Fantastic. I rarely use diltiazem because I was told it is also contraindicated in structural heart disease and often the patient with fast AF has had no recent echo
Many thanks for this. Very interesting as an occasional acute Afib patient. Flecanide IV seems to revert my rhythm back usually. Hate the condition though, detest the symptoms.
My own experience may be of interest, where I am fairly certain I had an external physical cause for a three month period of otherwise inexplicable Atrial Fibrillation (lasting up to 9 days at a time). (1) I had sleep problems, with repetitive nightmares associated with imagined chattering teeth (I was in fact suffocating, due to undiagnosed Sleep Apnoea). (2) One night I went into Atrial Flutter, and attended Hospital where this was diagnosed via ECG, and reversed via IV Fluids, Magnesium and a Beta Blocker, namely 5mg Bisoprolol Fumarate. Nobody then realised it was due to Sleep Apnoea, but I worked that out almost the next day. (3) I was put onto a daily precautionary dose of 5mg Bisoprolol Fumarate, which mainly seemed to cause Bradycardia, especially at night, so I halved that to 2.5 mg to reduce the Bradycardia, and later to 1.25 mg for the same reasons. I had various other tests, and my heart was found to be healthy with no structural issues. (4) I was eventually diagnosed with Severe Sleep Apnoea, and prescribed CPAP (Constant Positive Airway Pressure). I also have pretty severe Osteoarthritis in all lower joints from past injury, so cannot stop myself rolling on to my back, where I get the most relief from pain, but that is the worst position for Sleep Apnoea. For that reason, I find I need to run my CPAP Machine at the maximum pressure of 20 cm H20, which I find is fine, and stops most Apnoeas, but I struggle to stop my Face Mask from leaking air at that pressure. (5) I tried various CPAP Masks, and settled on the Prescribed ResMed F20. I have to keep the straps tight to stop leaks, but I can usually stop all leaks now. (6) Over the following 2 years, I experienced random irregular heart beats, which seemed to be Ectopic Beats or Premature Atrial Contractions (my own ECGs show an normal Lead I waveform, with what seems to be a premature malformed P wave, then normal QRS, then a normal T Wave, then a delayed P/QRS/T and then back to normal. This seemed to be linked to food as well, so I have to avoid anything with bad fats, such as Trans Fats or Palm Oil. That has to be some Vagal Gastro Cardiac link, but it happens 15 minutes after consuming such food (usually by accident until we work out what was in the food). (7) I had two acute Atrial Fibrillation sessions and had to return to Hospital, but both subsided without any intervention. I continued to struggle with night time Bradycardia due to the Beta Blocker, that I kept at 1.25 mg. (8) Early this year, I went into regular episodes of Atrial Fibrillation (mix of Brady and inappropriate Tachy), and despite a Hospital Visit that confirmed this, the only suggested help was to vary the dose of the Beta Blocker. That seemed to make things worse, and the Bradycardia became a real problem. (9) I felt that something was driving this, and my own small ECG was mainly showing a weird mixture of Bradycardia and inappropriate Tachycardia, as if my electrical system was misfiring, and unable to settle on a beat. (10) Trying to find a solution, I tried various things, including trying to stimulate a Vagus Reaction, such as thrusting my face into cold water, and also massaging the Vagus nerves either side of my neck. Bingo! The latter had an effect, and I noted my heart rate changed, and seemed to be linked to my Vagus nerves. (11) Then it all made sense. The tight Straps on my CPAP Mask, went right across my Vagus Nerves either side of my neck, just below my ears. This was always painful, and left deep welt marks by the morning. I felt that was a possible cause, as the Vagus Nerve is part of the body's parasympathetic system, so there is a link with heart rate control. (12) That day, I fabricated a Foam Neck pad from my wife's Yoga Mat, so 8mm open cell foam. This covered the back of my head, and also extended below my ears and onto my face, and was around 70mm wide over my Vagus Nerves to spread the Strap loading. (13) That worked, the Atrial Fibrillation stopped same night, and has not returned after some four Months. Also, the odd PACs died away, although I had many just afterwards, these reduced in frequency the longer I wore the neck pad. (14) I have since modified the design, and added plastic panels above the Foam where it goes over the Vagus