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".

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.

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.

The eyes may show retinal hemorrhage or an exudate. Papilledema must be present before a diagnosis of malignant hypertension can be made. The brain shows manifestations of increased intracranial pressure, such as headache, vomiting, and/or subarachnoid or cerebral hemorrhage. Patients will usually suffer from left ventricular dysfunction. The kidneys will be affected, resulting in hematuria, proteinuria, and acute renal failure. It differs from other complications of hypertension in that it is accompanied by papilledema. This can be associated with hypertensive retinopathy.

Other signs and symptoms can include:

- Chest pain

- Arrhythmias

- Headache

- Epistaxis

- Dyspnea

- Faintness or vertigo

- Severe anxiety

- Agitation

- Altered mental status

- Paresthesias

- Vomiting

Chest pain requires immediate lowering of blood pressure (such as with sodium nitroprusside infusions), while urgencies can be treated with oral agents, with the goal of lowering the mean arterial pressure (MAP) by 20% in 1–2 days with further reduction to "normal" levels in weeks or months. The former use of oral nifedipine, a calcium channel blocker, has been strongly discouraged as it has led to excessive falls in blood pressure with serious and fatal consequences.

Sometimes, the term hypertensive emergency is also used as a generic term, comprising both hypertensive "emergency", as a specific term for a serious and urgent condition of elevated blood pressure, and hypertensive urgency, as a specific term of a less serious and less urgent condition (the terminology hypertensive "crisis" is usually used in this sense).

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.

The term hypertensive emergency is primarily used as a specific term for a hypertensive crisis with a diastolic blood pressure greater than or equal to 120 mmHg or systolic blood pressure greater than or equal to 180 mmHg. Hypertensive emergency differs from hypertensive crisis in that, in the former, there is evidence of acute organ damage.

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.

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.

Diastolic heart failure and diastolic dysfunction refer to the decline in performance of one (usually the left ventricle) or both (left and right) ventricles during diastole. Diastole is the cardiac cycle phase during which the heart is relaxing and filling with incoming blood that is being returned from the body through the inferior (IVC) and superior (SVC) venae cavae to the right atrium and from lungs through pulmonary veins to the left atrium. In diastolic failure, if the patient has symptoms, there is a pathologic cause inducing them. Diastolic dysfunction can be found when doing a Doppler echocardiography in an apparently healthy patient, mainly in an elderly person.

High-output heart failure is a heart condition that occurs when the cardiac output is higher than normal due to increased peripheral demand. There is a circulatory overload which may lead to pulmonary edema secondary to an elevated diastolic pressure in the left ventricle. These individuals usually have a normal systolic function but symptoms are those of heart failure. With time, this overload causes systolic failure. Ultimately cardiac output can be reduced to very low levels.

It may occur in situations with an increased blood volume, from excess of water and salt (kidney pathology, excess of fluid or blood administration, treatment with retaining water steroids), chronic and severe anemia, large arteriovenous fistula or multiple small arteriovenous shunts as in HHT or Paget's disease of bone, some forms of severe liver or kidney disorders, hyperthyroidism, and wet beriberi, and acutely in septic shock, especially caused by Gram-negative bacteria.

Cardiac:

- constrictive pericarditis. One study found that pulsus paradoxus occurs in less than 20% of patients with constrictive pericarditis.

- pericardial effusion, including cardiac tamponade

- cardiogenic shock

Pulmonary:

- pulmonary embolism

- tension pneumothorax

- asthma (especially with severe asthma exacerbations)

- chronic obstructive pulmonary disease

Non-pulmonary and non-cardiac:

- anaphylactic shock

- hypovolemia

- superior vena cava obstruction

- pregnancy

- obesity

PP has been shown to be predictive of the severity of cardiac tamponade. Pulsus paradoxus may not be seen with cardiac tamponade if an atrial septal defect or significant aortic regurgitation is also present.

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.

People with TIC most often present with symptoms of congestive heart failure and/or symptoms related to their irregular heart rhythm. Symptoms of congestive heart failure can include shortness of breath, ankle swelling, fatigue, and weight gain. Symptoms of an irregular heart rhythm can include palpitations and chest discomfort.

