The primary symptoms of hypotension are lightheadedness or dizziness.

If the blood pressure is sufficiently low, fainting may occur.

Low blood pressure is sometimes associated with certain symptoms, many of which are related to causes rather than effects of hypotension:

- chest pain

- shortness of breath

- irregular heartbeat

- fever higher than 38.3 °C (101 °F)

- headache

- stiff neck

- severe upper back pain

- cough with sputum

- Prolonged diarrhea or vomiting

- dyspepsia (indigestion)

- dysuria (painful urination)

- adverse effect of medications

- acute, life-threatening allergic reaction

- seizures

- loss of consciousness

- profound fatigue

- temporary blurring or loss of vision

- Black tarry stools

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 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.

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).

Symptoms of cardiogenic shock include:

- Distended jugular veins due to increased jugular venous pressure

- Weak or absent pulse

- Abnormal heart rhythms, often a fast heart rate

- Pulsus paradoxus in case of tamponade

- Reduced blood pressure

Hypovolemia is a direct loss of effective circulating blood volume leading to:

- A rapid, weak, thready pulse due to decreased blood flow combined with tachycardia

- Cool, clammy skin due to vasoconstriction and stimulation of vasoconstriction

- Rapid and shallow breathing due to sympathetic nervous system stimulation and acidosis

- Hypothermia due to decreased perfusion and evaporation of sweat

- Thirst and dry mouth, due to fluid depletion

- Cold and mottled skin (Livedo reticularis), especially extremities, due to insufficient perfusion of the skin

The severity of hemorrhagic shock can be graded on a 1–4 scale on the physical signs. This approximates to the effective loss of blood volume. The "shock index" (heart rate divided by systolic blood pressure) is a stronger predictor of the impact of blood loss than heart rate and blood pressure alone. This relationship has not been well established in pregnancy-related bleeding.

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 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.

The hallmark sign of POTS is a measured increase in heart rate by at least 30 beats per minute within 10 minutes of assuming an upright position. For people aged between 12 and 19, the minimum increase for diagnosis is 40 beats per minute. This symptom is known as orthostatic (upright) tachycardia (fast heart rate). It occurs without any coinciding drop in blood pressure, as that would indicate orthostatic hypotension. It should be noted, however, that certain medications to treat POTS may cause orthostatic hypotension. It is accompanied by other features of orthostatic intolerance—symptoms which develop in an upright position and are relieved by reclining. These orthostatic symptoms include palpitations, light-headedness, chest discomfort, shortness of breath, nausea, weakness or "heaviness" in the lower legs, blurred vision and cognitive difficulties. Symptoms may be exacerbated with prolonged sitting, prolonged standing, alcohol, heat, exercise, or eating a large meal.

In up to one third of people with POTS, fainting occurs in response to postural changes or exercise. Migraine-like headaches are common, sometimes with symptoms worsening in an upright position (orthostatic headache). Some people with POTS develop acrocyanosis, or blotchy, red/blue skin upon standing, especially over the feet (indicative of blood pooling). 48% of people with POTS report chronic fatigue and 32% report sleep disturbances. Others exhibit only the cardinal symptom of orthostatic tachycardia.

POTS can co-occur in all types of Ehlers–Danlos syndrome (EDS), a hereditary connective tissue disorder marked by loose hypermobile joints prone to subluxations and dislocations, skin that exhibits moderate or greater laxity, easy bruising, and many other symptoms. A trifecta of POTS, EDS, and Mast Cell Activation Syndrome (MCAS) is becoming increasingly more common, with a genetic marker common among all three conditions. POTS is also often accompanied by vasovagal syncope, with a 25% overlap being reported. There is significant overlap between POTS and chronic fatigue syndrome, with evidence of POTS in 25–50% of CFS cases. Fatigue and reduced exercise tolerance are prominent symptoms of both conditions, and dysautonomia may underlie both conditions.

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).

Characteristic symptoms are:

- Sudden penetrating pain in the legs, lower back or abdomen

- Confusion, psychosis, slurred speech

- Severe lethargy

- Convulsions

- Fever

- Hyperkalemia (elevated potassium level in the blood)

- Hypercalcemia (elevated calcium level in the blood): the cause of hypercalcemia is a combination of increased calcium input into the extracellular space and reduced calcium removal by the kidney, this last caused by decreased glomerular filtration and increased tubular calcium reabsorption. Both renal factors are secondary to volume depletion and, in fact, improve rapidly during rehydration with saline infusion.

