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Case Study of Low Blood Pressure

Info: 5315 words (21 pages) Nursing Case Study Published: 12th Feb 2020

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  • Mr Jones has a BP of 90/60. Please name the appropriate health terminology in relation to his BP. Normal Range =

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  • Heart arrhythmias
  • Heart failure
  • Heat exhaustion or heat stroke
  • Hormonal issues such as an under-active thyroid, diabetes, or low blood sugar
  • Liver disease
  • Some over-the-counter drugs
  • Some prescription medications
  • Widening of the blood vessels
  • A reaction to alcohol or medication
  • Anaphylaxis, a severe allergic reaction
  • Heart muscle disease
  • High body temperature
  • Loss of blood
  • Low body temperature
  • Severe dehydration from diarrhoea, vomiting, or fever

Systolic pressure (mm Hg)

Diastolic pressure (mm Hg)

Pressure Range

90

60

Borderline Low blood Pressure

60

40

Too Low Blood Pressure

50

33

Dangerously Low Blood Pressure

Systolic pressure (mm Hg)

Diastolic pressure (mm Hg)

Pressure Range

130

85

High Normal Blood Pressure

120

80

Normal Blood Pressure

110

75

Low Normal Blood Pressure

Systolic pressure (mm Hg)

Diastolic pressure (mm Hg)

Stages of High Blood Pressure

210

120

Stage 4

180

110

Stage 3

160

100

Stage 2

140

90

Stage 1

case study on low blood pressure

116

76

122

78

126

82

136

86

120

85

120

79

121

80

122

81

123

82

125

83

127

84

129

85

131

86

134

87

80/34 – 120/75

83/38 – 117/76

88/47 – 128/84

88/50 – 122/83

92/53 – 130/90

93/55 – 129/88

  • Mr Jones has a HR of 153. Please name the appropriate health terminology in relation to his HR reading. Normal Range =

case study on low blood pressure

  • Atrial fibrillation (AF or AFib) is the most common SVT. During AF, the heartbeat produced by the atria is irregular and rapid, sometimes up to 4 times faster than normal. This impairs the heart’s ability to efficiently pump blood and increases the risk of developing blood clots which can cause a transient ischemic attack (TIA) or stroke.
  • Atrial flutter (AFL) is similar to atrial fibrillation in that it is characterised by a rapid heartbeat, sometimes up to 4 times faster than normal that originates in the atria. It differs from atrial fibrillation (AF) in that the heartbeat is regular, not irregular. Atrial flutter also carries the risk of developing blood clots, though not as great as with AF. With atrial flutter, the electrical signal becomes “trapped” in the right atrium. It repeatedly travels in a circular pattern inside the right atrium, only occasionally “escaping” through the AV node to the ventricles. This causes your atria to beat faster than the ventricles of your heart, at rates between 150 and 450 beats each minute.
  • Atrioventricular nodal re-entrant tachycardia (AVNRT) is the second most common SVT. In a normal heart, there is a single electrical pathway, or “gate”, called an atrioventricular node (AV node) that controls the timing and direction of the electrical signal as it travels from the upper chambers (atria) to the lower chambers (ventricles) of the heart. With AVNRT, an extra electrical pathway forms which allows the electrical signal to travel backward through the “gate” (AV Node) at the same time, starting another heartbeat. During AVNRT the electrical signals continuously go around the 2 pathways in a circular pattern called re-entry. This can lead to a very fast heart rate of 160 to 220 beats per minute.
  • Atrioventricular reciprocating tachycardia (AVRT) is similar to AVNRT in that an extra electrical pathway is formed that allows the electrical signal to travel backward from the ventricles to the atria. However, in AVRT the extra pathway circumvents the AV node, or “gate”. This extra pathway around the outside of the AV node is called an accessory pathway.

case study on low blood pressure

  • Ventricular Fibrillation (VF) is a tachycardia which causes the ventricles to contract in an irregular and very rapid manner. The heart immediately loses its ability to pump blood throughout the body. VF causes immediate loss of consciousness, and is invariably fatal within minutes unless it is stopped (usually by using a defibrillator.)