Nerves, to further spread the Strap load. I also no longer have any neck pain, nor any marks on my face by the morning. (15) I do not in effect now have Sleep Apnoea, because the CPAP is stopping the effects. So I had no evidence of any Sleep Apnoea triggering the Atrial Fibrillation, there were no signs of one impacting the other. So normal sleep, no Oxygen Drops, but random unrelated Atrial Fibrillation that seemed via my ECG to be a mixture of slow and fast beats. In summary Tight CPAP Mark Straps could be a cause of Atrial Fibrillation in some people. If Sleep Apnoea is diagnosed, and the patient is using CPAP at higher pressures, and has a CPAP Mask where narrow Straps go over the Vagus Nerve area in the neck, then any otherwise inexplicable Atrial Fibrillation may need to be investigated in terms of the CPAP Equipment. Sadly, I could not interest the local Cardiologist to consider this as a cause. I asked for help for the 3-4 Months this was happening, but did not even get a call for nearly 6 months, when he simply dismissed this explanation without looking at my many ECGs and well considered research! The fact is, the problem went away the very day I took steps to protect my Vagus Nerves. Unless I have missed something, I just cannot see that this is not the true cause in my case. I also stopped the Beta Blocker, which took some doing, and no longer now suffer from Bradycardia, and I also feel like a medicinal cosh has been lifted. I did try to point out the Bradycardia issues, and that the Beta Blocker may not be needed but, that too fell on deaf ears. As I understand it, a Beta Block is contraindicated in cases of Vagal Atrial Fibrillation. There is a cardiac link, as there are documented cases of premature babies being placed onto CPAP, and suffering Atrial Fibrillation until their CPAP Mask and Straps are adjusted, so as not to interfere with their Vagus Nerves in their necks. There are other documented cases where Vagus Nerve damage after, say, accident, has led to Atrial Fibrillation issues. I am not selling anything, and have nothing to gain from setting the above out. I am simply relaying my own experience in case this may help others.
Thank you for detailing your experience with A-Fib. I’m on a journey to find what is triggering my A-Fib and I found your comment very helpful. I appreciate you taking the time to share. Incidentally, my cardiologist taught me about the importance of the vagus nerve to brain, heart & gut health and he probably would not dismiss your conclusion.
I wish you had added some dosing regime for use of IV procainamide. This drug is only recently available here (and hard to get) and finding a consistent dosing protocol, and being familiar with it, is difficult. Otherwise, great video :)
It is mandatory to address the cause of atrial fibrillation prior to rate/rhythm control. Like Treat Anxiety, Pain, Anemia, Electrolytes like K/Mg, Respiratory problem, Infection etc.
I have one question: when the patient for instance presenting with afib with ventricular response ~ 150 bpm , sBP ~ 70 mmHg & known to have HFrEF with EF~ 25 , RV is involved, & enlarged left atrium ,, I'm not sure of cardioversion might be successful in restoring sinus rhythm (with risk of embolism) & even if SR was restored ,, mechanical LA contraction might not occur only after hours-days ... Wouldn't rate control be superior to cardioversion? (Digoxin might benefit but with ↑sympathetic tone is less likely to be effective & AKI is very common in such a case.. I'm thinking of amio + vasopressor [I know this might ↑VR] ) ..
Some of my patients who are diagnosed with afib and on anticoagulation appear to be in afib or irregular at times - yet asymptomatic. Is this emergent?
Certain situations can trigger an episode of atrial fibrillation, including: drinking excessive amounts of alcohol, particularly binge drinking. being overweight (read about how to lose weight) drinking lots of caffeine, such as tea, coffee or energy drinks. taking illegal drugs, particularly amphetamines or cocaine. 👍
As stated in the video, moderate amounts of caffeine (~2-3 cups of coffee) have consistently been shown to *not* trigger atrial fibrillation. However, you're correct about the others, with obesity being a risk factor for the development of a-fib in the long-term, stimulant abuse being a potential trigger for an acute episode, and alcohol abuse being both.
Dear Dr Strong, I have a doubt regarding cardioversion. If a patient has AF with RVR with Shock, do we really have the time to do transesophageal echo? What should be our immediate strategy here? THANKS.
