The behavioral symptoms are similar to those of an amphetamine, cocaine or caffeine overdose. Overstimulation of the central nervous system results in a state of hyperkinetic movement and unpredictable mental status including mania, rage and suicidal behavior.

Physical symptoms are more serious and include heart arrhythmias as well as outright heart attack or stroke in people who are at risk of coronary disease. Breathing is rapid and shallow while both pulse and blood pressure are dangerously elevated.

An adrenergic storm is a sudden and dramatic increase in serum levels of the catecholamines adrenalin and noradrenalin (also known as epinephrine and norepinephrine respectively), with a less significant increase in dopamine transmission. It is a life-threatening condition because of extreme tachycardia and hypertension, and is especially dire for those with prior heart problems. If treatment is prompt, prognosis is good; typically large amounts of diazepam or other benzodiazepines are administered alongside beta blockers. Beta blockers are contraindicated in some patients, so other anti-hypertensive medication such as clonidine may be used. It is usually caused by overdose of stimulants, especially cocaine or methamphetamine, or eating foods high in tyramine while taking monoamine oxidase inhibitors. A subarachnoid hemorrhage can also cause an adrenergic storm. A catecholamine storm is part of the normal course of Rabies infection, and is responsible for the severe feelings of agitation, terror, and dysautonomia present in the pre-coma stage of the disease.

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.

Characteristics of paroxysmal sympathetic hyperactivity include:

- fever

- tachycardia

- hypertension

- tachypnea

- hyperhidrosis or diaphoresis

- dystonic posturing

- pupillary dilation

- flushing

In cases where PSH episodes develop post-injury, specifically traumatic brain injury, symptoms typically develop quickly, usually within a week. Symptom onset has been seen to average 5.9 days post-injury. Episodes vary in duration and occurrence. Episodes can last as little as a few minutes or as long as ten hours, and they can occur multiple times a day. Episode duration has been seen to average 30.8 minutes and occur five to six times a day. Episodes can occur naturally or arise from external triggers. Common triggers include pain or stimulation, body turning or movements, and bladder distention. Bladder distention has been observed in patients being treated in intensive care units with the concurrent use of catheters. Symptoms of PSH can last from weeks to years following initial onset. As episodes persist over time, they have been found to become less frequent in occurrence but last for prolonged periods.

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.

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.

Paroxysmal sympathetic hyperactivity (PSH) is a syndrome that causes episodes of increased activity of the sympathetic nervous system. Hyperactivity of the sympathetic nervous system can manifest as increased heart rate, increased respiration, increased blood pressure, diaphoresis, and hyperthermia.

Previously, this syndrome has been identified as general dysautonomia but now is considered a specific form of it. It has also been referred to as paroxysmal sympathetic instability with dystonia, or PAID, and sympathetic storm. Recently, however, studies have adopted the name paroxysmal sympathetic hyperactivity to ensure specificity. PSH is observed more in younger patients than older ones. It is also seen more commonly in men than women. There is no known reason why this is the case, although it is suspected pathophysiological links may exist. In patients surviving traumatic brain injury, the occurrence of these episodes is one in every three. PSH can also be associated with severe anoxia, subarachnoid and intracerebral hemorrhage, and hydrocephalus.

Orthostatic hypotension is characterised by symptoms that occur after standing (from lying or sitting), particularly when this is done rapidly. Many report lightheadedness (a feeling that one might be about to faint), sometimes severe. Generalized weakness or tiredness may also occur. Some also report difficulty concentrating, blurred vision, tremulousness, vertigo, anxiety, palpitations (awareness of the heartbeat), feeling sweaty or clammy, and sometimes nausea. A person may look pale.

Cocaine increases alertness, feelings of well-being, euphoria, energy, competence, sociability, and sexuality. Common side effects include anxiety, increased temperature, paranoia, restlessness, and teeth grinding. With prolonged use, the drug can cause insomnia, anorexia, tachycardia, hallucinations, and paranoid delusions. Possible lethal side effects include rapid heartbeat, abnormal heart rhythms, tremors, convulsions, markedly increased core temperature, renal failure, heart attack, stroke and heart failure.

Depression with suicidal ideation may develop in heavy users. Finally, a loss of vesicular monoamine transporters, neurofilament proteins, and other morphological changes appear to indicate a long-term damage to dopamine neurons. Chronic intranasal usage can degrade the cartilage separating the nostrils (the septum nasi), which can eventually lead to its complete disappearance.