120-160

90-140

80-110

75-100

60-90

60-100

case study on low blood pressure

  • Mr Jones has oxygen saturations of 75%. Please name the appropriate health terminology in relation to his oxygen saturations. Normal Range =

case study on low blood pressure

Severity

% Saturation

None/Minimal

95-100%

Mild

90-94%

Moderate

80-89%

Severe

  • Mr Jones has a RR of 6. Please name the appropriate health terminology in relation to his RR reading. Normal Range =

case study on low blood pressure

35-40

30-50

25-32

20-30

16-20

12-20

  • Mr Jones has a temperature of 39 C. Please name the appropriate health terminology in relation to his temperature reading. Normal Range =

Measurement site

Mouth / Armpit

Ear / forehead

Rectum

Low temperature

Normal temperature

35.9 – 37.0 â-¦C

35.8 – 36.9 â-¦C

36.3 – 37.5 â-¦C

You are perfectly well

Increased temperature

37.1 – 37.5 â-¦C

37.0 – 37.5 â-¦C

37.6 – 38.0 â-¦C

You should get some rest

Light fever

37.6 – 38.0 â-¦C

37.6 – 38.0 â-¦C

38.1 – 38.5 â-¦C

Check your temperature regularly and rest

Moderate fever

38.1 – 38.5 â-¦C

38.1 – 38.5 â-¦C

38.6 – 39.0 â-¦C

Check your temperature regularly. Consult a doctor if you get worse or if the fever lasts for more than three days

High fever

38.6 – 39.5 â-¦C

38.6 – 39.4 â-¦C

39.1 – 39.9 â-¦C

Consult a doctor, especially if the fever lasts for more than one day

Very high fever

39.6 – 42.0 â-¦C

39.5 – 42.0 â-¦C

40.0 – 42.5 â-¦C

Go to emergency ward of a hospital

case study on low blood pressure

  • Please explain what the term dysphagia means in words that MR Jones can understand.

case study on low blood pressure

  • Please describe hemiplegia as if you were explaining what this term meant to a family member of Mr Jones and how would this impact on taking his blood pressure?

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  • Low blood pressure (hypotension)

To find out if you have low blood pressure, also called hypotension, your healthcare professional gives you a physical exam. You're also asked questions about your medical history. The exam includes checking your blood pressure.

You also can measure your blood pressure at home. Checking your blood pressure at home can help your healthcare professional diagnose high blood pressure earlier than usual. Ask a member of your healthcare team to:

  • Help you pick a blood pressure monitor.
  • Tell you how often to check your blood pressure.
  • Explain what blood pressure numbers should prompt you to call the medical office right away.

If you get a home blood pressure reading at or just below 90/60 mm Hg, it's not always a cause for concern. Your healthcare professional might tell you that the reading is OK for you, especially if you have no symptoms.

A tilt table test

  • Tilt table test

Someone having a tilt table test begins by lying flat on a table. Straps hold the person in place. After lying flat for a while, the table is tilted to a position that mimics standing. The healthcare professional watches how the heart and the nervous system that controls it respond to the changes in position.

Other tests may be done to find out the cause of low blood pressure.

  • Blood tests. Blood tests can help find symptoms of other conditions that can lower blood pressure. These include low blood sugar, also called hypoglycemia; high blood sugar, also called hyperglycemia or diabetes; and a low red blood cell count, also called anemia.
  • Electrocardiogram (ECG or EKG). This quick and painless test measures the electrical activity of the heart. During an ECG, sensors called electrodes are attached to the chest and sometimes to the arms or legs. Wires attached to the sensors connect to a machine that displays or prints out results. An ECG shows how fast or slow the heart is beating. It can be used to detect a current or previous heart attack.
  • Tilt table test. A tilt table test can study how the body reacts to changes in position. The test involves lying on a table that's tilted to raise the upper part of the body. This mimics the movement from lying down to standing up. Straps hold the body in place. Heart rate and blood pressure are tracked during the test.

More Information

  • Blood pressure test
  • Echocardiogram
  • Electrocardiogram (ECG or EKG)
  • Stress test

Compression stockings

Compression stockings

Compression stockings, also called support stockings, press on the legs, improving blood flow. A stocking butler may help with putting on the stockings.

Low blood pressure without symptoms or with only mild symptoms rarely requires treatment.

If low blood pressure causes symptoms, the treatment depends on the cause. For instance, if medicine causes low blood pressure, your healthcare professional may recommend changing or stopping the medicine. Or the dose of medicine might be lowered. Don't change or stop taking your medicine without first talking to your healthcare professional.