You are correct. If the patient requires emergent cardioversion due to shock or active ischemia, the only question is whether there is sufficient time for anesthesia to administer sedation; there is not usually time for a TEE - and even if there was enough time, one wouldn't delay cardioversion even if a left atrial clot was seen. So there's no point in doing the test. TEE is indicated in elective and urgent cardioversion (e.g. a-fib with RVR in the context of new onset heart failure but in the absence of cardiogenic shock; severe symptoms of palpitations, etc...)
It's not possible to tell what rhythm a person is experiencing just from the heart rate. I recommend speaking with your physician about personal health concerns; they can access all of the relevant data and provide you with more specific information.
Well I did cardioversion recently and I still feel the same way as before and now I’m in a state of angst. I want to feel normal again. This pronounced AFib is uncomfortable.
Sir, you listed rate not being controlled on oral meds as an indication for admission. Are oral meds tried before iv meds? Apart from diltiazem immediate release what all oral meds should be tried before switching to IV? After how much time of giving the drug can we call that a failure of not being controlled on oral meds?
If someone is presenting to the ED with a-fib and RVR and is without evidence of hemodynamic compromise and without cardiac history that would make RVR particularly dangerous (e.g. heart failure, severe CAD, and particularly WPW!), then I think it's very reasonable to try oral diltiazem. You're correct that if oral immediate-release dilt is ineffective, then other oral meds are unlikely to provide control quickly enough to avoid admission. But I think in general, clinicians too reflexively go straight to the IV dilt w/o even considering the possibility that oral dilt may be sufficient. Another big caveat here is that it depends on what's triggering the RVR. If someone's a-fib is complicating a larger acute problem (e.g. PE, COPD exac, etc...) that will be a reason for admission anyway, then it's less important whether one choose IV or oral up front. It's mostly about avoiding unnecessary hospital admissions.
@@StrongMed Thankyou for your reply. A follow-up question. After trying oral diltiazem if the heart rate hasn't slowed down for some time, after how long do we make a determination that it has not worked?
EECP is a pretty niche topic for general med ed channel, and I lack the expertise to do a deep dive on it without research. In what way do you think patients are being mislead?
@@StrongMed Few patients have been told that they don't require bypass even though their RCA and LAD are 90-95% blocked. My understanding of EECP is that it can help for minor block but not for critical one.
@@jerrypotter9070 Again, I'm not an expert on this specific issue (so take this with a grain of salt), but I'm not convinced in the effectiveness of EECP at improving objective, patient-centered outcomes. (Due to the nature of EECP, randomized controlled trials can't truly be blinded, so therefore, subjective trial endpoints such as self-reported frequency/severity of chest pain or exercise tolerance is arguably meaningless.) However, even if one accepts that there is clinically meaningful benefit from EECP, it should only be used as a primary modality in patients who are either too high risk to undergo invasive treatment (e.g. angioplasty/PCI or bypass), or whose coronary disease is not anatomically amenable to those options. Just my off-the-cuff 2 cents.
I agree that there has been a lot of caution over using DOACs in ESRD - not generally because they've been shown to be harmful but rather because most studies of DOACs have excluded patients with ESRD. Also, every country has its own process for approving and regulating medications, so it's very possible that apixaban may not be approved in ESRD where you practice/study. However, apixaban is approved by the FDA for use in such patients in the US. It's my understanding that the original approval for use in ESRD was based on extrapolation from pharmacologic data rather than a trial with clinically meaningful outcomes. However, there have since been a few studies just from the last 12 months demonstrating safety: www.acc.org/latest-in-cardiology/clinical-trials/2019/11/15/17/29/renal-af www.ncbi.nlm.nih.gov/pmc/articles/PMC7284084/ www.ncbi.nlm.nih.gov/pmc/articles/PMC6202193/
Watching this while having no medical insurance... I work 50hrs a week so I don't qualify for anything.... just waiting at this point for the big attack
Sort of. The newest approach to the influence of sex on stroke risk is that female sex isn't a risk factor as much as it is a modifier of other risk factors. There were 2 ways to account for this with the CHA2DS2-VASc score. In one way, female sex only gave a point if there were other risk factors (i.e. so a female with no other risk factors would still have a CHA2DS2-VASc score of 0, but a female with hypertension would have a score of 2). In the second way, female sex is not an official "risk factor" at all, but the cutoff for what CHA2DS2-VASc score should trigger anticoagulation is then different for males vs. females.
