24 hours, there is no hurry. If you start like sublingual nifedipine or Tlamyl. That is the most common practice done to reduce the BP unnecessarily. What is the problem? Rapid reduction. Rapid reduction, what is the problem? J -curve phenomenon. What is that J -curve response? Whenever rapid reduction BP, there will be sudden derangement in the perfusion of the body leading to cardiombolic events. Cardiombolic events? Cardio... Schemia. Schemia. So all your body system is set for that high BP. Your brain, your kidneys, all are set for that high BP. Suddenly if you are dropping your BP, kidneys and brain, these are the two organs which suffer mostly. They don't get blood. Regulation of blood will be completely distorted. There will be acute ischemia of kidney, acute ischemia of brain. Patient can develop problem of that. Cardiac events also more in that type of BP reduction. That is why that J -curve, if you see that, the curve increases. So the problem increases. As you reduce the BP, suddenly the problem part will increase. Mortality will increase. We are not supposed to reduce the BP like that. Slowly you can reduce the BP. Whereas conditions like high BP with pulmonary edema, high BP with cerebral hemorrhage, all those things, how do you manage? Usually... Pulmonary edema, so for example, commonest thing is pulmonary edema. In emergency room, high BP, pulmonary edema. What are the precautions you take? How do you manage this? Our target BP should be able to reduce the BP 10 to 20 % in the first one hour. Okay. And 10 to 20 % next 23 hours like that. There is a patient who is having very high BP like you told 220 by 130. What is the BP here? And he is having pulmonary edema. What do you do? Initially we will keep the patient in proper position, two lines we will keep. And we will start the patient on MDG infusions. The first one. Diuretic. Diuretic. Whatever may be your diagnosis, first thing is always diuretic. Okay. Second thing is MDG. MDG. Okay. What is the action of MDG? Both arterial and venous dilators. So lesser blood will go to heart, lesser pressure in the peripheral circulation. So heart can easily pump out blood to the peripheral circulation. Okay. There is an advantage of MDG. So any other drug can be given in that type of conditions? Any other drug? Other than MDG will reduce the BP. But any other drug to be started? And if you are starting what precautions you take? Nitroprus, Hydralysin. Hydralysin is the next line drug in that condition. If you want to start beta blocker what you have to rule out? Initially we have to rule out any heart blocks, anything is there. Bronchial asthma. Heart block is okay. Then second thing is? Asthma, bronchial asthma. Asthma is also okay. And then we need to attain the euvolemic status before starting beta blocker. You want to do an echo before starting beta blocker? You want to do an echo? Yes or no? What is the action of beta blocker? It decreases the heart rate and increases the diastolic interval. Decreases the contraction of the cardiac muscle. So before starting beta blocker in a patient who is having pulmonary edema. We don't know what is the reason of pulmonary edema. You have to always rule out the cardiac failure and you have to give beta blocker then only. Can cardiac failure produces diastolic BP high? Normally what we learned is cardiac failure means low systolic BP, low diastolic BP. In a cardiac failure what happens? Suppose somebody is having hypertension with cardiac failure. What happens to the BP? Hypertension with cardiac failure. Cardiac failure patients will not have good pumping. So systolic BP will be always low. But in a patient who is having hypertension with cardiac failure, diastolic BP increases. That is a problem. So if you see the diastolic BP you can probably know that whether the patient is having hypertension or not. Okay. But whatever it is, it is always better to do echo and rule out cardiac failure then only give beta blocker. That is very important. Okay. Hydrolysis, what is the action? What is the action of hydrolysis? It is a vasodilator. It is an arterial dilator better than any other drug. But IV preparations are not available at present. So we can give oral tablets. Okay. Calcium channel blocker? Can you give calcium channel blocker? What are the indications of calcium channel blocker in hypertension, urgency or emergency? Second line agents we usually give calcium channel blockers. As a second line agent you can give calcium channel blocker in patients who is having tachycardia. Okay. High BP with tachycardia. Again same problem. If the patient is having cardiac failure you cannot give calcium channel blocker. What is the action of calcium channel blocker in the heart muscles? What happened to the contraction? Contraction is a calcium channel blocker. Calcium is required. So contraction suddenly reduces. That is why when you give sublingual, what is that drug? Nifedipine. Nifedipine. The patient can deteriorate very fast. If the patient is having cardiac failure suddenly patient can deteriorate. Okay. So you should avoid such drugs. But if you want to give you have to do an effort and you can give. What you have given for this patient? We have given sir. Amlodipine was given sir. Amlodipine. What is the action of Amlodipine? What are the advantages of Amlodipine over other drugs? Where will you give Amlodipine? Don't give drugs like that. You should know the action. Then you will avoid all these things. Calcium channel blocker. It is a calcium channel blocker. Where all it can be used? Amlodipine is used in dash, dash, dash, dash. What are the conditions? In CKD patients we can perform. CKD patient normally we don't give. Why we don't give? We give suppose you want to give CKD patient calcium channel blocker Nifedipine is a choice. Why it is like that? Why it is like that? What is the duration of Amlodipine? Action duration. Amlodipine is given once daily or twice daily? Once. Once daily. It has got 24 hours action whereas Nifedipine it has got only 6 hours action. If you give Amlodipine in a patient with renal failure what will be the duration of action? Then it will extend more than 24 hours it may be 36 hours. So cumulative action will occur. So never give Amlodipine in a patient with renal failure. If you want to give calcium channel blocker better drug is Nifedipine. Normal tablets. Nifedipine there are two preparations. Sustained release and normal preparation. You have to give only normal tablets. So Amlodipine is not a good choice in renal failure. What are the other indications for Amlodipine?