The timecourse of TIC is most well-studied in experiments on animals. Researchers have found that animals began to exhibit abnormal changes in blood flow after just one day of an artificially generated fast heart rate (designed to simulate a tachyarrythmia). As their TIC progresses, these animals will have worsening heart function (e.g.: reduced cardiac output and reduced ejection fraction) for 3–5 weeks. The worsened heart function then persists at a stable state until the heart rate is returned to normal. With normal heart rates, these animals begin to demonstrate improving heart function at 1–2 days, and even complete recovery of ejection fraction at 1 month.

Human studies of the timecourse of TIC are not as robust as animal studies, though current studies suggest that the majority of people with TIC will recover a significant degree of heart function over months to years.

Pulsus paradoxus, also paradoxic pulse or paradoxical pulse, is an abnormally large decrease in stroke volume, systolic blood pressure and pulse wave amplitude during inspiration. The normal fall in pressure is less than 10 mmHg. When the drop is more than 10 mmHg, it is referred to as pulsus paradoxus. Pulsus paradoxus is not related to pulse rate or heart rate and it is not a paradoxical rise in systolic pressure. The normal variation of blood pressure during breathing/respiration is a decline in blood pressure during inhalation and an increase during exhalation. Pulsus paradoxus is a sign that is indicative of several conditions, including cardiac tamponade, chronic sleep apnea, croup, and obstructive lung disease (e.g. asthma, COPD).

The "paradox" in "pulsus paradoxus" is that, on physical examination, one can detect beats on cardiac auscultation during inspiration that cannot be palpated at the radial pulse. It results from an accentuated decrease of the blood pressure, which leads to the (radial) pulse not being palpable and may be accompanied by an increase in the jugular venous pressure height (Kussmaul's sign). As is usual with inspiration, the heart rate is slightly increased, due to decreased left ventricular output.

One particularity of diabetic cardiomyopathy is the long latent phase, during which the disease progresses but is completely asymptomatic. In most cases, diabetic cardiomyopathy is detected with concomitant hypertension or coronary artery disease. One of the earliest signs is mild left ventricular diastolic dysfunction with little effect on ventricular filling. Also, the diabetic patient may show subtle signs of diabetic cardiomyopathy related to decreased left ventricular compliance or left ventricular hypertrophy or a combination of both. A prominent “a” wave can also be noted in the jugular venous pulse, and the cardiac apical impulse may be overactive or sustained throughout systole. After the development of systolic dysfunction, left ventricular dilation and symptomatic heart failure, the jugular venous pressure may become elevated, the apical impulse would be displaced downward and to the left. Systolic mitral murmur is not uncommon in these cases. These changes are accompanied by a variety of electrocardiographic changes that

may be associated with diabetic cardiomyopathy in 60% of patients without structural heart disease, although usually not in the early asymptomatic phase. Later in the progression, a prolonged QT interval may be indicative of fibrosis. Given that diabetic cardiomyopathy’s definition excludes concomitant atherosclerosis or hypertension, there are no changes in perfusion or in atrial natriuretic peptide levels up until the very late stages of the disease, when the hypertrophy and fibrosis become very pronounced.

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.

In left ventricular dysfunction, the ejection fraction will decrease significantly, causing reduction in stroke volume, hence causing an increase in end-diastolic volume. As a result, during the next cycle of systolic phase, the myocardial muscle will be stretched more than usual and as a result there will be an increase in myocardial contraction, related to the Frank–Starling physiology of the heart. This results, in turn, in a stronger systolic pulse. There may initially be a tachycardia as a compensatory mechanism to try to keep the cardiac output constant.

Tachycardia-induced cardiomyopathy (TIC) is a disease where prolonged tachycardia (a fast heart rate) or arrhythmia (an irregular heart rhythm) cause an impairment of the myocardium (heart muscle), which can result in heart failure. People with TIC may have symptoms associated with heart failure (e.g. shortness of breath or ankle swelling) and/or symptoms related to the tachycardia or arrhythmia (e.g. palpitations). Though atrial fibrillation is the most common cause of TIC, several tachycardias and arrhythmias have been associated with the disease.