How do you know is Afib if the QRS is wide? ( I would assume is a ventricular tachycardia) Just because is iregular? If it would have been regular would you considered a V tach?
Yes, mostly. An irregularly irregular rhythm with no organized atrial activity (i.e. no P waves or flutter waves), with a wide and consistent QRS morphology must be a-fib with some form of aberrant conduction (e.g. bundle branch block, WPW). If the QRS duration was consistently wide, but the QRS morphology was changing from one beat to the next, it would suggest polymorphic ventricular tachycardia (of which torsades is the most well known subtype). A regular, wide complex tachycardia may not necessarily be VT. There is a significant amount of literature trying to figure out rules that allow one to differentiate VT from a supraventricular tachycardia with aberrancy, but in most clinical situations it's best to work on the assumption it is VT until you know definitively that it's something else.
Thank you Dr Strong , for taking time of your busy schedule to make this educational video.
medicine outside medschool is a totally different beast god help us all
Amen
Fantastic. I rarely use diltiazem because I was told it is also contraindicated in structural heart disease and often the patient with fast AF has had no recent echo
This video is very timely for this intern. Thank you!
Well explained. Very thorough!
This man is extremely knowledgeable.
Amazing and very informative. Thank you 😊
Many thanks for this. Very interesting as an occasional acute Afib patient. Flecanide IV seems to revert my rhythm back usually. Hate the condition though, detest the symptoms.
My own experience may be of interest, where I am fairly certain I had an external physical cause for a three month period of otherwise inexplicable Atrial Fibrillation (lasting up to 9 days at a time).
(1) I had sleep problems, with repetitive nightmares associated with imagined chattering teeth (I was in fact suffocating, due to undiagnosed Sleep Apnoea).
(2) One night I went into Atrial Flutter, and attended Hospital where this was diagnosed via ECG, and reversed via IV Fluids, Magnesium and a Beta Blocker, namely 5mg Bisoprolol Fumarate. Nobody then realised it was due to Sleep Apnoea, but I worked that out almost the next day.
(3) I was put onto a daily precautionary dose of 5mg Bisoprolol Fumarate, which mainly seemed to cause Bradycardia, especially at night, so I halved that to 2.5 mg to reduce the Bradycardia, and later to 1.25 mg for the same reasons. I had various other tests, and my heart was found to be healthy with no structural issues.
(4) I was eventually diagnosed with Severe Sleep Apnoea, and prescribed CPAP (Constant Positive Airway Pressure). I also have pretty severe Osteoarthritis in all lower joints from past injury, so cannot stop myself rolling on to my back, where I get the most relief from pain, but that is the worst position for Sleep Apnoea. For that reason, I find I need to run my CPAP Machine at the maximum pressure of 20 cm H20, which I find is fine, and stops most Apnoeas, but I struggle to stop my Face Mask from leaking air at that pressure.
(5) I tried various CPAP Masks, and settled on the Prescribed ResMed F20. I have to keep the straps tight to stop leaks, but I can usually stop all leaks now.
(6) Over the following 2 years, I experienced random irregular heart beats, which seemed to be Ectopic Beats or Premature Atrial Contractions (my own ECGs show an normal Lead I waveform, with what seems to be a premature malformed P wave, then normal QRS, then a normal T Wave, then a delayed P/QRS/T and then back to normal. This seemed to be linked to food as well, so I have to avoid anything with bad fats, such as Trans Fats or Palm Oil. That has to be some Vagal Gastro Cardiac link, but it happens 15 minutes after consuming such food (usually by accident until we work out what was in the food).
(7) I had two acute Atrial Fibrillation sessions and had to return to Hospital, but both subsided without any intervention. I continued to struggle with night time Bradycardia due to the Beta Blocker, that I kept at 1.25 mg.
(8) Early this year, I went into regular episodes of Atrial Fibrillation (mix of Brady and inappropriate Tachy), and despite a Hospital Visit that confirmed this, the only suggested help was to vary the dose of the Beta Blocker. That seemed to make things worse, and the Bradycardia became a real problem.
(9) I felt that something was driving this, and my own small ECG was mainly showing a weird mixture of Bradycardia and inappropriate Tachycardia, as if my electrical system was misfiring, and unable to settle on a beat.
