Clinically, it is often asymptomatic by itself and considered benign in nature.

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.

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.

Ashman phenomenon, also known as Ashman beats, describes a particular type of wide QRS complex, often seen isolated that is typically seen in atrial fibrillation. It is more often misinterpreted as a premature ventricular complex.

It is named for Richard Ashman (of New Orleans) (1890 –1969), after first being described by Gouaux and Ashman in 1947.

Management of multifocal atrial tachycardia consists mainly of the treatment of the underlying cause, but if clinically judged necessary, the rate may in some cases be reduced by administering the calcium channel blocker verapamil or the beta blocker metoprolol.

Administration of oxygen may play a role in the treatment of some patients.

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.

Therapy may be directed either at terminating an episode of the abnormal heart rhythm or at reducing the risk of another VT episode. The treatment for stable VT is tailored to the specific person, with regard to how well the individual tolerates episodes of ventricular tachycardia, how frequently episodes occur, their comorbidities, and their wishes. Individuals suffering from pulseless VT or unstable VT are hemodynamically compromised and require immediate electric cardioversion to shock them out of the VT rhythm.

MAT usually arises because of an underlying medical condition. Its prevalence has been estimated at about 3 per 1000 in adult hospital inpatients and is much rarer in paediatric practice; it is more common in the elderly, and its management and prognosis are both those of the underlying diagnosis.

It is mostly common in patients with lung disorders, but it can occur after acute myocardial infarction and can also occur in the setting of low blood potassium or low blood magnesium.

It is sometimes associated with digitalis toxicity in patients with heart disease.

It is most commonly associated with hypoxia and COPD. Additionally, it can be caused by theophylline toxicity, a drug with a narrow therapeutic index commonly used to treat COPD. Theophylline can cause a number of different abnormal heart rhythms when in excess, and thus further predisposes COPD patients to MAT. Theophylline toxicity often occurs following acute or chronic overtreatment or factors lowering its clearance from the body.

AV nodal reentrant tachycardia (AVNRT) is the most common reentrant tachycardia. It is a regular narrow complex tachycardia that usually responds well to the Valsalva maneuver or the drug adenosine. However, unstable patients sometimes require synchronized cardioversion. Definitive care may include catheter ablation.

AV reentrant tachycardia (AVRT) requires an accessory pathway for its maintenance. AVRT may involve orthodromic conduction (where the impulse travels down the AV node to the ventricles and back up to the atria through the accessory pathway) or antidromic conduction (which the impulse travels down the accessory pathway and back up to the atria through the AV node). Orthodromic conduction usually results in a narrow complex tachycardia, and antidromic conduction usually results in a wide complex tachycardia that often mimics ventricular tachycardia. Most antiarrhythmics are contraindicated in the emergency treatment of AVRT, because they may paradoxically increase conduction across the accessory pathway.

Coronary arteriovenous fistula between coronary artery and another cardiac chamber, like, the coronary sinus, right atrium, or right ventricle may cause steal syndrome under conditions like myocardial infarction and possible angina or ventricular arrhythmias, if the shunt is large in magnitude.

It can also be associated with new patterns of blood vessel growth.

It is usually seen when a physician performs ophthalmoscopy, during which a plaque will appear bright, refractile, and yellow. It is caused by an embolus lodged within the retinal vessel that originated from an atheromatous plaque in a more proximal (upstream) vessel, usually the internal carotid artery. It is often an indication of a previous ischemic episode in the eye and is a sign of severe atherosclerosis. The most important step in management is to identify and treat the originating plaque to prevent further embolization.

It is associated with dipyridamole. Hence, dipyridamole is a pharmacological success diagnostically, but a therapeutic failure because of the coronary steal phenomenon.

Coronary steal is also the mechanism in most drug-based cardiac stress tests; When a patient is incapable of doing physical activity they are given a vasodilator that produces a "cardiac steal syndrome" as a diagnostic procedure. The test result is positive if the patient's symptoms reappear or if ECG alterations are seen.

