Treatment for lightheadedness depends on the cause or underlying problem. Treatment may include drinking plenty of water or other fluids (unless the lightheadedness is the result of water intoxication in which case drinking water is quite dangerous). If a sufferer is unable to keep fluids down from nausea or vomiting, they may need intravenous fluid. Sufferers should try eating something sugary and lying down or sitting and reducing the elevation of the head relative to the body (for example, by positioning the head between the knees).

Other simple remedies include avoiding sudden changes in posture when sitting or lying and avoiding bright lights.

Several essential electrolytes are excreted when the body perspires. When people are out in unusual or extreme heat for a long time, sweating excessively can cause a lack of some electrolytes, which in turn can cause lightheadedness.

Lightheadedness can be simply (and most commonly) an indication of a temporary shortage of blood or oxygen to the brain due to a drop in blood pressure, rapid dehydration from vomiting, diarrhea, or fever. Other causes are: low blood sugar, hyperventilation, Postural Orthostatic Tachycardia Syndrome, panic attacks, and anemia. It can also be a symptom of many other conditions, some of them serious, such as heart problems (including abnormal heart rhythm or heart attack), respiratory problems such as pulmonary embolism, and also stroke, bleeding, and shock. If any of these serious disorders is present, the individual will usually have additional symptoms such as chest pain, a feeling of a racing heart, loss of speech or change in vision.

Many people, especially as they age, experience lightheadedness if they arise too quickly from a lying or seated position. Lightheadedness often accompanies the flu, hypoglycaemia, common cold, or allergies.

Dizziness could be provoked by the use of antihistamine drugs, like levocetirizine or by some antibiotics or SSRIs. Nicotine or tobacco products can cause lightheadedness for inexperienced users. Narcotic drugs, such as codeine can also cause lightheadedness.

Brief periods of unconsciousness do no harm and are seldom symptoms of disease.

The main danger of vasovagal syncope (or dizzy spells from vertigo) is the risk of injury by falling while unconscious. Medication therapy could possibly prevent future vasovagal responses; however, for some individuals medication is ineffective and they will continue to have fainting episodes.

Orthostatic hypotension may cause accidental falls. It is also linked to an increased risk of cardiovascular disease, heart failure, and stroke. There is also observational data suggesting that orthostatic hypotension in middle age increases the risk of eventual dementia and reduced cognitive function.

Many conditions cause dizziness because multiple parts of the body are required for maintaining balance including the inner ear, eyes, muscles, skeleton, and the nervous system.

Common physiological causes of dizziness include:

- inadequate blood supply to the brain due to:

- a sudden fall in blood pressure

- heart problems or artery blockages

- loss or distortion of vision or visual cues

- disorders of the inner ear

- distortion of brain/nervous function by medications such as anticonvulsants and sedatives

- result of side effect from prescription drugs, including proton-pump inhibitor drugs (PPIs) and Coumadin (warfarin) causing dizziness/fainting

The medication midodrine can benefit people with orthostatic hypotension, The main side-effect is piloerection ("goose bumps"). Fludrocortisone is also used, although based on more limited evidence.

A number of other measures have slight evidence to support their use indomethacin, fluoxetine, dopamine antagonists, metoclopramide, domperidone, monoamine oxidase inhibitors with tyramine (can produce severe hypertension), oxilofrine, potassium chloride, and yohimbine.

Dizziness is broken down into 4 main subtypes: vertigo (~50%), disequilibrium (less than ~15%), presyncope (less than ~15%) and lightheadedness (~10%).

The tilt table test is an evaluative clinical test to help identify postural hypotension, a common cause of presyncope or syncope. A tilt angle of 60 and 70 degrees is optimal and maintains a high degree of specificity. A positive sign with the tilt table test must be taken in context of patient history, with consideration of pertinent clinical findings before coming to a conclusion.

Presyncope is a state of lightheadedness, muscular weakness, blurred vision, and feeling faint (as opposed to a syncope, which is actually fainting). Presyncope is most often cardiovascular in cause. In many people, lightheadedness is a symptom of orthostatic hypotension. Orthostatic hypotension occurs when blood pressure drops significantly when the patient stands from a supine (horizontal) or seatted position. If loss of consciousness occurs in this situation, it is termed syncope.

