Magnesiumis a powerful anti-arrhythmic drug . It has a well established role in controlling VT when administered Intravenously especially in polymorphic VT .
Mechanism of action
It acts at the cell membrane.
It has a unique action of blocking calcium channels that reduces the number of oscillations of both early and late after potentials
Irregular wide qrs tachycardiais a fairly common clinical entity in any cardiac emergency room. The moment you ask about such tachycardia , 9/10 fellows will come out with a prompt answer ” AF with WPW syndrome” even before you complete the question ! It is not that common as we perceive .The problem is with our traditional teaching methods and the attraction of human brains to rare and exotic disorders.
traditionally SVT with aberrancy is diagnosed mainly in the setting of regular tachycardia .
We often forget “AF with aberrancy” is equally common , and it presents with a irregular wide qrs tachycardia .
I wonder whether this phenomenon can be termed as orthodromic aberrancy .This can directly compete in the differential diagnosis of antidromic AF with WPW !
It should also be mentioned antidromic AF can run into very high rates as accessory pathways do not check the incoming signals while orthodromic aberrancy the ventricular rates can not exceed 220 or so at least theoretically . (This simple clue can clinch the issue in favor of WPW )
There is no proper published data available for the true incidence of AF with orthodromic aberrancy in general population
In fact , there are many electrical environments for AF to become a wide qrs AF
1. AF with Antidromic conduction through accessory WPW pathway.
2. AF with Orthodromic aberrancy ( Non WPW – Similar to any SVT with aberrancy )
3. AF with pre existing LBBB
4. AF with Amiodarone effect. (Especially with DCM and cumulative load of Amiodarone )
5. AF with electrolytic / especially excess intra-cellualr potassium
6. Finally , even Atrial based pacing (DDD) can cause wide qrs irregular tachycardia when mode switching fails .Here the ventricles may track the atrial irregularity and respond with a wide qrs bizarre tachycardia .
Final message
There are many causes for wide qrs tachycardias in Atrial fibrillation . WPW with anti-dromic conduction is just one of them .We need to approach the issue with an open mind .Please be reminded , once contemplated WPW syndrome can be a powerful thought blocker !
Note : *We are not including polymorphic ventricular tachycardia here .It is an important subset of wide qrs irregular tachycardia.
** VT can co-exist with AF .This is not surprising as many of the diffuse cardiomyopathies involve both atria and ventricle with extensive scarring and fibrosis a perfect trigger for both atrial and ventricular arrhythmias .
Interventions in Eisenmenger syndrome or severe PAH in left to right shunt continues to be a major diagnostic issue.The challenge lies not only in assessing whether the progression of PAH can be prevented by blocking the left to right shunt , but also to assess it’s impact on survival.
The factors involved are
Pulmonary artery pressures
Pulmonary blood flow
Pulmonary vascular resistance
RV function
Co-morbid /general condition of the patient
While cardiologists worry more about LV , surgeons have different issue . In left to right shunts with PAH RV function bothers them more , as the high pulmonary artery pressure may never allow the surgeons to come off the pump , once the decompression provided by ASD/ VSD is removed
How relevant is Ohm’s Law in complex shunt with leaky valves and bidirectional shunting ?
The fundamental hemodynamic equation is derived from Ohm’s law .How relevant is Ohm’s law in Eisenmenger is not clear. For decades we have been using complicated calculations with many presumed and assumed parameters. The calculation of effective pulmonary blood flow in bidirectional shunt may be most complex equation in clinical cardiology. One can only imagine how one error could amplifies the other.
The hemodynamic equivalent of Ohm’s law states
R = Pressure / Flow .The current thinking is If the PVR is between 6-8 it is operable .
Is it really that simple ?
We know pressures can be measured with a fair degree of accuracy . Flow and resistance are subjected to change in a moment to moment basis .They are determined by a gamut of neural and humoral factors.
Ironically , we are not yet clear , whether flow determines the pressure or pressure determine the flow .
