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.

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.

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

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.

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.

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.

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.

The choice of fluids for resuscitation remains an area of research, the Surviving Sepsis Campaign an international consortium of experts, did not find adequate evidence to support the superiority crystalloid fluids versus colloid fluids. Drugs such as, pyridoxalated hemoglobin polyoxyethylene, which scavenge nitric oxide from the blood have been investigated. As well as methylene blue which may inhibit the nitric oxide-cyclic guanosine monophosphate (NO-cGMP) pathway which has been suggested to play a significant role in distributive shock.

Septic shock is associated with significant mortality and is the leading non cardiac cause of death in intensive care units (ICUs).

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

The best evidence exists for the treatment of septic shock in adults and as the pathophysiology appears similar in children and other types of shock treatment this has been extrapolated to these areas. Management may include securing the airway via intubation if necessary to decrease the work of breathing and for guarding against respiratory arrest. Oxygen supplementation, intravenous fluids, passive leg raising (not Trendelenburg position) should be started and blood transfusions added if blood loss is severe. It is important to keep the person warm as well as adequately manage pain and anxiety as these can increase oxygen consumption.

Aggressive intravenous fluids are recommended in most types of shock (e.g. 1–2 liter normal saline bolus over 10 minutes or 20 ml/kg in a child) which is usually instituted as the person is being further evaluated. Which intravenous fluid is superior, colloids or crystalloids, remains undetermined. Thus as crystalloids are less expensive they are recommended. If the person remains in shock after initial resuscitation packed red blood cells should be administered to keep the hemoglobin greater than 100 g/l.

For those with haemorrhagic shock the current evidence supports limiting the use of fluids for penetrating thorax and abdominal injuries allowing mild hypotension to persist (known as permissive hypotension). Targets include a mean arterial pressure of 60 mmHg, a systolic blood pressure of 70–90 mmHg, or until their adequate mentation and peripheral pulses.

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).

Not required for physiologic sinus tachycardia. Underlying causes are treated if present.

Acute myocardial infarction. Sinus tachycardia can present in more than a third of the patients with AMI but this usually decreases over time. Patients with sustained sinus tachycardia reflects a larger infarct that are more anterior with prominent left ventricular dysfunction, associated with high mortality and morbidity. Tachycardia in the presence of AMI can reduce coronary blood flow and increase myocardial oxygen demand, aggravating the situation. Beta blockers can be used to slow the rate, but most patients are usually already treated with beta blockers as a routine regimen for AMI.

Practically, many studies showed that there is no need for any treatment.

IST and POTS. Beta blockers are useful if the cause is sympathetic overactivity. If the cause is due to decreased vagal activity, it is usually hard to treat and one may consider radiofrequency catheter ablation.

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.

In those that are unstable with a narrow complex tachycardia, intravenous adenosine may be attempted. In all others immediate cardioversion is recommended.

Neurogenic shock can result from severe central nervous system damage (brain injury, cervical or high thoracic spinal cord). In more simple terms: the trauma causes a sudden loss of background sympathetic stimulation to the blood vessels. This causes them to relax (vasodilation) resulting in a sudden decrease in blood pressure (secondary to a decrease in peripheral vascular resistance).

Neurogenic shock results from damage to the spinal cord above the level of the 6th thoracic vertebra. It is found in about half of people who suffer spinal cord injury within the first 24 hours, and usually doesn't go away for one to three weeks.

Some causes of tachycardia include:

- Adrenergic storm

- Alcohol

- Amphetamine

- Anaemia

- Antiarrhythmic agents

- Anxiety

- Atrial fibrillation

- Atrial flutter

- Atrial tachycardia

- AV nodal reentrant tachycardia

- Brugada syndrome

- Caffeine

- Cocaine

- Exercise

- Fear

- Fever

- Hypoglycemia

- Hypovolemia

- Hyperthyroidism

- Hyperventilation

- Infection

- Junctional tachycardia

- Methamphetamine

- Multifocal atrial tachycardia

- Nicotine

- Pacemaker mediated

- Pain

- Pheochromocytoma

- Sinus tachycardia

- Tricyclic antidepressants

- Wolff–Parkinson–White syndrome

While CSWS usually appears within the first week after brain injury and spontaneously resolves in 2–4 weeks, it can sometimes last for months or years. In contrast to the use of fluid restriction to treat SIADH, CSWS is treated by replacing the urinary losses of water and sodium with hydration and sodium replacement. The mineralocorticoid medication fludrocortisone can also improve the low sodium level.

Neurogenic shock is a distributive type of shock resulting in low blood pressure, occasionally with a slowed heart rate, that is attributed to the disruption of the autonomic pathways within the spinal cord. It can occur after damage to the central nervous system such as spinal cord injury. Low blood pressure occurs due to decreased systemic vascular resistance resulting in pooling of blood within the extremities lacking sympathetic tone. The slowed heart rate results from unopposed vagal activity and has been found to be exacerbated by hypoxia and endobronchial suction.