- Hypoglycemia (reduced level of blood glucose)

- Hyponatremia (low sodium level in the blood)

- Hypotension (low blood pressure)

- Hypothyroid (low T4 level)

- Severe vomiting and diarrhea, resulting in dehydration

- Syncope (loss of consciousness and ability to stand)

The body has several feedback mechanisms to maintain adequate blood flow and blood pressure. If blood pressure decreases, the heart beats faster in an attempt to raise it. This is called reflex tachycardia. This can happen in response to a decrease in blood volume (through dehydration or bleeding), or an unexpected change in blood flow. The most common cause of the latter is orthostatic hypotension (also called postural hypotension). Fever, hyperventilation, diarrhea and severe infections can also cause tachycardia, primarily due to increase in metabolic demands.

An increase in sympathetic nervous system stimulation causes the heart rate to increase, both by the direct action of sympathetic nerve fibers on the heart and by causing the endocrine system to release hormones such as epinephrine (adrenaline), which have a similar effect. Increased sympathetic stimulation is usually due to physical or psychological stress. This is the basis for the so-called fight-or-flight response, but such stimulation can also be induced by stimulants such as ephedrine, amphetamines or cocaine. Certain endocrine disorders such as pheochromocytoma can also cause epinephrine release and can result in tachycardia independent of nervous system stimulation. Hyperthyroidism can also cause tachycardia. The upper limit of normal rate for sinus tachycardia is thought to be 220 bpm minus age.

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.

Usually in women with no heart problems, this syndrome is characterized by normal resting heart rate but exaggerated postural sinus tachycardia with or without orthostatic hypotension.

The symptoms of POTS can be caused by several distinct pathophysiological mechanisms. These mechanisms are poorly understood, and can overlap, with many people showing features of multiple POTS types. Many people with POTS exhibit low blood volume (hypovolemia), which can decrease the rate of blood flow to the heart. To compensate for this, the heart increases its cardiac output by beating faster, leading to the symptoms of presyncope and reflex tachycardia.

In the 30% to 60% of cases classified as "hyperadrenergic POTS", norepinephrine levels are elevated on standing, often due to hypovolemia or partial autonomic neuropathy. A smaller minority of people with POTS have (typically very high) standing norepinephrine levels that are elevated even in the absence of hypovolemia and autonomic neuropathy; this is classified as "central hyperadrenergic POTS". The high norepinephrine levels contribute to symptoms of tachycardia. Another subtype, "neuropathic POTS", is associated with denervation of sympathetic nerves in the lower limbs. In this subtype, it is thought that impaired constriction of the blood vessels causes blood to pool in the veins of the lower limbs. Heart rate increases to compensate for this blood pooling.

Genetics likely plays a role, with one study finding that 1 in 8 POTS patients reported a history of orthostatic intolerance in their family. In up to 50% of cases, POTS is associated with recent viral illness. It may also be associated with physical deconditioning or chronic fatigue syndrome. During viral illness or prolonged bed rest, the body may become conditioned to orthostatic intolerance and excitability of the central nervous system, resulting in a failure to re-adapt to the normal demands of standing or exercise.

POTS is more common in females than males. It has also been shown to be linked in patients with acute stressors such as pregnancy, recent surgery, or recent trauma. POTS has been also linked to patients with a history of autoimmune diseases, IBS, anemia, hyperthyroidism, fibromyalgia, diabetes, amyloidosis, sarcoidosis, systemic lupus erythmatosus, and cancer.

If POTS is caused by another condition, it may be classified as "secondary POTS". Chronic diabetes mellitus is one frequently seen primary cause. POTS can also be secondary to gastrointestinal disorders that are associated with low fluid intake due to nausea or fluid loss through diarrhea, leading to hypovolemia.

There are a subset of patients that present with both POTS and mast cell activation syndrome (MCAS), and it is not yet clear whether MCAS is a secondary cause of POTS or simply comorbid, however treating MCAS for these patients can significantly improve POTS symptoms.

POTS can sometimes be a paraneoplastic syndrome associated with cancer. Autoantibodies have been found in some cases which occur after a viral infection raising the possibility of some cases being autoimmune in nature.

Tachycardia is often asymptomatic. If the heart rate is too high, cardiac output may fall due to the markedly reduced ventricular filling time. Rapid rates, though they may be compensating for ischemia elsewhere, increase myocardial oxygen demand and reduce coronary blood flow, thus precipitating an ischemic heart or valvular disease. Sinus tachycardia accompanying a myocardial infarction may be indicative of cardiogenic shock.

