Ad

Tricuspid regurgitation

Tricuspid regurgitation (TR)
Trivial (small) TR is frequently detected by echocardiography in normal subjects, and should never be interpreted as an abnormal finding. 
Pathological TR is more often secondary (not due to a disorder of the valve structure) and less often it is attributed to a primary (structural) valve lesion. 
Secondary TR is due to annular dilatation and increased tricuspid leaflet tethering and is caused by:
1) Right ventricular (RV) pressure overload (usually caused by pulmonary hypertension as a consequence of left sided heart disease, chronic pulmonary disease, connective tissue disease, congenital heart disease, or idiopathic pulmonary hypertension) 
or
2) RV volume overload (dilatation of the right ventricle due to an atrial septal defect, or due to intrinsic right ventricular disease with systolic dysfunction, as in right ventricular cardiomyopathy).

Primary TR (caused by structural alterations of the valve) can be caused by
 Infective endocarditis (especially in intravenous drug addicts),
Myxomatous disease (leading to prolapse of the valve leaflets)
Rheumatic heart disease,
Iatrogenic causes (
occasionally TR occurs after pacemaker implantation or after endomyocardial biopsy)
Carcinoid syndrome
( carcinoid syndrome, is  a type of neuroendocrine tumor, usually in the small bowel or appendix, with metastases to the liver, which releases serotonin metabolites into the bloodstream. These metabolites are responsible for the formation of endocardial plaques in the right heart chambers. Involvement of the tricuspid valve causes thickening and immobilization of the leaflets, resulting in significant tricuspid regurgitation and, less often tricuspid stenosis.)
Ebstein’s anomaly is a congenital malformation characterized by apical displacement of the annular insertion of the septal and posterior leaflets of the tricuspid valve and atrialization of a portion of the ventricular myocardium.
Endomyocardial fibrosis,
Ergot-like drugs,
Thoracic trauma
Symptoms
Often, even severe TR can be tolerated for a long period of time without significant symptoms. Symptoms of the causative disorder may be present. Eventually, severe TR will produce symptoms of right heart failure, such as fatigue, exercise intolerance, edema, vague abdominal discomfort due to hepatomegaly.
Physical examination in TR
The most common physical signs of severe TR are prominent v waves in the jugular veins and a pulsatile liver. Both these signs are due to regurgitation of right ventricular blood into the systemic veins. 
The systolic murmur of TR is heard at the lower left sternal border and at the xiphoid area. The holosystolic murmur of tricuspid regurgitation (TR) is often soft (and may be absent in many cases of severe TR, if flow is not turbulent enough) and it becomes louder on inspiration.
In severe cases peripheral (ankle or leg) edema, or even ascites may be present.
ECG
Frequent findings are an incomplete right bundle branch block and atrial fibrillation.
Echocardiography in tricuspid regurgitation (TR)
TR is identified using color flow mapping of the systolic
regurgitant jet in the right atrium.
Evaluation of the pulmonary systolic pressure from the measurement of the peak velocity of the TR jet should be carried out in all cases. This may be inaccurate in the presence of severe TR (with a large regurgitant volume) because this leads to a lower pressure difference (pressure gradient) between the right ventricle and the right atrium .
The presence of associated lesions, particularly left ventricular systolic or diastolic dysfunction and lesions of the left-sided cardiac valves, should be assessed.
In primary TR, valve morphology can help determine the etiology: vegetations in endocarditis, leaflet retraction and thickened leaflet tips in rheumatic valve disease, prolapsing thickened leaflets in myxomatous disease, a flail leaflet in myxomatous or post-traumatic valve involvement.
In secondary TR annular dilatation or leaflet tethering is observed:
Significant tricuspid annular dilatation is defined in the apical 4 chamber echocardiographic view by a diastolic diameter ≥40 mm , or >21 mm/ mof body surface area. 
Significant tethering of the valve, in secondary TR, is characterized by a coaptation distance > 8 mm. This is the distance between the tricuspid annular plane and the point of coaptation of the valve leaflets in mid-systole from the apical 4-chamber view.
Evaluation of the right ventricular (RV) dimensions and function should be performed.  Indications of RV systolic dysfunction are: Tricuspid annular plane systolic excursion (TAPSE) <15 mm,
 pulse wave TDI-derived peak systolic velocity of the lateral tricuspid annulus <11 cm/s, and
 RV end-systolic area >20 cm2
Tricuspid regurgitation (TR) severity is estimated from the extent of the jet, or better by vena contracta width (vena contracta is the narrowest portion of the jet, near its origin from the valve leaflets). In many cases, just a visual estimate can allow judgment on the severity of regurgitation.  In case of TR with an eccentric jet, a large eccentric jet reaching the posterior wall of the right atrium indicates significant TR.  Conversely, small jets and a normal size of the right atrium and right ventricle usually indicate mild TR.
Regurgitant jet area correlates roughly with the severity of regurgitation:mild <5 cm2 
moderate 6-10 cm2
severe >10 cm2.  

