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.

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.

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.

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

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.

The medical literature suggests a number of treatments that have been proven effective for specific cases of needle phobia, but provides very little guidance to predict which treatment may be effective for any specific case. The following are some of the treatments that have been shown to be effective in some specific cases.

- Ethyl Chloride Spray (and other freezing agents). Easily administered, but provides only superficial pain control.

- Jet Injectors. Jet Injectors work by introducing substances into the body through a jet of high pressure gas as opposed to by a needle. Though these eliminate the needle, some people report that they cause more pain. Also, they are only helpful in a very limited number of situations involving needles i.e. insulin and some inoculations.

- Iontophoresis. Iontophoresis drives anesthetic through the skin by using an electric current. It provides effective anesthesia, but is generally unavailable to consumers on the commercial market and some regard it as inconvenient to use.

- EMLA. EMLA is a topical anesthetic cream that is a eutectic mixture of lidocaine and prilocaine. It is a prescription cream in the United States, and is available without prescription in some other countries. Although not as effective as iontophoresis, since EMLA does not penetrate as deeply as iontophoresis-driven anesthetics, EMLA provides a simpler application than iontophoresis. EMLA penetrates much more deeply than ordinary topical anesthetics, and it works adequately for many individuals.

- Ametop. Ametop gel appears to be more effective than EMLA for eliminating pain during venepuncture.

- Lidocaine/tetracaine patch. A self-heating patch containing a eutectic mixture of lidocaine and tetracaine is available in several countries, and has been specifically approved by government agencies for use in needle procedures. The patch is sold under the trade name "Synera" in the United States and "Rapydan" in European Union. Each patch is packaged in an air-tight pouch. It begins to heat up slightly when the patch is removed from the packaging and exposed to the air. The patch requires 20 to 30 minutes to achieve full anesthetic effect. The Synera patch was approved by the United States Food and Drug Administration on 23 June 2005.

- Behavioral therapy. Effectiveness of this varies greatly depending on the person and the severity of the condition. There is some debate as to the effectiveness of behavioral treatments for specific phobias (like blood, injection, injury type phobias), though some data are available to support the efficacy of approaches like exposure therapy. Any therapy that endorses relaxation methods may be contraindicated for the treatment of fear of needles as this approach encourages a drop in blood pressure that only enhances the vasovagal reflex. In response to this, graded exposure approaches can include a coping component relying on applied tension as a way to prevent complications associated with the vasovagal response to specific blood, injury, injection type stimulus.

- Nitrous Oxide (Laughing Gas). This will provide sedation and reduce anxiety for the patient, along with some mild analgesic effects.

- Inhalation General Anesthesia. This will eliminate all pain and also all memory of any needle procedure. On the other hand, it is often regarded as a very extreme solution. It is not covered by insurance in most cases, and most physicians will not order it. It can be risky and expensive and may require a hospital stay.

- Benzodiazepines, such as diazepam (Valium) or lorazepam, may help alleviate the anxiety of needle phobics, according to Dr. James Hamilton. These medications have an onset of action within 5 to 15 minutes from ingestion. A relatively large oral dose may be necessary.

The neurotransmitter acetylcholine is known to decrease sympathetic response by slowing the heart rate and constricting the smooth muscle tissue. Ongoing research and successful clinical trials have shown that agents such as diphenhydramine, atropine and Ipratropium bromide (all of which act as receptor antagonists of muscarinic acetylcholine receptors) are effective for treating asthma and COPD-related symptoms .

Following a declination or total extinction in response to a previously therapeutic dose of an antidepressant, the issue is clinically addressed as stemming from tolerance development. Several strategies are available, such as exploring drug options from a different drug class used to treat depression. The patient can also choose to switch to another SSRI (or MAOI, if applicable) while maintaining proportionate dose. If tolerance develops in a drug from the same class, the clinician may recommend a regular cycle consisting of all effective treatments within the SSRI or MAOI classes, in order to minimize transitional side effects while maximizing therapeutic efficacy.

Other options include increasing dose of the same medication, or supplementation with another antidepressant. Dual reuptake inhibitors, also known as tricyclic antidepressants have been shown to have lower rates of tachyphylaxis.

Beta2-adrenergic agonists are recommended for bronchospasm.