It is also associated with the administration of Isoflurane, which is an inhaled anesthetic. Hydralazine can potentially cause this condition as well, as it is a direct arteriolar vasodilator.

It has been associated with nitroprusside.

The Lazarus phenomenon raises ethical issues for physicians, who must determine when medical death has occurred, resuscitation efforts should end, and postmortem procedures such as autopsies and organ harvesting may take place.

Medical literature has recommended observation of a patient's vital signs for five to ten minutes after cessation of resuscitation before certifying death.

The phenomenon is named after the American ophthalmologist Dr. Robert Hollenhorst (1913–2008) who first described their significance in 1961. N

The microscopic examination of tissue (histology) gives the definitive diagnosis. The diagnostic histopathologic finding is intravascular cholesterol crystals, which are seen as cholesterol clefts in routinely processed tissue (embedded in paraffin wax). The cholesterol crystals may be associated with macrophages, including giant cells, and eosinophils.

The sensitivity of small core biopsies is modest, due to sampling error, as the process is often patchy. Affected organs show the characteristic histologic changes in 50-75% of the clinically diagnosed cases. Non-specific tissue findings suggestive of a cholesterol embolization include ischemic changes, necrosis and unstable-appearing complex atherosclerotic plaques (that are cholesterol-laden and have a thin fibrous cap). While biopsy findings may not be diagnostic, they have significant value, as they help exclude alternate diagnoses, e.g. vasculitis, that often cannot be made confidently based on clinical criteria.

Lazarus syndrome, (the Lazarus heart) also known as autoresuscitation after failed cardiopulmonary resuscitation, is the spontaneous return of circulation after failed attempts at resuscitation. Its occurrence has been noted in medical literature at least 38 times since 1982. It takes its name from Lazarus who, as described in the New Testament of The Bible, was raised from the dead by Jesus.

Occurrences of the syndrome are extremely rare and the causes are not well understood. One hypothesis for the phenomenon is that a chief factor (though not the only one) is the buildup of pressure in the chest as a result of cardiopulmonary resuscitation (CPR). The relaxation of pressure after resuscitation efforts have ended is thought to allow the heart to expand, triggering the heart's electrical impulses and restarting the heartbeat. Other possible factors are hyperkalemia or high doses of epinephrine.

In studies, white coat hypertension can be defined as the presence of a defined hypertensive average blood pressure in a clinic setting, although it isn't present when the patient is at home.

Diagnosis is made difficult as a result of the unreliable measures taken from the conventional methods of detection. These methods often involve an interface with health care professionals and frequently results are tarnished by a list of factors including variability in the individual’s blood pressure, technical inaccuracies, anxiety of the patient, recent ingestion of pressor substances, and talking, amongst many other factors. The most common measure of blood pressure is taken from a noninvasive instrument called a sphygmomanometer. "A survey showed that 96% of primary care physicians habitually use a cuff size too small," adding to the difficulty in making an informed diagnosis. For such reasons, white coat hypertension cannot be diagnosed with a standard clinical visit. It can be reduced (but not eliminated) with automated blood pressure measurements over 15 to 20 minutes in a quiet part of the office or clinic.

Patients with white coat hypertension do not exhibit the signs indicative of trepidation and their increased blood pressure is often not accompanied by tachycardia. This is supported by studies that repeatedly indicate that 15%–30% of those thought to have mild hypertension as a result of clinic or office recordings display normal blood pressure and no unusual response to pressure stimulus. These persons did not show any specific characteristics such as age that may be indicative of a higher susceptibility to white coat hypertension.

Ambulatory blood pressure monitoring and patient self-measurement using a home blood pressure monitoring device is being increasingly used to differentiate those with white coat hypertension or experiencing the white coat effect from those with chronic hypertension. This does not mean that these methods are without fault. Daytime ambulatory values, despite taking into account stresses of everyday life when taken during the patient's daily routine, are still susceptible to the effects of daily variables such as physical activity, stress and duration of sleep. Ambulatory monitoring has been found to be the more practical and reliable method in detecting patients with white coat hypertension and for the prediction of target organ damage. Even as such, the diagnosis and treatment of white coat hypertension remains controversial.

