Digoxin toxicity is often divided into acute or chronic toxicity. In both of these toxicity, cardiac effects are of the greatest concern. With an acute ingestion, symptoms such as nausea, vertigo, and vomiting are prominent. On the other hand, nonspecific symptoms are more predominate in chronic toxicity. These symptoms include fatigue, malaise, and visual disturbances.

The classic features of digoxin toxicity are nausea, vomiting, abdominal pain, headache, dizziness, confusion, delirium, vision disturbance (blurred or yellow vision). It is also associated with cardiac disturbances including irregular heartbeat, ventricular tachycardia, ventricular fibrillation, sinoatrial block and AV block.

In individuals with suspected digoxin toxicity, a serum digoxin concentration, serum potassium concentration, creatinine, BUN, and serial electrocardiograms is obtained.

Most people who have taken too much of a calcium channel blocker, especially diltiazem, get slow heart rate and low blood pressure. This can progress to the heart stopping altogether. CCBs of the dihydropyridine group, as well as flunarizine, predominantly cause reflex tachycardia as a reaction to the low blood pressure. For verapamil, despite it having a similar mechanism of action as diltiazem, both fast and slow heart rhythm are described.

Other potential symptoms include: nausea and vomiting, a decreased level of consciousness, and breathing difficulties. Symptoms usually begin within 6 hours of taking the medication by mouth. With extended release formulations symptoms may not occur for up to a day. Seizures are rare in adults but in children occur more often.

The peripheral autonomic nervous system, central nervous system and the heart are the main systems that are affected following overdose. Initial or mild symptoms typically develop within 2 hours and include tachycardia, drowsiness, a dry mouth, nausea and vomiting, urinary retention, confusion, agitation, and headache. More severe complications include hypotension, cardiac rhythm disturbances, hallucinations, and seizures. Electrocardiogram (ECG) abnormalities are frequent and a wide variety of cardiac dysrhythmias can occur, the most common being sinus tachycardia and intraventricular conduction delay resulting in prolongation of the QRS complex and the PR/QT intervals. Seizures, cardiac dysrhythmias, and apnea are the most important life-threatening complications.

Calcium channel blocker toxicity is the taking of too much of the medications known as calcium channel blockers (CCBs) either by accident or on purpose. This often causes a slow heart rate and low blood pressure. This can progress to the heart stopping altogether. Some CCBs can also cause a fast heart rate as a result of the low blood pressure. Other symptoms may include nausea, vomiting, sleepiness, and shortness of breath. Symptoms usually occur in the first six hours but with some forms of the medication may not start until 24 after hours.

There are a number of treatments that may be useful. These include efforts to reduce absorption of the drug including: activated charcoal taken by mouth if given shortly after the ingestion or whole bowel irrigation if an extended release formula was taken. Efforts to cause vomiting are not recommended. Medications to treat the toxic effects include: intravenous fluids, calcium gluconate, glucagon, high dose insulin, vasopressors and lipid emulsion. Extracorporeal membrane oxygenation may also be an option.

More than ten thousand cases of calcium channel blocker toxicity were reported in the United States in 2010. Along with beta blockers and digoxin calcium channel blockers have one of the highest rates of death in overdose. These medications first became available in the 1970s and 1980s. They are one of the few types of medication in which one pill can result in the death of a child.

Tricyclic antidepressant overdose is poisoning caused by excessive medication of the tricyclic antidepressant (TCA) type. Symptoms may include elevated body temperature, blurred vision, dilated pupils, sleepiness, confusion, seizures, rapid heart rate, and cardiac arrest. If symptoms have not occurred within six hours of exposure they are unlikely to occur.

TCA overdose may occur by accident or purposefully in an attempt to cause death. The toxic dose depends on the specific TCA. Most are non-toxic at less than 5 mg/kg except for desipramine, nortriptyline, and trimipramine which are generally non-toxic at less than 2.5 mg/kg. In small children one or two pills can be fatal. An electrocardiogram (ECG) should be included in the assessment when there is concern of an overdose.

In overdose activated charcoal is often recommended. People should not be forced to vomit. In those who have a wide QRS complex () sodium bicarbonate is recommended. If seizures occur benzodiazepines should be given. In those with low blood pressure intravenous fluids and norepinephrine may be used. The use of intravenous lipid emulsion may also be tried.

In the early 2000s TCAs were one of the most common cause of poisoning. In the United States in 2004 there was more than 12,000 cases. In the United Kingdom they resulted in about 270 deaths a year. An overdose from TCAs was first reported in 1959.

The most common symptom is dizziness or syncope which often occurs during exercise or as a response to emotional stress.

Symptoms reported by patients vary in frequency and severity.