- Short acting (SABA)

- Terbutaline

- Salbutamol

- Levosalbutamol

- Long acting (LABA)

- Formoterol

- Salmeterol

- Others

- Dopamine

- Norepinephrine

- Epinephrine

Among the choices for vasopressors, norepinephrine is superior to dopamine in septic shock. Norepinephrine is the preferred vasopressor, while epinephrine may be added to norepinephrine when needed. Low-dose vasopressin also may be used as an addition to norepinephrine, but is not recommended as a first-line treatment. Dopamine may cause rapid heart rate and arrhythmias, and is only recommended in combination with norepinephrine in those with slow heart rate and low risk of arrhythmia. In the initial treatment of low blood pressure in septic shock, the goal of vasopressor treatment is a mean arterial pressure (MAP) of 65 mm Hg. In 2017, the FDA approved angiotensin II injection for intravenous infusion to increase blood pressure in adults with septic or other distributive shock.

Treatment guidelines call for the administration of broad-spectrum antibiotics within the first hour following recognition of septic shock. Prompt antimicrobial therapy is important, as risk of dying increases by approximately 10% for every hour of delay in receiving antibiotics. Time constraints do not allow the culture, identification, and testing for antibiotic sensitivity of the specific microorganism responsible for the infection. Therefore, combination antimicrobial therapy, which covers a wide range of potential causative organisms, is tied to better outcomes.

Numerous compounds alleviate the pain from allodynia. Some are specific for certain types of allodynia while others are general. They include:

- Dynamic mechanical allodynia - compounds targeting different ion channels; opioids

- Mexiletine

- Lidocaine (IV/topical)

- Tramadol

- Morphine (IV)

- Alfentanil (IV)

- Ketamine (IV)

- Methylprednisone (intrathecal)

- Adenosine

- Glycine antagonist

- Desipramine

- Venlafaxine

- Lyrica

- Static mechanical allodynia - sodium channel blockers, opioids

- Lidocaine (IV)

- Alfentanil (IV)

- Adenosine (IV)

- Ketamine (IV)

- Glycine antagonist

- Venlafaxine

- Gabapentin (may also be helpful in cold and dynamic allodynias)

- Cold allodynia

- Lamotrigine

- Lidocaine (IV)

The list of compounds that can be used to treat allodynia is even longer than this. For example, many non-steroidal anti-inflammatory drugs, such as naproxen, can inhibit COX-1 and/or COX-2, thus preventing the sensitization of the central nervous system. Another effect of naproxen is the reduction of the responsiveness of mechano- and thermoreceptors to stimuli.

Other compounds act on molecules important for the transmission of an action potential from one neuron to another. Examples of these include interfering with receptors for neurotransmitters or the enzymes that remove neurotransmitters not bound to receptors.

Endocannabinoids are molecules that can relieve pain by modulating nociceptive neurons. When anandamide, an endocannabinoid, is released, pain sensation is reduced. Anandamide is later transported back to the neurons releasing it using transporter enzymes on the plasma membrane, eventually disinhibiting pain perception. However, this re-uptake can be blocked by AM404, elongating the duration of pain inhibition.

Fear of needles, especially in its more severe forms, is often comorbid with other phobias and psychological ailments; for example, iatrophobia, or an irrational fear of doctors, is often seen in needle phobic patients.

A needle phobic patient does not need to physically be in a doctor's office to experience panic attacks or anxiety brought on by needle phobia. There are many triggers in the outside world that can bring on an attack through association. Some of these are blood, injuries, the sight of the needle physically or on a screen, paper pins, examination rooms, hospitals, white lab coats, hospital gowns, doctors, dentists, nurses, the antiseptic smell associated with offices and hospitals, the sight of a person who physically resembles the patient's regular health care provider, or even reading about the fear.

Patients are typically sent to therapy for BII phobia in order to receive therapeutic treatments to calm their levels of anxiety and stress. Therapists use a combination of psychological and physical measures, such as applying muscle tension, in order to help the patient to be aware that there is certainly a needle in front of them.

A popular method of treatment for BII phobics is Cognitive-Behavior Therapy (CBT), which is a technique that allows the patient to become immune to their fear by being exposed to it. For BII phobics, patients are given pictures of needles or blood, they are also asked to draw pictures of these needles and speak about it. Afterwards, they are given an actual needle, and the goal is: by that point, that the patient is to be comfortable enough with their fear of needles and blood.