Other more accurate indications of severe TR are:
Vena contracta ≥ 7 mm

In continuous wave Doppler examination of TR, a dense/triangular TR Doppler signal with early peaking.
PISA radius >9 mm, at color Doppler examination with baseline shift, with a Nyquist limit (aliasing velocity) of 28 cm/s towards the direction of the regurgitation.
Effective regurgitant orifice area (EROA) ≥40 mm².
Regurgitant Volume ≥45 ml/beat.
In severe TR, enlargement of the right atrium, right ventricle, and inferior vena cava is almost always present.


Treatment 
Diuretics improve signs of congestion. Specific therapy of the underlying disease is necessary, when feasible.
Surgery (usually tricuspid annuloplasty with a prosthetic ring) is indicated in :
Symptomatic patients with severe primary TR without severe right ventricular dysfunction. 
In asymptomatic or mildly symptomatic patients with severe isolated primary TR and progressive right ventricular (RV) dilatation or progressive deterioration of RV function (class IIa indication).
In patients with severe (indication class I) or moderate (indication class IIa) primary TR, or moderate secondaryTR with dilated annulus (for limits of annular diameter see above) undergoing left-sided valve surgery.
The surgical operation performed is usually annuloplasty with a prosthetic ring, but in advanced forms of tethering and RV dilatation, or in a severe valve deformity that cannot be corrected, valve replacement should be considered. Valve replacement is performed with large bioprostheses (these are preferred than mechanical valves in the tricuspid position).

Tricuspid regurgitation (color doppler echocardiography). A video-link (by dr Luke Howard) :
https://www.youtube.com/watch?v=UHNKYKyorJo


Mitral stenosis


Mitral stenosis (MS)
Causes 

The most common underlying cause of MS is prior rheumatic fever
occurring, on average, 20 years before presentation of mitral stenosis. 

Rheumatic valve disease is characterized by fibrous thickening and calcification of the valve leaflets, fusion of  the commissures (the borders where the leaflets meet), shortening and thickening of the chordae tendineae.
 Other more rare etiologies of MS include calcification of  the mitral annulus that extends onto the leafets, infective endocarditis with large vegetations obstructing the valve orifice, and rare congenital mitral stenosis (parachute mitral valve, supravalvular mitral ring). In parachute mitral valve, there is a single papillary muscle to which chordae to both leaflets attach. It results in mitral stenosis or mitral regurgitation.
Some systemic diseases can cause valvular fibrosis and stenosis (carcinoid, systemic lupus erythematosus, rheumatoid arthritis, healed endocarditis, mucopolysaccharidosis. 
Mitral valvular fibrosis and stenosis can also be caused by prior anorectic drug use.

