Affected patients demonstrate no structural problems of the heart upon echocardiographic, CT or MRI imaging.

CPVT diagnosis is based on reproducing irregularly shaped ventricular arrhythmias during ECG exercise stress testing, syncope occurring during physical activity and acute emotion, and a history of exercise or emotion-related palpitations and dizziness with an absence of structural cardiac abnormalities.

Because its symptoms are usually only triggered when the body is subjected to intense emotional or physical stress, the condition is often not detected by the traditional methods of electrophysiologic examination such as a resting electrocardiogram.

The absence of a pulse confirms a clinical diagnosis of cardiac arrest, but PEA can only be distinguished from other causes of cardiac arrest with a device capable of electrocardiography (ECG/EKG). In PEA, there is organised or semi-organised electrical activity in the heart as opposed to asystole (flatline)or to the disorganised electrical activity of either ventricular fibrillation or ventricular tachycardia.

ARVD is an autosomal dominant trait with reduced penetrance. Approximately 40–50% of ARVD patients have a mutation identified in one of several genes encoding components of the desmosome, which can help confirm a diagnosis of ARVD. Since ARVD is an autosomal dominant trait, children of an ARVD patient have a 50% chance of inheriting the disease causing mutation. Whenever a mutation is identified by genetic testing, family-specific genetic testing can be used to differentiate between relatives who are at-risk for the disease and those who are not. ARVD genetic testing is clinically available.

In recent reports, left cardiac sympathetic denervation and bilateral thoracoscopic sympathectomy have shown promising results in individuals whose symptoms cannot be controlled by beta blockers.

Canadian genetic testing guidelines and recommendations for individuals diagnosed with HCM are as follows:

- The main purpose of genetic testing is for screening family members.

- According to the results, at-risk relatives may be encouraged to undergo extensive testing.

- Genetic testing is not meant for confirming a diagnosis.

- If the diagnosed individual has no relatives that are at risk, then genetic testing is not required.

- Genetic testing is not intended for risk assessment or treatment decisions.

- Evidence only supports clinical testing in predicting the progression and risk of developing complications of HCM.

For individuals "suspected" of having HCM:

- Genetic testing is not recommended for determining other causes of left ventricular hypertrophy (such as "athlete's heart", hypertension, and cardiac amyloidosis).

- HCM may be differentiated from other hypertrophy-causing conditions using clinical history and clinical testing.

Genetic testing for Brugada syndrome is clinically available and may help confirm a diagnosis, as well as differentiate between relatives who are at risk for the disease and those who are not. Some symptoms when pinpointing this disease include fainting, irregular heartbeats, and chaotic heartbeats. However, just detecting the irregular heartbeat may be a sign of another disease, so the doctor must detect another symptom as well.

In general, the minimal evaluation of atrial fibrillation should be performed in all individuals with AF. The goal of this evaluation is to determine the general treatment regimen for the individual. If results of the general evaluation warrant it, further studies may then be performed.

Limited studies have suggested that screening for atrial fibrillation in those 65 years and older increases the number of cases of atrial fibrillation detected.

There are no specific diagnostic criteria for TIC, and it can be difficult to diagnose for a number of reasons. First, in patients presenting with both tachycardia and cardiomyopathy, it can be difficult to distinguish which is the causative agent. Additionally, it can occur in patients with or without underlying structural heart disease. Previously normal left ventricular ejection fraction or left ventricular systolic dysfunction out of proportion to a patient’s underlying cardiac disease can be important clues to possible TIC. The diagnosis of TIC is made after excluding other causes of cardiomyopathy and observing resolution of the left ventricular systolic dysfunction with treatment of the tachycardia.

Specific tests that can be used in the diagnosis and monitoring of TIC include:

- electrocardiography (EKG)

- Continuous cardiac rhythm monitoring (e.g. Holter monitor)

- echocardiography

- Radionuclide imaging

- Endomyocardial biopsy

- Cardiac magnetic resonance imaging (CMR)

- N-terminal pro-B-type natriuretic peptide (NT-pro BNP)

Cardiac rhythm monitors can be used to diagnose tachyarrhythmias. The most common modality used is an EKG. A continuous rhythm monitor such as a Holter monitor can be used to characterize the frequency of a tachyarrhythmia over a longer period of time. Additionally, some patients may not present to the clinical setting in an abnormal rhythm, and continuous rhythm monitor can be useful to determine if an arrhythmia is present over a longer duration of time.