Neurogenic shock can be a potentially devastating complication, leading to organ dysfunction and death if not promptly recognized and treated. It is not to be confused with spinal shock, which is not circulatory in nature.

Sinus tachycardia is usually a response to normal physiological situations, such as exercise and an increased sympathetic tone with increased catecholamine release—stress, fright, flight, anger. Other causes include:

- Pain

- Fever

- Anxiety

- Dehydration

- Malignant hyperthermia

- Hypovolemia with hypotension and shock

- Anemia

- Heart failure

- Hyperthyroidism

- Mercury poisoning

- Kawasaki disease

- Pheochromocytoma

- Sepsis

- Pulmonary embolism

- Acute coronary ischemia and myocardial infarction

- Chronic obstructive pulmonary disease

- Hypoxia

- Intake of stimulants such as caffeine, theophylline, nicotine, cocaine, or amphetamines

- Hyperdynamic circulation

- Electric shock

- Drug withdrawal

- Porphyria

- Acute inflammatory demyelinating polyradiculoneuropathy

- Postural orthostatic tachycardia syndrome

Untreated individuals with DβH deficiency should avoid hot environments, strenuous exercise, standing still, and dehydration.

Pharmacological methods of treatment include fludrocortisone, midodrine, somatostatin, erythropoietin, and other vasopressor agents. However, often a patient with pure autonomic failure can mitigate his or her symptoms with far less costly means. Compressing the legs and lower body, through crossing the legs, squatting, or the use of compression stockings can help. Also, ingesting more water than usual can increase blood pressure and relieve some symptoms.

Since the conversion of dihydroxyphenylserine (Droxidopa; trade name: Northera; also known as L-DOPS, L-threo-dihydroxyphenylserine, L-threo-DOPS and SM-5688), to norepinephrine bypasses the dopamine beta-hydroxylation step of catecholamine synthesis, L-Threo-DOPS is the ideal therapeutic agent. In humans with DβH deficiency, L-Threo-DOPS, a synthetic precursor of noradrenaline, administration has proven effective in dramatic increase of blood pressure and subsequent relief of postural symptoms.

L-DOPS continues to be studied pharmacologically and pharmacokinetically and shows an ability to increase the levels of central nervous system norepinephrine by a significant amount. This is despite the fact that L-DOPS has a relative difficulty crossing the blood-brain barrier when compared to other medications such as L-DOPA. When used concurrently, there is evidence to show that there is increased efficacy as they are both intimately involved and connected to the pathway in becoming norepinephrine.

There is hope and evidence that L-DOPS can be used much more widely to help other conditions or symptoms such as pain, chronic stroke symptoms, and progressive supranuclear palsy, amongst others. Clinically, L-DOPS has been already shown to be helpful in treating a variety of other conditions related to hypotension including the following:

- Diabetes induced orthostatic hypotension

- Dialysis-induced hypotension

- Orthostatic intolerance

- Familial amyloidotic polyneuropathy

- Spinal Cord Injury related hypotension

Empirical evidence of mild effectiveness has been reported using mineralocorticoids or adrenergic receptor agonists as therapies.

Other medications that can bring relief to symptoms include:

- phenylpropanolamine- due to pressor response to vascular α-adrenoceptors

- indomethacin

Vitamin C (ascorbic acid) is also a required cofactor for the Dopamine beta hydroxylase enzyme. Recent research has shown that vitamin C rapidly catalyzes the conversion of dopamine to norepinephrine through stimulation of the dopamine beta hydroxylase enzyme.

IST has been treated both pharmacologically and invasively, with varying degrees of success. IST, in and of itself, is not indicative of higher rates of mortality, and non-treatment is an option chosen by many if they have minimal symptoms.

Some types of medication tried by cardiologists and other physicians include: beta blockers, selective sinus node I channel inhibitors (ivabradine), calcium channel blockers and antiarrhythmic agents. Some SSRI drugs are also occasionally tried and also treatments more commonly used to treat postural orthostatic tachycardia syndrome such as fludrocortisone. This approach is very much "trial-and-error". Patients with IST are often intolerant to beta blockers. A new selective sinus node inhibitor ivabradine is also being used to treat IST.

Invasive treatments include forms of catheter ablation such as sinus node modification (selective ablation of the sinus node), complete sinus node ablation (with associated implantation of a permanent artificial pacemaker) and AV node ablation in very resistant cases (creation of iatrogenic complete heart block, necessitating implantation of a permanent artificial pacemaker).

However invasive treatments can also make the symptoms worse, not cure it. Treatment should be chosen with care as the patient could become in need of a pacemaker or have more extensive symptoms.