Pathophysiology of mitral stenosis (MS)
In the normal heart, the mitral valve opens in early diastole  and blood flows freely rom the left atrium (LA) into the left ventricle (LV). Normally the pressure difference between these two chambers in diastole is negligible (the LA and the LV have almost the same diastolic pressure). The normal cross sectional area of the mitral valve orifice is 4-6 cm2
 In MS, there is obstruction to blood flow across the mitral valve. This produces an abnormal pressure gradient (pressure difference)
between the LA and LV, resulting in an icreased  left atrial (LA) pressure. Hemodynamic changes (a rise in transvalvular pressure gradient) begin when the cross-sectional area of  the valve,  is reduced to less than 2 
cm2.
In MS the high LA pressure is transmitted retrograde to the pulmonary circulation, resulting in increased pulmonary venous and capillary pressures. The elevated pressure in the pulmonary vasculature may cause transudation of  plasma into the lung interstitium and alveoli. This causes symptoms of heart failure, such as exertional dyspnea and paroxysmal nocturnal dyspnea, or orthopnea. 
In MS, chronic pressure overload of the LA (i.e. the chronically elevated LA pressure) leads to left atrial dilatation. This stretches the atrial conduction fibers and may adversely affect intra-atrial conduction of electric impulses, resulting in atrial fibrillation.
Atrial fibrillation due to the increased heart rate leads to a shortened diastolic period. The contribution of atrial systole to diastolic filling is also lost. These factors worsen the patient's clinical condition, because they result in a further elevation in atrial and pulmonary venous pressures and in a diminished cardiac output. 

Auscultatory findings in MS 
The opening snap is an early diastolic sound of short duration, and it is considered as the most characteristic auscultatory finding of mitral stenosis (MS). You can hear the opening snap near the cardiac apex, but it is more easily heard along the lower left sternal border. However, as the disease progresses and the valve becomes more calcified and immobile, the opening snap may be lost. Also the first heart sound (S1), which is usually accentuated (loud) in MS, for the same reason can become softer at a later stage of the disease. The murmur of MS is a low-pitched rumbling mid-diastolic murmur. It is best heard with the bell of the stethoscope with the patient in the left lateral decubitus position. Presystolic accentuation of the murmur can be present if the patient is in sinus rhythm. Auscultation after a brief period of exercise usually accentuates the murmur of MS, because exercise increases the transvalvular gradient, due to the increased cardiac output and heart rate.
 The  length of the murmur correlates better with the severity of MS than the loudness. MS is more severe when the murmur is longer and when the time interval from the second heart sound (S2) to the opening snap is short.
ECG
The electrocardiogram (ECG) in MS, if the rhythm is sinus, shows left atrial enlargement. Atrial fibrillation may be present (it is common in MS). If  pulmonary hypertension has developed, then there is also ECG evidence of right ventricular hypertrophy.
 Echocardiography in MS 
It shows structural abnormalities of the valve (in rheumatic MS  mitral leaflets are thickened with abnormal fusion of  their commissures). Echocardiography also shows restricted separation
of the valve leaflets and doming of leaflets during diastole.
 Left atrial enlargement is also present.
The mitral valve area (MVA) can be measured directly from the parasternal short axis view at the level of the tips of the mitral valve. Optimal positioning of the echocardiographic view, in order to obtain this measurement, is done by first obtaining a parasternal long-axis view and placing the mitral valve orifice in the center of the scan plane. The transducer is then rotated 90° to obtain the short-axis view. Measurements are obtained at the tips of the mitral leaflets. Three-dimensional echocardiography can provide a more accurate determination of the mitral valve area (MVA).
MVA can also be calculated from Doppler velocity measurements (the diastolic pressure half time). In general, the pressure half time (PHT) represents the time in which the peak pressure gradient between two adjacent chambers decreases to the half of its value. Thus,The PHT is the time it takes for the pressure gradient across the valve to fall to one-half the starting value. (This is equal to the time for the velocity of the mitral E wave to decrease to 70% of peak velocity). The mitral inflow E wave is used in this calculation.
 MVA (in cm2) = 220/PHT.
Another method to determine the mitral valve area (MVA) is the PISA (proximal isovelocity surface area) method, a method also used (more commonly) for the calculation of the effective regurgitant oriffice in cases of mitral regurgitation. In mitral stenosis (MS) the PISA method can be used to calculate the MVA and it offers the advantage of being still accurate in case of concomitant mitral or aortic regurgitation. 
On the atrial side of the stenotic mitral valve, diastolic flow converges towards the stenotic valvular orifice, producing multiple hemispheres of isovelocity (the velocity of blood is the same in every point of the surface of each of these converging hemispheres). As blood accelerates towards the stenotic orifice, the velocity at the outer hemispheres is lower than the velocity on the smaller inner hemispheres. If π=3.14, r (in cm) is the PISA radius (the radius of flow convergence) which is the radius of the hemisphere where blood velocity is the aliasing velocity  and a is the opening angle of mitral leaflets, i.e. the angle between the two mitral leaflets at the atrial surface (in degrees), aliasing velocity is the velocity at which aliasing of color doppler occurs in the direction of flow through the mitral valve (this is set by the echocardiographer to 20-45 cm/s), then we can use the equation: 
MVA= 2π r2  x (aliasing velocity/peak MS velocity) x (a/180).
Thus,
 MVA=6,28 r2  x (aliasing velocity/peak MS velocity) x (a/180)