Studies have shown that cocaine usage during pregnancy triggers premature labor and may lead to abruptio placentae.

Dopamine beta (β)-hydroxylase deficiency is a condition that affects the autonomic nervous system (ANS). The ANS works via two opposing branches, the sympathetic and parasympathetic, both of which antagonistically control involuntary processes that regulate bodily homeostasis. Problems related to DβH deficiency often first appear as complications shortly after birth. Postnatal episodes may include vomiting, dehydration, hypotension, muscle hypotonia, hypothermia, and hypoglycemia.

Due to the deficiency of norepinephrine and epinephrine those affected by dopamine β-hydroxylase deficiency may present with droopy eyelids (ptosis), nasal congestion, and hypotension. The most common complaint of individuals with dopamine β-hydroxylase deficiency is orthostatic hypotension. The symptoms associated with orthostatic hypotension are dizziness, blurred vision, or fainting upon standing. Therefore, DβH deficiency patients may have an inability to stand for a prolonged period of time. This phenomenon is especially pronounced when going from supine to upright positions, such as getting out of bed in the morning. It is also worsened by extreme climates due to loss of fluid through excessive sweating. The inability to maintain normal blood pressure makes it difficult for people with DβH deficiency to exercise (exercise intolerance). Males with DβH deficiency may experience retrograde ejaculation, a discharge of semen backward into the bladder due to dysmotility of their smooth muscle, which as innervated by the ANS. A subset of DβH deficiency patients present with hypermobility. Postural orthostatic tachycardia syndrome, another form of dysautonomia, also sees this comorbidity with hypermobility in the form of a rare connective tissue disorder called Ehlers Danlos syndrome.

Another commonly experienced symptom is hypoglycemia, which is thought to be caused by adrenomedullary failure. In looking at the cardiovascular system, a loss of noradrenergic control is seen as T-wave abnormalities on electrocardiogram. Prolactin is frequently suppressed by excessive dopamine found in the patient's central nervous system. Excess dopamine can also affect digestion, producing vomiting and inhibiting motor signaling to the GI tract.

Orthostatic hypotension, also known as postural hypotension, occurs when a person's blood pressure falls when suddenly standing up from a lying or sitting position. It is defined as a fall in systolic blood pressure of at least 20 mm Hg or diastolic blood pressure of at least 10 mm Hg when a person assumes a standing position. It occurs predominantly by delayed constriction of the lower body blood vessels, which is normally required to maintain an adequate blood pressure when changing position to standing. As a result, blood pools in the blood vessels of the legs for a longer period and less is returned to the heart, thereby leading to a reduced cardiac output. Mild orthostatic hypotension is common and can occur briefly in anyone, although it is prevalent in particular among the elderly and those with known low blood pressure. Severe drops in blood pressure can lead to fainting, with a possibility of injury.

There are numerous possible causes for orthostatic hypotension, such as certain medications (e.g. alpha blockers), autonomic neuropathy, decreased blood volume, and age-related blood vessel stiffness.

Apart from addressing the underlying cause, orthostatic hypotension may be treated with a recommendation to increase salt and water intake (to increase the blood volume), wearing compression stockings, and sometimes medication (fludrocortisone, midodrine or others).

The symptoms include many of the symptoms associated with milder degrees of hypoglycemia, especially the adrenergic symptoms, but do not progress to objective impairment of brain function, seizures, coma, or brain damage.

- Shakiness

- Sense of weakness

- Altered or depressed mood

- Confusion

- Fatigue

- Anxiety

- Paleness

- Perspiration

- Increased pulse or respiratory rate

- Hunger

Thyroid storm is characterized by an acute onset of symptoms of hyperthyroidism (fast heart rate, restlessness, agitation) accompanied by other features such as fever (temperatures often above 40 °C/104 °F), mental status changes, diarrhea, and vomiting.

Individuals can exhibit varying signs of organ dysfunction. Patients may experience liver dysfunction, and yellow discoloration of the skin is considered a poor prognostic sign. Heart (cardiac) symptoms include abnormal heart rhythms, decreased blood flow to the heart and heart attacks, and congestive heart failure, which may lead to cardiovascular collapse. Mortality can be as high as 20-30%.

