Tuesday, August 20, 2019
Scandinavian Clinical practice guidelines for therapeutic hypothermia and post-resuscitation care after cardiac arrest
A little bit of an older article on TTM, but nevertheless a nice overview
The Art of Medicine
My prior TED Talk Blog entry reminded me of a patient I saw in my clinic, many years ago as a Cardiologist when I was still practicing in a Multi-Specialty Group as well as another "beautiful" TED Talk by Dr Abraham Verhgese ( I published on another Blog I ran during those years) .....
" I recently saw a young woman referred to me for shortness of breath. She had been seen by several physicians and had a recent ER visit for this problem. A week prior she reported some atypical chest pain and a CT scan of the chest was done. She was diagnosed with a "small pneumonia" and given antibiotics. She was told everything else was fine. Her shortness of breath failed to improve, however. She was then referred by her primary care physician to me, because surely there was something wrong with her heart.
As I walked into the exam room, I noticed she was very pale looking and very anxious appearing. As part of her history she told me that several years ago, she underwent gastric bypass surgery. I asked her if she had blood work done, because my immediate suspicion was that she was anemic. She told me she had it done as recently at the time of her ER visit . My nurse started looking for the labs accessing another database ( even in the community I work, several "Electronic Medical Records" don't "talk" to each other) and not surprisingly, the young woman was profoundly anemic with a hemoglobin of 7.4 ( normal greater then 12), explaining her shortness of breath.
I don't know what's the saddest part of this story: the fact we don't "look" and "examine" our patients anymore, or being enamored by a CAT scan and completely forgetting to look at a basic blood count or being seen by several physicians, not one of them picking up on the fact that she is a set up for iron deficiency and other micro-nutritional abnormalities because of her gastric bypass surgery and then being referred to a Cardiologist. This is far from being an isolated case in our current outpatient model of HealthCare. The irony of course is that seeing 30-40 patient a day in clinic is bound to increase the cost rather than curtail it and surely with poorer overall outcomes."
" I recently saw a young woman referred to me for shortness of breath. She had been seen by several physicians and had a recent ER visit for this problem. A week prior she reported some atypical chest pain and a CT scan of the chest was done. She was diagnosed with a "small pneumonia" and given antibiotics. She was told everything else was fine. Her shortness of breath failed to improve, however. She was then referred by her primary care physician to me, because surely there was something wrong with her heart.
As I walked into the exam room, I noticed she was very pale looking and very anxious appearing. As part of her history she told me that several years ago, she underwent gastric bypass surgery. I asked her if she had blood work done, because my immediate suspicion was that she was anemic. She told me she had it done as recently at the time of her ER visit . My nurse started looking for the labs accessing another database ( even in the community I work, several "Electronic Medical Records" don't "talk" to each other) and not surprisingly, the young woman was profoundly anemic with a hemoglobin of 7.4 ( normal greater then 12), explaining her shortness of breath.
I don't know what's the saddest part of this story: the fact we don't "look" and "examine" our patients anymore, or being enamored by a CAT scan and completely forgetting to look at a basic blood count or being seen by several physicians, not one of them picking up on the fact that she is a set up for iron deficiency and other micro-nutritional abnormalities because of her gastric bypass surgery and then being referred to a Cardiologist. This is far from being an isolated case in our current outpatient model of HealthCare. The irony of course is that seeing 30-40 patient a day in clinic is bound to increase the cost rather than curtail it and surely with poorer overall outcomes."
Sunday, August 18, 2019
Tuesday, August 13, 2019
Smartphone electrocardiograms reveal painful left bundle branch block syndrome and illustrate associated electrophysiological phenomena
EP Europace Painfull LBBB syndrome
A 69-year-old lady presented with exertional chest discomfort. A 12-lead ECG indicated anteroseptal T wave inversion (TWI) (Panel A, left), suspicious for Wellens’ syndrome. However, cardiac catheterization (Panel A, right) and echocardiography were normal. Her symptoms persisted and she purchased a smartphone electrocardiogram (EGM) device (AliveCor KardiaMobile™, USA). Recordings revealed that her pain coincided with the sudden onset and resolution of left bundle branch block (LBBB) (Panel B, top EGM). ‘Painful LBBB Syndrome’ is an increasingly recognized entity and is easily missed following a reassuring ischaemic evaluation. These single lead recordings also illustrate associated electrophysiological phenomena. The LBBB is rate related (Panel B, top EGM), suggesting a phase 3 block. Resolution occurs at a lower rate than onset, due to ‘linking phenomenon’ whereby concealed retrograde invasion of the bundle occurs from the contralateral side. Premature ventricular contractions allowed time for the LBBB to recover (Panel B, middle), consistent with aforementioned explanations for ‘functional’ block. The TWI was also demonstrated on the KardiaMobile™ by recording an anterior precordial lead (Panel B, bottom). Known as ‘cardiac memory’, TWI transiently occurs after a period of abnormal ventricular activation.