 Measurement of the opening angle is demanding, however it has
been demonstrated that there is only a slight difference in the angle
between patients and the use of a fixed angle of 100 degrees can provide an accurate estimation of MVA.
Current guidelines define clinically important, severe, MS as a valve area ≤1.5cm2  , because this valve area is typically accompanied by left atrial enlargement and elevated pulmonary artery systolic pressure. A valve area ≤1.0 cm2 is termed "very severe" MS.
The transvalvular mean gradient (assessed by means of tracing mitral inflow continuous wave doppler signal) provides an estimate of stenosis severity. In mild stenosis : mean gradient < 5 mm Hg Moderate stenosis : mean gradient between 5 and 10 mm Hg.
 Severe MS : mean gradient > 10 mm Hg. 
Treatment of MS
 Symptoms due to vascular congestion can be improved by restriction of salt intake and diuretic therapy.
Heart rate slowing agents, such as beta-blockers or nondihydropyridine calcium channel blockers (diltiazem or verapamil), increase diastolic left ventricular filling time and so they there decrease symptoms with exercise. These drugs, or digoxin, are also used to slow the ventricular rate in patients with rapid atrial brillation. Anticoagulant therapy to prevent thromboembolism is indicated  in MS patients with atrial fibrillation, or an identied LA thrombus, or a prior embolic event.
Percutaneous or surgical valve interventions are the only treatments that alter the natural history of severe MS. They are indicated in patients with severe (see above for the echocardiographic criteria of MS severity), symptomatic MS. Percutaneous mitral balloon 
 valvuloplasty is the treatment of  choice in appropriately selected patients (those without advanced anatomic deformity of  the valve, and without moderate or severe mitral regurgitation, or left atrial thrombus). Transesophageal echocardiography (TEE) is indicated to exclude LA thrombus prior to valvuloplasty.
Percutaneous mitral valvuloplasty (PMV) is also indicated for asymptomatic patients with severe MS (valve area  ≤1.5cm2) , who have pulmonary hypertension (pulmonary artery systolic pressure > 50 mm Hg at rest or > 60 mm Hg with exercise) if valve morphology is favorable for PMV, in the absence of left atrial thrombus or moderate to severe mitral regurgitation.
In patients with severe MS causing symptoms, not suitable for percutaneous valvuloplasty, surgical treatment is indicated. This is true for patients with severe subvalvular disease or severe valvular calcification, or concomitant mitral regurgitation (moderate or severe). Surgical treatment choices include: 
Open mitral valvotomy: It involves direct visualization of the mitral valve (with cardiopulmonary bypass), debridement of calcium, and splitting of fused commissures and chordae.
 Mitral valve replacement.with a prosthetic valve is often required, when there is extensive fibrosis and calcification or concomitant moderate to severe mitral regurgitation.

LINKS : 
Mitral stenosis and echocardiography. A good video by 123sonography
https://www.youtube.com/watch?v=MQ5UyGoYhZ8


An echocardiogram of a patient with mitral stenosis (by dr Maged Al Ali)
https://www.youtube.com/watch?v=9yPfTxBAq3s



Bradyarrhythmias-Bradycardia : Diagnosis and treatment and a case-quiz

Note: The site is under develoment and content is continuously expanding
Cardiology free e-book online ECG QUIZ 1. An electrocardiography CASE-QUIZ:  A patient with weakness and lightheadedness. What is the diagnosis and which should be the management ?
Watch the video and answer the question. Click on the symbol [] at the lower right corner of the video to see it enlarged: full screen)