Presyncope is frequently reported in people with autonomic dysfunctions such as the postural orthostatic tachycardia syndrome (POTS).

Most patients experience an improvement of their symptoms, but for some, OI can be gravely disabling and can be progressive in nature, particularly if it is caused by an underlying condition which is deteriorating. The ways in which symptoms present themselves vary greatly from patient to patient; as a result, individualized treatment plans are necessary.

OI is treated both pharmacologically and non-pharmacologically. Treatment does not cure OI; rather, it controls symptoms.

Physicians who specialize in treating OI agree that the single most important treatment is drinking more than two liters (eight cups) of fluids each day. A steady, large supply of water or other fluids reduces most, and for some patients all, of the major symptoms of this condition. Typically, patients fare best when they drink a glass of water no less frequently than every two hours during the day, instead of drinking a large quantity of water at a single point in the day.

For most severe cases and some milder cases, a combination of medications are used. Individual responses to different medications vary widely, and a drug which dramatically improves one patient's symptoms may make another patient's symptoms much worse. Medications focus on three main issues:

Medications that increase blood volume:

- Fludrocortisone (Florinef)

- Erythropoietin

- Hormonal contraception

Medications that inhibit acetylcholinesterase:

- Pyridostigmine

Medications that improve vasoconstriction:

- Stimulants: (e.g., Ritalin or Dexedrine)

- Midodrine (ProAmatine)

- Ephedrine and pseudoephedrine (Sudafed)

- Theophylline (low-dose)

- Selective serotonin reuptake inhibitors (SSRI's - Prozac, Zoloft, and Paxil)

Behavioral changes that patients with OI can make are:

- Avoiding triggers such as prolonged sitting, quiet standing, warm environments, or vasodilating medications

- Using postural maneuvers and pressure garments

- Treating co-existing medical conditions

- Increasing fluid and salt intake

- Physical therapy and exercise unless contraindicated by an underlying condition such as chronic fatigue syndrome where traditional exercise can worsen the condition

POTS treatment involves using multiple methods in combination to counteract cardiovascular dysfunction, address symptoms, and simultaneously address any associated disorders. For most patients, water intake should be increased, especially after waking, in order to expand blood volume (reducing hypovolemia). 8–10 cups of water daily are recommended. Increasing salt intake, by adding salt to food, taking salt tablets, or drinking sports drinks and other electrolyte solutions is an effective way to raise blood pressure by helping the body retain water. Different physicians recommend different amounts of sodium to their patients. Salt intake is not appropriate for people with high blood pressure. Combining these techniques with gradual physical training enhances their effect. In some cases, when increasing oral fluids and salt intake is not enough, intravenous saline or the drug desmopressin is used to help increase fluid retention.

Large meals worsen symptoms for some people. These people may benefit from eating small meals frequently throughout the day instead. Alcohol and food high in carbohydrates can also exacerbate symptoms of orthostatic hypotension. Excessive consumption of caffeine beverages should be avoided, because they can promote urine production (leading to fluid loss) and consequently hypovolemia. Exposure to extreme heat may also aggravate symptoms.

Prolonged physical inactivity can worsen the symptoms of POTS. Techniques that increase a person's capacity for exercise, such as endurance training or graded exercise therapy, can relieve symptoms for some patients. Aerobic exercise performed for 20 minutes a day, three times a week, is sometimes recommended for patients who can tolerate it. Exercise may have the immediate effect of worsening tachycardia, especially after a meal or on a hot day. In these cases, it may be easier to exercise in a semi-reclined position, such as riding a recumbent bicycle, rowing or swimming.

When changing to an upright posture, finishing a meal or concluding exercise, a sustained hand grip can briefly raise the blood pressure, possibly reducing symptoms. Compression garments can also be of benefit by constricting blood pressures with external body pressure.

Medium-term (and less well-demonstrated) treatments of hypotension include:

- Blood sugar control (80–150 by one study)

- Early nutrition (by mouth or by tube to prevent ileus)

- Steroid support

If nonpharmacological methods are ineffective, medication may be necessary. As of 2013, no medication has been approved by the U.S. Food and Drug Administration to treat POTS, but a variety are used off-label. Their efficacy has not yet been examined in long-term randomized controlled trials.