Recent studies showed that home blood pressure monitoring is as accurate as a 24-hour ambulatory monitoring in determining blood pressure levels. Researchers at the University of Turku, Finland studied 98 patients with untreated hypertension. They compared patients using a home blood pressure device and those wearing a 24-hour ambulatory monitor. Researcher Dr. Niiranen said that "home blood pressure measurement can be used effectively for guiding anti-hypertensive treatment". Dr. Stergiou added that home tracking of blood pressure "is more convenient and also less costly than ambulatory monitoring."

Use of breathing patterns has been proposed as a technique for identifying white coat hypertension.

In one Turkish study of 438 consecutive patients, 38% were normotensive, 43% had white coat hypertension, 2% had masked hypertension, and 15% had sustained hypertension. Even patients taking medication for sustained hypertension who are normotensive at home may exhibit white coat hypertension in the office setting.

Treatment of an episode of cholesterol emboli is generally symptomatic, i.e. it deals with the symptoms and complications but cannot reverse the phenomenon itself. In kidney failure resulting from cholesterol crystal emboli, statins (medication that reduces cholesterol levels) have been shown to halve the risk of requiring hemodialysis.

Before root canal treatment or extraction are carried out, the clinician should have thorough knowledge about the root canal morphology to avoid complications.

It is important to distinguish Raynaud's "disease" (primary Raynaud's) from "phenomenon" (secondary Raynaud's). Looking for signs of arthritis or vasculitis as well as a number of laboratory tests may separate them. If suspected to be secondary to systemic sclerosis, one tool which may help aid in the prediction of systemic sclerosis is thermography.

A careful medical history will often reveal whether the condition is primary or secondary. Once this has been established, an examination is largely to identify or exclude possible secondary causes.

- Digital artery pressure: pressures are measured in the arteries of the fingers before and after the hands have been cooled. A decrease of at least 15 mmHg is diagnostic (positive).

- Doppler ultrasound: to assess blood flow.

- Full blood count: this may reveal a normocytic anaemia suggesting the anaemia of chronic disease or renal failure.

- Blood test for urea and electrolytes: this may reveal renal impairment.

- Thyroid function tests: this may reveal hypothyroidism.

- An autoantibody screen, tests for rheumatoid factor, Erythrocyte sedimentation rate, and C-reactive protein, which may reveal specific causative illnesses or a generalised inflammatory process.

- Nail fold vasculature: this can be examined under the microscope.

To aid in the diagnosis of Raynaud's phenomenon, multiple sets of diagnostic criteria have been proposed. Table 1 below provides a summary of these various diagnostic criteria.

Recently, International Consensus Criteria were developed for the diagnosis of primary Raynaud's phenomenon by a panel of multiple experts in the fields of rheumatology and dermatology.

Lucio's phenomenon is treated by anti-leprosy therapy (dapsone, rifampin, and clofazimine), optimal wound care, and treatment for bacteremia including antibiotics. In severe cases exchange transfusion may be helpful.

Secondary Raynaud's is managed primarily by treating the underlying cause and as primary Raynaud's, avoiding triggers, such as cold, emotional and environmental stress, vibrations and repetitive motions, and avoiding smoking (including passive smoking) and sympathomimetic drugs.

Mees' lines appear after an episode of poisoning with arsenic, thallium or other heavy metals, and can also appear if the subject is suffering from renal failure. They have been observed in chemotherapy patients.

CREST is not easily diagnosed as it closely mimics symptoms of other connective tissue and autoimmune diseases. Diagnoses are usually given when a patient presents three or more of the five major clinical symptoms. Additionally, blood exams can be given to test for a positive ANAs and ACAs or skin biopsies can be given to help confirm a diagnosis.