THE ANSWER 


Heart rate (ventricular rate) 30- 35/min. P waves are more frequent than the QRS complexes and they do not have any temporal relation with QRS complexes (some P waves even fall in the ST segment). This is a case of complete atrioventricular block.  QRS has a right bundle branch block morphology. In general, complete atrioventricular (AV) block would be an indication for permanent pacing, but in this case the complete (third degree) AV block could be possibly caused by verapamil, which the patient has been taking for hypertension. So there is a potentially reversible cause for the AV block. When we suspect a reversible cause we do not implant a permanent pacemaker. Instead there is an indication for temporary pacing and discontinuation of the causal drug. The patient was admitted to the hospital, verapamil was discontinued and replaced by another antihypertensive agent, with no effect on conduction. The patient remained under observation with temporary transvenous pacing for 2 days. Two days after the discontinuation of verapamil the normal heart rhythm (normal atrioventricular conduction) recovered. So a permanent pacemaker was not implanted. 
In cases, where the complete AV block persists and is not reversible, or if there is no revesible cause for the block, implantation of a permanent pacemaker is absolutely indicated.


Bradycardia is a ventricular rate (at rest) < 50 beats per minute (bpm)  (cycle length 1200 ms). Some cardiologists use 60 bpm (cycle length 1000 ms) as the lower limit of the  normal resting heart rate. Bradycardia is not always an abnormal finding. It can be normal, especially in the absence of symptoms. Trained athletes, especially endurance athletes, usually have bradycardia at rest and this is normal.
Bradycardia due to an abnormality of the conducting system of the heart is called "bradyarrhythmia". Many of these rhythm disorders are asymptomatic and benign, requiring no treatment, whereas some cause symptoms and need treatment with pacemaker implantation and others can be life threatening requiring rapid intervention.
Symptoms of bradycardia or bradyarrhythmias are nonspecific (i.e. the symptom is not always directly correlated to the bradycardia and other causes should also be sought). Symptoms include: fatigue, generalized weakness,  lightheadedness, presyncope, syncope, dyspnea on exertion. 

Bradyarrhythmias arise from abnormalities in one or more of three locations in the heart's conducting system: sinoatrial node, atrioventricular node, or infranodal (the His -Purkinje system).

A female patient 78 years old with a history of hypertension and one-vessel coronary artery disease treated with a percutaneous coronary intervention (PCI) of the right coronary artery 3 years before (because of effort angina). She also has a history of asthma. One year before she had a myocardial perfusion scintigraphy (a technetium 99m SPECT scan) which did not reveal any ischemia of significant extent or any myocardial scar. She complains of episodes of fainting, or near-fainting (one episode of syncope and two presyncopal episodes during the last month). She is currently on medication with irbesartan -hydrochlorothiazide 300/25 mg per day, aspirin 100 mg per day ,atorvastatin 20 mg per day and an inhaled bronchodilator. Physical examination is normal and it also did not reveal orthostatic hypotension. Her blood tests revealed no significant abnormalities. Her 12 lead  ECG shows sinus rhythm, a prolonged PR interval (first degree AV block) and a LBBB . Here is a part of her 24-hours Holter ECG recording. The patient did not have any symptoms during the recording. What are the findings ?  Which  could be the most probable cause ?  What treatment do you propose ?







THE ANSWER

The presence of PR prolongation and/or a bundle branch block in a patient with presyncopal or syncopal episodes, should raise a suspicion of a bradyarrhytmic cause (e.g. pauses due to sinus node dysfunction, or a transient second or third degree atrioventicular block). In this case the holter ECG recording shows sinus pauses with a duration of about 3-3,5 seconds. The most probable cause of sinus node dysfunction in this age group is idiopathic degenerative fibrosis of the conductive system. The patient does not take any medications whith an influence on sinus node function. A permanent pacemaker (type DDDR) was implanted and the patient is asymptomatic since then. (There was a class II indication for permanent pacing, since there is ECG evidence of sinus node dysfunction and symptoms compatible with the disorder are present, in the absense of another identifiable cause. If the patient had symptoms at the time of the recorded pauses, then the indication for pacing would be absolute- class I).