We cannot throw the drugs like that. We should know what is the indication, what are the contraindications. Whether it is useful, not useful. It definitely reduces the BP. There is no question of that. Where will you give? Tell me indications for Amlodipine.

Amlodipine is indicated in high systolic BP. Isolated systolic hypertension that is a drug of choice. Elderly individuals that is a drug of choice. It is not a drug of choice in diastolic BP. It is not a drug of choice in renal failure. But effect wise it is a very good drug. Amlodipine there is no adverse effects. Only thing it can produce some fetal edema. That is clinically not that important. So you should be very careful. This patient Amlodipine may not be a very good choice. Since she has come to emergency room, acute attack. Amlodipine once you give you cannot withdraw the drug. If you want to give a calcium channel blocker then nifedipine oral tablets are better. Not sustained release oral tablets not subliminal. That will be better because the action will subside within 6 hours. Suppose there is a problem occurring due to your calcium channel blocker. Then you can immediately withdraw the drug. After 6 hours the effect will go off. What happens to the heart rate because of Amlodipine and nifedipine? Heart rate decreases or increases? Decreases. In decreases. You have to tell properly. Amlodipine decreases the heart rate. Sure. Amlodipine increases the heart rate. It increases the heart rate. That is why it is always combined with beta blocker. Amlodipine is an ethanol combination. Amlodipine actually increases the heart rate. What is the heart rate here? 85. So you can safely give. The only thing is in acute condition you try to avoid. Because you don't know what happens to the patient. Whether the patient's BP crashes after some time. Once you give Amlodipine it is for 24 hours. You have already given. So never try to give Amlodipine in an emergency. Once the patient is stabilized you can give Amlodipine. That is the only problem. Otherwise Amlodipine can be continued. What else you can give here? You are given a choice. You take ACD rule only. AC inhibitor ARB. AC is calcium cyanoblocker. D. What will you give here in this patient?

You can select A. What is A? AC inhibitor ARB. Can we give in this patient? There is no contraindication. Because renal failure is not there. She is not pregnant. She is not having renal atresia. You can safely give AC inhibitor. Or ARB can be given. Calcium cyanoblocker which one you prefer? Nifedipine. Nifedipine oral tablet not sublingual. Not sustained release. Once the patient is stabilized you can go for Amlodipine or Nifedipine sustained release. Diuretic? You have to give diuretic in this patient. Because high BP the safest drug will be diuretic. Because that will not produce drastic reduction in the BP. That removes the sodium and water from the body. What is the sodium level in this patient? Sodium is normal. Do you think that patients who are in hypertension, sodium levels will be high in blood. And we should advise not to take salt to the patient. Patient will be admitted here. Patient want to take salt. Will you see the sodium level and advise or not like that?