The right heart blood flow can get complicated by not only bi-directional shunt but also by pulmonary and tricuspid regurgitation ,
There is a huge perception problem here . We are tuned to think , reversibilty of PAH is same as operability of shunt lesion . Definitively not ! This is the reason why there is a vast difference in ultimate outcome with little correlation with PVR !
In Eisenmenger physiology , critical decisions regarding surgery are made outside the cath lab
Good clinical acumen,
A meticulous echocardiography
Hard parameters like pulmonary artery diastolic pressure and pulse pressure
Above all a harmonious Cardiologist – Cardiac surgeon team is vital to plan this complex surgery
So, now it would seem cath studies are primarily done for academic pursuit , and it rarely helps in genuine decision-making process.
The following table synthesized in our hospital (Mainly with clinical data ) can be a useful tool.
Reference: Learnt in the bedside from poor children of India
We had a situation like this . A patient was in class 3 or 4 and calculated PVR was less than 6 Wood units what will you do ?
Never give importance to numbers . These patients will 99% of times won’t survive a shunt closure surgery.
Future development
With the availability of modern drugs like Nitric oxide, prostocyclins, Sildenafil analogues medical management has a potential to improve upon surgical results. Unfortunately large studies are not possible in these population . In the surgical front, fenestrated VSD closures peri-operative intensive nitric oxide show some promise.
Final message
I think we are about to say a final good-bye* to oxymetry ( or even cath study ) in the work up of PAH due to shunts.
*Still, pressures of right heart chambers and pulmonary artery is vital .Echo can not be expected to provide accurate measure of PA pressure .(Even though there some echo studies available to calculate qp/qs and PVR non invasive)
Sons are too glad to inherit wealth from their father . But destiny maintains a fine balance . It makes sure they do inherit adverse biological events as well .
A 68 year old man who had a TIA and was completely evaluated . Except for a mild elevation of systolic bl0od pressure and dyslipidemia (Hgh TGL) other parameters were normal. Carotid vertebral Doppler study were normal even though the Intimal-medial thickness was borderline. His CRP was normal . His neurologists warned him about possibility of recurrent TIA or cardiac events and prescribed statins /Amlodipine .
Even as every one was worried about their father his eldest son aged 44 developed a full fledged stroke just a month later !
What is the inference and final message ?
The vascular risk is a continuum .The risk is transmitted vertically to the family members. After all , the father and son share at least 30 % of vascular endothelium by means of structural and genetic blue print.
“Father’s Aorta could continue as son’s carotid artery ! (What a crazy statement ! )
So , whenever you have an elderly man with a vascular event , screen entire family and preferably start vascular prophylaxis. The problem with vascular inheritance is , the children may be conferred more or less risk . The exact quantum can not be predicted.
Final message
Beware , children can inherit diseases form their parents even before the parent manifest the full expression of the index disease.It was an example of instantaneous inheritance here .
The irony is complete as the father develops warning shots (TIA) and the son suffers permanent damage (Stroke )
We can’t expect genes to behave in rational way . More importantly genes do get modified with environment in a significant fashion. What is preventing two biological system created by same genes one goes for full-blown vascular event other escapes with a minor event . One simple explanation is , while vascular aging is physiological , the younger vascular system faces much more stress and strain due to altered living conditions.
Jugular vein is a natural non invasive right heart catheter inserted permanently in the right atrium . It faithfully reflects the right heart hemo-dynamics during every heart beat.
The information you gather is dependent upon the time you spend and mind you you apply on this biological catheter.Wenke back did so nicely he was able to identify progressive a and c interval and a drop of c wave before even the ECG machine was invented.
Acute rheumatic fever classically involves large joints of lower or upper limbs referred to as fleeting migratory polyarthritis .But this pattern is not exclusive. In fact acute rheumatic fever commonly present with atypical features .The incidence can be up to 25 % in various series .The most surprising thing is , it can involve spinal as well as hip joints . Mono arthritis is also possible.
The only contention is , atypical features are frequently labelled by some as post streptococal reactive arthritis instead of rheumatic fever .
