Wide Complex Tachyarrythmia || Brugada Algorithm || ACLS Guidelines || #aetcm ||

Added: 2026-05-22

[00:00:25]Welcome to ATCM the emergency medicine channel.

[00:00:29]Presenting the case of a 65year-old male who came to ER uh with complaints of fever since 3 days uh with lower abdominal pain uh since the last 2 days and also uh dissura since the last 2 days on in and uh he also comping difficulty since last one day. On initial 10-second assessment, uh the patient's airway was patent. There was no pooling of secretions. The patient was conscious oriented and he was talking in full complete sentences. On assessment of breathing, the patient had a saturation of uh 90%age in room. uh with uh also uh with that here respirator rate was 24 breaths per minute and an oscultation there was bilateral basal reputations also present for this patient and on assess and following which we had directly intervened we had started him on O2 uh we had kept him in propped up position and we had started him on O2 support uh via O2 mask following which uh we had assessed the circulation part uh the patient's uh BP was uh 70 bar 40 mm of mercury uh with a uh capillary refill time less than 3 seconds.

[00:01:37]>> Okay.

[00:01:37]>> And also an assessment of the heart rate was around 160 and following which we had went to the disability. The GCS was E4 E5 M6. Uh the pupils were equal and reactive. We had assessed the GRBS. The GRBs was 87 and also following which we had gone to the exposure. the exposure the patient was a fabbral there was no and then followed which we had uh taken as adjunct to the primary survey uh initially we had taken an ECG for this patient uh in the ECG the patient had uh wide complex rhythms uh with uh which had with a heart rate of 160. So this was the uh finding which we had got for this uh patient and following this we had taken a mean art blood gas for this patient and the patient had a pa2 of 56 with the PCO of 34 and by carb of 17 uh with the creatinine of two so and lactate of four so this was the finding which he had got in the AG and we had also taken a CBC CRP a patient had a total counts of 16,000 uh with a plate of uh 1 lakh 60,000 and a CRP more than 230.

[00:02:53]So following which uh um when we got the CCG we had a white complex teicardia and then we had initially looked for signs of instability. So for this patient uh the patient came with complaints of breathlessness also there was bilateral basal cuts. We did a pocus pocus showing diffuse B lines across all R1, R2, R3, L1, L2, L3. So there was a B profile along the lung status and also uh patient uh was having desaturation.

[00:03:22]There was no chest discomfort. Um but we had sent cardiac and same uh drop point of care which was also elevated. Uh so uh when we look for signs of instability, it was going for to the it was positive for the signs of instability. Uh so we had uh treated him according to the ACLS algorithm as a white complex teicardia with u patient having uh signs of instability and >> what do you mean by white complex ticardia white complex white complex >> more than 120 millconds. Yes.

[00:04:00]>> Okay. Three small boxes. So this patient then >> tell me three reasons for white complex tech. Four reasons.

[00:04:08]>> Uh four reasons. Uh one of the possibility is ventricular one is ventricular other three are >> other three are muscle bundle br with lb with >> there are four reasons at least we should know but the most important thing is we treat it as wide complex according to we don't see whether it is VT or SU with abency but if you know like uh the rhythm in a better way you can treat it with basic drugs that is advantage.

[00:04:43]>> Yes. So this patient we had gone we had uh taken consent for synchronized cardio from the patient and the bystander uh we had given him injection fentinel 30 micrograms uh sat and following which we had given injection uh then at termed it. We had given 8 mg following which we had given synchronized cardio version with a shock of 100 jewit shock of 100 jewles. Then we had again reassessed but still patient was still in ventricular teicardia. So we had gone for a second shock.

[00:05:17]>> Uh second shock was given at 150 jewles but still the patient's uh ventricular the teicardia persisted while complex teicardia. We had increased the jewels to 200 jewles. Uh we had given three shocks but still the ventricular teicardia was persisting. So we had uh started in one amodon 150 mg. uh we had given ballous dose IV over 10 minutes and then we had started on infusion.

[00:05:40]>> Okay.

[00:05:40]>> Following which the ventricle teicardia episode the white complex teardia had resolved.

[00:05:46]>> Okay.

[00:05:46]>> So we came to a diagnosis that by the ECG that the patient had a um ventricle teicardia because of the following reasons the mainly the reasons were uh he had like it was more than or equal to three VP VPC. So ventricle premature compress is more than or equal to three with a rate of more than 130 beats per minute. So that's a criteria of ventricle teicardia and if it's more than if it is lasting for more than 30 seconds it is a sustained ventricle. So for this patient he had a sustained ventricle it was persistent for more than 30 seconds and can can be monomorphic or polymorphic. In this patient the face was always upright.