Then why we are restricting sodium? What is the action of sodium? There are two types of hypertension. One is salt dependent hypertension. One is salt independent hypertension. Some patients are not taking salt. There are some reasons for that. BP will increase after taking salt. Some patients BP will not increase with salt. Even if you tell the patient to take salt nothing will happen. Only problem is salt can retain water. Salt can increase the renin -angiotensin -aldosterone mechanism and retain water. But some patients BP will be dependent on the sodium. Their BP increases with sodium. But that does not mean that serum sodium will be elevated. Serum sodium will be always normal. What is the difference between sodium chloride and potassium chloride? Both are salt only. Sodium chloride is what we are taking, normal salt. Some doctors prescribe potassium chloride. It is available everywhere. Both are having that same taste. What is the difference? Where will you advise potassium chloride? Hypokalemia. What is the action of potassium on blood vessels? A patient who is having hypertension, low potassium, we make some diagnosis. Aldosterone. Potassium is one element which can increase the BP. Potassium can really dilate the blood vessels. If potassium is not there, constriction occurs and patient will have hypertension. Potassium chloride is another type of salt that can be advised if the patient does not have renal failure. Along with your regular salt, we can advise potassium chloride salt also. Do not avoid salt for any patient in your ICU. What advice do you give when the patient is having hypertension in your ICU? How do you control the salt? Your ICU patients are there. With high BP, they are admitted. Will you give salt or not give salt? That is the question. Yes or no? Give salt. You have to give salt. Salt is very much required for your brain. Normal diet has to be given. You should restrict salt. What is restriction of salt? Additional salt should not be given to the patient. Whatever they are taking in curry, they can take. Additional salt like pappad, achar should be avoided. That is all. Salt restricted diet, not salt reduced diet. Salt has got minimal role in hypertension management. That you should understand. Due to some reason, it can retain water and other things that can add on your BP. You should avoid taking extra salt. What happened after that? The patient was admitted and echoed. Ophthal consultation, 24 hours, urine protein. Ophthal consultation is given for what? Thurglot, hypertensia, retinopathy. What are the grades of hypertension, retinopathy? Kth Wagner classification, we will take grade 1. There will be arteriole construction. Grade 2, we can see, grade 2 and 3, we can see cotton wool sports, X -rays. Grade 2, we will see AV nicking. Grade 3, we will see cotton wool sports. Grade 4, we will see optic disc edema. So, this patient is normal? Normal, sir. Then all the lab parameters was also normal. RFT was normal, renal Doppler was done, USG was done. Where will you ask for renal Doppler in patients? Which are the type of patients you ask for renal Doppler? Every patient admitted with high BP, you should not ask. Either clinically you should get a like renal brewery, otherwise there are indications for that. Elevated creatinine. Either young patient or elderly individual. Young patients can have renal artery stenosis. Elderly individual BP starting after 60 years, 70 years, then there also renal artery stenosis is one of the important factor. In that two conditions, you have to really look for that. And elevated creatinine, early elevation of creatinine is another reason for that. All the parameters was normal. Ultrasound kidney was done? Yes, there was no asymmetry in the kidneys. There was? No, no asymmetry was there. Normal kidneys. Normal kidneys. What happens to the kidney in ultrasound in high BP? What are the changes you anticipate? Why you are looking for the kidneys? One is in the symmetry of the kidney, whether we can understand whether it is a long standing hypertension or not. Corticomedullary differentiation will be lost in chronic kidney disease. Then suppose the size is large, what else you look for? Cysts are there in the kidney. Polycystic kidney disease. Polycystic kidney disease. They are more prone for? They are more prone for aneurysm. It is very important. So all these things you have to look. Then what else was done? Potassium is done? Potassium was done or not? Potassium was done. Potassium level was 3 .5. 3 .5 is low. What are the conditions you get low potassium with high potassium? Primary hyperhidrosis. That is the first thing you are going to see. You tell common things first, then only you think rare things. What is the commonest condition you get high BP with low potassium? Diuretics. Patients who are taking diuretics, that is the commonest cause. Second thing only, you have Kohn's syndrome. That is a rare condition where first itself patient is having hypokalemia. Urine potassium will be high. What will happen to urine potassium in elastics? There also it will be high. So that you have to think. So unnecessarily do not do all investigation. If you have already given elastics, then urine will definitely show high potassium. What do you mean by high potassium in urine? More than 20. More than 20 millikarons is high potassium in urine. Then what is the magnesium level? Magnesium is also normal. Only potassium is low. So what do you do for that? Urine spot potassium was done and it was normal. Potassium low in hypertension is not a good situation. Even if it is 3 .5, it is not good. Then how do you manage it? Workup was done. Urine spot potassium was around normal. 18 was there. Potassium correction was done. How do you correct potassium in this case? Every 0 .3 corresponds to 100 millikarons loss. So how much loss is there? 100 millikarons. So how do you correct it? We can correct either by IV correction or oral correction. IV correction is required here? What are the indications for IV correction of potassium? Patients having symptoms like weakness. Muscle weakness, cardiac arrhythmias. These are the two indications. That is not there. So you have to give oral. Why we avoid IV correction? Slow. If it is there, it can cause cardiac arrhythmia. I will give 100 millikarons through your IV. What will happen? Vessels will get... Thrombophlebitis. Thrombophlebitis. So we avoid. We do not want to give that potassium through peripheral line at all. Unless until there is an emergency, we do not want. And more than 40 millikarons, we never give through an IV line. So that we have to keep in mind. Unnecessarily IV potassium should not be given. You can give. Easily you can correct it with oral potassium or you can give lemon juice. That is enough. More than enough. Then? Then last the patient was sent for sleep study. What happened in sleep study? Diagnosed of OSS. Patient was started on CPAP. CPAP is already started. Then BP control. BP control. Time, sleepiness all. So what tablet you have given for this patient? Initially patient was started on Fumasortan, sir. 8 centimeters initially it was started. Okay. ARB. ARB is started. 16 g was started. Okay. Then that is all. That is enough. Then only the CPAP the patient tolerated well. Okay. What else you wanted to tell something about BP?