In summary, smartphone-based EGM’s continue to improve our diagnostic capability and can illustrate complex electrophysiological phenomena
Painful left bundle branch block syndrome: Clinical and electrocardiographic features and further directions for evaluation and treatment- Heart Rhythm Society
Monday, August 12, 2019
Narrow QRS tachycardia ("SVT") in the ICU
Supraventricular tachycardias should be described as long RP or short RP tachycardia.
SVT is a general term and has no reference to the underlying pathophysiology or mechanism causing narrow QRS tachycardia. Short RP tachycardias, are most commonly seen in clinical practice, long RP tachycardias to a lesser extent (the latter more frequently in the ICU setting)
.
One should always look at the initiation of the tachycardia, i.e. is there warm up or ramp-up phase. How does the tachycardia terminate: is there a P before conversion to sinus tachycardia after administration of adenosine, or does the tachycardia terminate without a P-wave? What is the axis of the P-wave during narrow QRS tachycardia, i.e. is axis inferior or superior?
Adenosine should always be administered both as a diagnostic and possible therapeutic agent in the setting of sudden onset hemodynamically stable narrow QRS tachycardia ( and regular monomorphic VT- see below) . Adenosine terminates close to 100% of short RP ( narrow QRS) tachycardias (slow-fast AVNRT as most common rhythm).
Long RP (narrowQRS) tachycardia's are seen less common but deserve some further attention (higher incidence in the ICU setting) :
1. Fast-slow AV nodal reentry tachycardia
2. AV reentry tachycardia with retrograde conduction over accessory pathway
3. Ectopic atrial tachycardia/focal atrial tachycardia
4. Sinus tachycardia
Adenosine will terminate AV nodal reentry tachycardia, but very uncommonly there is an adenosine sensitive accessory pathway. It will not terminate sinus tachycardia but can cause slowing of the rate.
However, some ectopic atrial tachycardias can be terminated by adenosine.(60-80%)
Of note, adenosine can also be administered for hemodynamically stable regular monomorphic wide complex QRS tachycardia, as it will break AV reentry tachycardia with antegrade conduction over accessory pathway as well as some forms of ventricular tachycardia
The new ACLS guidelines now has adenosine given up to 2 times instead of 3 times. The first dose of adenosine should be 6 mg administered rapidly over 1-3 seconds followed by a 20 cc normal saline bolus ( use 3 -way stopcock). If the patient's rhythm does not convert within 1 to 2 minutes, a second 12 mg dose may be given similar fashion.
A lower initial dose of 3 mg should be used in patients taking dipyridamole or carbamazepine as these 2 medications potentiate the effect of adenosine.
Also, prolonged asystole has been seen with the use of normal doses of adenosine in heart transplant patients and central line use. Therefore, the lower, 3 mg dose should be considered for patient's with a central venous line or history of heart transplant
Sometimes termination is followed by an immediate return of the tachycardia, even in AVNRT. In these patients, intravenous verapamil 5-10 mg slow push can be used. Diltiazem, 20 mg IV as a loading dose followed by 10 mg/min continuous infusion, can be used but is less effective than verapamil. Intravenous beta blockers i.e. metoprolol, esmolol, can be used as an alternative to verapamil or diltiazem in patients who do not not convert with or are intolerant to adenosine.
This case report in the New England Journal of Medicine is an interesting presentation of focal atrial tachycardia secondary to hyperthyroidism ( Graves' disease).