(10) Trying to find a solution, I tried various things, including trying to stimulate a Vagus Reaction, such as thrusting my face into cold water, and also massaging the Vagus nerves either side of my neck. Bingo! The latter had an effect, and I noted my heart rate changed, and seemed to be linked to my Vagus nerves.
(11) Then it all made sense. The tight Straps on my CPAP Mask, went right across my Vagus Nerves either side of my neck, just below my ears. This was always painful, and left deep welt marks by the morning. I felt that was a possible cause, as the Vagus Nerve is part of the body's parasympathetic system, so there is a link with heart rate control.
(12) That day, I fabricated a Foam Neck pad from my wife's Yoga Mat, so 8mm open cell foam. This covered the back of my head, and also extended below my ears and onto my face, and was around 70mm wide over my Vagus Nerves to spread the Strap loading.
(13) That worked, the Atrial Fibrillation stopped same night, and has not returned after some four Months. Also, the odd PACs died away, although I had many just afterwards, these reduced in frequency the longer I wore the neck pad.
(14) I have since modified the design, and added plastic panels above the Foam where it goes over the Vagus Nerves, to further spread the Strap load. I also no longer have any neck pain, nor any marks on my face by the morning.
(15) I do not in effect now have Sleep Apnoea, because the CPAP is stopping the effects. So I had no evidence of any Sleep Apnoea triggering the Atrial Fibrillation, there were no signs of one impacting the other. So normal sleep, no Oxygen Drops, but random unrelated Atrial Fibrillation that seemed via my ECG to be a mixture of slow and fast beats.
In summary
Tight CPAP Mark Straps could be a cause of Atrial Fibrillation in some people.
If Sleep Apnoea is diagnosed, and the patient is using CPAP at higher pressures, and has a CPAP Mask where narrow Straps go over the Vagus Nerve area in the neck, then any otherwise inexplicable Atrial Fibrillation may need to be investigated in terms of the CPAP Equipment.
Sadly, I could not interest the local Cardiologist to consider this as a cause. I asked for help for the 3-4 Months this was happening, but did not even get a call for nearly 6 months, when he simply dismissed this explanation without looking at my many ECGs and well considered research!
The fact is, the problem went away the very day I took steps to protect my Vagus Nerves. Unless I have missed something, I just cannot see that this is not the true cause in my case.
I also stopped the Beta Blocker, which took some doing, and no longer now suffer from Bradycardia, and I also feel like a medicinal cosh has been lifted. I did try to point out the Bradycardia issues, and that the Beta Blocker may not be needed but, that too fell on deaf ears. As I understand it, a Beta Block is contraindicated in cases of Vagal Atrial Fibrillation.
There is a cardiac link, as there are documented cases of premature babies being placed onto CPAP, and suffering Atrial Fibrillation until their CPAP Mask and Straps are adjusted, so as not to interfere with their Vagus Nerves in their necks. There are other documented cases where Vagus Nerve damage after, say, accident, has led to Atrial Fibrillation issues.
I am not selling anything, and have nothing to gain from setting the above out. I am simply relaying my own experience in case this may help others.
Thank You for the details of your issues. If you find a cure for something that nobody has an incentive to sell to someone it will be ignored.
Thank you for detailing your experience with A-Fib. I’m on a journey to find what is triggering my A-Fib and I found your comment very helpful. I appreciate you taking the time to share. Incidentally, my cardiologist taught me about the importance of the vagus nerve to brain, heart & gut health and he probably would not dismiss your conclusion.
Great video.Thank you Sir.I have stated clicking the like symbol even before watching them.
Brilliant, thank you.
I wish you had added some dosing regime for use of IV procainamide. This drug is only recently available here (and hard to get) and finding a consistent dosing protocol, and being familiar with it, is difficult.
Otherwise, great video :)
It is mandatory to address the cause of atrial fibrillation prior to rate/rhythm control. Like Treat Anxiety, Pain, Anemia, Electrolytes like K/Mg, Respiratory problem, Infection etc.
Always look for other causes of instability among patients with AF and shock or difficulty controlling the ventricular rate.