Symptoms associated with IST include:

- Frequent or sustained palpitations

- Dyspnea (shortness of breath) and palpitations on exertion

- Pre-syncope (feeling as if about to faint)

- Fatigue (physical)

- Dizziness

- Exercise intolerance

- Occasional paresthesia and cramping

- Symptoms associated with autonomic nervous system disturbance, including GI disturbance

Hypermagnesemia is an electrolyte disturbance in which there is a high level of magnesium in the blood. It is defined as a level greater than 1.1 mmol/L. Symptoms include weakness, confusion, decreased breathing rate, and cardiac arrest.

Hypermagnesemia can occur in kidney failure and those who are given magnesium salts or who take drugs that contain magnesium (e.g. some antacids and laxatives). It is usually concurrent with other electrolyte disturbances such as a low blood calcium and/or high blood potassium level. Specific electrocardiogram (ECG) changes may be present.

Treatment when levels are very high include calcium chloride, intravenous normal saline with furosemide, and hemodialysis.

Hypermagnesemia occurs rarely because the kidney is very effective in excreting excess magnesium.

Symptoms may include palpitations, feeling faint, sweating, shortness of breath, and chest pain. Episodes start and end suddenly.

CPVT typically start manifesting during the first or second decade of life. The majority of events occur during childhood with more than 60% of affected individuals having their first episode of syncope or cardiac arrest by age 12-20.

For infants, bradycardia is defined as a heart rate less than 100 BPM (normal is around 120–160). Premature babies are more likely than full-term babies to have apnea and bradycardia spells; their cause is not clearly understood. The spells may be related to centers inside the brain that regulate breathing which may not be fully developed. Touching the baby gently or rocking the incubator slightly will almost always get the baby to start breathing again, which increases the heart rate. Medications (theophylline or caffeine) can be used to treat these spells in babies if necessary. Neonatal intensive-care unit (NICU) standard practice is to electronically monitor the heart and lungs for this reason.

Abnormal heart rhythms and asystole are possible complications of hypermagnesemia related to the heart. Magnesium acts as a physiologic calcium blocker, which results in electrical conduction abnormalities within the heart.

Clinical consequences related to serum concentration:

- 4.0 mEq/l decreased reflexes

- >5.0 mEq/l Prolonged atrioventricular conduction

- >10.0 mEq/l Complete heart block

- >13.0 mEq/l Cardiac arrest

Note that the therapeutic range for the prevention of the pre-eclampsic uterine contractions is: 4.0-7.0 mEq/L. As per Lu and Nightingale, serum Mg concentrations associated with maternal toxicity (also neonate depression - hypotonia and low Apgar scores) are:

- 7.0-10.0 mEq/L - loss of patellar reflex

- 10.0-13.0 mEq/L - respiratory depression

- 15.0-25.0 mEq/L - altered atrioventricular conduction and (further) complete heart block

- >25.0 mEq/L - cardiac arrest

Bradycardia in an adult is any heart rate less than (BPM), although symptoms usually manifest only for heart rates less than 50 BPM.

Afterdepolarizations are abnormal depolarizations of cardiac myocytes that interrupt phase 2, phase 3, or phase 4 of the cardiac action potential in the electrical conduction system of the heart. Afterdepolarizations may lead to cardiac arrhythmias.

Cocaine intoxication refers to the immediate and deleterious effects of cocaine on the body. Although cocaine intoxication and cocaine dependence can be present in the same individual, these syndromes present with different symptoms.

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.

Multifocal atrial tachycardia is characterized by an electrocardiogram (ECG) strip with 3 or more P-waves of variable morphology and varying P–R intervals, plus tachycardia, which is a heart rate exceeding 100 beats per minute. Narrow QRS complexes are visible as well.

Inappropriate Sinus Tachycardia (IST) is a rare type of cardiac arrhythmia, within the category of supraventricular tachycardia (SVT). IST may be caused by the sinus node itself having an abnormal structure or function, or it may be part of a problem called dysautonomia, a disturbance and/or failure of the autonomic nervous system. Research into the mechanism and etiology (cause) of Inappropriate Sinus Tachycardia is ongoing.

IST is viewed by most to be a benign condition in the long-term. Symptoms of IST however, may be distracting and warrant treatment. The heart is a strong muscle and typically can sustain the higher-than-normal heart rhythm, though monitoring the condition is generally recommended.

The mechanism and primary etiology of Inappropriate Sinus Tachycardia has not been fully elucidated. An autoimmune mechanism has been suggested as several studies have detected autoantibodies that activate beta adrenoreceptors in a portion of patients. The mechanism of the arrhythmia primarily involves the sinus node and peri-nodal tissue and does not require the AV node for maintenance. Treatments in the form of pharmacological therapy or catheter ablation are available, although it is currently difficult to treat successfully.