It is pure semantics at play . Whether you agree with the terminology or not , never hesitate to diagnose rheumatic fever when the joint involvement is atypical . If you ignore this you are bound to be guilty for damaging few hearts later.
What are the unusual joint involvement in acute rheumatic fever ?
Small joints of the feet
Small joints of the hands
Cervical spine
Wrist
Elbow
Shoulder
Hip
Thoracic spine
Calcaneus
Lumbar spine
The involvement of above joint can be up to 25%
Here is an excellent paper from Brazil about the huge variation in the pattern of joint involvement in acute rheumatic fever.
How can it correct the rhythm alone ? If the rhythm is corrected , rate will automatically be controlled, unless Amiodarone converts AF into Sinus tachycardia which is very unlikely !
Of course Amidarone is not a magic drug .The success rate of Amiodarone restoring sinus rhythm is far . . . far less . . . than our expectations ! . It fails to convert to sinus rhythm in a significant chunk *. Interestingly , it may still control the ventricular response by its beta blocking action .
*Our estimate is , the failure rate Amiodarone is between 30-40% or even higher , as bulk of AF we witness is due to Rheumatic heart disease.
Which is the best drug for “ventricular rate control”in atrial fibrillation ?
Digoxin alone
Diltiazem alone
Atenolol alone
Digoxin +Atenolol
Digoxin + Diltiazem
The answer is 4.
This is based on a study done by Bramh N Singh and his team from California published in 1999 . (http://content.onlinejacc.org/cgi/reprint/33/2/304.pdf )It was a wonderful study involving just 12 patients , still good enough to prove a point . It was a sequential cross over study a rare theme in medical trials ! where same patients act as control .Hence bias and host variations are nil. Few excerpts from the study .
It is very clear, for optimal rate control we need a combination regimen , Digoxin must be one of them .Atenolol combined well with Digoxin , even as though Diltiazem resulted in maximum dip in nocturnal heart rate.
Digoxin + Atenolol is clear winner in rate control during exertion as well ! Note Digoxin has absoutely no control over the heart rate at times of exercise !
Few thoughts about this study
This study has clearly documented superiority of combined drug regimen for rate control in AF .
Still it leaves a lingering question ! Why verapamil was not used as an agent in this study ?
If only , verapamil was used (As we do in our hospital ) Digoxin -Atenolol combination would have faced a really tough competiton.
Another curiosity is , what would have been the power of a unique combination of Atenolol and Diltiazem in controlling ventricular rate in AF ?
Any way , it was a wonderful cross over study . Such studies are a rare breed, always welcome in this world of funny pharma trials wherein a new drug is compared with a dud drug called placebo !
Now . . . Try this one
Amiodarone
Corrects rhythm
Controls ventricular rate
Does both ?
How can it correct the rhythm alone ? If rhythm is corrected , rate will automatically be controlled unless Amiodarone converts AF into Sinus tachyardia !
Of course Amidarone fais to convert to sinus rhthm in many , still it may control the rate by its beta blocking action.
Ventricular tachycardia is a major cardiac electrical disorder. Even though it connotes a deadly meaning the prognosis and outcome vastly vary.It can be a benign arrhythmia in structurally normal heart that present as occasional fasicular VT or Exercise induced RVOT , to dangerous ischemic polymorphic VT which rapidly degenerate to VF and SCD if not reverted . It is ironical we are trained to put all VTs in a single basket and propagate fear psychosis among physicians and patients .
Management of VT has certain broad principles.
Identify the cause
Whether specific structural heart diseases present or not
Identify the mechanism if possible
Rule out transient metabolic cause as a trigger
Therapeutic targets
Stabilising the cell of origin
Passifying the scars
Interrupting bundle branches in BBR mediated tachycardia
Ischemia related Focus – Re-perfusion
Reversing LV dysfunction
Management
General
Correct Cell hypoxia /Acidois
Pharmacological ( Class 1A/1B /1C , class 3 and Beta blockers , Magnesium )
Role of beta blockers for VT management is largely under recognised.It has an important role to play in both acute and chronic VTs)
Electrical (DC shock ,Ablation and ICD)
DC shock is treatment of choice all emergency VTs
Ablation aims at preventing episodes of VT .Ablation needs EP study and expertise of an electro physiologist.
