The main pumping chamber, the ventricle, is protected (to a certain extent) against excessively high rates arising from the supraventricular areas by a "gating mechanism" at the atrioventricular node, which allows only a proportion of the fast impulses to pass through to the ventricles. In Wolff-Parkinson-White syndrome, a "bypass tract" avoids this node and its protection and the fast rate may be directly transmitted to the ventricles. This situation has characteristic findings on ECG.

In normal individuals, the AV node slows the conduction of electrical impulse through the heart. This is manifest on a surface electrocardiogram (ECG) as the PR interval. The normal PR interval is from 120 ms to 200 ms in length. This is measured from the initial deflection of the P wave to the beginning of the QRS complex.

In first-degree heart block, the diseased AV node conducts the electrical activity more slowly. This is seen as a PR interval greater than 200 ms in length on the surface ECG. It is usually an incidental finding on a routine ECG.

First-degree heart block does not require any particular investigations except for electrolyte and drug screens, especially if an overdose is suspected.

Investigations may also be warranted with a prolonged interval that is greater than 0.2 sec.

The criteria to diagnose a right bundle branch block on the electrocardiogram:

- The heart rhythm must originate above the ventricles (i.e. sinoatrial node, atria or atrioventricular node) to activate the conduction system at the correct point.

- The QRS duration must be more than 100 ms (incomplete block) or more than 120 ms (complete block)

- There should be a terminal R wave in lead V1 (e.g. R, rR', rsR', rSR' or qR)

- There should be a slurred S wave in leads I and V6.

The T wave should be deflected opposite the terminal deflection of the QRS complex. This is known as appropriate T wave discordance with bundle branch block. A concordant T wave may suggest ischemia or myocardial infarction.

A mnemonic to distinguish between ECG signatures of left bundle branch block (LBBB) and right, is WiLLiaM MaRRoW; i.e., with LBBB, there is a W in lead V1 and an M in lead V6, whereas, with RBBB, there is an M in V1 and a W in V6.

The management includes identifying and correcting electrolyte imbalances and withholding any offending medications. This condition does not require admission unless there is an associated myocardial infarction. Even though it usually does not progress to higher forms of heart block, it may require outpatient follow-up and monitoring of the ECG, especially if there is a comorbid bundle branch block. If there is a need for treatment of an unrelated condition, care should be taken not to introduce any medication that may slow AV conduction. If this is not feasible, clinicians should be very cautious when introducing any drug that may slow conduction; and regular monitoring of the ECG is indicated.

The prognosis of patients with complete heart block is generally poor without therapy. Patients with 1st and 2nd degree heart block are usually asymptomatic.

In otherwise healthy patients, occasional premature atrial contractions are a common and normal finding and do not indicate any particular health risk. Rarely, in patients with other underlying structural heart problems, PACs can trigger a more serious arrhythmia such as atrial flutter or atrial fibrillation. In otherwise healthy people, PACs usually disappear with adolescence.

PVCs are usually diagnosed after the patient has described "skipped beats", pauses or palpitations. Typically the palpitations felt by PVC patients are very irregular and less sustained than patients with other types of arrhythmia. They are likely to have "flip flopping" sensations where it feels like the heart is flipping over or pounding due to there being a pause after the premature contraction and then a powerful contraction after the pause. There is a possibility that they might feel a ‘fluttering’ in their chest or a pounding in their neck but these two types of palpitations aren't very common in PVC patients.

A physical examination should be conducted after a full history has been taken. This is useful in determining any possible heart defects that might be causing the palpitations. For example, some cases of premature ventricular contraction have a mitral-valve prolapse which can be determined through the physical examination.

