• In ventricular tachycardia, HV interval is always negative? No, it may be short positive, if the focus is near the His bundle.
• During a wide complex tachycardia, His potentials dissociated from ventricular potentials indicate that it is ventricular tachycardia.
• For inducing ventricular tachycardia during electrophysiological stimuli, the premature stimulus used is early, not late.
• In coronary artery disease patients, ventricular tachycardia is more in the morning.
• Commonest cause of ventricular tachycardia is coronary artery disease. Next commonest is cardiomyopathy, hypertrophic or dilated.
• Patients with ventricular tachycardia are more likely than patients with ventricular fibrillation to have previous myocardial infarction and low ejection fraction.
• The best non-invasive marker of prognosis in ventricular tachycardia is low ejection fraction.
• The best electrophysiological marker of prognosis in ventricular tachycardia is inducibility.
• The best upcoming ECG indicator of prognosis in ventricular tachycardia is T wave alternans.

• Primary prevention ICD trials- spot the trials with the following findings-
  • After CABG, ICD did not reduce mortality in patients with abnormal signal averaged ECG.
  • After MI,
    • ICD reduced mortality in patients with low ejection fraction, NSVT and inducible VT,
    • ICD reduced mortality in patients with low ejection fraction and NSVT,
    • ICD reduced mortality in patients with low ejection fraction and frequent VPCs but
    • ICD did not reduce mortality in low ejection fraction alone when implanted immediate post MI.
  • In heart failure,
    • ICD reduced mortality in wide QRS and NYHA 3 to 4,
    • ICD reduced mortality in low ejection fraction with VPCs or NSVT and
    • ICD reduced mortality in low ejection fraction with NYHA 2 to 3.
• Primary prevention ICD trials- answers-
  • After CABG, ICD did not reduce mortality in patients with abnormal signal averaged ECG (CABG-PATCH)
  • After MI,
    • ICD reduced mortality in patients with low ejection fraction, NSVT and inducible VT (MADIT)
    • ICD reduced mortality in patients with low ejection fraction and NSVT (MUSTT)
    • ICD reduced mortality in patients with low ejection fraction and frequent VPCs (MADIT II)
    • ICD did not reduce mortality in low ejection fraction alone when implanted immediate post MI (DINAMIT)
  • In heart failure,
    • ICD reduced mortality in wide QRS and NYHA 3 to 4 (COMPANION)
    • ICD reduced mortality in low ejection fraction with VPCs or NSVT (DEFINITE)
    • ICD reduced mortality in low ejection fraction with NYHA 2 to 3 (SCD-HeFT).

• The trials which showed that ICD is better than drugs for secondary prevention of cardiac arrest are CASH, AVID and CIDS.
• Propranolol was found to reduce total and sudden deaths post MI in the BHAT trial.
• Amiodarone was found to reduce mortality in low ejection fraction patients in the GESICA trial.

1. Compensatory- usual.
2. Non-compensatory- if retrograde conduction.
3. No pause- interpolated.
4. Postponed compensatory- first degree block in next beat causes complete heart block in the next.

• Ventricular premature complexes may be narrow if-

1. Arising high in the IVS
2. Fusion of two ventricular premature complexes or one ventricular premature complex and a supraventricular aberrant beat.

• Frequent ventricular premature complexes can cause heart failure!
• Tea, coffee or alcohol may be the cause of ventricular premature complexes.
• The ventricular premature complex may have a first heart sound, without a second heart sound.
• The electrolyte imbalance which causes ventricular premature complexes is hypokalemia.
• The drug of choice to acutely suppress ventricular premature complexes is lignocaine. If it does not work, try procainamide and then propranolol or magnesium
• Ventricular premature complexes are more in males.

while on amiodarone

8 months after stopping amiodarone

This can occur in 5% of patients who receive amiodarone. It is fatal in 5% of cases.

There are two types- insidious onset and sudden onset. Insidious onset is also called interstitial pneumonitis and sudden onset is also called ARDS. In insidious onset variety, chest X-ray shows mainly interstitial shadows while in the sudden onset variety, alveolar shadows predominate.