Sinus nodal or sinoatrial nodal (SA nodal) dysfunction (sick sinus syndrome) 
Causes of sinus node dysfunction have been classified as intrinsic or extrinsic. This classification is practical because extrinsic causes are often reversible. In this case they should be corrected (if it is possible) and this way unnecessary pacemaker therapy can be avoided. The most common causes of extrinsic sinus node dysfunction are drugs and influences of the autonomic nervous system (stimulation of the parasympathetic nervous system via the vagus nerve or inhibition of the activity of the sympathetic nervous system can suppress automaticity and/or slow conduction).
Drugs that can cause sinus node dysfunction are beta-blockers, non-dihydropyridine calcium channel blockers (verapamil, diltiazem), digoxin, ivabradine, antiarrhythmic drugs, such as type IA (quinidine, procainamide, disopyramide) ,Type IC (flecainide and propafenone) Type III (sotalol and amiodarone), sympatholytic antihypertensives (clonidine, methyldopa, reserpine) and other miscellaneous drugs (lithium, cimetidine, amitriptyline, phenytoin).
Causes of sinus node dysfunction related to effects of the autonomic nervous system include vasovagal syncope and generally situations of excessive vagal tone, the carotid sinus syndrome and endotracheal suctioning (via activation of the vagus nerve).
 Other extrinsic causes include hypothyroidism, sleep apnea, hyperkalemia, increased intracranial pressure, sepsis, hypothermia and hypoxia.
Intrinsic sinus node dysfunction is often degenerative due to fibrous replacement of the sinus node or its connections to the atrium. This is more common in elderly individuals.
Other causes of intrinsic sinus node dysfunction are :
Acute and chronic coronary artery disease (in the setting of acute myocardial infarction, typically inferior, the abnormality can be transient).
 Inflammatory processes such as myocarditis (e.g viral myocarditis), rheumatic heart disease, systemic lupus erythematosus (SLE), rheumatoid arthritis and mixed connective tissue disease. 
Congenital heart disease (transposition of the great arteries/Mustard and Fontan repairs)

Familial causes of sinus node disease (miscellaneous genetic causes and also in rare familial syndromes such as Kearns-Sayre syndrome and myotonic dystophy.
Iatrogenic damage of the sinus node from direct injury in cardiothoracic surgical procedures, or radiotherapy.
Sinus node dysfunction (sick sinus syndrome) can be manifested with: sinus bradycardia (with heart rate ≤ 50/min)
Sinus pauses, of duration > 2 seconds ( Generally pauses < 3 seconds are not a serious concern. However, pauses > 3 seconds while the patient is awake are generally concidered abnormal). For a description of sinus pauses and sinoatrial exit block see below.
Chronotropic incompetence: inability to attain 80% of the maximum predicted heart rate in response to exercise. It can be  associated with symptoms (such as fatigue, reduced exercise toleralce, dizziness with exercise). 
The "tachy-brady" (tachycardia-bradycardia) syndrome: when there are alternating periods of a supraventricular tachycardia (most commonly atrial fibrillation, but atrial flutter, or atrial tachycardia can also occur) with periods of sinus bradycardia or sinus pauses > 2 seconds. In patients with tachycardia-bradycardia syndrome after conversion of tachyarrhythmias, long pauses may occur (post-conversion pause). Sinus bradycardia in some patients can facilitate the occurence of reentrant tachycardias, by magnifying discrepancies in the duration of the refractory period between different areas of the cardiac tissue. This is a phenomenon that occurs with longer cycle lengths.
 Sinus pauses
The sinus node may fail to deliver an electrical impulse to the atria for a time interval and this is manifested on the ECG by the absence of P waves and also absence of cardiac electical activity, until a sinus impulse appears, or until an escape pacemaker (an other focus of conductive tissue) depolarizes and generates an impulse. This can happen because of a sinus arrest or sinus pause, which occurs when the sinus node does not depolarize on time, or because of sinoatrial (SA) exit block. In SA exit block the sinus node generates electrical impulses, some of which are blocked on their exit from the sinus node to the atrial tissue. SA exit block produces on the ECG an abnormality very similar to sinus arrest. SA exit block may be distinguished from sinus arrest by the fact that the pause is a multiple of the sinus PP interval (the interval between two consecutive sinus P waves before the pause)
Brief, asymptomatic sinus pauses are a common finding and do not require treatment. Generally pauses < 3 seconds are not a serious concern and can be seen in Holter ECG monitoring in up to approximately 10% of normal persons. They are also more common in athletes. Pauses lasting > 3 seconds, especially if they occur while the patient is awake are considered abnormal.