The next step in diagnosis is a 12 lead ECG which can be performed in the doctors’ office over a short period of time; however this is often non-conclusive in diagnosis because it is not very sensitive and there is only a small chance of a premature ventricular contraction occurring in the short period of time. Holter monitoring is a far better method for diagnosis as it is continuous recording of the heart’s rhythm over a period of 24 hours, or event monitoring which records noncontinuously for 30 days or indefinitely. This increases the likelihood of a premature ventricular contraction occurring during the recording period and is therefore more useful in diagnosis. Another method of detection of PVCs is a portable electrocardiogram device known as an event recorder that can be carried around for home monitoring of the heart's activity. Both the Holter monitor and the event recorder can help to identify the pattern of a PVC. The significance of a patient's PVCs can be monitored and diagnosed through exercise stress electrocardiogram. If the premature beats go away during the exercise test then they are considered to be harmless, but if the exercise provokes the extra beats than it may indicate higher risk of serious heart rhythm problems.

When looking at an electrocardiograph, premature ventricular contractions are easily spotted and therefore a definitive diagnosis can be made. The QRS and T waves look very different from normal readings. The spacing between the PVC and the preceding QRS wave is a lot shorter than usual and the time between the PVC and the following QRS is a lot longer. However, the time between the preceding and ing QRS waves stays the same as normal due to the compensatory pause.

PVCs can be distinguished from premature atrial contractions because the compensatory pause is longer following premature ventricular contractions.

There are four different named patterns of regularly occurring PVCs. Depending whether there are 1, 2, or 3 normal beats between each PVC, the rhythm is called bigeminy, trigeminy, or quadrigeminy. Unifocal PVCs are triggered from a single site in the ventricle, causing the peaks on the ECG to look the same. Multifocal PVCs arise when more than one site in the ventricles initiate depolarization, causing each peak on the ECG to have a different shape. If 3 or more PVCs occur in a row it may be called ventricular tachycardia.

Ambulatory monitoring of the electrocardiogram (ECG) may be necessary because arrhythmias are transient. The ECG may show any of the following:

- Inappropriate sinus bradycardia

- Sinus arrest

- Sinoatrial block

- Tachy-Brady Syndrome

- Atrial fibrillation with slow ventricular response

- A prolonged asystolic period after a period of tachycardias

- Atrial flutter

- Ectopic atrial tachycardia

- Sinus node reentrant tachycardia

- Wolff-Parkinson-White syndrome

Electrophysiologic tests are no longer used for diagnostic purposes because of their low specificity and sensitivity. Cardioinhibitory and vasodepressor forms of sick sinus syndrome may be revealed by tilt table testing.

Sinoatrial blocks are typically well-tolerated. They are not as serious as an AV block and most often do not require treatment. In some people, they can cause fainting, altered mental status, chest pain, hypoperfusion, and signs of shock. They can also lead to cessation of the SA node and more serious dysrhythmias. Emergency treatment, if deemed necessary, consists of administration of atropine sulfate or transcutaneous pacing.

The treatment for diffuse distal conduction system disease is insertion of a pacemaker. If the PR prolongation is due to AV nodal disease, a case may be made for observation, as it may never progress to complete heart block with life threateningly low heart rates.

Regardless of where in the conduction system the block is, if the block is believed to be the cause of syncope in an individual, a pacemaker is an appropriate treatment.

Third degree AV block can be treated with Cilostazol which acts to increase Ventricular escape rate

Some people with bundle branch blocks are born with this condition. Many other acquire it as a consequence of heart disease. People with bundle branch blocks may still be quite active, and may have nothing more remarkable than an abnormal appearance to their ECG. However, when bundle blocks are complex and diffuse in the bundle systems, or associated with additional and significant ventricular muscle damage, they may be a sign of serious underlying heart disease. In more severe cases, a pacemaker may be required to restore an optimal electrical supply to the heart muscle.

An electrocardiogram can be used to identify a ventricular escape beat. The QRS portion of the electrocardiogram represents the ventricular depolarisation; in normal circumstances the QRS complex forms a sharp sudden peak. For a patient with a ventricular escape beat, the shape of the QRS complex is broader as the impulse can not travel quickly via the normal electrical conduction system.

Ventricular escape beats differ from ventricular extrasystoles (or premature ventricular contractions), which are spontaneous electrical discharges of the ventricles. These are not preceded by a pause; on the contrary they are often followed by a compensatory pause.