Sir, according to now we will follow the 2018 European Society of Cardiology guidelines, sir. Where the optimal BP is less than 120. Normal is 120 to 129. High normal is 130 to 140. And further we divide into grade 1, grade 2 and grade 3, sir. Normal is? 120 to 129, sir. And systolic BP will be 80 to 84, sir. Then as I said earlier the Indian Society of Hypertension for diagnosis of hypertension we made in first visit, second visit and third visit. The main criteria for looking at the target organ damage is the central systolic blood pressure. We are not prescribing beta blockers now because it is the drug that increases the central systolic blood pressure whereas terrestri agents will decrease the central systolic blood pressure, sir. So the mainstay drugs are ACE inhibitors or ARBs and calcine. Where all you cannot use beta blocker? Tell me. One is now it is removed from the first line drug. In emergency room where all you cannot use beta blockers? Accidentally you have already given there is no issue. Okay, long term we don't continue. Where all you cannot give? Tell some solid contraindications for beta blockers. Heart blocks also, sir. Heart blocks you cannot give. Bronchial asthma. Bronchial asthma you cannot give. COPD also better avoid. Will beta blockers produce asthma in any patient? Exacerbate. Sometimes, some patients it will exacerbate, not in all patients. But we better avoid. Cardiac failure. Whether acute or chronic better avoid high dose of beta blockers. You are not telling the most important reason. You should not give beta blockers as a first line drug in this condition. What is that? But you have to give beta blockers but not as a first line drug. What is that? What is the treatment options for pheochromocytoma? Alpha blockers. First alpha blockers, second only beta blockers. If you start beta blockers what will happen? Anapostosis. Anapostosis. You have to be very careful. If you are giving beta blockers BP increases. This is called as paradoxical hypertension. Where all you get paradoxical hypertension? Tell me two conditions where you get paradoxical hypertension. Paradoxical hypertension means you are doing something good for reducing the BP. Renal artery stenosis. Renal artery stenosis, ACA and beta. Here because of pheochromocytoma, beta blockers, both can increase the BP. Sometimes, not always. Okay. So then according to the BP targets are like less than 120 bar 80. According to the SPRINT trial that was latestly conducted, the target BP is less than 120 bar 80 in the absence of diabetes and helps reduce the cardiovascular risk and the mortality. Okay. Then coming to the hypertensive emergencies, all firstly diagnosed hypertension we need to rule out. We need to rule out the secondary cause of hypertension, mainly the endocrine and the renal causes. According to the ESI 2020 guidelines, we need to suspect primary hyperaldosirionism in a patient with young hypertension, resistant hypertension, hypertension that is out of proportion to target organ damage, hypokalemia with hypertension and mainly diastolic hypertension. And 2021 they modified us, every newly diagnosed hypertension must be screened for primary hyperaldosirionism. And… Now we rule out primary hyperaldosirionism. We will send the aldosirone and the renin levels. What happened to aldosirone and renin? Hyporenemic hyperaldosirionism. That is primary hyperaldosirionism. If the renin is high… That is secondary. Hyperrenemic hyperaldosirionism. Due to hypolemia, hyperperfusion, the system will get activated. Okay. So there are conditions where renin alone is elevated, especially like what you told is correct, then kidney diseases. That is also one important reason for hyperrenemic hypertension. They also will have tachycardia, hypertension, all these things. There what is a drug of choice? Alisper. Alisper. That is a new drug. It is not available. It may be available now. But you can give AC inhibitors or ARPs. Okay. Then also the Endocrine Society of India recommends the screening of Cushy syndrome, sir. What is the… I understand that this Cushy syndrome clinically. Most common syndrome will be the central obesity, sir. But most discriminating features will be proximal myopathy, muscle weakness, facial plethora and osteoporosis at a young age, bruising and diagnosed cardiomyopathy like that. Central obesity with these discriminatory features are present. So, it is suspected Cushy syndrome and has to be screened in the patients. So, this patient is okay. The reason for hypertension is here. Here it is OSA, sir. OSA is the reason for hypertension. So, clinical features of OSA are hypertension, obesity, then daytime sleepiness, headache and personality and mood changes. Hypothyroidism is ruled out? Yes, sir. Okay. Thank you. BSCKI.Nhatduy (talk) 15:31, 17 March 2024 (UTC)