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.
I wonder this question is being asked over many generations in medical schools , yet to be answered clearly. The traditional explanation given is ” mitral valve is kept open wide till onset of systole and it closes with a bang due to a long excursion it has to make ” This concept is no longer tenable and acceptable ( For the simple reason if the valve is wide open . . . hemodynamically significant mitral stenosis cease to exist !)
There are two major factors that determine the loudness of S1 in mitral stenosis
Hemodynamic
Valve structure and morphology
Mitral valve closes whenever the ventricular pressure curve crosses above the LA mean pressure . This is the pressure crossover point (LV/LA) .
In normal persons it happens very early after the onset of ventricular contraction .(ie the LV pressure has to raise only to about 8-12mmhg . At this point the LV pressure curve has certain force of contraction (Dp/Dt) .Since in mitral stenosis the mean pressure is raised well above normal (Often 20-30mmhg) the LV pressure cross over point is slightly delayed and more importantly occur at a higher slope of LV pressure curve . Even this slight delay adds a punch in the ventricular contractility .The impact of LV contractility on mitral valve closure especially the AML is forceful .
(Imagine the force of impact of a stone hitting you from a distance of 1 meter from above , is different from a stone hitting you from 10 meter above as it gains the momentum )
The second phenomenon is probably more important as it involves acoustics the final step in the genesis of loud S1 .
The mitral valve need to be not only pliable but also the conduction properties should be intact.
Acoustic principles state that even a speck of calcium in the AML can dampen the sound that is generated by leaflet motion.
(Try touching a speaker cone while it is playing .The sound immediately drops and dampens.)
Similarly for S1 to be loud the valve should pliable without any significant calcification or extreme rigidity or subvalvular fusion .)
It is important to realize the PML contributes less to the intensity of S1 . Hence even if some calcium present in PML it won’t affect the intensity of S1
Other important factors that affect the intensity of S1 include
LV function ( Onset of LV dysfunction elevates LVEDP reduces the net gradient across mitral valve )
Presence of mitral regurgitation .
Aortic valve disease (Especially AR )
Heart rate
Rarely associated Tricuspid stenosis make T 1 component of S 1 louder
Final message
The loud S 1 is due to both physiological and anatomical factors of mitral valve .The condition of valve may be more important for the simple reason , whatever be the hemodynamic predispoistion for loud S1 , the prevailing valve morphology has a potential to nullify it !
A 55 year old man came with a BP of 1o0/70 with vague symptoms of back pain to our ER.
Troponin T was positive
Can we thrombolyse ?
There is a minimal ST elevation in inferior leads but not amounting to the required criteria 1 mm
Technically No , Academically yes , scientifically No , logically yes
*I wont thromolyse but i will take him to cath lab maybe the modern answer
What we did ?
We did neither !
Just observed in CCU with heparin infusion , Aspirin and clopidogrel .
Note: The ECG becomes almost normal .The initial suggestion of inferior MI is stands questionable
Serial ECGs were taken .
And now . . . after 24 hours a new complete heart block appear with classical evolved pattern of inferior MI.The most interesting feature is patient has been comfortable all along even as his posterior aspect of heart is experiencing terrible electrical earth quakes.
Is troponin Guided thrombolyis an accepted concept ?
Yes , only in few situations like , posterior MI , LBBB , pacemaker rhythm, re infarction .(Note , true posterior MI do not elevate the ST segment but depress it ) .
One may be surprised why we shouldn’t lyse a patient whenever troponin is elevated in acute coronary syndrome (After all it denotes myocardial necrosis and infarct !) The point here is , troponin can raise in all forms of MI (NSTEMI, even in some cases of chronic stable angina ) Read in this link Why thrombolysis is contrindicated in UA/NSTEMI
The benefits of thrombolysis is not proven in small and micro infarcts. ECG ST eelvation remain the sole criteria for thromolysis for STEMI because of high degree of correlation with total coronary occlusion .
In this era of rapid interventions the treatment concepts has blurred as we tend to do PCI and stenting most cases of ACS including UA/Unstable angina
OK , what happened to this patient ?
Temporary pacer was kept stand by with a sheath and catheter in situ.
Next day morning AV block disappeared .Patient was comfortable .
To our surprise , in the same evening his ECG showed a complete heart block with AV dissociation . Still the heart rate was good . The demand temporary pacemaker didn’t take over .
On the third day , every conduction disturbance disappeared and patient was sent to the wards. He is being discharged in a stable condition with std drugs .there was a minimal wall motion defect in infero-posterior segments with an ejection fraction of 50 % . He is scheduled for coronary angiogram 2 weeks later.
What is the pathology ?
Pathologicallyit could be a small focal area of Infarct incidenataly invloving the AV node .(This is alss refered to as vital area Infarct” )It is hard to differentiate whether AV block is due to revrible ischemia or necrosis , simple tissue edema , high vagal tone . or combination of above .If the block recovers it can be concluded necrosis is not the dominant theme.
Final message
STEMI presenting primarily as heart block is less common . When such a presentation occurs extra caution is required.
Many of these patients may not show a classical ST elevation and hence do not permit us to thrombolyse as per criteria.