If the cause of low blood pressure isn't clear or if no treatment exists, the goal is to raise blood pressure and relieve symptoms. Depending on your age, health and the type of low blood pressure you have, there are various ways to do this:

  • Use more salt. Experts usually recommend limiting table salt and foods high in sodium. That's because salt and sodium can raise blood pressure, sometimes by a lot. For people with low blood pressure, though, that can be a good thing. But too much salt or sodium can lead to heart failure, especially in older adults. So it's important to check with a healthcare professional before eating more salt or high-sodium foods.
  • Drink more water. Fluids increase blood volume and help prevent dehydration, both of which are important in treating hypotension.
  • Wear compression stockings. Also called support stockings, these elastic stockings are often used to relieve the pain and swelling of varicose veins. They improve blood flow from the legs to the heart. Some people have an easier time using compression belts around the stomach area than they do using compression stockings. The compression belts are called abdominal binders.

Medicines. Various medicines can treat low blood pressure that occurs when standing up, also called orthostatic hypotension. For example, the drug fludrocortisone boosts blood volume. It's often used to treat orthostatic hypotension.

If you have long-term orthostatic hypotension, midodrine (Orvaten) may be prescribed to raise standing blood pressure levels. This medicine lessens the ability of the blood vessels to expand, which raises blood pressure.

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Lifestyle and home remedies

Depending on the reason for low blood pressure, the following lifestyle and home remedies might help ease or prevent symptoms:

  • Drink more water, less alcohol. Alcohol is dehydrating and can lower blood pressure, even in moderation. Water boosts the amount of blood in the body and prevents dehydration.

Pay attention to body positions. Gently move from lying flat or squatting to a standing position. Don't sit with legs crossed.

If symptoms of low blood pressure begin while standing, cross the thighs like a pair of scissors and squeeze. Or put one foot on a ledge or chair and lean as far forward as you can. These moves encourage blood flow from the legs to the heart.

Eat small, low-carb meals. To help prevent blood pressure from dropping sharply after meals, eat small meals several times a day. Limit high-carbohydrate foods such as potatoes, rice, pasta and bread.

A healthcare professional also might recommend drinking one or two strong cups of caffeinated coffee or tea with breakfast. Caffeine can cause dehydration, though, so be sure to drink plenty of water and other fluids without caffeine.

  • Exercise regularly. As a general goal, work up to at least 150 minutes of moderate aerobic exercise a week. For example, you could aim to get about 30 minutes of activity most days. Also, aim to do strength-training exercises at least twice a week. But try not to exercise in hot, humid conditions.

Preparing for your appointment

You don't have to take any special steps to prepare to have your blood pressure checked. Don't stop taking medicines you think might affect your blood pressure without a healthcare professional's advice.

Here's some information to help you get ready for your appointment.

What you can do

Make a list of:

  • Symptoms. Include any that do not seem related to low blood pressure, and when they occur.
  • Blood pressure readings. If you track your blood pressure at home, keep a log of your blood pressure readings. Note multiple readings at different times of day. Also note when you have symptoms and whether they happened when your blood pressure was low.
  • Important personal information. Include any family history of low blood pressure and major stresses or recent life changes.
  • All medicines, vitamins or other supplements you use. Include the doses you take.
  • Questions to ask your healthcare professional.

For low blood pressure, basic questions to ask your healthcare professional include:

  • What is likely causing my symptoms or condition?
  • What are other possible causes?
  • What tests will I need?
  • What's the most appropriate treatment?
  • How often should I be screened for low blood pressure?
  • I have other health conditions. How can I best manage them together?
  • Are there restrictions I need to follow?
  • Should I see a specialist?
  • Are there brochures or other printed materials I can have? What websites do you recommend?

Feel free to ask other questions.

What to expect from your doctor

Your healthcare professional is likely to ask you questions, including:

  • Do you always have symptoms of low blood pressure, or do they come and go?
  • How severe are your symptoms?
  • What, if anything, seems to improve your symptoms?
  • What, if anything, appears to make your symptoms worse?
  • Do you have a family history of heart disease?
  • Low blood pressure. National Heart, Lung, and Blood Institute. https://www.nhlbi.nih.gov/health-topics/low-blood-pressure. Accessed Feb. 10, 2022.
  • Understanding blood pressure readings. American Heart Association. https://www.heart.org/en/health-topics/high-blood-pressure/understanding-blood-pressure-readings. Accessed Feb. 10, 2022.
  • AskMayoExpert. Orthostatic hypotension. Mayo Clinic; 2021.
  • Palma JA, et al. Mechanisms, causes, and evaluation of orthostatic hypotension. https://www.uptodate.com/contents/search. Accessed Jan. 24, 2022.
  • Low blood pressure: When blood pressure is too low. American Heart Association. https://www.heart.org/en/health-topics/high-blood-pressure/the-facts-about-high-blood-pressure/low-blood-pressure-when-blood-pressure-is-too-low. Accessed Feb. 10, 2022.
  • Orthostatic hypotension. Merck Manual Professional Version. https://www.merckmanuals.com/professional/cardiovascular-disorders/symptoms-of-cardiovascular-disorders/orthostatic-hypotension. Accessed March 3, 2022.
  • Palma JA, et al. Treatment of orthostatic and postprandial hypotension. https://www.uptodate.com/contents/search. Accessed Jan. 24, 2022.
  • Sheikh AB, et al. Blood pressure variability in clinical practice: Past, present and the future. Journal of the American Heart Association. 2023; doi:10.1161/JAHA.122.029297.
  • Physical Activity Guidelines for Americans. 2nd ed. U.S. Department of Health and Human Services. https://health.gov/our-work/physical-activity/current-guidelines. Accessed Jan. 24, 2022.
  • AskMayoExpert. Physical activity (adult). Mayo Clinic; 2021.
  • Laughlin EA, et al. Increased salt intake for orthostatic intolerance syndromes: A systematic review and meta-analysis. The American Journal of Medicine. 2020; doi:10.1016/j.amjmed.2020.05.028.
  • Rosei EA, et al. How important is blood pressure variability? European Heart Journal Supplements. 2020; doi:10.1093/eurheartj/suaa061.
  • Lopez-Jimenez F (expert opinion). Mayo Clinic. Dec. 13, 2023.

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  • Heart Health

Low Blood Pressure (Hypotension): Symptoms, Causes, and Treatment

case study on low blood pressure

  • What Is Low Blood Pressure?

Hypotension is the medical term for low blood pressure . You have it when a reading shows your blood pressure is much lower than expected. 

A blood pressure reading appears as two numbers. The top number is a measure of systolic pressure, or the pressure in the arteries when the heart beats and fills them with blood. The bottom number measures diastolic pressure, the pressure in the arteries when the heart rests between beats. The optimal blood pressure level is less than 120/80. (You may also see it written as 120/80 mmHg). 

What is considered low blood pressure?

Doctors consider you to have low blood pressure when your reading is less than 90/60. 

The risk of both low and high blood pressure increases with age due in part to normal changes during aging. 

Is low blood pressure serious?

In healthy people, low blood pressure without any symptoms isn't usually a concern and doesn't require treatment. But low blood pressure can be a sign of an underlying problem -- especially in older people -- and could reduce blood flow to the heart, brain, and other vital organs.

Long-lasting low blood pressure with no symptoms is almost never serious. But you can have health problems when your blood pressure drops suddenly and your brain doesn't have an adequate blood supply. This can lead to dizziness , lightheadedness, and sometimes fainting. 

Types of low blood pressure

There are several types of low blood pressure:

  • Postural hypotension. Sudden drops in blood pressure most often happen when you rise from a lying or sitting position to standing. This is called postural hypotension or orthostatic hypotension. It happens when your cardiovascular or nervous system doesn't react appropriately to sudden position changes. An estimated 10% to 20% of people over 65 have postural hypotension.
  • Neurally mediated hypotension . You can get this type when you stand up for a long time. It's thought to happen because of communication problems between your brain and your heart. It's more common in younger people.
  • Postprandial hypotension. Sometimes, your blood pressure drops an hour or two after a meal. It’s thought to be caused by blood pooling into the vessels of the stomach and intestines . It's most common in older people with high blood pressure or nervous system conditions like Parkinson's disease. It tends to happen after large meals containing  lots of carbohydrates. 
  • Multiple system atrophy with orthostatic hypotension. This rare type of low blood pressure happens when you're lying down. It involves your involuntary nervous system, which controls things like your blood pressure, breathing, and heart rate. 