ICDs revert it only after the VT emanates from the focus . ICD can be implanted without knowing the focus .May not require a EP consult.
Surgical
CABG + Surgical scar excision , Aneurysectomy might help in certain refractory VT.
ASD device closure is rapidly gaining popularity . Amplatzer device occluder has become a de-facto standard. Contraindications are declining . More and more young cardiologists want to indulge in this play . Fortunately cost of device is acts as a major deterrent .
The pre procedural evaluation seems to be many fold important than the procedure itself.
* You ask any cardiac surgeon , How variable the shape and size of ASD can be ? To complicate the issue the LA side may show an entirely different shape and diameter compared to RA aspect. The orifice by itself may travel obliquely.
Currently the thickness of IAS* is not taken into account in device selection . It may be unwise to do so , because the thickness of the rim and its interaction with device determines which direction the device will drag (Homing in ) in the long run .
The potential dead space between the device and the septum can be a late focus for thrombosis. CVAs have been reported following ASD device closure.
Classification with reference to size
ASDs can be small (3 to <6 mm), medium (6 to <12 mm), or large (>12 mm),
What is the shape of Ostium secundum ASD ?
Round (perfect round very rare)
Oval
Irregularity oval
Irregularly round
Combinations
How is the orifice orientation with reference to plane of IAS ?
Horizontal
Oblique
Combination of the two
Which is the best method to measure the ASD size ?
Trans-thoracic Echo
2DTrans-Esophageal Echo
Balloon estimated ASD size in fluoroscopy
Real Time 3D TEE
Intra-cardiac Echocardiogram
Currently there is some degree of confusion about utility value of balloon sizing . Opinion differs. A meticulously done TEE may be the winner
How do you tackle an elongated and Oval ASD ?
A large ASD with an adjacent daughter ASD . It is very difficult identify this daughter defect by conventional imaging . Intra cardiac Echo may help . Failure to recognize fenestrated defects especially in the edge can lead to poor device approximation
Con-founders in ASD size measurement.
Stretched ASD diameter. (How much stretch ? )
Systolic vs diastolic ASD size
Practical tips for ASD sizing
Add 2mm to balloon/TEE estimated waist.
TEE may be more accurate than the balloon .
Balloon has a inherent issue of over stretching the ASD and false high diameter.
Waists are often circular in the device We do not have oval Amplatzer device.
Accurate sizing is very difficult to achieve , so which side is better to err ? lesser or over size ?
Dangers of under-sizing
Mushrooming of the device
Dislodgment & Embolisation
Residual shunts
Thrombosis over metal gutter created by intending device
Dangers of over sizing
Aortic erosion
AV blocks
Newer modalities for ASD imaging
Intra cardiac echo and real time 3D TEE will facilitate the ASD device procedures Image source : Heart 2010;96:1409e1417
Final message
ASD device closure is rapidly gaining popularity . Contraindications are declining . More and more young cardiologists want to indulge in this play . Though more children are getting benefited in this non surgical modality , complications are also increasing .
Small centers should not be allowed to carry out these procedures. Fortunately cost of device acts as a major deterrent . A few centers (one or two per state ) is to be developed for high degree of expertise .
Without mastering the art of TEE never touch the ASD device .
The most critical step in ASD device closure lies before the procedure and . . . it is often outside the cath lab !
Always refer large defects and complex ASDs which are adjacent to Aorta and AV to a good surgeon .Get an operative photograph of the defect and re analyse whether device would have been possible in retrospect .
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Please Note
The author acknowledges all the queries posted by the readers and wishes to answer them .Due to logistic reasons only few could be responded. Inconvenience caused is regretted.
Dr.S.Venkatesan MD 