Fludrocortisone may be used to enhance sodium retention and blood volume which may be beneficial not only by augmenting sympathetically-mediated vasoconstriction but also because a large subset of POTS patients appear to have low absolute blood volume.

While POTS patients typically have normal or even elevated arterial blood pressure, the neuropathic form of POTS is presumed to constitute a selective sympathetic venous denervation. In these patients the selective Alpha-1 Adrenergic receptor agonist Midodrine may increase venous return, enhance stroke volume and improve symptoms. Midodrine should only be taken during the daylight hours as it may promote supine hypertension.

Ivabradine can successfully restrain heart rate in POTS without affecting blood pressure and approximately 60% of POTS patients treated in an open-label trial of ivabradine experienced symptom improvement.

Pyridostigmine has been reported to restrain heart rate and improve chronic symptoms in about half of patients.

The selective alpha 1 agonist phenylephrine has been used successfully to enhance venous return and stroke volume in some people with POTS. However, this medication may be hampered by poor oral bioavailability.

Treatment for reflex syncope focuses on avoidance of triggers, restoring blood flow to the brain during an impending episode, and measures that interrupt or prevent the pathophysiologic mechanism described above.

The treatment for hypotension depends on its cause. Chronic hypotension rarely exists as more than a symptom. Asymptomatic hypotension in healthy people usually does not require treatment. Adding electrolytes to a diet can relieve symptoms of mild hypotension. A morning dose of caffeine can also be effective. In mild cases, where the patient is still responsive, laying the person in dorsal decubitus (lying on the back) position and lifting the legs increases venous return, thus making more blood available to critical organs in the chest and head. The Trendelenburg position, though used historically, is no longer recommended.

Hypotensive shock treatment always follows the first four following steps. Outcomes, in terms of mortality, are directly linked to the speed that hypotension is corrected. Still-debated methods are in parentheses, as are benchmarks for evaluating progress in correcting hypotension. A study on septic shock provided the delineation of these general principles. However, since it focuses on hypotension due to infection, it is not applicable to all forms of severe hypotension.

1. Volume resuscitation (usually with crystalloid)

2. Blood pressure support with a vasopressor (all seem equivalent with respect to risk of death, with norepinephrine possibly better than dopamine). Trying to achieve a mean arterial pressure (MAP) of greater than 70 mmHg does not appear to result in better outcomes than trying to achieve a MAP of greater than 65 mm Hg in adults.

3. Ensure adequate tissue perfusion (maintain SvO2 >70 with use of blood or dobutamine)

4. Address the underlying problem (i.e., antibiotic for infection, stent or CABG (coronary artery bypass graft surgery) for infarction, steroids for adrenal insufficiency, etc...)

The best way to determine if a person will benefit from fluids is by doing a passive leg raise followed by measuring the output from the heart.

Symptoms of OI are triggered by the following:

- An upright posture for long periods of time (e.g. standing in line, standing in a shower, or even sitting at a desk).

- A warm environment (such as in hot summer weather, a hot crowded room, a hot shower or bath, after exercise).

- Emotionally stressful events (seeing blood or gory scenes, being scared or anxious).

- Astronauts returning from space not yet re-adapted to gravity.

- Extended bedrest

- Inadequate fluid and salt intake.

Increased and regimented aerobic exercise such as running have been shown to have a positive effect in combating panic anxiety. There is evidence that suggests that this effect is correlated to the release of exercise-induced endorphins and the subsequent reduction of the stress hormone cortisol.

There remains a chance of panic symptoms becoming triggered or exacerbated due to increased respiration rate that occurs during aerobic exercise. This increased respiration rate can lead to hyperventilation and hyperventilation syndrome, which mimics symptoms of a heart attack, thus inducing a panic attack. Benefits of incorporating an exercise regimen have shown best results when paced accordingly.

Definitive treatment depends on the underlying cause of vertigo. Ménière's disease patients have a variety of treatment options to consider when receiving treatment for vertigo and tinnitus including: a low-salt diet and intratympanic injections of the antibiotic gentamicin or surgical measures such as a shunt or ablation of the labyrinth in refractory cases.