[00:06:22]There was no downward no dual faces. So it was a monomorphic ventricular ticardia. So >> monomorphic means what? Sorry, polymorphic means what?

[00:06:32]>> Multiple morphology.

[00:06:33]>> Multiple morphology.

[00:06:34]>> What is the most common diagnos for that?

[00:06:39]>> So this patient had a monomorphic ventricular teicardia and we card and sims are also elevated. So most probably we are class telling that most probably the ventricle teicardia could be due to the underly infection. uh and uh if it's polymorphic usually the QRS will be uh like white QRS with rate will be more than 200 per minute and also which will change the axis axis. So that is the main thing to look into uh usually predisposing conditions involve underlying uh in schemic heart disease. So underlying myioardial infection is one of the cause. Second cause includes tanalopathy. So tanalopathys usually involves uh like romano wart syndrome regard syndrome. So these are the uh chandelopathies which are the causes. So we should look for QT prolongation. So basically uh QT prolongation is one of the criteria which will lead to VT in the subsequent VT. So other effect is >> there are other things like you have told about ectopic. Yes. How do how do you classify ectopic and what stage onwards it will become VT? uh is usually class the classification is called as launch classification. Uh it is classified into grade zero to grade five. So usually the grade five is the RT phenomenon where it's coming from. So >> Ron phenomena is a very dangerous thing and it can proceed to VT >> even uh like polymorphic ectopics also can produce bgeiny trigeminy polymorphic ectopics all those things can lead to wing. Other causes are the drugs that cause UT prolongation. So usually the drugs are usually the common antibiotics like acetrome, clarithroycin. These are the orthroycin and even drugs like metropomoride oretron haloperod or even uh TCA. TCA TCA is known for wide QRS more than 200 millconds. Okay.

[00:08:37]>> So it can cause very wide QRS >> and alert disturbances. So elite disturbance is one thing which you have to check in our blood gas. the patient had a potassium of three.

[00:08:46]>> Okay.

[00:08:47]>> So the hypocalemia was also there for this uh patient uh with hypoalemia or hypercalemia both can cause vt or hypomagnesmia hypocalcemia. So these are the causes or even temperature. So when we assess the temperature patient is in hypothermia patient has an increased propensity to go for a vendicular ticardia. Then uh MIA or structural heart disease ho. So that also can be hypertrophic oxy cardiammyopy can also be one of the cause of end takardia.

[00:09:17]Then usually the most common confusion which we come across is when we have a white complex SVT like SV with abency or with a VT. So then we have a criteria called.

[00:09:28]>> So you have SVT you have ST with abency.

[00:09:32]You have to differentiate these two.

[00:09:34]Okay. then probably you can use drugs like uh uh uh like beta blockers, calcium channel blockers and all SVT with LBV or RBV again it is a question questionable thing in WPW.

[00:09:47]>> So that criteria is mainly the bugata criteria. So bugata criteria consist of four steps. So the first one is usually we should check whether the RS complex is present in any lead. If RS complex is present it is not WT. If it is not present the rhythm is VT.

[00:10:02]>> So that is the first thing. Then we should look for the RS duration.

[00:10:05]>> That means VTs are always monomorphic monopacic.

[00:10:09]>> Monophasing >> either positive or negative negative.

[00:10:12]Okay. But SVT will follow the ECG pattern like normal ECG pattern. Some it will be R some it will be some it will be RS. So if you're seeing RS it is SV with a >> uh second one is RS duration. So if the RS duration is more than 100 in any lead then the rhythm is VT.

[00:10:30]Then third one is we should look for AV dissociation. Uh and we should look whether the patient is having fusion or capture beats. So the capture beats is usually a narrow QRS complex which will be present in between the white QRS complexes. So that's one capture one beat one uh wave which is captured by the syn. So in that way we'll get a narrow complex. So uh that is usually finally found in ventricular ticard >> and if the and we should check the rhythm.

[00:11:02]>> Yeah. So then we should also check whether the patient's rhythm is morphologically consistent with the SVT.

[00:11:07]>> Okay.

[00:11:07]>> So that is the other criteria to look into. So these four >> consistent with the SVT with the pattern >> pattern.

[00:11:14]>> So if RBV pattern or LBV pattern is there then you have to suspect that >> yes. So these four are the uh criterias which we look into the uh VT. So in case of if there's an RS rdash pattern if the left side uh RS R pattern if it's larger than the uh right side then it is set to be >> rabbit ears rabbit right or left rabbit.

[00:11:38]>> So if it's RS Rash V1 if you get that R left side R is larger in amplitude than right then we tell it as it is V_T. So these are the criterias which we look into as per bugar.

[00:11:52]>> Why should we know all these things?

[00:11:53]>> So uh the management >> what is the what is the idea?

[00:11:57]>> Yeah you say the beta blockers or so if you know it in a better way you can use drugs like beta blockers blockers all those things.

[00:12:06]>> But according to ACLS we actually no need to see all these things. We should take it as a wide complex teicardia with or without cardiac instability. Okay. If instability is there like you told shock has to be delivered. If uh if patient is stable then amidron is the choice.

[00:12:23]Amidron can can be given in VT amidron can be given in SV with abency SV with WPW center everywhere can be given that is advantage but if you know better like like what you told like buga this not buga that criteria >> yeah bugata criteria >> buga criteria algorithm has to be followed then you can uh treat it in a better way >> yes so usually the management according to the SLS algorithm uh the first thing is we should look whether the patient has a pulse or pulses. So if it's a pulsus, if you have a white complex rhythm, we should look for the pulse. If the patient's pulse is preset, then we should look for signs of instability. So the patient signs of instability mainly includes patient going having a hypotension. Our patient patient had a hypotension uh patient having features of pulmonary edema features showing complaints of chest discomfort.

[00:13:17]>> GCS also >> yeah also altered sensory. Our patient's sensory was full but other three criterias were fulfilling. Uh so for such patients we should go for if pulse is present we should go for synchronized cardio version. If pulse is absent in case of white complaciardia we go for defibrillation. So that is the uh difference. So what is the basic difference between defibrillation and cardioverion?

[00:13:41]>> In cardio there will be synchronized we have to >> we have to press the synchronized button and deliver the shock and >> so they'll be usually delivering the shock at the peak of the hour.

[00:13:51]>> What what we have to do as a >> we have to keep for 10 seconds that is very important. Defibrillation means immediately the shock will be delivered and it will be delivered in the highest juice. But here we can gradually increase.

[00:14:05]>> So that is usually the uh ACS protocol.

[00:14:08]And uh this shock is usually uh we give it thrice in case of pulsus VT. After the third shock we go with amador 300 mg >> and we should exclude the reversible causes of uh arrest.

[00:14:22]>> Okay. Did you send cardiac in?

[00:14:24]>> Yes. In this patient card >> before or after shock?

[00:14:26]>> Before shock. After shock.

[00:14:27]>> It has to be sent before giving shock.

[00:14:30]after shock anyway it will be elevated so he cannot depend on that value.

[00:14:35]>> Uh then uh usually if the single the single is also done only thrice if it is done more than three times if still patient is having takaria we can start on amodderone that is usually in 5 mg per kg infusion dose. So usually start dose will be 150 >> 150 mg IV which is given over 10 minutes then uh we start with 1 mg per minute over the last over the 6 hours then followed by.5 mg per minute over uh 18 hours. So this is what is the criteria which goes for amodor but there are also other drugs which we can use into so other drug is usually the lidocaine or linocine both are actually same.

[00:15:15]>> Okay. uh yeah even the constituents are also same now we can say that now lidocine is the actual the term which is used in case of uh we >> all preparations are slightly different subcutaneous >> yes here uh we give usually in the IV in the dose of 1 mg 1 to 1.5 mg per kg I basis doses which we give and we assess for five every 5 minutes and we can give a maximum dose of 3 mg per kg uh and following which we give a infusion at the rate of uh the usually the increment is by.5 to 75 mg per kg. So that is the usual uh increment which we look into and then the second drug which you can give is promid is another drug which is usually given at a dose of 50 mg per minute and third drug is silo silo is beta block.

[00:16:05]>> So that can be given 1 mg per kg. So these are the three uh drugs which like three additional drugs which we can give it when required takaria u so these are the management way >> what happened to the patient after the rhythm has come back to normal >> yeah yeah following the infusion dose patient's rhythm had come back to the normal >> what are the adverse effects of amron >> I mean >> that is longterm shortterm >> we should look in the thyroid status of the patient so patient >> hyper thyroid ISM because of thyroiditis later hypothyroidism because of fibrosis. Then lung fibrosis is very late.

[00:16:43]>> It can also affect the liver liver transmit.

[00:16:47]>> So we have to be when we are we are giving highdose infusion we have to monitor all those things. Yes.

[00:16:52]>> Okay.

[00:16:54]>> Okay.