 Causes of Low Blood Pressure

The cause of low blood pressure isn't always clear. It may be linked to:

  • Hormonal problems such as an underactive thyroid (hypothyroidism), diabetes, or low blood sugar (hypoglycemia)
  • Some over-the-counter medications
  • Some prescription medicines such as for high blood pressure, depression, or Parkinson’s disease
  • Heart failure
  • Heart arrhythmias (abnormal heart rhythms)
  • Heart valve disease
  • Widening, or dilation, of the blood vessels
  • Heat exhaustion or heat stroke
  • Liver disease
  • Bed rest for long periods
  • Anemia caused by shortages of vitamin B12, iron, and folate

What Causes a Sudden Drop in Blood Pressure?

Sudden drops in blood pressure can be life-threatening. Causes of this type of hypotension include:

  • Loss of blood from bleeding
  • Low body temperature
  • High body temperature
  • Heart muscle disease causing heart failure
  • Sepsis, a severe blood infection
  • Severe dehydration from vomiting, diarrhea, or fever
  • A reaction to medication or alcohol
  • A severe allergic reaction called anaphylaxis that causes an irregular heartbeat

Postural Hypotension

Postural hypotension, which causes dizziness upon standing, can happen to anyone for a variety of reasons, such as dehydration, lack of food, or being overly fatigued. It can also be influenced by:

  • Psychological factors
  • Conditions like infection and allergy

Postural hypotension happens most often in people who are taking drugs to control high blood pressure (hypertension). It can also be related to pregnancy, strong emotions, hardening of the arteries (atherosclerosis), or diabetes . Older people are particularly affected, especially those who have high blood pressure or autonomic nervous system dysfunction.

Several drugs are linked to postural hypotension. They can be divided into two main categories:

  • Drugs used to treat high blood pressure, such as diuretics, beta-blockers, calcium-channel blockers, and angiotensin-converting enzyme (ACE) inhibitors
  • Drugs that have hypotension as a side effect, including nitrates, erectile dysfunction (ED) medications, drugs for Parkinson's disease, antipsychotics, neuroleptics, anti-anxiety agents, sedative-hypnotics, and tricyclic antidepressants

Common causes of naturally occurring postural hypotension include:

  • Dehydration and electrolyte loss, which may result from diarrhea, vomiting, excessive blood loss during your period, or other conditions
  • Age-related declines in blood pressure regulation, which may be made worse by certain health conditions or medications

Certain diseases can also cause postural hypotension. These include:

  • Nerve problems, such as peripheral neuropathy or autonomic neuropathy
  • Cardiovascular disorders
  • Nutritional diseases

What Are the Symptoms of Low Blood Pressure? 

Low blood pressure symptoms can include:

  • Lightheadedness
  • Unsteadiness
  • Dimming or blurring of vision
  • Agitation or other behavior changes
  • Fatigue or lethargy
  • Cold, clammy skin

If your blood pressure gets seriously low, your body might not get enough oxygen to carry out its normal functions. That can impair the functioning of your heart and brain and cause breathing problems. You could lose consciousness or go into shock (when the organs shut down). Shock symptoms may include: 

  • Turning pale
  • Skin that feels cold
  • Fast breathing
  • Weak, quick pulse

How Do I Know if I Have Low Blood Pressure?

Low blood pressure doesn't always signal a problem. But if you have signs of low blood pressure, your doctor can diagnose the condition and uncover the cause. Then you can get the right treatment.

The doctor will look at your medical history, age, and symptoms, and do a  physical exam . They may repeatedly check your blood pressure and pulse rate -- after you've been lying down for a few minutes, right after you stand up, and within a few minutes after you stand quietly.

You might have other tests, such as an ECG (electrocardiogram) to measure heart rate and rhythm and an echocardiogram (an ultrasound test to visualize the heart). You may also have blood tests to look for anemia or problems with your blood sugar levels.

Your doctor might recommend more sophisticated home ECG monitoring (a Holter monitor or "event" monitor) to check for heart problems that come and go or an irregular heartbeat that can cause your blood pressure to drop suddenly.

An  exercise stress test or, less commonly, an electrophysiology test (EP test) may also be helpful.

With some types of postural hypotension, you may need a "tilt table" test. It evaluates your body's reaction to changes in position. You lie on a table,  safely strapped in, and the table is raised to an upright position for up to an hour. Your blood pressure, heart rate, and symptoms are recorded. You might be given a drug that helps your doctor figure out what's going on.

What Are the Treatments for Low Blood Pressure?