The main symptoms are dyspnoea, non-productive cough, pleuritic chest pain and weight loss. Fever is more likely to occur in the sudden onset group. The main sign is crepitations. Sometimes, pleural rub is also heard.

Total WBC count may be elevated. ESR is usually elevated, absence of which questions the diagnosis.

Chest X-ray shows bilateral diffuse changes- usually a combination of infiltrative and alveolar shadows, though either of these may predominate. Pleural effusion and hilar adenopathy are conspicuous by their absence.

Pulmonary function tests show restrictive lung disease with reduction in total lung capacity and in diffusion capacity of carbon monoxide.

CT chest is sensitive to diagnose lung disease. It can also quantify the amount of iodine in the lungs, although this does not imply causation.

Gallium scan shows inflammatory activity in the lungs.

CT chest and gallium scan are not specific enough for diagnosing amiodarone lung disease.

Bronchoalveolar lavage shows two important findings- foam cells and CD8+ cells. Foam cells are macrophages having lamellar phospholipid laden bodies in the cytoplasm. Absence of foam cells rules out amiodarone induced lung disease while presence does not diagnose it as it can occur in other diseases also. CD8+ lymphocyte predominance also is highly sensitive for the diagnosis.

Bronchoscopic biopsy shows fibrosis in interstitium and alveoli.

When the disease is diagnosed, amiodarone should be stopped unless there is a pressing indication in which case, it may be given at a lower dose. Steroids are useful, the usually given agent being prednisolone 40 to 60 mg/day tapered to stop over 2 to 6 months.

Prevention is by close monitoring for symptoms by careful history taking every 3 months. Before starting amiodarone, a baseline chest X-ray should be taken for future reference. The chance of developing amiodarone induced lung disease is increased 10 fold in those with baseline lung disease. So, in these patients, some other drug should be given, if possible. The chance of amiodarone induced lung disease is more if amiodarone is given in a dose of 400 mg/day or more. So, if possible a lower dose is to be given, even though it is now being appreciated that even with a dose of 200 mg/day amiodarone induced lung disease can occur, even though the chance is lesser than with a higher dose. Also, the chance of amiodarone induced lung disease is more if amiodarone is given for a long duration. So, we have to carefully monitor patients on long term amiodarone.

Pacemaker nomenclature

The code for pacemaker is called NASPE/BPEG code. These stand for North American Society of Pacing and Electrophysiology and British Pacing and Electrophysiology Group. The first code was in 1974. Present code was made in 2002. Positions are in the order- chamber paced, chamber sensed, response to sensing, rate modulation and multisite pacing. For 1,2 and 5, codes may be OAVD- none, atrial, ventricular and dual. For 3, code may be OTID- none, triggered, inhibited or dual. For 4, OR- none or rate modulation present.

Indications for permanent pacing (PP)

Commonest indication for PP is sinus node disease, second commonest being AV node disease.

For complete heart block, PP is always indicated. There is some confusion about congenital CHB, with some experts of the opinion that PP is indicated here only if there is (CBSEE)

• Congestive heart failure
• Bradycardia of less than 50 when awake
• Syncope or presyncope
• Ectopy from ventricles or
• Exercise intolerance.

If second degree heart block is symptomatic, PP is indicated. If asymptomatic, PP is indicated if

• Asystole > 3 sec when awake
• Rate < 40 when awake

And may be indicated if

• Due to neuromuscular disorder
• Intra or infra Hisian block (not for supra Hisian).

For bi or tri fascicular block, PP is indicated if there is transient CHB and PP may be indicated if symptomatic.

For sinus node dysfunction, PP is indicated if symptomatic and is not indicated if asymptomatic. For reversible causes like Lyme disease, PP is naturally not indicated.

For neurocardiogenic syncope (VVS & carotid sinus hypersensitivity), if the predominant cause is cardioinhibitory rather than vasodepressor (this can be made more clear by tilt table testing), PP is indicated if drugs such as beta blockers are ineffective. Dual chamber pacing was found to be useful in this setting in some studies (VPS-I and VASIS) but not in others (VPS-II).

