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.

Low blood pressure can be caused by low blood volume, hormonal changes, widening of blood vessels, medicine side effects, anemia, heart problems or endocrine problems.

Reduced blood volume, hypovolemia, is the most common cause of hypotension. This can result from hemorrhage; insufficient fluid intake, as in starvation; or excessive fluid losses from diarrhea or vomiting. Hypovolemia is often induced by excessive use of diuretics. Low blood pressure may also be attributed to heat stroke. The body may have enough fluid but does not retain electrolytes. Absence of perspiration, light headedness and dark coloured urine are also indicators.

Other medications can produce hypotension by different mechanisms. Chronic use of alpha blockers or beta blockers can lead to hypotension. Beta blockers can cause hypotension both by slowing the heart rate and by decreasing the pumping ability of the heart muscle.

Decreased cardiac output despite normal blood volume, due to severe congestive heart failure, large myocardial infarction, heart valve problems, or extremely low heart rate (bradycardia), often produces hypotension and can rapidly progress to cardiogenic shock. Arrhythmias often result in hypotension by this mechanism.

Some heart conditions can lead to low blood pressure, including extremely low heart rate (bradycardia), heart valve problems, heart attack and heart failure. These conditions may cause low blood pressure because they prevent the body from being able to circulate enough blood.

Excessive vasodilation, or insufficient constriction of the resistance blood vessels (mostly arterioles), causes hypotension. This can be due to decreased sympathetic nervous system output or to increased parasympathetic activity occurring as a consequence of injury to the brain or spinal cord or of dysautonomia, an intrinsic abnormality in autonomic system functioning. Excessive vasodilation can also result from sepsis, acidosis, or medications, such as nitrate preparations, calcium channel blockers, or AT1 receptor antagonists (Angiotensin II acts on AT1 receptors). Many anesthetic agents and techniques, including spinal anesthesia and most inhalational agents, produce significant vasodilation.

Meditation, yoga, or other mental-physiological disciplines may reduce hypotensive effects.

Lower blood pressure is a side effect of certain herbal medicines, which can also interact with hypotensive medications. An example is the theobromine in "Theobroma cacao", which lowers blood pressure through its actions as both a vasodilator and a diuretic, and has been used to treat high blood pressure.

Orthostatic hypotension may be caused by low blood volume, resulting from bleeding, the excessive use of diuretics, vasodilators, or other types of drugs, dehydration, or prolonged bed rest(immobility); as well as occurring in people with anemia.

Orthostatic hypotension, also called "postural hypotension", is a common form of low blood pressure. It occurs after a change in body position, typically when a person stands up from either a seated or lying position. It is usually transient and represents a delay in the normal compensatory ability of the autonomic nervous system. It is commonly seen in hypovolemia and as a result of various medications. In addition to blood pressure-lowering medications, many psychiatric medications, in particular antidepressants, can have this side effect. Simple blood pressure and heart rate measurements while lying, seated, and standing (with a two-minute delay in between each position change) can confirm the presence of orthostatic hypotension. Orthostatic hypotension is indicated if there is a drop in 20 mmHg of systolic pressure (and a 10 mmHg drop in diastolic pressure in some facilities) and a 20 beats per minute increase in heart rate.

Vasovagal syncope is a form of dysautonomia characterized by an inappropriate drop in blood pressure while in the upright position. Vasovagal syncope occurs as a result of increased activity of the vagus nerve, the mainstay of the parasympathetic nervous system .

Another, but rarer form, is postprandial hypotension, a drastic decline in blood pressure that occurs 30 to 75 minutes after eating substantial meals. When a great deal of blood is diverted to the intestines (a kind of "splanchnic blood pooling") to facilitate digestion and absorption, the body must increase cardiac output and peripheral vasoconstriction to maintain enough blood pressure to perfuse vital organs, such as the brain. Postprandial hypotension is believed to be caused by the autonomic nervous system not compensating appropriately, because of aging or a specific disorder.

Hypotension is a feature of Flammer syndrome which is characterized by cold hands and feet and predisposes to normal tension glaucoma.

Haemorrhagic shock occurs in about 1–2% of trauma cases. Up to one-third of people admitted to the intensive care unit (ICU) are in circulatory shock.

The prognosis of shock depends on the underlying cause and the nature and extent of concurrent problems. Hypovolemic, anaphylactic and neurogenic shock are readily treatable and respond well to medical therapy. Septic shock however, is a grave condition with a mortality rate between 30% and 50%. The prognosis of cardiogenic shock is even worse with a mortality rate between 70% and 90%.

POTS has a favorable prognosis when managed appropriately. Symptoms improve within five years of diagnosis for many patients, and 60% return to their original level of functioning. About 90% of people with POTS respond to a combination of pharmacological and physical treatments. Those who develop POTS in their early to mid teens during a period of rapid growth will most likely see complete symptom resolution in two to five years. Outcomes are more guarded for adults newly diagnosed with POTS. Some people do not recover, and a few even worsen with time. The hyperadrenergic type of POTS typically requires continuous therapy. If POTS is caused by another condition, outcomes depend on the prognosis of the underlying disorder.

The prevalence of POTS is unknown. One study estimated a minimal rate of 170 POTS cases per 100,000 individuals, but the true prevalence is likely higher due to underdiagnosis. Another study estimated that there were between 500,000 and 3,000,000 cases in the United States. POTS is more common in women, with a female-to-male ratio of 5:1. Most people with POTS are aged between 20 and 40, with an average onset of 30. Diagnoses of POTS beyond age 40 are rare, perhaps because symptoms improve with age.

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

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.

Hahner et al. investigated the frequency, causes and risk factors for adrenal crisis in patients with chronic adrenal insufficiency. Annane et al.'s landmark 2002 study found a very high rate of relative adrenal insufficiency among the enrolled patients with septic shock.