To assess cardiac structure and function, echocardiography is the most commonly available and utilized modality. In addition to decreased left ventricular ejection fraction, studies indicate that patients with TIC may have a smaller left ventricular end-diastolic dimension compared to patients with idiopathic dilated cardiomyopathy. Radionuclide imaging can be used as a non-invasive test to detect myocardial ischemia. Cardiac MRI has also been used to evaluate patients with possible TIC. Late-gadolinium enhancement on cardiac MRI indicates the presence of fibrosis and scarring, and may be evidence of cardiomyopathy not due to tachycardia. A decline in serial NT-pro BNP with control of tachyarrhythmia indicates reversibility of the cardiomyopathy, which would also suggest TIC.

People with TIC display distinct changes in endomyocardial biopsies. TIC is associated with the infiltration of CD68 macrophages into the myocardium while CD3 T-cells are very rare. Furthermore, patients with TIC display significant fibrosis due to collagen deposition. The distribution of mitochondria has found to be altered as well, with an enrichment at the intercalated discs (EMID-sign).

TIC is likely underdiagnosed due to attribution of the tachyarrhythmia to the cardiomyopathy. Poor control of the tachyarrhythmia can result in worsening of heart failure symptoms and cardiomyopathy. Therefore, it is important to aggressively treat the tachyarrhythmia and monitor patients for resolution of left ventricular systolic dysfunction in cases of suspected TIC.

If the symptoms are present while the person is receiving medical care (e.g., in an emergency department), an electrocardiogram (ECG/EKG) may show typical changes that confirm the diagnosis. If the palpitations are recurrent, a doctor may request a Holter monitor (24-hour or longer portable ECG) recording. Again, this will show the diagnosis if the recorder is attached at the time of the symptoms. In rare cases, disabling but infrequent episodes of palpitations may require the insertion of a small microchip-based device (e.g., Reveal Plus) under the skin that continuously record heart activity, and can be read through the skin after an episode. All these ECG-based technologies also enable the distinction between AVNRT and other abnormal fast heart rhythms such as atrial fibrillation, atrial flutter, sinus tachycardia, ventricular tachycardia and tachyarrhythmias related to Wolff-Parkinson-White syndrome, all of which may have symptoms that are similar to AVNRT.

Blood tests commonly performed in people with palpitations are:

- thyroid function tests (TFTs) - an overactive thyroid increases the risk of AVNRT

- electrolytes - disturbances in potassium, calcium and magnesium may predispose to AVNRT

- cardiac markers - if there is a concern that myocardial infarction (heart attack) has occurred either as a cause or as a result of the AVNRT; this is usually only the case if the patient has experienced chest pain

A recent study by Salcido et al. (2010) ascertained rearrest in all initial and rearrest rhythms treated by any level of Emergency Medical Service (EMS), finding a rearrest rate of 36% and a lower but not significantly different rate of survival to hospital discharge in cases with rearrest compared to those without rearrest.

All first degree family members of the affected individual should be screened for ARVD. This is used to establish the pattern of inheritance. Screening should begin during the teenage years unless otherwise indicated. Screening tests include:

- Echocardiogram

- EKG

- Signal averaged EKG

- Holter monitoring

- Cardiac MRI

- Exercise stress test

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.

Current research seeks to predict the event of rearrest after patients have already achieved ROSC. Biosignals, such as electrocardiogram (ECG), have the potential to predict the onset of rearrest and are currently being investigated to preemptively warn health care providers that rearrest could be imminent.

A stronger pulse detector would also contribute to lowering the rate of rearrest. If the resuscitator could accurately know when the patient has achieved ROSC, there would be less instances of chest compressions being provided when a native pulse is present.

In some cases, the disease can be detected by observing characteristic patterns on an electrocardiogram. These patterns may be present all the time, they might be elicited by the administration of particular drugs (e.g., Class IA, such as ajmaline or procainamide, or class 1C, such as flecainide or pilsicainide, antiarrhythmic drugs that block sodium channels and cause appearance of ECG abnormalities), or they might resurface spontaneously due to as-yet unclarified triggers.

Brugada syndrome has three different ECG patterns:

- Type 1 has a coved type ST elevation with at least 2 mm (0.2 mV) J-point elevation and a gradually descending ST segment followed by a negative T-wave.

- Type 2 has a saddle-back pattern with a least 2 mm J-point elevation and at least 1 mm ST elevation with a positive or biphasic T-wave. Type 2 pattern can occasionally be seen in healthy subjects.

- Type 3 has either a coved (type 1 like) or a saddle-back (type 2 like) pattern, with less than 2 mm J-point elevation and less than 1 mm ST elevation. Type 3 pattern is not rare in healthy subjects.