In some situations, individuals may not experience the classic signs of restlessness and agitation, but instead present with apathetic signs of weakness and confusion.

Dopamine beta (β)-hydroxylase deficiency (DβH deficiency) is a condition involving inadequate Dopamine beta-hydroxylase. It is characterized by increased amounts of serum dopamine and the absence of norepinephrine (NE) and epinephrine. Dopamine is released, as a false neurotransmitter, in place of norepinephrine. Other names for norepinephrine include noradrenaline (NA) and noradrenalin. This condition is also sometimes referred to as "norepinephrine deficiency". Researchers of disorders such as depression, schizophrenia, and migraines are very interested in studying this disorder, as patients with these specific diseases generally have a threefold increase in the amount of dopamine in their system and yet are generally normal. This is in contrast to patients with DβH deficiency.

Dopamine beta-hydroxylase deficiency is a very rare form of dysautonomia. It belongs to the class of rare diseases, with "a prevalence of fewer than 20 affected individuals, all of Western European descent", as described in the scientific literature. It is an caused by a mutation in the DβH gene, which results in the production of a nonfunctional dopamine β-hydroxylase enzyme. Without this enzyme, the patients with DβH deficiency end up having a large number of clinical manifestations which greatly affect their daily lives.

Idiopathic postprandial syndrome, colloquially but incorrectly known by some as hypoglycemia, describes a collection of clinical signs and symptoms similar to medical hypoglycemia but without the demonstrably low blood glucose levels which characterise said condition.

People with this condition suffer from recurrent episodes of altered mood and cognitive efficiency, often accompanied by weakness and adrenergic symptoms such as shakiness. The episodes typically occur a few hours after a meal, rather than after many hours of fasting. The principal treatments recommended are extra small meals or snacks and avoidance of excessive simple sugars.

The signs and symptoms of a pheochromocytoma are those of sympathetic nervous system hyperactivity, including:

- Skin sensations

- Flank pain

- Elevated heart rate

- Elevated blood pressure, including paroxysmal (sporadic, episodic) high blood pressure, which sometimes can be more difficult to detect; another clue to the presence of pheochromocytoma is orthostatic hypotension (a fall in systolic blood pressure greater than 20 mmHg or a fall in diastolic blood pressure greater than 10 mmHg upon standing)

- Palpitations

- Anxiety often resembling that of a panic attack

- Diaphoresis (excessive sweating)

- Headaches – most common symptom

- Pallor

- Weight loss

- Localized amyloid deposits found microscopically

- Elevated blood glucose level (due primarily to catecholamine stimulation of lipolysis (breakdown of stored fat) leading to high levels of free fatty acids and the subsequent inhibition of glucose uptake by muscle cells. Further, stimulation of beta-adrenergic receptors leads to glycogenolysis and gluconeogenesis and thus elevation of blood glucose levels).

A pheochromocytoma can also cause resistant arterial hypertension. A pheochromocytoma can be fatal if it causes a hypertensive emergency, that is, severely high blood pressure that impairs one or more organ systems (formerly called "malignant hypertension"). This hypertension is not well controlled with standard blood pressure medications.

Not all patients experience all of the signs and symptoms listed. The most common presentation is headache, excessive sweating, and increased heart rate, with the attack subsiding in less than one hour.

Tumors may grow large, but most are smaller than .

Thyroid storm or thyrotoxic crisis is a rare but severe and potentially life-threatening complication of hyperthyroidism (overactivity of the thyroid gland). It is characterized by a high fever (temperatures often above 40 °C/104 °F), fast and often irregular heart beat, vomiting, diarrhea, and agitation. Heart failure and heart attack may occur. Death may occur despite treatment. Most episodes occur either in those with known hyperthyroidism whose treatment has been stopped or become ineffective, or in those with untreated mild hyperthyroidism who have developed an intercurrent illness (such as an infection).

The primary treatment of thyroid storm is with organic iodine and antithyroid drugs (propylthiouracil or methimazole) to reduce synthesis and release of thyroid hormone. Temperature control and intravenous fluids are also mainstays of management. Beta blockers are often used to reduce the effects of thyroid hormone. Patients often require admission to the intensive care unit.