Cardiac arrhythmia are often first detected by simple but nonspecific means: auscultation of the heartbeat with a stethoscope, or feeling for peripheral pulses. These cannot usually diagnose specific arrhythmia but can give a general indication of the heart rate and whether it is regular or irregular. Not all the electrical impulses of the heart produce audible or palpable beats; in many cardiac arrhythmias, the premature or abnormal beats do not produce an effective pumping action and are experienced as "skipped" beats.

The simplest "specific" diagnostic test for assessment of heart rhythm is the electrocardiogram (abbreviated ECG or EKG). A Holter monitor is an EKG recorded over a 24-hour period, to detect arrhythmias that may happen briefly and unpredictably throughout the day.

A more advanced study of the heart's electrical activity can be performed to assess the source of the aberrant heart beats. This can be accomplished in an electrophysiology study, an endovascular procedure that uses a catheter to "listen" to the electrical activity from within the heart, additionally if the source of the arrhythmias is found, often the abnormal cells can be ablated and the arrhythmia can be permanently corrected. "" (TAS) instead uses an electrode inserted through the esophagus to a part where the distance to the posterior wall of the left atrium is only approximately 5–6 mm (remaining constant in people of different age and weight). Transesophageal atrial stimulation can differentiate between atrial flutter, AV nodal reentrant tachycardia and orthodromic atrioventricular reentrant tachycardia. It can also evaluate the risk in people with Wolff–Parkinson–White syndrome, as well as terminate supraventricular tachycardia caused by re-entry.

Depending on the anatomical location of the defect which leads to a bundle branch block, the blocks are further classified into:

- Right bundle branch block

- Left bundle branch block

The left bundle branch block can be further sub classified into:

- Left anterior fascicular block. In this case only the anterior half of the left bundle branch (fascicle) is involved

- Left posterior fascicular block. Only the posterior part of the left bundle branch is involved

Other classifications of bundle branch blocks are;

- Bifascicular block. This is a combination of right bundle branch block (RBBB) and either left anterior fascicular block (LAFB) or left posterior fascicular block (LPFB)

- Trifascicular block. This is a combination of right bundle branch block with either left anterior fascicular block or left posterior fascicular block together with a first degree AV block

- Tachycardia-dependent bundle branch block

Subtypes of SVT can usually be distinguished by their electrocardiogram (ECG) characteristics

Most have a narrow QRS complex, although, occasionally, electrical conduction abnormalities may produce a wide QRS complex that may mimic ventricular tachycardia (VT). In the clinical setting, the distinction between narrow and wide complex tachycardia (supraventricular vs. ventricular) is fundamental since they are treated differently. In addition, ventricular tachycardia can quickly degenerate to ventricular fibrillation and death and merits different consideration. In the less common situation in which a wide-complex tachycardia may actually be supraventricular, a number of algorithms have been devised to assist in distinguishing between them. In general, a history of structural heart disease markedly increases the likelihood that the tachycardia is ventricular in origin.

- Sinus tachycardia is physiologic or "appropriate" when a reasonable stimulus, such as the catecholamine surge associated with fright, stress, or physical activity, provokes the tachycardia. It is identical to a normal sinus rhythm except for its faster rate (>100 beats per minute in adults). Sinus tachycardia is considered by most sources to be an SVT.

- Sinoatrial node reentrant tachycardia (SANRT) is caused by a reentry circuit localised to the SA node, resulting in a P-wave of normal shape and size (morphology) that falls before a regular, narrow QRS complex. It cannot be distinguished electrocardiographically from sinus tachycardia unless the sudden onset is observed (or recorded on a continuous monitoring device). It may sometimes be distinguished by its prompt response to vagal maneuvers.