The pattern seen on the ECG is persistent ST elevations in the electrocardiographic leads V-V with a right bundle branch block (RBBB) appearance, with or without the terminal S waves in the lateral leads that are associated with a typical RBBB. A prolongation of the PR interval (a conduction disturbance in the heart) is also frequently seen. The ECG can fluctuate over time, depending on the autonomic balance and the administration of antiarrhythmic drugs. Adrenergic stimulation decreases the ST segment elevation, while vagal stimulation worsens it. (There is a case report of a patient who died while shaving, presumed due to the vagal stimulation of the carotid sinus massage.)

The administration of class Ia, Ic, and III drugs increases the ST segment elevation, as does fever. Exercise decreases ST segment elevation in some people, but increases it in others (after exercise, when the body temperature has risen). The changes in heart rate induced by atrial pacing are accompanied by changes in the degree of ST segment elevation. When the heart rate decreases, the ST segment elevation increases, and when the heart rate increases, the ST segment elevation decreases. However, the contrary can also be observed.

Studies have shown that patients with Pacemaker syndrome and/or with sick sinus syndrome are at higher risk of developing fatal complications that calls for the patients to be carefully monitored in the ICU. Complications include atrial fibrillation, thrombo-embolic events, and heart failure.

The diagnosis of ventricular tachycardia is made based on the rhythm seen on either a 12-lead ECG or a telemetry rhythm strip. It may be very difficult to differentiate between ventricular tachycardia and a wide-complex supraventricular tachycardia in some cases. In particular, supraventricular tachycardias with aberrant conduction from a pre-existing bundle branch block are commonly misdiagnosed as ventricular tachycardia. Other rarer phenomena include ashman beats and antedromic atrioventricular re-entry tachycardias.

Various diagnostic criteria have been developed to determine whether a wide complex tachycardia is ventricular tachycardia or a more benign rhythm. In addition to these diagnostic criteria, if the individual has a past history of a myocardial infarction, congestive heart failure, or recent angina, the wide complex tachycardia is much more likely to be ventricular tachycardia.

The proper diagnosis is important, as the misdiagnosis of supraventricular tachycardia when ventricular tachycardia is present is associated with worse prognosis. This is particularly true if calcium channel blockers, such as verapamil, are used to attempt to terminate a presumed supraventricular tachycardia. Therefore, it is wisest to assume that all wide complex tachycardia is VT until proven otherwise.

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.

At the time of pacemaker implantation, AV synchrony should be optimized to prevent the occurrence of pacemaker syndrome. Where patients with optimized AV synchrony have shown great results of implantation and very low incidence of pacemaker syndrome than those with suboptimal AV synchronization.

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.

Myofibre break-up, abbreviated MFB, is associated with ventricular fibrillation leading to death. Histomorphologically, MFB is characterized by fractures of the cardiac myofibres perpendicular to their long axis, with squaring of the myofibre nuclei.

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.

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.

The ECG tracing in torsades demonstrates a "polymorphic ventricular tachycardia" with a characteristic illusion of a twisting of the QRS complex around the isoelectric baseline (peaks, which are at first pointing up, appear to be pointing down for subsequent "beats" when looking at ECG traces of the "heartbeat"). It is hemodynamically unstable and causes a sudden drop in arterial blood pressure, leading to dizziness and fainting. Depending on their cause, most individual episodes of torsades de pointes revert to normal sinus rhythm within a few seconds; however, episodes may also persist and possibly degenerate into ventricular fibrillation, leading to sudden death in the absence of prompt medical intervention. Torsades de pointes is associated with long QT syndrome, a condition whereby prolonged QT intervals are visible on an ECG. Long QT intervals predispose the patient to an , wherein the R-wave, representing ventricular depolarization, occurs during the relative refractory period at the end of repolarization (represented by the latter half of the T-wave). An R-on-T can initiate torsades. Sometimes, pathologic T-U waves may be seen in the ECG before the initiation of torsades.

A "short-coupled variant of torsade de pointes", which presents without long QT syndrome, was also described in 1994 as having the following characteristics:

- Drastic rotation of the heart's electrical axis

- Prolonged QT interval (LQTS) - may not be present in the short-coupled variant of torsade de pointes

- Preceded by long and short RR-intervals - not present in the short-coupled variant of torsade de pointes

- Triggered by a premature ventricular contraction (R-on-T PVC)

There can be similar patterns depending on the frequency of abnormal beats. If every other beat is abnormal, it is described as bigeminal. If every third beat is aberrant, it is trigeminal; every fourth would be quadrigeminal. Typically, if every fifth or more beat is abnormal, the aberrant beat would be termed occasional.

Bigeminy is contrasted with couplets, which are paired abnormal beats. Groups of three abnormal beats are called triplets and are considered as a brief run of non-sustained ventricular tachycardia (NSVT) and if the grouping last for more than 30 seconds, it is ventricular tachycardia (VT).