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

Adrenal crisis is triggered by physiological stress (such as trauma). Activities that have an elevated risk of trauma are best avoided. Treatment must be given within two hours of trauma and consequently it is advisable to carry injectable hydrocortisone in remote areas.

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.

It is difficult to determine the incidence of TACO, but its incidence is estimated at about one in every 100 transfusions using active surveillance, and in one in every 10000 transfusions using passive surveillance. TACO is the most commonly reported cause of transfusion-related death and major morbidity in the UK, and second most common cause in the USA.

The risk increases with patients over the age of 60, patients with cardiac or pulmonary failure, renal impairment, hypoalbuminemia or anemia.

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.

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.

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).

Because it causes a loss of sympathetic tone, which plays a major role in other forms of shock, neurogenic shock causes a unique and atypical presentation.

Typically, in other forms of shock, the sympathetic nervous system triggers various compensatory mechanisms by releasing epinephrine and norepinephrine, its major chemical mediators. These neurotransmitters trigger an increased heart rate, faster breathing, and sweating. They also trigger vasoconstriction, to shunt blood away from the extremities and to the vital organs.

In neurogenic shock, the body loses its ability to activate the sympathetic nervous system and cannot trigger these compensatory mechanisms. Only parasympathetic tone remains. Consequently, neurogenic shock's unique presentation includes:

- Instantaneous hypotension due to sudden, massive vasodilation

- Warm, flushed skin due to vasodilation and inability to vasoconstrict

- Priapism, also due to vasodilation

- The patient will be unable to get tachycardic, and may become bradycardic

- If the injury is below the 5th cervical vertebra, the patient will exhibit diaphragmatic breathing due to loss of nervous control of the intercostal muscles (which are required for thoracic breathing).

- If the injury is above the 3rd cervical vertebra, the patient will go into respiratory arrest immediately following the injury, due to loss of nervous control of the diaphragm.

In mostly European experience with 69 patients during 1996-2016, the 5- and 10-year survival rates for SCLS patients were 78% and 69%, respectively, but the survivors received significantly more frequent preventive treatment with IVIG than did non-survivors. Five- and 10-year survival rates in patients treated with IVIG were 91% and 77%, respectively, compared to 47% and 37% in patients not treated with IVIG. Moreover, better identification and management of this condition appears to be resulting in lower mortality and improving survival and quality-of-life results as of late.

Transfusion associated circulatory overload is prevented by avoiding unnecessary transfusions, closely monitoring patients receiving transfusions, transfusing smaller volumes of blood at a slower rate, and considering the use of diuretics. A pre-transfusion TACO checklist can be used to assess patients' risk of developing TACO.

The decreased heart rate can cause a decreased cardiac output resulting in symptoms such as lightheadedness, dizziness, hypotension, vertigo, and syncope. The slow heart rate may also lead to atrial, junctional, or ventricular ectopic rhythms.

Bradycardia is not necessarily problematic. People who regularly practice sports may have sinus bradycardia, because their trained hearts can pump enough blood in each contraction to allow a low resting heart rate. Sinus bradycardia can also be an adaptive advantage; for example, diving seals may have a heart rate as low as 12 beats per minute, helping them to conserve oxygen during long dives.

Sinus bradycardia is a common condition found in both healthy individuals and those who are considered well conditioned athletes.

Heart rates considered bradycardic vary by species; for example, in the common housecat, a rate of under 120 beats per minute is abnormal. Generally, smaller species have higher heart rates while larger species have lower rates.

The initial stage is the capillary leak phase, lasting from 1 to 3 days, during which up to 70% of total plasma volume may invade cavities especially in the extremities. The most common clinical features are flu-like symptoms such as fatigue; runny nose; lightheadedness up to and including syncope (fainting); limb, abdominal or generalized pain; facial or other edema; dyspnea; and hypotension that results in circulatory shock and potentially in cardiopulmonary collapse and other organ distress or damage. Acute renal dysfunction or failure is a common risk due to acute tubular necrosis consequent to hypovolemia and rhabdomyolysis.

The loss of fluid out of the capillaries has similar effects on the circulation as dehydration, slowing both the flow of oxygen delivered to tissues and organs as well as the output of urine. Urgent medical attention in this phase consists of fluid resuscitation efforts, mainly the intravenous administration of saline solution plus hetastarch or albumin and colloids (to increase the remaining blood flow to vital organs like the kidneys), as well as glucocorticoids (steroids like methylprednisolone, to reduce or stop the capillary leak). However effective on blood pressure, the impact of fluid therapy is always transient and leads to increased extravascular fluid accumulation, engendering multiple complications especially compartment syndrome and thus limb-destructive rhabdomyolysis. Consequently, patients experiencing episodes of SCLS should be closely monitored in a hospital intensive-care setting, including for orthopedic complications requiring surgical decompression, and their fluid therapy should be minimized as much as possible.

The symptoms of sedative/hypnotic toxidrome include ataxia, blurred vision, coma, confusion, delirium, deterioration of central nervous system functions, diplopia, dysesthesias, hallucinations, nystagmus, paresthesias, sedation, slurred speech, and stupor. Apnea is a potential complication. Substances that may cause this toxidrome include anticonvulsants, barbiturates, benzodiazepines, gamma-Hydroxybutyric acid, Methaqualone, and ethanol. While most sedative-hypnotics are anticonvulsant, some such as GHB and methaqualone instead lower the seizure threshold, and so can cause paradoxical seizures in overdose.

The symptoms of an opiate toxidrome include the classic triad of coma, pinpoint pupils, and respiratory depression as well as altered mental states, shock, pulmonary edema and unresponsiveness. Complications include bradycardia, hypotension, and hypothermia. Substances that may cause this toxidrome are opioids.