Blood pressure is determined by the sympathetic nervous system, renin–angiotensin–aldosterone system and plasma volume. The majority of hypertension is primary or ‘essential’ and mediated by genetic and environmental factors. Risk factors to develop hypertension are advancing age, family history, obesity, physical inactivity, high sodium diet, excess alcohol intake, and presence of other cardiovascular risk factors.

Primary hypertension is the most common reason for elevated BP. Major secondary causes are medications, alcohol, nicotine, stimulant drugs, chronic renal disease, obstructive sleep apnea, and less commonly endocrine disorders, hyperaldosteronism, pheochromocytoma.

Medications usually cause BP elevation within the normal range but sometimes can cause overt hypertension. See table for nonpsychotropic medications that can elevate BP .

Psychotropic agents raise BP by their effect on cholinergic, dopaminergic, and adrenergic systems. They also indirectly increase risk for hypertension by causing obesity and metabolic syndrome.

A psychotropic medication usually does not induce overt hypertension but if patient already has risk factors or a borderline high BP, the BP rise may be clinically significant.

Stimulants raise BP by 5–7 mmHg [1]. Mean BP rise with amphetamines is slightly higher than with methylphenidate. Atomoxetine causes a modest 2 mmHg BP elevation.

Among antidepressants, tricyclic antidepressants (TCAs) and serotonin norepinephrine reuptake inhibitors (SNRIs) are associated with a mean increase in blood pressure [2]. Venlafaxine causes a sustained increase in DBP; the risk is strongly dose dependent with incidence <2% at <100 mg/day and 9% at >300 mg/day [3]. Duloxetine causes a modest elevation in BP at higher doses [4]. With both medications, mean rise in BP is <10 mmHg. Bupropion, a norepinephrine dopamine reuptake inhibitor, also causes a <10 mmHg elevation in BP [1]. Monoamine oxidase inhibitors (MAOIs) rarely cause a hypertensive crisis when foods containing tyramine are ingested.

Clozapine is associated with hypertension while olanzapine is not [5]. There is uncertainty over whether the BP elevation is by a direct effect on the vasculature or indirectly through weight gain.

Even though the direct effect on BP from psychotropic medications is small, antipsychotic-induced weight gain can contribute to a rise in BP and metabolic syndrome. In patients with preexisting hypertension, addition of other risk factors such as obesity, diabetes, dyslipidemia worsens overall cardiovascular risk.

In the absence of coexisting factors like obesity, BP elevation from medications will reverse when the medication is stopped.

Patients with hypertension are generally asymptomatic until they develop complications of end-organ damage, which may only occur several years after onset of illness. A significantly elevated blood pressure (considered as SBP ≥180 and/or DBP ≥120) may cause symptoms of end-organ damage like nausea/vomiting, headache, delirium, seizures, focal weakness, visual disturbance, chest pain, dyspnea, and severe back pain.

Hypertension should only be diagnosed after at least three separate measurements. Preferably this should be supplemented by home-based testing to eliminate predominant white coat hypertension. If there is persistent discordance between office and home measurements, 24-h ambulatory BP monitoring is recommended but this is rarely available in clinician offices. In the office, both upper arms should be alternatively used for measurement as a pressure difference >5 mmHg could signify increased risk of cardiac complications.

Previous national guidelines defined prehypertension as BP 120–139/80–89 and hypertension as 140/90 or higher. Current guidelines do not use these categories and instead define goals for therapy that are based on age and other risk factors. These are however subject to change and clinicians are encouraged to refer to the most updated Joint National Committee (JNC) guidelines .