Some patients may refuse professional help for their phobia. Instead, a different type of treatment solely revolves around motivation and whether or not the patient is willing to undergo through treating their phobia with self-help. Similar to CBT, patients treat themselves by completing exercises to become immune to their fear. This requires no professional assistance and merely relies on the person.

Research on hypnotherapy has been looked upon to treat patients with BII phobia. Hypnotherapists are known for using relaxing therapies towards individuals with common anxiety issues. A form of therapy given to patients with BII phobia include the “Applied Tension” method, which was developed by Lars-Göran Öst and his colleagues at the University of Uppsala in Sweden. This “coping method involves creating tension on a person’s arms, legs, and chest until they start to feel their body temperature rising,” (Robertson) which usually occurs within 10 to 20 seconds. These sessions of muscle tension is repeated 5 times with 20 to 30 second breaks. Patients should complete this form of therapy over the course of 5 weeks. This helps to prevent the patient from fainting by applying tension to the body, the blood pressure steadily rises, preventing any sudden drop until their vaccination is complete. By using this treatment, there was a noticeable improvement by 90% of patients with BII phobia. Compared to patients that only used the relaxation methods, where only 60% showed noticeable improvement.

Along with muscle tension,there are several methods of physical maneuvers that can help with the treatment of BII phobia. Therapists suggest that while being injected, patients should perform movements, such as: leg crossing, muscle tensing, and holding in the breath. Patients are instructed by their therapist to perform these maneuvers simultaneously while being injected with a needle. It’s also recommended that the patient stays seated with their head lowered while performing these movements.

ADT tachyphylaxis specifically occurs in depressed patients using SSRIs and MAOIs. Currently, SSRIs are the preferred treatment for depression among clinicians, as MAOIs require the patient to avoid certain foods and other medications due to the potential for interactions capable of inducing dangerous side effects. Provided is a list of medications known to be subject to Poop-out.

Hyperalgesia is similar to other sorts of pain associated with nerve irritation or damage such as allodynia and neuropathic pain, and consequently may respond to standard treatment for these conditions, using various drugs such as SSRI or tricyclic antidepressants, Nonsteroidal anti-inflammatory drugs (NSAIDs), glucocorticoids, gabapentin or pregabalin, NMDA antagonists, or atypical opioids such as tramadol. Where hyperalgesia has been produced by chronic high doses of opioids, reducing the dose may result in improved pain management. However, as with other forms of nerve dysfunction associated pain, treatment of hyperalgesia can be clinically challenging, and finding a suitable drug or drug combination that is effective for a particular patient may require trial and error. The use of a transcutaneous electrical nerve stimulation device has been shown to alleviate hyperalgesia.

Postpartum chills is a physiological response that occurs within two hours of childbirth. It appears as uncontrollable shivering that is not under voluntary control. It is seen in many women after delivery and can be unpleasant. It lasts for a short time. It is thought to be a result of a nervous system response. It may also be related to fluid shifts and the actual strenuous work of labor. It is considered a normal response and there is no accompanying fever. If a fever does develop further assessments may reveal the presence of an infection. Treatment consists of an explanation from clinicians that the shivering is a normal response and that it only lasts for a short time. Warm blankets are given to the women and fluid replacement is encouraged. It has been described as a fairly common and normal occurrence.

After discharge to home with the baby, chills that accompany uncontrolled bleeding, shortness of breath, cold clammy skin, dizziness, heart pain, and racing heart can be a sign of shock that needs immediate medical attention. Mastitis can also cause shivering.

In a patient fully withdrawn from opioids, going back to an intermittent schedule or maintenance dosing protocol, a fraction of the old tolerance level will rapidly develop, usually starting two days after therapy is resumed and, in general, leveling off after day 7. Whether this is caused directly by opioid receptors modified in the past or affecting a change in some metabolic set-point is unclear. Increasing the dose will usually restore efficacy; relatively rapid opioid rotation may also be of use if the increase in tolerance continues.