Tachyphylaxis is characterized by the rate sensitivity: the response of the system depends on the rate with which a stimulus is presented. To be specific, a high-intensity prolonged stimulus or often-repeated stimulus may bring about a diminished response also known as desensitization.

Because of the ubiquity of arsenic in ground water supplies and its effect on cardiovascular health, low dose arsenic poisoning should be inferred as a part of the pathogenesis of idiopathic hypertension. Idiopathic and essential are both somewhat synonymous with primary hypertension. Arsenic exposure has also many of the same signs of primary hypertension such as headache, somnolence,

confusion, proteinuria

visual disturbances, and nausea and vomiting

Tachyphylaxis (Greek ταχύς, "tachys", "rapid", and φύλαξις, "phylaxis", "protection") is a medical term describing an acute, sudden decrease in response to a drug after its administration, i.e. a rapid and short-term onset of drug tolerance. It can occur after an initial dose or after a series of small doses. Increasing the dose of the drug may be able to restore the original response.

The upper threshold of a normal human resting heart rate is based on age. Cutoff values for tachycardia in different age groups are fairly well standardized; typical cutoffs are listed below:

- 1–2 days: Tachycardia > 159 beats per minute (bpm)

- 3–6 days: Tachycardia >166 bpm

- 1–3 weeks: Tachycardia >182 bpm

- 1–2 months: Tachycardia >179 bpm

- 3–5 months: Tachycardia >186 bpm

- 6–11 months: Tachycardia >169 bpm

- 1–2 years: Tachycardia >151 bpm

- 3–4 years: Tachycardia >137 bpm

- 5–7 years: Tachycardia >133 bpm

- 8–11 years: Tachycardia >130 bpm

- 12–15 years: Tachycardia >119 bpm

- >15 years – adult: Tachycardia >100 bpm

Heart rate is considered in the context of the prevailing clinical picture. For example: in sepsis >90 bpm is considered tachycardia.

When the heart beats excessively or rapidly, the heart pumps less efficiently and provides less blood flow to the rest of the body, including the heart itself. The increased heart rate also leads to increased work and oxygen demand by the heart, which can lead to rate related ischemia.

Relative tachycardia involves a greater increase in rate than would be expected in a given illness state.

Junctional tachycardia is an automatic tachycardia originating in the AV junction. It tends to be a regular, narrow complex tachycardia and may be a sign of digitalis toxicity.

Another common and under-recognized sign of hypertension is sleep apnea, which is often best treated with nocturnal nasal continuous positive airway pressure (CPAP), but other approaches include the Mandibular advancement splint (MAS), UPPP, tonsillectomy, adenoidectomy, septoplasty, or weight loss.

Another cause is an exceptionally rare neurological disease called Binswanger's disease, causing dementia; it is a rare form of multi-infarct dementia, and is one of the neurological syndromes associated with hypertension.

Hypertensive encephalopathy is most commonly encountered in young and middle-aged people who have hypertension. Overall, the condition is rare even among people with hypertension. Studies report that from 0.5 to 15% of people with malignant hypertension develop hypertensive encephalopathy. With the development of methods for detection and treatment of hypertension, hypertensive encephalopathy has been becoming more rare.

Symptoms of hypertensive encephalopathy typically start to occur 12–48 hours after a sudden and sustained increase in blood pressure. The first manifestation of these symptoms is a severe headache. Headache occurs in greater than 75% of patients. The patient becomes restless. Alterations in consciousness may follow several hours later, which include impaired judgement and memory, confusion, somnolence and stupor. If the condition is not treated, these neurological symptoms may worsen and ultimately turn into a coma. Other symptoms may include increased irritability, vomiting, diplopia, seizures, twitching and myoclonus of the limbs. Alterations in vision (vision blurring, hemivisual field defects, color blindness, cortical blindness) are common. They occur in 4 out of 11 cases (Jellinek et al. 1964). Hemiparesis, intracerebral hemorrhage, aphasia may also occur, but they are less common.

The differential diagnoses of pheochromocytoma include:

- Anxiety disorders, including Benzodiazepine withdrawal syndrome

- Paragangliomas

- Von Hippel–Lindau Disease

- Essential hypertension

- Hyperthyroidism

- Insulinoma

- Mercury poisoning

- Paroxysmal supraventricular tachycardia

- Renovascular hypertension

- Carcinoid