There are no formal diagnostic criteria for TIC. Thus, TIC is typically diagnosed when (1) tests have excluded other causes of cardiomyopathy and (2) there is improvement in myocardial function after treatment of the tachycardia or arrhythmia. Treatment of TIC can involve treating the heart failure as well as the tachycardia or arrhythmia. TIC has a good prognosis with treatment, with most people recovering some to all of their heart function.

The number of cases that occur is unclear. TIC has been reported in all age groups.

Untreated hearts with RCM often develop the following characteristics:

- M or W configuration in an invasive hemodynamic pressure tracing of the RA

- Square root sign of part of the invasive hemodynamic pressure tracing Of The LV

- Biatrial enlargement

- Thickened LV walls (with normal chamber size)

- Thickened RV free wall (with normal chamber size)

- Elevated right atrial pressure (>12mmHg),

- Moderate pulmonary hypertension,

- Normal systolic function,

- Poor diastolic function, typically Grade III - IV Diastolic heart failure.

Those afflicted with RCM will experience decreased exercise tolerance, fatigue, jugular venous distention, peripheral edema, and ascites. Arrhythmias and conduction blocks are common.

Symptoms usually include one or more of the following: orthopnea (difficulty breathing while lying flat), dyspnea (shortness of breath on exertion), pitting edema (swelling), cough, frequent night-time urination, excessive weight gain during the last month of pregnancy (1-2+ kg/week; two to four or more pounds per week), palpitations (sensation of racing heart-rate, skipping beats, long pauses between beats, or fluttering), and chest pain.

The shortness of breath is often described by PPCM patients as the inability to take a deep or full breath or to get enough air into the lungs. Also, patients often describe the need to prop themselves up overnight by using two or more pillows in order to breathe better. These symptoms, swelling, and/or cough may be indications of pulmonary edema (fluid in the lungs) resulting from acute heart failure and PPCM.

Unfortunately, patients and clinicians sometimes dismiss early symptoms because they appear to be typical of normal pregnancy. Yet, early detection and treatment are critically important to the patient with PPCM. Delays in diagnosis and treatment of PPCM are associated with increased morbidity and mortality.

It is important to note that occasionally patients present with other signs or symptoms. This is demonstrated by one report of a woman with liver failure five weeks postpartum who was being considered for liver transplant. An echocardiogram was performed and revealed PPCM and heart failure as the cause of her severe liver failure. Conventional heart failure medications were administered. She survived and completely recovered from both the liver failure and PPCM.

It is also quite common for women to present with evidence of having an embolus (clot) passing from the heart to a vital organ, causing such complications as stroke, loss of circulation to a limb, even coronary artery occlusion (blockage) with typical myocardial infarction (heart attack).

For these reasons, it is paramount that clinicians hold a high suspicion of PPCM in any peri- or postpartum patient where unusual or unexplained symptoms or presentations occur.

Any condition or process that leads to stiffening of the left ventricle can lead to diastolic dysfunction. Causes of left ventricular stiffening include:

- A long-standing hypertension where, as a result of left ventricular muscle hypertrophy caused by the high pressure, the left ventricle has become stiff.

- Aortic stenosis of any cause where the ventricular muscle becomes hypertrophied, and thence stiff, as a result of the increased pressure load placed on it by the stenosis.

- Diabetes

- Age – elderly patients mainly if they have hypertension.

Causes of isolated right ventricular diastolic failure are uncommon. These causes include:

- Constrictive pericarditis

- Restrictive cardiomyopathy, which includes Amyloidosis (most common restrictive), Sarcoidosis and fibrosis.

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

Restrictive cardiomyopathy (RCM) is a form of cardiomyopathy in which the walls of the heart are rigid (but not thickened). Thus the heart is restricted from stretching and filling with blood properly. It is the least common of the three original subtypes of cardiomyopathy: hypertrophic, dilated, and restrictive.

It should not be confused with constrictive pericarditis, a disease which presents similarly but is very different in treatment and prognosis.

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.