It is the individual physician’s discretion to do so ( or not to do ! ) . No body is going to fault. After all 5 % of thrombolyis world over is for benign early repolarisation syndromes.
The above description is an example of complicated inferior MI . . . still managed effectively by conventional methods.
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 .
Echo helps us to confirm the valvular, myocardial or congenital heart diseases in the evaluation of PAH. Apart from these etiological diagnosis of PAH predominantly lies in a systematic medical work up .(Read Dana Point classification )
2-D features
RA RV dilates
RVH*may occur (Dilation is more common )
IVS assumes a D shape ( RV pressure is close to or even > than LV pressure )
Tricuspid annulus dilates
* For some reason RVH does not occur commonly in pulmonary hypertension , while LV hypertrophies promptly in systemic hypertension .
Doppler
Tricuspid valve begins to leak and RV ejects with giant “cv” waves into RA/JVP
Other Echo findings
MPA may dilate
Pulmonary regurgitation
At what pressure RV begins to dilate in PAH ?
It is not known .It is highly variable . But most will dilate their RV at a systolic pressure > 50mmg.
It is also possible the onset of TR and the magnitude of TR has a major say in the timing of RV enlargement .
We know RV is more sensitive to volume overload than pressure overload .
Paradoxically , it is often observed acute elevation in RV pressure dilate the RV faster than chronic ones.
Right atrium and right ventricle are significantly
The tricuspid annulus is dilated .Note the severe TR with twin jet morphology.
Estimating Pulmonary artery pressure
PA systolic pressure : TR jet + 10 mmhg
PA diastolic pressure : PR end diastolic jet + 10
PA mean pressure : Peak PR gradient
Other complex methods to arrive ar PAP in the absence of TR or PR
The Dabestani -Mahan ‘s equation* – The mean PA pressure = 90 – (0.62 X acceleration time).
It is popular for calculating PAP by measuring pulmonary artery Doppler acceleration time .
Many believe it is neither sensitive nor practical in real clinical setting.
*Even though Dabestani is the first author of this paper Mahan got the full credits for the simple reason his name is easily remembered !
Note the peak TR jet is around 50mmhg and predicted RVSP would be 60mmhg.One would have expected still higher RV pressure but since the RV is dysfunctional the true PAP may be underestimated.
The classical D shaped IVS during systole . D shape indicates RV pressure during systole is almost equal or even higher than LV. ( Please recall D shape occurs in Volume overload also but the timing is in diastole !)
Pulmonary valve M-Mode
According to Wyeman the following M mode signs are useful in diagnosing PAH.
Presence or absence and the amplitude of the “a” wave
magnitude of the e-f slope
presence of mid-systolic closure or notching
fluttering of the posterior pulmonic leaflet
Currently , one may consider M-Mode echo to be an obsolete , but still the foundations help us understand the hemo-dynamics.
The most important principle in the motion of pulmonary valve , is the relationship between pulmonary “a” wave and right atrial “a” wave
Normally atrial contraction produce an inward movement* on the closing pulmonary leaflet . This happens because the MPA end diastolic pressure is usually lower than right atrial a wave .In severe PAH the elevated pulmonary diastolic pressure does not allow the atrial contraction to intend the pulmonary leaflet in pre-systolic atrial contraction .Hence pulmonary valve a wave in m -mode is diminished or even absent .
In PAH even premature closure of pulmonary valve may occur resulting in mid systolic notch .This is referred to as flying “W” -Mid systolic notch. (See below)
* The motion we see in short axis M-Mode is that of left pulmonary cusp that moves posteriorly.
Absence of a dip is a hemo-dyanmicaly important sign pf PAH but with one important caveat .This absence of a dip is valid only until RV failure occur.In th presence of elevated RVEDP a begin to appear again
RR interval in Atrial fibrillation is irregular because . . .
The Atria fires irregularly
AV node conducts irregularly
Atria confuses the AV node with its random firing and varying penetration *
The ventricle just reflects irregular response of atria .
The answer is all of the above. Response 3 explains best.
*Please note , the AV nodal property is predominantly responsible for the irregular RR interval in AF . Atria confuses the AV node with its random firing .The varying penetration into different depths of AV nodal structure and the resultant concealed conduction make the the AV nodal refractory period into continuous oscillation .This random delays in AV node is reflected in RR interval as irregularity )
The response we get in ventricles in AF can be summed up as “A filtered atrial rhythm”
Paradoxically, amidst the chaos in atria the rate is fairly constant within the atria (Fibrillatory wave firing at up-to 600/mt ) Of course , the FF interval in the atria will also be varying . At a rate of 450-600 this is difficult to quantitate especially in fine AF.
When does RR interval becomes regular in AF ?
When the patient develops complete heart block.
Digoxin toxicity
Associated Sinus node dysfunction
For advanced readers in EP : A mystery explanation for irregular rhythm in AF in the offing ?
AV node is a physiological and electrical sink .
When atria fires at 600/mt it absorbs about 60-70 % of the atrial response .Whether it releases the original impulse or initiate a new rhythm in the junction is not clear.
There is some evidence to suggest the rhythm that control the ventricle in AF may not be filtered original rhythm from the atria .Instead it could be a fast junctional escape rhythm (Is that a junctional fibrillation ?)
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Dr.S.Venkatesan MD 