The treatment of coronary artery ectasia is normally done in conjunction with therapies of other heart disorders such as atherosclerosis and hypertension. To prevent the formation of blood clots and the blockage of the vessels, patients are commonly placed on anticoagulant therapy (e.g. warfarin, and aspirin), as well as anti-spasm therapy of calcium channel blockers. Coronary artery ectasia also responds to statins and ACE inhibitors.

Use of intranasal decongestants (such as oxymetazoline) for more than three days leads to tachyphylaxis of response and rebound congestion, caused by alpha-adrenoceptor mediated down-regulation and desensitization of response. Oxymetazoline-induced tachyphylaxis and rebound congestion are reversed by intranasal fluticasone.

This disorder may resolve itself with time or may develop into a more severe disorder such as PTSD. However, results of Creamer, O'Donnell, and Pattison's (2004) study of 363 patients suggests that a diagnosis of acute stress disorder had only limited predictive validity for PTSD. Creamer et al. did find that re-experiences of the traumatic event and arousal were better predictors of PTSD. Early pharmacotherapy may prevent the development of posttraumtic symptoms.

Studies have been conducted to assess the efficacy of counselling and psychotherapy for people with ASD. Cognitive behavioral therapy which included exposure and cognitive restructuring was found to be effective in preventing PTSD in patients diagnosed with ASD with clinically significant results at 6 months follow-up. A combination of relaxation, cognitive restructuring, imaginal exposure, and in vivo exposure was superior to supportive counseling. Mindfulness based stress reduction programs also appear to be effective for stress management.

In a wilderness context where counseling, psychotherapy, and cognitive behavioral therapy is unlikely to be available, the treatment for acute stress reaction is very similar for the treatment of cardiogenic shock, vascular shock, and hypovolemic shock; that is, allowing the patient to lie down, providing reassurance, and removing the stimulus for the occurrence of the reaction. In traditional shock cases, this is generally the relieving of pain from injuries or the stopping of blood loss. In an acute stress reaction, this may be pulling a rescuer away from the emergency to calm down, or blocking the sight of an injured friend from a patient.

Exercise hypertension is an excessive rise in blood pressure during exercise. Many of those with exercise hypertension have spikes in systolic pressure to 250 mmHg or greater.

A rise in systolic blood pressure to over 200 mmHg when exercising at 100 W is pathological and a rise in pressure over 220 mmHg needs to be controlled by the appropriate drugs.

Similarly, in healthy individuals the response of the diastolic pressure to 'dynamic' exercise (e.g. walking, running or jogging) of moderate intensity is to remain constant or to fall slightly (due to the improved blood flow), but in some individuals a rise of 10 mmHg or greater is found.

Recent work at Johns Hopkins involving a group of athletes aged 55 to 75 with mild hypertension has found a correlation of those with exercise hypertension to a reduced ability of the major blood vessels to change in size in response to increased blood flow (probably due to impaired function of the endothelial cells in the vessel walls). This is to be differentiated from stiffness of the blood-vessel walls, which was not found to be correlated with the effect.

The standard approach to treatment is the same as with other phobias - cognitive-behavioral therapy, desensitization, and possibly medications to help with the anxiety and discomfort. In recent years, the technique known as "applied tension", applying tension to the muscles in an effort to increase blood pressure, has increasingly gained favor as an often effective treatment for blood phobia associated with drops in blood pressure and fainting.

Because the fear of blood is extremely common, it is frequently exploited in popular culture. Horror movies and Halloween events prey on our natural aversion to blood, often featuring large quantities of fake blood.

In theory, avoidance is simply a matter of preventing hyperinsulinemia. In practice, the difficulty for a diabetic person to aggressively dose insulin to keep blood sugars levels close to normal and at the same time constantly adjust the insulin regimen to the dynamic demands of exercise, stress, and wellness can practically assure occasional hyperinsulinemia. The pharmacokinetic imperfections of all insulin replacement regimens is a severe limitation.

Some practical behaviors which are useful in avoiding chronic Somogyi rebound are:

- frequent blood glucose monitoring (8–10 times daily);

- continuous blood glucose monitoring;

- logging and review of blood glucose values, searching for patterns of low blood sugar values;

- conservative increases in insulin delivery;

- awareness to the signs of hypoglycemia;

- awareness to hyperglycemia in response to increased delivery of insulin;

- use of appropriate types of insulin (long-acting, short-acting, etc.) in appropriate amounts.