Pacing for the prevention of tachyarrhythmias- PP is indicated in pause-dependent VT and PP may be indicated for congenital long QT syndrome.

Pacing to prevent atrial fibrillation (AF)- Atrial pacing has been studied for prevention of AF. The concept is that it decreases the refractoriness of dispersion in the atrium. Various techniques are used. Usual single site atrial pacing, strial septal pacing and Bachmann’s bundle pacing are single site pacing techniques. Dual site pacing is with one lead in usual RA position and other lead in the coronary sinus. Many pacing algorithms have been developed too. Prevention of AF by pacing was shown in ADOPT trial, but was not shown in the ASPECT trial.

Cardiac resynchronization therapy- CRT is a technique to reestablish synchronous contraction between LV free wall and IVS. Usually, biventricular pacing is needed, but LV pacing alone can achieve this in some persons. Trials have shown that this improves functional status, but not longevity. The indication for CRT is if all of the following are met-

• NYHA III or IV
• Optimized medical therapy
• LVEF 0.35
• NSR
• QRS more than 120 msec

PP in HCM- Dual chamber PP for HCM has not been shown to improve symptoms, though it does decrease the LVOT gradient, presumably due to RV apical pacing causing altered septal activation leading to less LVOT narrowing and hence less Venturi effect causing less SAM. So, it is only a IIb indication.

Selection of appropriate pacing mode

For patients with sinus node dysfunction AAI is preferred to VVI due to definite morbidity benefit (thromboembolism, AF, HF) and controversial mortality benefit. (The main studies are MOST and Andersen et al.)

For heart blocks, DDD does not offer benefit over VVI (UKPACE study).

Along with an ICD, when antibradycardia pacing is not needed, VVI is better than DDD (DAVID study)!

Modes and timing cycles

VVI- after a ventricular event, the pacemaker delivers a ventricular spike only after waiting for a time interval called lower rate interval. If a ventricular activity occurs within this time, the LR timer is reset, but activity in an initial part of the LRI called the ventricular refractory period (VRP) will not reset the LR timer.

AAI- Like for VVI, there is a LR interval and an atrial refractory period. Before implanting an AAI for a sinus node disease, we have to be sure of good AV nodal conduction by demonstrating 1:1 conduction of atrial beats at a rate of 140/mt.

DDI- This is like a combination of AAI and VVI, but there is not VAT function, presence of which would have made it a DDD. VAT function (or tracking of P) refers to pacing of ventricle after a P wave if there is AV conduction (after waiting for an interval called the AVI or AV interval) to produce an intrinsic QRS. DDI is usually a programmable option in DDD pacemakers and is switched on if atrial tachyarrhythmias are causing problems.

VDD- This is used for heart blocks. Its advantage is use of a single lead only- the atrial sensor is at the atrial position of the ventricular lead. It essentially functions as a VVI, with the additional option of P tracking- that is, if an intrinsic P occurs, the ventricular lead will wait for AVI and will pace only if the P is not conducted to produe a QRS (if a P conducts in spite of the heart block, it is allowed to work!).

 DDD- In addition to the settings for VDD, there is a new setting to decide when atrial pacing should start if there is no atrial activity. After ventricular activity, if there is no atrial activity at the end of an interval called the VA interval, an atrial pacing spike is given. But, as for the VRP of VVI, there is an interval after the QRS when atrial activity is not sensed by the atrial sensor- this is called PVARP or post ventricular atrial refractory period. Since the atrial sensor is also not allowed to sense during the entire AVI, AVI + PVARP constitutes total atrial refractory period or TARP. The need for a PVARP is to avoid a retrograde P from being sensed and initiate an AVI, this again producing a retrograde P which is again sensed- thus causing an endless loop or pacemaker mediated tachycardia. If still this is occurring, just increase the PVARP so that the retrograde P would not be sensed.

 DDD is especially useful for AV block (even though, as told earlier, no benefit over VVI was shown in studies). DDD is not useful in SSS and AF.

DDD can manifest as

• NSR,
• atrial pacing if no atrial activity and normal AV conduction,
• P synchronous pacing if normal atrial activity and no AV conduction and
• AV sequential pacing if no atrial activity and no AV conduction.