While a few seconds may not result in problems longer periods are dangerous. Short periods may occur without symptoms or present with lightheadedness, palpitations, or chest pain. Ventricular tachycardia may result in cardiac arrest and turn into ventricular fibrillation.

Even though many types of sick sinus syndrome produce no symptoms, a person may present with one or more of the following signs and symptoms:

- Stokes-Adams attacks – fainting due to asystole or ventricular fibrillation

- Dizziness or light-headedness

- Palpitations

- Chest pain or angina

- Shortness of breath

- Fatigue

- Headache

- Nausea

Paroxysmal supraventricular tachycardia (PSVT) is a type of supraventricular tachycardia. Often people have no symptoms. Otherwise symptoms may include palpitations, feeling lightheaded, sweating, shortness of breath, and chest pain. Episodes start and end suddenly.

The cause is not known. Risk factors include alcohol, caffeine, nicotine, psychological stress, and Wolff-Parkinson-White syndrome which often is inherited from a person's parents. The underlying mechanism typically involves an accessory pathway that results in re-entry. Diagnosis is typically by an electrocardiogram (ECG) which shows narrow QRS complexes and a fast heart rhythm typically between 150 and 240 beats per minute.

Vagal maneuvers, such as the valsalva maneuver, are often used as the initial treatment. If not effective and the person has a normal blood pressure the medication adenosine may be tried. If adenosine is not effective a calcium channel blockers or beta blocker may be used. Otherwise synchronized cardioversion is the treatment. Future episodes can be prevented by catheter ablation.

About 2.3 per 1000 people have paroxysmal supraventricular tachycardia. Problems typically begin in those 12 to 45 years old. Women are more often affected than men. Outcomes in those who otherwise have a normal heart are generally good. An ultrasound of the heart may be done to rule out underlying heart problems.

Ventricular tachycardia (V-tach or VT) is a type of regular and fast heart rate that arises from improper electrical activity in the ventricles of the heart. Although a few seconds may not result in problems, longer periods are dangerous. Short periods may occur without symptoms or present with lightheadedness, palpitations, or chest pain. Ventricular tachycardia may result in cardiac arrest and turn into ventricular fibrillation. Ventricular tachycardia is found initially in about 7% of people in cardiac arrest.

Ventricular tachycardia can occur due to coronary heart disease, aortic stenosis, cardiomyopathy, electrolyte problems, or a heart attack. Diagnosis is by an electrocardiogram (ECG) showing a rate of greater than 120 bpm and at least three wide QRS complexes in a row. It is classified as non-sustained versus sustained based on whether or not it lasts less than or more than 30 seconds. The term "ventricular tachycardias" refers to the group of irregular heartbeats that includes ventricular tachycardia, ventricular fibrillation, and torsades de pointes.

In those who have a normal blood pressure and strong pulse, the antiarrhythmic medication procainamide may be used. Otherwise immediate cardioversion is recommended. In those in cardiac arrest due to ventricular tachycardia cardiopulmonary resuscitation (CPR) and defibrillation is recommended. Biphasic defibrillation may be better than monophasic. While waiting for a defibrillator, a precordial thump may be attempted in those on a heart monitor who are seen going into an unstable ventricular tachycardia. In those with cardiac arrest due to ventricular tachycardia survival is about 45%. An implantable cardiac defibrillator or medications such as calcium channel blockers or amiodarone may be used to prevent recurrence.

Many people with long QT syndrome have no signs or symptoms.

Some people may experience the following symptoms:

- Fainting (or syncope). This may occur when the patient is emotionally or physically stressed. It is unusual in QT syndrome to have any signs before the person actually faints.

- Seizures

- Sudden death. If there is sudden death, and doctors suspect long QT syndrome as the cause, they may recommend that the family members of the deceased get tested for the disease.

The clinical signs of milk fever can be divided into three distinct stages:

Stage 1: Cows are mobile but show signs of hypersensitivity and excitability such as restlessness, tremors, ear twitching, head bobbing and mild ataxia. If not treated, symptoms usually progress to stage 2.

Stage 2: Cows can no longer stand and present in sternal recumbency. Tachycardia, weakened heart contraction and peripheral pulses. Cows appear dull, have dry muzzles, cold extremities and a lower than normal body temperature. Smooth muscle paralysis can cause bloat, and the inability to urinate or defecate. Cows often tuck their heads into their flanks.

Stage 3: Lateral recumbency, muscle flaccidity, unresponsiveness to stimuli, and loss of consciousness progressing to coma. Heart rate can approach 120 bpm, with peripheral pulses becoming undetectable. If untreated, progression will continue to death.