It also highlights that performing contrast studies will cause temporary suppression of thyroid production due to administration of a high iodine load and " masque" hyperthyroidism for certain period of time.
SVT is a general term and has no reference to the underlying pathophysiology or mechanism causing narrow QRS tachycardia. Short RP tachycardias, are most commonly seen in clinical practice, long RP tachycardias to a lesser extent (the latter more frequently in the ICU setting)
.
One should always look at the initiation of the tachycardia, i.e. is there warm up or ramp-up phase. How does the tachycardia terminate: is there a P before conversion to sinus tachycardia after administration of adenosine, or does the tachycardia terminate without a P-wave? What is the axis of the P-wave during narrow QRS tachycardia, i.e. is axis inferior or superior?
Adenosine should always be administered both as a diagnostic and possible therapeutic agent in the setting of sudden onset hemodynamically stable narrow QRS tachycardia ( and regular monomorphic VT- see below) . Adenosine terminates close to 100% of short RP ( narrow QRS) tachycardias (slow-fast AVNRT as most common rhythm).
Long RP (narrowQRS) tachycardia's are seen less common but deserve some further attention (higher incidence in the ICU setting) :
1. Fast-slow AV nodal reentry tachycardia
2. AV reentry tachycardia with retrograde conduction over accessory pathway
3. Ectopic atrial tachycardia/focal atrial tachycardia
4. Sinus tachycardia
Adenosine will terminate AV nodal reentry tachycardia, but very uncommonly there is an adenosine sensitive accessory pathway. It will not terminate sinus tachycardia but can cause slowing of the rate.
However, some ectopic atrial tachycardias can be terminated by adenosine.(60-80%)
Of note, adenosine can also be administered for hemodynamically stable regular monomorphic wide complex QRS tachycardia, as it will break AV reentry tachycardia with antegrade conduction over accessory pathway as well as some forms of ventricular tachycardia
The new ACLS guidelines now has adenosine given up to 2 times instead of 3 times. The first dose of adenosine should be 6 mg administered rapidly over 1-3 seconds followed by a 20 cc normal saline bolus ( use 3 -way stopcock). If the patient's rhythm does not convert within 1 to 2 minutes, a second 12 mg dose may be given similar fashion.
A lower initial dose of 3 mg should be used in patients taking dipyridamole or carbamazepine as these 2 medications potentiate the effect of adenosine.
Also, prolonged asystole has been seen with the use of normal doses of adenosine in heart transplant patients and central line use. Therefore, the lower, 3 mg dose should be considered for patient's with a central venous line or history of heart transplant
Sometimes termination is followed by an immediate return of the tachycardia, even in AVNRT. In these patients, intravenous verapamil 5-10 mg slow push can be used. Diltiazem, 20 mg IV as a loading dose followed by 10 mg/min continuous infusion, can be used but is less effective than verapamil. Intravenous beta blockers i.e. metoprolol, esmolol, can be used as an alternative to verapamil or diltiazem in patients who do not not convert with or are intolerant to adenosine.
This case report in the New England Journal of Medicine is an interesting presentation of focal atrial tachycardia secondary to hyperthyroidism ( Graves' disease).
It also highlights that performing contrast studies will cause temporary suppression of thyroid production due to administration of a high iodine load and " masque" hyperthyroidism for certain period of time.
Thursday, July 4, 2019
Cardiac Amyloidosis: Not a Rare Disease Anymore
- Transthyretin amyloid cardiomyopathy is a life-threatening, progressive disease that is often underdiagnosed and misdiagnosed
- Certain clinical scenarios have been identified that now warrants screening for transthyretin amyloid cardiomyopathy
- Once transthyretin cardiomyopathy suspected definitive diagnosis can usually be achieved noninvasively
- Accurate, early diagnosis of transthyretin cardiomyopathy ischemic to enabling appropriate patient care
screening for transthyretinamyloid cardiomyopathy in everyday practice, published in JACC HF failure, July 2019
Journal of the American College of cardiology state-of-the-art review:
transthyretin amyloid cardiomyopathy
The following Webinar from the European Society of Cardiology ( ESC) which gives a good overview about the diagnosis and treatment various forms of cardiac amyloidosis, presenting several case reports
Tuesday, July 2, 2019
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