 Rate adaptive pacing- The sensors usually measure activity, minute ventilation or QT. Activity sensors are most commonly used and may be accelerometers or piezoelectric crystals, the former being more physiological.

Nowadays DDDR is most commonly used. These can be reprogrammed to AAIR in cases of sinus node dysfunction only. VVIR is used instead of DDDR in patients with AF.

VVI is contraindicated if it causes hypotension or VA conduction.

Pacemakers are implanted epicardially if there is no access to the right ventricle or if there is an intracardiac shunt that could predispose to thromboembolism. A lateral subclavian approach is preferred to medial to avoid crush injury to lead and pneumothorax.

Pacemaker programming

Pulse width- usually triple the threshold is used.

Voltage- usually double the threshold is used.

Microjoules- not usually done- if done, usually triple the threshold is used.

Mode switching- If a rapid atrial rhythm occurs in a PP capable of P tracking (DDD or VDD), to avoid rapid ventricular rhythm the PP automatically switches off P tracking- that is, in effect it becomes DDI or VVI (note that if DDD/VDD – VAT = DDI/VVI).

AVI- is programmed in such a way as to support intrinsic AV conduction.

Pacemaker complications

During implantation, complications like pneumothorax, hemothorax, arterial puncture, AV fistula, thoracic duct injury and brachial plexus injury can occur.

For hematoma, aspiration is not advised. Evacuation is done only if absolutely necessary.

Lead entry into the LV, via a PFO, is recognized by posterior position on lateral view and by RBBB pacing pattern. It can cause embolization.

Lead perforation may manifest as cardiac tamponade, pericardial effusion, pericarditis, friction rub, increased threshold, RBBB pacing pattern or intercostal muscle or diaphragmatic contraction. Withdraw lead and reposition.

Subclavian vein thrombosis is usually asymptomatic.

Lead dislodgement may be macro or micro, former being visible radiographically.

Loose connector pin can cause loss of output.

Insulation break can cause sensing or pacing problems.

Lead fracture can occur, especially at the costoclavicular space.

VPCs can occur in the first two days of pacemaker implantation due to mechanical stimulation. They have the same configuration as the pacemaker induced complex. They resolve.

Diaphragmatic stimulation may be due to direct stimulation, when the left hemidiaphragm is paced, or due to phrenic nerve stimulation, when the right hemidiaphragm is paced. Try decreasing voltage or pulse width. If that does not work, reposition.

Pacemaker infection is usually local rather than septicemic. Early infection is caused by Staph aureus and is aggressive while late infection is caused by Staph epidermidis and is usually indolent. Local antibiotic irrigation helps to prevent infection. Treatment is removal of the entire system including leads.

Pacemaker erosion may be due to infection or a tight pocket. Treatment is removal of the system. The same system cannot be reimplanted at another site- a new one has to be used. So impending erosion is an emergency- revise the pocket and reimplant.

Troubleshooting

Failure to capture- Means a pacing artifact is present without depolarization. Causes are high threshold, lead fracture, insulation break, lead dislodgement, lead perforation, impending battery depletion, functional noncapture, and high threshold due to drugs or metabolic problems. Functional noncapture refers to failure to capture due to pacing spike falling in refractory period of a beat.

Failure to output- Means that there is no pacing artifact. Causes are oversensing, battery depletion, loose set screw, lead fracture, internal insulation failure in a bipolar lead and air in the pocket of a unipolar pacemaker.

True undersensing occurs due to lead dislodgement, lead fracture or battery depletion. Functional undersensing occurs when a cardiac activity falls within a programmed refractory period of the pacemaker.

Fusion beat is a hybrid of intrinsic and pacemaker induced activities. Pseudofusion beat is due to pacemaker spike falling on intrinsic activation, without pacemaker induced activation. It occurs in two situations- when pacing rate and intrinsic rate are similar and when there is an intraventricular conduction defect. In the former situation, it occurs because the initial part of the intrinsic activation is not sensed by the pacemaker and hence it discharges.