- Ectopic (unifocal) atrial tachycardia arises from an independent focus within the atria, distinguished by a consistent P-wave of abnormal shape and/or size that falls before a narrow, regular QRS complex. It is caused by "automaticity", which means that some cardiac muscle cells, which have the primordial ("primitive, inborn, inherent") ability to generate electrical impulses that is common to all cardiac muscle cells, have established themselves as a 'rhythm center' with a natural rate of electrical discharge that is faster than the normal SA node.

- Multifocal atrial tachycardia (MAT) is tachycardia arising from at least three ectopic foci within the atria, distinguished by P-waves of at least three different morphologies that all fall before irregular, narrow QRS complexes. This rhythm is most commonly seen in elderly people with COPD.

- Atrial fibrillation meets the definition of SVT when associated with a ventricular response greater than 100 beats per minute. It is characterized as an "irregularly irregular rhythm" both in its atrial and ventricular depolarizations and is distinguished by its fibrillatory atrial waves that, at some point in their chaos, stimulate a response from the ventricles in the form of irregular, narrow QRS complexes.

- Atrial flutter, is caused by a re-entry rhythm in the atria, with a regular atrial rate often of about 300 beats per minute. On the ECG this appears as a line of "sawtooth" waves preceding the QRS complex. The AV node will not usually conduct 300 beats per minute so the P:QRS ratio is usually 2:1 or 4:1 pattern, (though rarely 3:1, and sometimes 1:1 where class IC antiarrhythmic drug are in use). Because the ratio of P to QRS is usually consistent, A-flutter is often regular in comparison to its irregular counterpart, atrial fibrillation. Atrial flutter is also not necessarily a tachycardia unless the AV node permits a ventricular response greater than 100 beats per minute.

- AV nodal reentrant tachycardia (AVNRT) involves a reentry circuit forming next to, or within, the AV node. The circuit most often involves two tiny pathways one faster than the other. Because the node is immediately between the atria and ventricle, the re-entry circuit often stimulates both, appearing as a backward (retrograde) conducted P-wave buried within or occurring just "after" the regular, narrow QRS complexes.

- Atrioventricular reciprocating tachycardia (AVRT), also results from a reentry circuit, although one physically much larger than AVNRT. One portion of the circuit is usually the AV node, and the other, an abnormal accessory pathway (muscular connection) from the atria to the ventricle. Wolff-Parkinson-White syndrome is a relatively common abnormality with an accessory pathway, the bundle of Kent crossing the AV valvular ring.

- In orthodromic AVRT, atrial impulses are conducted down through the AV node and retrogradely re-enter the atrium via the accessory pathway. A distinguishing characteristic of orthodromic AVRT can therefore be a P-wave that follows each of its regular, narrow QRS complexes, due to retrograde conduction.

- In antidromic AVRT, atrial impulses are conducted down through the accessory pathway and re-enter the atrium retrogradely via the AV node. Because the accessory pathway initiates conduction in the ventricles outside of the bundle of His, the QRS complex in antidromic AVRT is often wider than usual, with a delta wave.

- Finally, junctional ectopic tachycardia (JET) is a rare tachycardia caused by increased automaticity of the AV node itself initiating frequent heart beats. On the ECG, junctional tachycardia often presents with abnormal morphology P-waves that may fall anywhere in relation to a regular, narrow QRS complex. It is often due to drug toxicity.

The criteria to diagnose a left bundle branch block on the electrocardiogram:

- The heart rhythm must be supraventricular in origin

- The QRS duration must be ≥ 120 ms

- There should be a QS or rS complex in lead V1

- There should be a notched ('M'-shaped) R wave in lead V6.

The T wave should be deflected opposite the terminal deflection of the QRS complex. This is known as appropriate T wave discordance with bundle branch block. A concordant T wave may suggest ischemia or myocardial infarction.

There are also partial blocks of the left bundle branch: "left anterior fascicular block" (LAFB) and a "left posterior fascicular block" (LPFB). This refers to the bifurcation of the left bundle branch.