Treatment:
For sinus node dysfunction (sick sinus syndrome) implantation of a  permanent pacemaker is generally indicated only when symptoms that correlate to this disorder 
are present -this is a class I indication (or it may be indicated if symptoms compatible with the disorder are present, in the absense of another identifiable cause-a class II indication). These pacing indications are valid for cases where sinus node dysfunction is not the result of a reversible cause. 3) Sinus node disease. 
Pacing is not indicated in patients with sinus node dysfunction, or sinus bradycardia which is asymptomatic or due to reversible causes.
Atrioventricular (AV) node or His-Purkinje system disorders (disorders of atrioventricular conduction)
Their etiologies  can classified as functional (which are often reversible) or structural.  The most common cause of atrioventricular (AV) block is idiopathic fibrosis of the heart's conductive system (Lenegre’s disease and Lev’s disease). This, of course, is a structural cause and it is not reversible also.
Other structural causes include: Acute myocardial infarction (MI) : AV block in patients with acute inferior MI is more common (occuring approximately in 14%-15 % of patients) and less common in those with anterior infarction, (2%). AV block occurs usually within the first 24 hours of an acute MI, most commonly, it is first-or second-degree AV block, but complete heart block can also occur. In acute inferior MI the level of block is usually in the AV node, resulting in more stable, escape rhythms with narrow QRS complex . In contrast in acute anterior MI  the level of block is usually  in the His bundle, or bundle branches resulting in unstable escape rhythm with a wide QRS complex and a worse prognosis (high mortality rates).
Chronic coronary artery disease can also cause AV block.
Calcific valvular disease
Cardiomyopathies and infiltrative diseases of the heart can also cause disorders of AV conduction (AV block). Infiltrative diseases are conditions caused by the accumulation in tissues of substances or cells  not normally found in those tissues, such as amyloidosis, hemochromatosis and sarcoidosis 
Infectious and inflammatory disorders such as endocarditis myocarditis (Chagas disease, Lyme disease, rheumatic fever, etc)
Collagen vascular diseases (scleroderma, rheumatoid arthritis, systemic lupus erythematosus, Reiter’s syndrome, ankylosing spondylitis, and polymyositis)
Iatrogenic AV block is not uncommon. It may occur as a consequence of mitral or aortic valve surgery, or catheter ablation.
Congenital heart disease, such as congenital complete heart block ostium primum atrial septal defect and transposition of the great vessels can also cause AV block
Functional causes of AV block are common and include drugs ( beta-blockers, nondihydropyridine calcium channel blockers digoxin, antiarrhythmic drugs)
Effects exerted via the autonomic nervous system ( vasovagal syncope, carotid sinus syndrome) hyperkalemia, hypermagnesemia.

Atrioventricular (AV) node or His-Purkinje system disorders can be manifested as:
A first-degree AV blockPR interval prolongation  (PR duration >200 ms).
A second-degree AV block, which is further classified in two types:
Mobitz I (Wenckebach): The ECG shows progressive PR interval
prolongation followed by a single blocked P wave. In some cases the progressive lengthening of the PR interval may be subtle. The best way to assess it is to measure the PR interval of the beat which is immediately prior to a blocked P wave and the PR of the beat  immediately after a blocked P wave. The latter should be shorter.
In this type of atrioventricular (AV) block, the most common site of block is in the AV node.
Mobitz II: There is no progressive PR interval prolongation
before a blocked P wave. The PR interval is constant but there is intermittent conduction of the atrial electrical impulses to the ventricles, so that some P waves are not followed by a QRS complex. In Mobitz II AV block, the most common site of block
is infranodal (in the His-Purkinje system).