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.

ECG characteristics

- Rate: Less than 60 beats per minute.

- Rhythm: Regular.

- P waves: Upright, consistent, and normal in morphology and duration.

- P-R Interval: Between 0.12 and 0.20 seconds in duration.

- QRS Complex: Less than 0.12 seconds in width, and consistent in morphology.

Adrenal crisis (also known as Addisonian crisis and acute adrenal insufficiency) is a medical emergency and potentially life-threatening situation requiring immediate emergency treatment. It is a constellation of symptoms that indicate severe adrenal insufficiency caused by insufficient levels of the hormone cortisol. This may be the result of either previously undiagnosed or untreated Addison's disease, a disease process suddenly affecting adrenal function (such as bleeding from the adrenal glands in Waterhouse-Friderichsen syndrome), suddenly stopping intake of glucocorticoids or an intercurrent problem (e.g. infection, trauma, in fact any form of physical or mental stress) in someone known to have Addison's disease or congenital adrenal hyperplasia (CAH).

The symptoms of a cholinergic toxidrome include bronchorrhea, confusion, defecation, diaphoresis, diarrhea, emesis, lacrimation, miosis, muscle fasciculations, salivation, seizures, urination, and weakness. Complications include bradycardia, hypothermia, and tachypnea. Substances that may cause this toxidrome include carbamates, mushrooms, and organophosphates.

Common mnemonics for organophosphate poisoning include the "killer B's" of bradycardia, bronchorrhea and bronchospasm because they are the leading cause of death, and SLUDGE - Salivation, Lacrimation, Urination, Diarrhea, Gastrointestinal distress, and Emesis.

An alternative mnemonic is DUMBBELLSS - Diarrhea, Urination, Miosis, Bradycardia, Bronchospasm, Emesis, Lacrimation, Lethargy, Salivation and Seizures.

Most SCLS patients report having flu-like symptoms (like a runny nose), or else gastro-intestinal disorders (diarrhea or vomiting), or a general weakness or pain in their limbs, but others get no particular or consistent warning signs ahead of their episodes. They subsequently develop thirst and lightheadedness and the following conditions measurable in a hospital emergency-room setting:

- hemoconcentration (elevated hematocrit or hemoglobin readings, with hematocrit levels >49% in men and >43% in women, not because of an absolute increase in them but because of the leak of plasma);

- very low blood pressure (profound arterial hypotension, with systolic blood pressure levels <90 mm Hg);

- albumin deficiency (hypoalbuminemia measuring <3.0 g/dL);

- partial or generalized edema, and cold extremities;

- a paraprotein in the blood (an MGUS in approximately 80% of cases).

Symptoms reported by patients vary in frequency and severity.

Symptoms associated with IST include:

- Frequent or sustained palpitations

- Dyspnea (shortness of breath) and palpitations on exertion

- Pre-syncope (feeling as if about to faint)

- Fatigue (physical)

- Dizziness

- Exercise intolerance

- Occasional paresthesia and cramping

- Symptoms associated with autonomic nervous system disturbance, including GI disturbance

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.

Signs and symptoms of CSWS include large amounts of urination (at least 3 liters of urine output over a 24-hour period for adults) due to inadequate sodium retention in the body, high amounts of sodium in the urine, low blood sodium concentration, excessive thirst, extreme salt cravings, dysfunction of the autonomic nervous system, and dehydration. Patients often self-medicate by naturally gravitating toward a high-sodium diet and by dramatically increasing their water intake. Advanced symptoms include muscle cramps, lightheadedness, dizziness or vertigo, feelings of anxiety or panic (not mentally induced), increased heart rate or slowed heart rate, low blood pressure and orthostatic hypotension sometimes resulting in fainting. Other symptoms frequently associated with dysautonomia include: headaches, pallor, malaise, facial flushing, constipation or diarrhea, nausea, acid reflux, visual disturbances, numbness, nerve pain, trouble breathing, chest pains, loss of consciousness and seizures.

CSWS is usually caused by brain injury/trauma or cerebral lesion, tumor, or hematoma. CSWS is a diagnosis of exclusion and may be difficult to distinguish from the syndrome of inappropriate antidiuretic hormone (SIADH), which develops under similar circumstances and also presents with hyponatremia. The main clinical difference is that of total fluid status of the patient: CSWS leads to a relative or overt low blood volume whereas SIADH is consistent with a normal or high blood volume. If blood-sodium levels increase when fluids are restricted, SIADH is more likely.