If an affected individual begins to experience severe TDBBB, then medical intervention is often advised. Suggested therapy for the treatment of TDBBB can include the prescription of certain medications or the implantation of a pacemaker device. Advised medications would possess anti-coagulant mechanisms to reduce the risk of blood clot formation ensuring that no further restriction of arteries would deprive the heart of oxygen and further damage the bundle branches. The use of a pacemaker would ensure that the heart receives a constant rhythmic electrical input that never changes in frequency. While this would effectively eliminate the occurrence of TDBBB, the pacemaker would restrict the patient's heart to a permanent rhythm, eliminating the ability of patients to perform physical activity. Future pacemakers that adaptively respond to physiological requirements are being developed in order to negate the limitations observed with their current use.

Premature atrial contractions are often benign, requiring no treatment. Occasionally, the patient having the PAC will find these symptoms bothersome, in which case the doctor may treat the PACs. Sometimes the PACs can indicate heart disease or an increased risk for other cardiac arrhythmias. In this case the underlying cause is treated. Often a beta blocker will be prescribed for symptomatic PACs.

Treatment in emergency situations ultimately involves electrical pacing. Pharmacological management of suspected beta-blocker overdose might be treated with glucagon, calcium channel blocker overdose treated with calcium chloride and digitalis toxicity treated with the digoxin immune Fab.

Third-degree AV block can be treated by use of a dual-chamber artificial pacemaker. This type of device typically listens for a pulse from the SA node via lead in the right atrium and sends a pulse via a lead to the right ventricle at an appropriate delay, driving both the right and left ventricles. Pacemakers in this role are usually programmed to enforce a minimum heart rate and to record instances of atrial flutter and atrial fibrillation, two common secondary conditions that can accompany third-degree AV block. Since pacemaker correction of third-degree block requires full-time pacing of the ventricles, a potential side effect is pacemaker syndrome, and may necessitate use of a biventricular pacemaker, which has an additional 3rd lead placed in a vein in the left ventricle, providing a more coordinated pacing of both ventricles.

The 2005 Joint European Resuscitation and Resuscitation Council (UK) guidelines state that atropine is the first line treatment especially if there were any adverse signs, namely: 1) heart rate 3 seconds. Mobitz Type 2 AV block is another indication for pacing.

As with other forms of heart block, secondary prevention may also include medicines to control blood pressure and atrial fibrillation, as well as lifestyle and dietary changes to reduce risk factors associated with heart attack and stroke.

Treatment is aimed at slowing the rate by correcting acidosis, correcting electrolytes (especially magnesium and calcium), cooling the patient, and antiarrhythmic medications. Occasionally pacing of the atrium at a rate higher than the JET may allow improved cardiac function by allowing atrial and ventricular synchrony.

A 1994 study at the Adolph Basser Institute of Cardiology found that amiodarone, an antiarrhythmic agent, could be used safely and relatively effectively.

JET occurring after the first six months of life is somewhat more variable, but may still be difficult to control. Treatment of non-post-operative JET is typically with antiarrhythmic medications or a cardiac catheterization with ablation (removal of affected tissue). A cardiac catheterization may be performed to isolate and ablate (burn or freeze) the source of the arrhythmia. This can be curative in the majority of cases. The use of radiofrequency energy is infrequently associated with damage to the normal conduction due to the close proximity to the AV node, the normal conduction tissue. The use of cryotherapy (cold energy) appears to be somewhat safer, and can also be effective for the treatment of JET.

An atrial septal defect is one possible cause of a right bundle branch block. In addition, a right bundle branch block may also result from Brugada syndrome, right ventricular hypertrophy, pulmonary embolism, ischaemic heart disease, rheumatic heart disease, myocarditis, cardiomyopathy or hypertension.

The method of cardiac rhythm management depends firstly on whether or not the affected person is stable or unstable. Treatments may include physical maneuvers, medications, electricity conversion, or electro- or cryo-cautery.

In the United States, people admitted to the hospital with cardiac arrhythmia and conduction disorders with and without complications were admitted to the intensive care unit more than half the time in 2011.