A special case is a 2:1 AV block, where every second P wave is conducted to the ventricles (followed by a QRS).

Third-degree (complete) AV block, or complete heart block
There is no temporal association between P waves and QRS
complexes, because there is no conduction of atrial impulses (P waves) to the ventricles. Thus, the ventricular rhythm is an escape rhythm originating from a secondary pacing site and not from transmission of sinus impulses.
This ventricular escape rhythm, if it is characterized by narrow QRS complexes, is called a junctional escape rhythm. Usually in these cases the site of block is in the AV node.
If QRS complexes are wide (≥ 120 msec) the block is infranodal, i.e. below the AV node,  in the His- Purkinje system.
The autonomic nervous system exerts an important effect on the function of the AV node but it only minimally influences the His bundle and the distal conducting system. Thus, the influence of the autonomic system on the production and conduction of electrical impulses in the heart is mainly on the sinus node and the AV node.
The AV node is highly innervated with postganglionic sympathetic and parasympathetic nerves.
Treatment of bradycardia and heart block is needed if there are symptoms such as syncope, lightheadedness, dyspnea (shortness of breath), ischemic chest pain and/or evidence of hemodynamic compromise or low cardiac output. If bradycardia is attributed to the effect of a drug, then this drug should be discontinued, if possible.However, if cessation of drug therapy considered as the cause of the bradycardia for a reasonable duration of time does not result in improvement, or drug therapy is needed for an indication (e.g. a paroxysmal tachyarrhythmia) then the implantation of a permanent pacemaker should be considered.
If rapid treatment of bradycardia is needed, because of the presense of serious symptoms, or hypotension the next step is intravenous administration of atropine. Infusion of isoproterenol, may be required in acutely decompensated patients if atropine fails, until pacing can be initiated. Temporary pacing is more effective than atropine or isoproterenol for decompensated patients with serious bradycardia. Temporary pacing includes:
External transcutaneous pacing, which can be rapidly and easily instituded, but it is used only for a short period of time, due to the unpredictable transcutaneous capture and also because it is poorly tolerated by the patient.
Transvenous temporary pacing, via the insertion of a pacing electrode through the subclavian or the internal jugular vein into the right ventricle. This is the most effective and reliable method of temporary pacing.

Implantation of a permanent pacemaker is indicated in all patients with symptomatic bradycardia (caused by sinus node dysfunction, or any type of second or third degree AV block-even Mobitz I if it results in symptoms), when bradycardia is not due to a reversible cause. When symptomatic sinus bradycardia, sinus pauses, or AV block is attributed to the effects of drug treatment (for examle treatment with beta blockers, diltiazem, verapamil, or antiarrhythmic agents) the following general rules should be followed : 
If this treatment is not absolutely necessary, these drugs should be disontinued. Then, if the bradyarrhythmia terminates, no pacemaker is indicated. 
If symptomatic bradycardia is attributed to an absolutely necessary drug treatment, then a permanent pacemaker is implanted and drug treatment is continued.
 A permanent pacemaker is also indicated  in asymptomatic patients with aqcuired Mobitz type 2 block,  or complete (third degree) AV block, because these types of block are assossiated with a high risk for the development of profound bradycardia and syncope (This is a class I indication according to ESC guidelines on cardiac pacing-2013).
 Permanent pacing is also indicated in 2:1 infranodal block, and it  should be considered in patients with second-degree type 1 AV block if it causes symptoms or if it is found to be located at intra- or infra-His levels at an electrophysiologic study.(This is a class IIa indication, according to the ESC guidelines on cardiac pacing-2013). Pacing is not indicated in patients with AV block which is due to reversible causes (i.e. a class III indication).

Bibliography and useful links :

AHA Guideline: Management of Symptomatic Bradycardia and of Symptomatic Tachycardia in the acute setting.



ESC (2013) Guidelines on cardiac pacing and cardiac resynchronization therapy


Deal N.Evaluation And Management Of Bradydysrhythmias In The Emergency Department. Emergency Medicine Practice, 2013;15:1-16.
LINK http://www.ebmedicine.net/topics.php?paction=showTopic&topic_id=377


Focused Update Incorporated Into the ACCF/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities


ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities