Hypertension with certain specific additional signs and symptoms may suggest secondary hypertension, i.e. hypertension due to an identifiable cause. For example, Cushing's syndrome frequently causes truncal obesity, glucose intolerance, moon face, a hump of fat behind the neck/shoulder (referred to as a buffalo hump), and purple abdominal stretch marks. Hyperthyroidism frequently causes weight loss with increased appetite, fast heart rate, bulging eyes, and tremor. Renal artery stenosis (RAS) may be associated with a localized abdominal bruit to the left or right of the midline (unilateral RAS), or in both locations (bilateral RAS). Coarctation of the aorta frequently causes a decreased blood pressure in the lower extremities relative to the arms, or delayed or absent femoral arterial pulses. Pheochromocytoma may cause abrupt ("paroxysmal") episodes of hypertension accompanied by headache, palpitations, pale appearance, and excessive sweating.

Hypertension is rarely accompanied by symptoms, and its identification is usually through screening, or when seeking healthcare for an unrelated problem. Some with high blood pressure report headaches (particularly at the back of the head and in the morning), as well as lightheadedness, vertigo, tinnitus (buzzing or hissing in the ears), altered vision or fainting episodes. These symptoms, however, might be related to associated anxiety rather than the high blood pressure itself.

On physical examination, hypertension may be associated with the presence of changes in the optic fundus seen by ophthalmoscopy. The severity of the changes typical of hypertensive retinopathy is graded from I–IV; grades I and II may be difficult to differentiate. The severity of the retinopathy correlates roughly with the duration or the severity of the hypertension.

In medicine, systolic hypertension is defined as an elevated systolic blood pressure (SBP).

If the systolic blood pressure is elevated (>140) with a normal (<90) diastolic blood pressure (DBP), it is called "isolated systolic hypertension".

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.

A recent classification recommends blood pressure criteria for defining normal blood pressure, prehypertension, hypertension (stages I and II), and isolated systolic hypertension, which is a common occurrence among the elderly. These readings are based on the average of seated blood pressure readings that were properly measured during 2 or more office visits. In individuals older than 50 years, hypertension is considered to be present when a person's blood pressure is consistently at least 140 mmHg systolic or 90 mmHg diastolic. Patients with blood pressures over 130/80 mmHg along with Type 1 or Type 2 diabetes, or kidney disease require further treatment.

Resistant hypertension is defined as the failure to reduce blood pressure to the appropriate level after taking a three-drug regimen. Guidelines for treating resistant hypertension have been published in the UK, and US.

Systolic hypertension may be due to reduced compliance of the aorta with increasing age. This increases the load on the ventricle and compromises coronary blood flow, eventually resulting in left ventricular hypertrophy, coronary ischemia, and heart failure.

Contemporary science shows an immersed boundary method of computational illustration of a single heartbeat. Applied to physiologic models, immersed boundary theory sees the heart as a great folded semisolid sail fielding and retrieving a viscous blood mass. The sail, likened to Windkessel effect physiology, gives and receives a load under time-ordered phases. Decreasing compliance of the sail heralds the onset of systolic hypertension.

Essential hypertension (also called primary hypertension or idiopathic hypertension) is the form of hypertension that by definition has no identifiable cause. It is the most common type of hypertension, affecting 95% of hypertensive patients, it tends to be familial and is likely to be the consequence of an interaction between environmental and genetic factors. Prevalence of essential hypertension increases with age, and individuals with relatively high blood pressure at younger ages are at increased risk for the subsequent development of hypertension.

Hypertension can increase the risk of cerebral, cardiac, and renal events.

The symptoms of pulmonary hypertension include the following:

Less common signs/symptoms include non-productive cough and exercise-induced nausea and vomiting. Coughing up of blood may occur in some patients, particularly those with specific subtypes of pulmonary hypertension such as heritable pulmonary arterial hypertension, Eisenmenger syndrome and chronic thromboembolic pulmonary hypertension. Pulmonary venous hypertension typically presents with shortness of breath while lying flat or sleeping (orthopnea or paroxysmal nocturnal dyspnea), while pulmonary arterial hypertension (PAH) typically does not.

Other typical signs of pulmonary hypertension include an accentuated pulmonary component of the second heart sound, a right ventricular third heart sound, and parasternal heave indicating a hypertrophied right atrium. Signs of systemic congestion resulting from right-sided heart failure include jugular venous distension, ascites, and hepatojugular reflux. Evidence of tricuspid insufficiency and pulmonic regurgitation is also sought and, if present, is consistent with the presence of pulmonary hypertension.

The symptoms and signs of hypertensive heart disease will depend on whether or not it is accompanied by heart failure. In the absence of heart failure, hypertension, with or without enlargement of the heart (left ventricular hypertrophy) is usually symptomless.

Symptoms, signs and consequences of Congestive heart failure can include:

- Fatigue

- Irregular pulse or palpitations

- Swelling of feet and ankles

- Weight gain

- Nausea

- Shortness of breath

- Difficulty sleeping flat in bed (orthopnea)

- Bloating and abdominal pain

- Greater need to urinate at night

- An enlarged heart (cardiomegaly)

- Left ventricular hypertrophy and left ventricular remodeling

- Diminished coronary flow reserve and silent myocardial ischemia

- Coronary heart disease and accelerated atherosclerosis

- Heart Failure With Normal Left Ventricular Ejection Fraction (HFNEF), often termed diastolic heart failure

- Atrial fibrillation, other cardiac arrhythmias, or sudden cardiac death

Heart failure can develop insidiously over time or patients can present acutely with acute heart failure or acute decompensated heart failure and pulmonary edema due to sudden failure of pump function of the heart. Sudden failure can be precipitated by a variety of causes, including myocardial ischemia, marked increases in blood pressure, or cardiac arrhythmias.

Symptoms of renovascular hypertension include the following:

- High blood pressure (early age)

- Kidney dysfunction

- Narrowing of arteries elsewhere in the body

- Pulmonary edema

Other conditions can share features with hypertensive heart disease and need to be considered in the differential diagnosis. For example:

- Coronary artery disease or ischemic heart disease due to atherosclerosis

- Hypertrophic cardiomyopathy

- Left ventricular hypertrophy in athletes

- Congestive heart failure or heart failure with normal ejection fraction due to other causes

- Atrial fibrillation or other disorders of cardiac rhythm due to other causes

- Sleep apnea

Renovascular hypertension (or "renal hypertension") is a condition in which high blood pressure is caused by the kidneys' hormonal response to narrowing of the arteries supplying the kidneys. When functioning properly this hormonal axis regulates blood pressure. Due to low local blood flow, the kidneys mistakenly increases blood pressure of the entire circulatory system. It is a form of secondary hypertension - a form of hypertension whose cause is identifiable.

Pulmonary hypertension (PH or PHTN) is a condition of increased blood pressure within the arteries of the lungs. Symptoms include shortness of breath, syncope, tiredness, chest pain, swelling of the legs, and a fast heartbeat. The condition may make it difficult to exercise. Onset is typically gradual.

The cause is often unknown. Risk factors include a family history, prior blood clots in the lungs, HIV/AIDS, sickle cell disease, cocaine use, COPD, sleep apnea, living at high altitudes, and problems with the mitral valve. The underlying mechanism typically involves inflammation of the arteries in the lungs. Diagnosis involves first ruling out other potential causes.

There is no cure. Treatment depends on the type of disease. A number of supportive measures such as oxygen therapy, diuretics, and medications to inhibit clotting may be used. Medications specifically for the condition include epoprostenol, treprostinil, iloprost, bosentan, ambrisentan, macitentan, and sildenafil. A lung transplant may be an option in certain cases.

While the exact frequency of the condition is unknown, it is estimated that about 1,000 new cases occur a year in the United States. Females are more often affected than males. Onset is typically between 20 and 60 years of age. It was first identified by Ernst von Romberg in 1891.

Signs and symptoms of portal hypertension include:

In addition, a widened portal vein as seen on a CT scan or MRI may raise the suspicion about portal hypertension. A cutoff of 13 mm is widely used in this regard, but the diameter is often larger than this is in normal individuals as well.

Because of the ubiquity of arsenic in ground water supplies and its effect on cardiovascular health, low dose arsenic poisoning should be inferred as a part of the pathogenesis of idiopathic hypertension. Idiopathic and essential are both somewhat synonymous with primary hypertension. Arsenic exposure has also many of the same signs of primary hypertension such as headache, somnolence,

confusion, proteinuria

visual disturbances, and nausea and vomiting

Portal hypertension is hypertension (high blood pressure) in the hepatic portal system – made up of the portal vein and its branches, that drain from most of the intestines to the liver. Portal hypertension is defined as a hepatic venous pressure gradient. Cirrhosis (a form of chronic liver failure) is the most common cause of portal hypertension; other, less frequent causes are therefore grouped as non-cirrhotic portal hypertension. When it becomes severe enough to cause symptoms or complications, treatment may be given to decrease portal hypertension itself or to manage its complications.

Due to the role of intracellular potassium in regulation of cellular pressures related to sodium, establishing potassium balance has been shown to reverse hypertension.

White coat hypertension, more commonly known as white coat syndrome, is a phenomenon in which patients exhibit a blood pressure level above the normal range, in a clinical setting, though they don't exhibit it in other settings. It is believed that the phenomenon is due to anxiety that those afflicted experience during a clinic visit.

The patient's daytime ambulatory blood pressure is used as a reference as it takes into account ordinary levels of daily stress. Many problems have been incurred in the diagnosis and treatment of white coat hypertension.

The term "masked hypertension" can be used to describe the contrasting phenomenon, where a patient's blood pressure is above the normal range during daily living, although it isn't above the normal range when the patient is in a clinic setting.

Heart failure with preserved ejection fraction (HFpEF) is a form of congestive heart failure where in the amount of blood pumped from the heart's left ventricle with each beat (ejection fraction) is greater than 50%. Approximately half of people with heart failure have HFpEF, while the remainder display a reduction in ejection fraction, or heart failure with reduced ejection fraction (HFrEF).

HFpEF is characterized by abnormal diastolic function, which manifests as an increase in the stiffness of the heart's left ventricle and a decrease in left ventricular relaxation when filling with blood before the next beat. There is an increased risk for atrial fibrillation and pulmonary hypertension. Risk factors for HFpEF include hypertension, hyperlipidemia, diabetes, smoking, and obstructive sleep apnea. There is a query about the relationship between diastolic heart failure and HFpEF.

Clinical manifestations of HFpEF are similar to those observed in HFrEF and include shortness of breath including exercise induced dyspnea, paroxysmal nocturnal dyspnea and orthopnea, exercise intolerance, fatigue, elevated jugular venous pressure, and edema.

Patients with HFpEF poorly tolerate stress, particularly hemodynamic alterations of ventricular loading or increased diastolic pressures. Often there is a more dramatic elevation in systolic blood pressure in HFpEF than is typical of HFrEF.

In studies, white coat hypertension can be defined as the presence of a defined hypertensive average blood pressure in a clinic setting, although it isn't present when the patient is at home.

Diagnosis is made difficult as a result of the unreliable measures taken from the conventional methods of detection. These methods often involve an interface with health care professionals and frequently results are tarnished by a list of factors including variability in the individual’s blood pressure, technical inaccuracies, anxiety of the patient, recent ingestion of pressor substances, and talking, amongst many other factors. The most common measure of blood pressure is taken from a noninvasive instrument called a sphygmomanometer. "A survey showed that 96% of primary care physicians habitually use a cuff size too small," adding to the difficulty in making an informed diagnosis. For such reasons, white coat hypertension cannot be diagnosed with a standard clinical visit. It can be reduced (but not eliminated) with automated blood pressure measurements over 15 to 20 minutes in a quiet part of the office or clinic.

Patients with white coat hypertension do not exhibit the signs indicative of trepidation and their increased blood pressure is often not accompanied by tachycardia. This is supported by studies that repeatedly indicate that 15%–30% of those thought to have mild hypertension as a result of clinic or office recordings display normal blood pressure and no unusual response to pressure stimulus. These persons did not show any specific characteristics such as age that may be indicative of a higher susceptibility to white coat hypertension.

Ambulatory blood pressure monitoring and patient self-measurement using a home blood pressure monitoring device is being increasingly used to differentiate those with white coat hypertension or experiencing the white coat effect from those with chronic hypertension. This does not mean that these methods are without fault. Daytime ambulatory values, despite taking into account stresses of everyday life when taken during the patient's daily routine, are still susceptible to the effects of daily variables such as physical activity, stress and duration of sleep. Ambulatory monitoring has been found to be the more practical and reliable method in detecting patients with white coat hypertension and for the prediction of target organ damage. Even as such, the diagnosis and treatment of white coat hypertension remains controversial.

Recent studies showed that home blood pressure monitoring is as accurate as a 24-hour ambulatory monitoring in determining blood pressure levels. Researchers at the University of Turku, Finland studied 98 patients with untreated hypertension. They compared patients using a home blood pressure device and those wearing a 24-hour ambulatory monitor. Researcher Dr. Niiranen said that "home blood pressure measurement can be used effectively for guiding anti-hypertensive treatment". Dr. Stergiou added that home tracking of blood pressure "is more convenient and also less costly than ambulatory monitoring."

Use of breathing patterns has been proposed as a technique for identifying white coat hypertension.

In one Turkish study of 438 consecutive patients, 38% were normotensive, 43% had white coat hypertension, 2% had masked hypertension, and 15% had sustained hypertension. Even patients taking medication for sustained hypertension who are normotensive at home may exhibit white coat hypertension in the office setting.

Clinical symptoms and signs are often non-specific or absent in early CTEPH, with signs of right heart failure only in advanced disease. The main symptom of CTEPH is exertional breathlessness (shortness of breath during exertion such as exercise), which is unspecific and may often be attributed to other, more common, diseases by physicians. When present, the clinical symptoms of CTEPH may resemble those of acute PE, or of idiopathic pulmonary arterial hypertension (iPAH). Leg oedema (swelling) and haemoptysis (blood in mucus) occur more often in CTEPH, while syncope (fainting) is more common in iPAH.

Chronic thromboembolic pulmonary hypertension (CTEPH) is a long-term disease caused by a blockage in the blood vessels that deliver blood from the heart to the lungs (pulmonary arteries), resulting in increased pressure in these arteries (pulmonary hypertension). The blockage either results from a hardened blood clot that is thought to originate from the deep veins of the body (thromboembolism) and remains in the arteries, or from a scar that forms at the site where the clot has damaged the arteries, causing permanent fibrous obstruction (blood flow blockage). Most patients have a combination of microvascular (small vessel) and macrovascular (large vessel) obstruction. Some patients may present with normal or near-normal pulmonary pressures at rest despite symptomatic disease. These patients are labelled as having chronic thromboembolic disease (CTED).

Diagnosis is based on findings obtained after at least 3 months of effective anticoagulation therapy (blood thinners) in order to discriminate this condition from ‘subacute’ pulmonary embolism (blood clot in the lungs, PE). Diagnostic findings for CTEPH are:

1. Invasively (i.e., in the blood) measured mean pulmonary arterial pressure (mPAP) ≥25 mmHg;

2. Mismatched perfusion defects on lung ventilation/perfusion (V/Q) scan and specific diagnostic signs for CTEPH seen by multidetector computed tomography angiography (MDCT), magnetic resonance imaging (MRI) or conventional pulmonary cineangiography (PAG), such as ring-like stenoses, webs/slits, chronic total occlusions (pouch lesions, or tapered lesions) and tortuous lesions.

For many people cardiomegaly is asymptomatic. For others, if the enlarged heart begins to affect the body's ability to pump blood effectively, then symptoms associated with congestive heart failure may arise.

- Heart palpitations – irregular beating of the heart, usually associated with a valve issue inside the heart.

- Severe shortness of breath (especially when physically active) – irregularly unable to catch one's breath.

- Chest pain

- Fatigue

- Swelling in legs

- Increased abdominal girth

- Weight gain

- Edema – swelling

- Fainting

Although there are many signs and symptoms associated with PVCs, PVCs may have no symptoms at all. An isolated PVC is hard to catch without the use of a Holter monitor. PVCs may be perceived as a skipped heart beat, a strong beat, or a feeling of suction in the chest. They may also cause chest pain, a faint feeling, fatigue, or hyperventilation after exercise. Several PVCs in a row becomes a form of ventricular tachycardia (VT), which is a potentially fatal abnormal heart rhythm. Overall it has been seen that the symptom felt most by patients experiencing a PVC is the mere perception of a skipped heartbeat. The more frequently these contractions occur, the more likely there are to be symptoms, despite the fact that these beats have little effect of the pumping action of the heart and therefore cause minimal if any symptoms.

Some other possible signs and symptoms of PVCs:

- Abnormal ECG

- Irregular heart beat

- Dyspnea

- Dizziness

- Feeling your heart beat (palpitations)

- Feeling of occasional, forceful beats

- Increased awareness of your heart beat

- Perception of a skipped heartbeat