The presence of LBBB results in that electrocardiography (ECG) cannot be used to diagnose left ventricular hypertrophy or Q wave infarction, because LBBB in itself results in widened QRS complex, and changes in the ST-T segment consistent with ischemia or injury.

As an overall medical condition PVCs are normally not very harmful to patients that experience them, but frequent PVCs may put patients at increased risk of developing arrhythmias or cardiomyopathy, which can greatly impact the functioning of the heart over the span of that patient's life. On a more serious and severe scale, frequent PVCs can accompany underlying heart disease and lead to chaotic, dangerous heart rhythms and possibly sudden cardiac death.

Asymptomatic patients that do not have heart disease have long-term prognoses very similar to the general population, but asymptomatic patients that have ejection fractions greater than 40% have a 3.5% incidence of sustained ventricular tachycardia or cardiac arrest. One drawback comes from emerging data that suggests very frequent ventricular ectopy may be associated with cardiomyopathy through a mechanism thought to be similar to that of chronic right ventricular pacing associated cardiomyopathy. Patients that have underlying chronic structural heart disease and complex ectopy, mortality is significantly increased.

In meta-analysis of 11 studies, people with frequent PVC (≥1 time during a standard electrocardiographic recording or ≥30 times over a 1-hour recording) had risk of cardiac death 2 times higher than persons without frequent PVC. Although most studies made attempts to exclude high-risk subjects, such as those with histories of cardiovascular disease, they did not test participants for underlying structural heart disease.

In a study of 239 people with frequent PVCs (>1000 beats/day) and without structural heart disease (i.e. in the presence of normal heart function) there were no serious cardiac events through 5.6 years on average, but there was correlation between PVC prevalence and decrease of ejection fraction and increase of left ventricular diastolic dimension. In this study absence of heart of disease was excluded by echocardiography, cardiac magnetic resonance imaging in 63 persons and Holter monitoring.

Another study has suggested that in the absence of structural heart disease even frequent (> 60/h or 1/min) and complex PVCs are associated with a benign prognosis. It was study of 70 people followed by 6.5 years on average. Healthy status was confirmed by extensive noninvasive cardiologic examination, although cardiac catheterization of a subgroup disclosed serious coronary artery disease in 19%. Overall survival was better than expected.

On the other hand, the Framingham Heart Study reported that PVCs in apparently healthy people were associated with a twofold increase in the risk of all-cause mortality, myocardial infarction and cardiac death. In men with coronary heart disease and in women with or without coronary heart disease, complex or frequent arrhythmias were not associated with an increased risk. The at-risk people might have subclinical coronary disease. These Framingham results have been criticised for the lack of rigorous measures to exclude the potential confounder of underlying heart disease.

In the ARIC study of 14,783 people followed for 15 to 17 years those with detected PVC during 2 minute ECG, and without hypertension or diabetes on the beginning, had risk of stroke increased by 109%. Hypertension or diabetes, both risk factors for stroke, did not change significantly risk of stroke for people with PVC. It is possible that PVCs identified those at risk of stroke with blood pressure and impaired glucose tolerance on a continuum of risk below conventional diagnostic thresholds for hypertension and diabetes. Those in ARIC study with any PVC had risk of heart failure increased by 63% and were >2 times as likely to die due to coronary heart disease (CHD). Risk was also higher for people with or without baseline CHD.

In the Niigata study of 63,386 people with 10-year follow-up period those with PVC during a 10-second recording had risk of atrial fibrillation increased nearly 3 times independently from risk factors: age, male sex, body mass index, hypertension, systolic and diastolic blood pressure, and diabetes.

Reducing frequent PVC (>20%) by antiarrhythmic drugs or by catheter ablation significantly improves heart performance.

Recent studies have shown that those subjects who have an extremely high occurrence of PVCs (several thousand a day) can develop dilated cardiomyopathy. In these cases, if the PVCs are reduced or removed (for example, via ablation therapy) the cardiomyopathy usually regresses.

Also, PVCs can permanently cease without any treatment, in a material percentage of cases.