Common drug treatment options for vertigo may include the following:

- Anticholinergics such as hyoscine hydrobromide (scopolamine)

- Anticonvulsants such as topiramate or valproic acid for vestibular migraines

- Antihistamines such as betahistine, dimenhydrinate, or meclizine, which may have antiemetic properties

- Beta blockers such as metoprolol for vestibular migraine

- Corticosteroids such as methylprednisolone for inflammatory conditions such as vestibular neuritis or dexamethasone as a second-line agent for Ménière's disease

All cases of decompression sickness should be treated initially with 100% oxygen until hyperbaric oxygen therapy (100% oxygen delivered in a high-pressure chamber) can be provided. Several treatments may be necessary, and treatment will generally be repeated until either all symptoms resolve, or no further improvement is apparent.

Caffeine may cause or exacerbate panic anxiety. Anxiety can temporarily increase during withdrawal from caffeine and various other drugs.

Many drugs taken to relieve typical symptoms of motion sickness (including nausea, dizziness, etc.) contain compounds that may exacerbate drowsiness. Antihistamines are commonly used to treat motion sickness; however, side effects include drowsiness and impaired cognitive abilities. Anticholinergics such as scopolamine have also proved effective against motion sickness, but may induce drowsiness. These treatments may be combined with stimulants to counteract typical motion-induced nausea and dizziness while also preventing sedation.

However, many stimulants possess addictive properties, which result in a high potential for substance abuse. Some stimulants also tend to interfere with normal sleep patterns. Modafinil has been studied as a possible treatment for the sopite syndrome that does not appear to have the same side effects of normal stimulants. Modafanil appears to be effective when taken in combination with anticholinergics such as scopolamine, but studies of Modafanil-only treatments for motion sickness remain inconclusive.

For those who are stable with a monomorphic waveform the medications procainamide or sotalol may be used and are better than lidocaine. Evidence does not show that amiodarone is better than procainamide.

As a low magnesium level in the blood is a common cause of VT, magnesium sulfate can be given for torsades de pointes or if a low blood magnesium level is found/suspected.

Long-term anti-arrhythmic therapy may be indicated to prevent recurrence of VT. Beta-blockers and a number of class III anti-arrhythmics are commonly used, such as the beta-blockers carvedilol, metoprolol, and bisoprolol, and the Potassium-Channel-Blockers amiodarone, dronedarone,bretylium, sotalol, ibutilide, and dofetilide. Angiotensin-converting-eynsyme (ACE) inhibitors and aldostrone antatagonists are also sometimes used in this setting.

Arrhythmias due to medications have been reported since the 1920s with the use of quinine. In the 1960s and 1970s problems with antihistamines and antipsychotics were discovered. It was not until the 1980s that the underlying issue, QTc prolongation was determined.

Knowledge that TdP may occur in patients taking certain prescription drugs has been both a major liability and reason for retirement of these medications from the marketplace. Examples of compounds linked to clinical observations of TdP include amiodarone, fluoroquinolones, methadone, lithium, chloroquine, erythromycin, amphetamine, ephedrine, pseudoephedrine, methylphenidate, and phenothiazines. It has also been shown as a side effect of certain anti-arrhythmic medications, such as sotalol, procainamide, and quinidine. The gastrokinetic drug cisapride (Propulsid) was withdrawn from the US market in 2000 after it was linked to deaths caused by long QT syndrome-induced torsades de pointes. In many cases, this effect can be directly linked to QT prolongation mediated predominantly by inhibition of the hERG channel.

In September 2011 (subsequently updated in March 2012 and February 2013), the FDA issued a warning concerning increased incidence of QT prolongation in patients prescribed doses of the antidepressant Celexa (citalopram) above 40 mg per day, considered the maximum allowable dosage, thereby increasing the risk of Torsades. However, a study, "Evaluation of the FDA Warning Against Prescribing Citalopram at Doses Exceeding 40 mg," reported no increased risk of abnormal arrhythmias, thus questioning the validity of the FDA's warning.

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.

There are many classes of antiarrhythmic medications, with different mechanisms of action and many different individual drugs within these classes. Although the goal of drug therapy is to prevent arrhythmia, nearly every anti arrhythmic drug has the potential to act as a pro-arrhythmic, and so must be carefully selected and used under medical supervision.