Brilliant thank you, needed for this 1st year med student 🤗
great cme update keep up dtay blessed
Sooo well explained!!! Many thanks 🙏🏻 please do a video on diabetes... treatment... how to proceed!!!
Great insights
Very useful information!
Well explained! Tqsm!
Hi I favorite your videos and I would like to ask you if it possible: Could you share an video low rate A-Fib? Thank you so much.
I have one question: when the patient for instance presenting with afib with ventricular response ~ 150 bpm , sBP ~ 70 mmHg & known to have HFrEF with EF~ 25 , RV is involved, & enlarged left atrium ,, I'm not sure of cardioversion might be successful in restoring sinus rhythm (with risk of embolism) & even if SR was restored ,, mechanical LA contraction might not occur only after hours-days ... Wouldn't rate control be superior to cardioversion? (Digoxin might benefit but with ↑sympathetic tone is less likely to be effective & AKI is very common in such a case.. I'm thinking of amio + vasopressor [I know this might ↑VR] ) ..
Some of my patients who are diagnosed with afib and on anticoagulation appear to be in afib or irregular at times - yet asymptomatic. Is this emergent?
Certain situations can trigger an episode of atrial fibrillation, including:
drinking excessive amounts of alcohol, particularly binge drinking.
being overweight (read about how to lose weight)
drinking lots of caffeine, such as tea, coffee or energy drinks.
taking illegal drugs, particularly amphetamines or cocaine.
👍
As stated in the video, moderate amounts of caffeine (~2-3 cups of coffee) have consistently been shown to *not* trigger atrial fibrillation. However, you're correct about the others, with obesity being a risk factor for the development of a-fib in the long-term, stimulant abuse being a potential trigger for an acute episode, and alcohol abuse being both.
You've talked olabout rate control in this video,
How about rythm control?
Dear Dr Strong, I have a doubt regarding cardioversion. If a patient has AF with RVR with Shock, do we really have the time to do transesophageal echo? What should be our immediate strategy here? THANKS.
Shock >> Emergency >> Elektrokardioversion , there is no Time to make Diagnostik or to treat it with Medikation. That what i would do
You are correct. If the patient requires emergent cardioversion due to shock or active ischemia, the only question is whether there is sufficient time for anesthesia to administer sedation; there is not usually time for a TEE - and even if there was enough time, one wouldn't delay cardioversion even if a left atrial clot was seen. So there's no point in doing the test. TEE is indicated in elective and urgent cardioversion (e.g. a-fib with RVR in the context of new onset heart failure but in the absence of cardiogenic shock; severe symptoms of palpitations, etc...)
@@StrongMed Thank you for your response sir!
Hi i had an at home sleep study and have mild sleep apnea but had a BPM go as high as 129 is this afib?
It's not possible to tell what rhythm a person is experiencing just from the heart rate. I recommend speaking with your physician about personal health concerns; they can access all of the relevant data and provide you with more specific information.
@@StrongMed oh okay will do and thank you
awesome
Well I did cardioversion recently and I still feel the same way as before and now I’m in a state of angst. I want to feel normal again. This pronounced AFib is uncomfortable.
Sir, you listed rate not being controlled on oral meds as an indication for admission. Are oral meds tried before iv meds? Apart from diltiazem immediate release what all oral meds should be tried before switching to IV? After how much time of giving the drug can we call that a failure of not being controlled on oral meds?
If someone is presenting to the ED with a-fib and RVR and is without evidence of hemodynamic compromise and without cardiac history that would make RVR particularly dangerous (e.g. heart failure, severe CAD, and particularly WPW!), then I think it's very reasonable to try oral diltiazem. You're correct that if oral immediate-release dilt is ineffective, then other oral meds are unlikely to provide control quickly enough to avoid admission. But I think in general, clinicians too reflexively go straight to the IV dilt w/o even considering the possibility that oral dilt may be sufficient. Another big caveat here is that it depends on what's triggering the RVR. If someone's a-fib is complicating a larger acute problem (e.g. PE, COPD exac, etc...) that will be a reason for admission anyway, then it's less important whether one choose IV or oral up front. It's mostly about avoiding unnecessary hospital admissions.
@@StrongMed Thankyou for your reply. A follow-up question. After trying oral diltiazem if the heart rate hasn't slowed down for some time, after how long do we make a determination that it has not worked?
It depends how busy the ER is... ;) (EDIT: That's actually sort of the truth, not just a joke!)
Could you please do a video on EECP? People are misguiding patients.
EECP is a pretty niche topic for general med ed channel, and I lack the expertise to do a deep dive on it without research. In what way do you think patients are being mislead?
@@StrongMed Few patients have been told that they don't require bypass even though their RCA and LAD are 90-95% blocked. My understanding of EECP is that it can help for minor block but not for critical one.
@@jerrypotter9070 Again, I'm not an expert on this specific issue (so take this with a grain of salt), but I'm not convinced in the effectiveness of EECP at improving objective, patient-centered outcomes. (Due to the nature of EECP, randomized controlled trials can't truly be blinded, so therefore, subjective trial endpoints such as self-reported frequency/severity of chest pain or exercise tolerance is arguably meaningless.)
However, even if one accepts that there is clinically meaningful benefit from EECP, it should only be used as a primary modality in patients who are either too high risk to undergo invasive treatment (e.g. angioplasty/PCI or bypass), or whose coronary disease is not anatomically amenable to those options.
Just my off-the-cuff 2 cents.
Thanks alot but i know that Apixaban cannot be used by Endstage renal Failur
I agree that there has been a lot of caution over using DOACs in ESRD - not generally because they've been shown to be harmful but rather because most studies of DOACs have excluded patients with ESRD. Also, every country has its own process for approving and regulating medications, so it's very possible that apixaban may not be approved in ESRD where you practice/study. However, apixaban is approved by the FDA for use in such patients in the US. It's my understanding that the original approval for use in ESRD was based on extrapolation from pharmacologic data rather than a trial with clinically meaningful outcomes. However, there have since been a few studies just from the last 12 months demonstrating safety:
www.acc.org/latest-in-cardiology/clinical-trials/2019/11/15/17/29/renal-af
www.ncbi.nlm.nih.gov/pmc/articles/PMC7284084/
www.ncbi.nlm.nih.gov/pmc/articles/PMC6202193/
@@StrongMed Sir...Is it true that it can be used above the eGFR of 15 ..not below that?
Omg the intro music. RIP headphone users
This is for Dr. Not for self health
Ablation be useful?
In some patients, yes, but it would almost never be done in an acutely ill patient.
Watching this while having no medical insurance... I work 50hrs a week so I don't qualify for anything.... just waiting at this point for the big attack
The latest determination, as of 2023, is that the female patient does NOT have assigned a score for her sex.
Sort of. The newest approach to the influence of sex on stroke risk is that female sex isn't a risk factor as much as it is a modifier of other risk factors. There were 2 ways to account for this with the CHA2DS2-VASc score. In one way, female sex only gave a point if there were other risk factors (i.e. so a female with no other risk factors would still have a CHA2DS2-VASc score of 0, but a female with hypertension would have a score of 2). In the second way, female sex is not an official "risk factor" at all, but the cutoff for what CHA2DS2-VASc score should trigger anticoagulation is then different for males vs. females.
sir ,we want more concise lectures from you.
No we don't.
Does 18:29 count as concise? In other words, is this video a good length and amount of content?
Good length but still comprehensive enough. Thank you so much
@@StrongMed man this video was awesome, thank you
How do you know is Afib if the QRS is wide? ( I would assume is a ventricular tachycardia) Just because is iregular? If it would have been regular would you considered a V tach?
Yes, mostly. An irregularly irregular rhythm with no organized atrial activity (i.e. no P waves or flutter waves), with a wide and consistent QRS morphology must be a-fib with some form of aberrant conduction (e.g. bundle branch block, WPW). If the QRS duration was consistently wide, but the QRS morphology was changing from one beat to the next, it would suggest polymorphic ventricular tachycardia (of which torsades is the most well known subtype).
A regular, wide complex tachycardia may not necessarily be VT. There is a significant amount of literature trying to figure out rules that allow one to differentiate VT from a supraventricular tachycardia with aberrancy, but in most clinical situations it's best to work on the assumption it is VT until you know definitively that it's something else.
@@StrongMed Thank you very much. Again, i really apreciate your videos.
Omg the intro music. RIP headphone users
Apixiban is for the heart or blood thinner.