For many people, chronic low blood pressure can be effectively treated with diet and lifestyle changes. Others need medication to manage their symptoms.

Lifestyle changes to lower blood pressure

 Depending on the cause of your symptoms, your doctor may tell you to increase your blood pressure by making these simple changes:

  • Eat a diet higher in salt.
  • Drink lots of nonalcoholic fluids.
  • Limit  alcoholic beverages.
  • Drink more fluids during hot weather and while sick with a viral illness, such as a cold or the flu.
  • Have your doctor check your prescription and over-the-counter medications to see if any of them are causing your symptoms.
  • Get regular exercise to promote blood flow.
  • Be careful when rising from lying down or sitting. To improve circulation, pump your feet and ankles a few times before standing up. Then go slowly. When you get out of bed, sit upright on the edge of the bed for a few minutes before standing.
  • Raise the head of your bed at night by placing bricks or blocks under it.
  • Avoid heavy lifting.
  • Avoid straining while on the toilet.
  • Avoid standing still for long periods.
  • Avoid prolonged exposure to hot water, such as hot showers and spas. If you get dizzy, sit down. It may help to keep a chair or stool in the shower in case you need to sit. To prevent injury, use a nonslip chair or stool designed for use in showers and bath tubs.
  • To avoid problems with low blood pressure and lessen episodes of  dizziness after meals, try eating smaller, more frequent meals. Cut back on carbohydrates. Rest after eating. Avoid taking drugs to lower blood pressure before meals.

If needed, use elastic support (compression) stockings that cover the calf and thigh. These help restrict blood flow to your legs, thus keeping more blood in your upper body.

Medications for low blood pressure

If these steps don't lessen the problem, you may need medication. These drugs are sometimes used to treat low blood pressure:

  • Fludrocortisone. This medication seems to help some types of low blood pressure. It works by promoting sodium retention by your  kidneys . This causes fluid retention and some swelling, which is necessary to improve blood pressure. But sodium retention also causes a loss of potassium. So when taking fludrocortisone, make sure you get enough potassium each day. Fludrocortisone has none of the anti-inflammatory properties of cortisone or prednisone and doesn't build muscle like anabolic steroids.
  • Midodrine. This drug activates receptors on your smallest arteries and veins to boost blood pressure. It's used to increase standing blood pressure in people who have postural hypotension related to problems with the nervous system . 

Complications of Low Blood Pressure

Complications you could develop because of low blood pressure include:

  • Falls. Dizziness caused by low blood pressure can make you fall or faint. Falls can result in injuries, sometimes serious ones.
  • Heart problems or stroke : Your heart might try to make up for low blood pressure by pumping too hard or too fast. That can lead to problems like heart failure, stroke, or deep vein thrombosis (DVT).
  • Shock. Seriously low blood pressure can limit blood supply to your organs so much that you go into shock. If you have symptoms of shock, call 911 right away.

Low blood pressure during pregnancy can lead to an increased risk of falls. But there's no scientific evidence that low blood pressure by itself is harmful to your baby unless it gets low enough to send you into shock. 

 When to Call a Doctor

Call your doctor if:

  • You have any of the symptoms listed above.
  • You've been diagnosed with low blood pressure and are more often having symptoms, such as falling down or passing out.
  • You have symptoms as a result of taking prescription or nonprescription medication .

Low blood pressure often has no symptoms and doesn't require treatment. But seriously low blood pressure can lead to complications. See your doctor if you have low blood pressure symptoms.   

Low Blood Pressure FAQs

What are the reasons for low blood pressure?

Many different things can cause low blood pressure, including:

  • Dehydration
  • Fear, stress, or pain
  • Donating blood
  • Some injuries and illnesses
  • Certain medications 

What is considered a dangerously low blood pressure?

Blood pressure under 90/60 is considered low. But some people normally have low blood pressure. Most doctors think of low blood pressure as dangerous only if it causes noticeable symptoms. 

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case study on low blood pressure

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Study on diastolic blood pressure could change how doctors treat some patients with hypertension

Medical pills for hypertension next to equipment for measuring blood pressure in the background.

Intensive lowering of diastolic blood pressure—the bottom reading in blood pressure measurements— does not appear to be linked to an increased risk of heart attacks and other adverse cardiovascular outcomes, according to a large new study. The findings could change how physicians interpret this reading and how some patients with hypertension are treated in the future, researchers suggest.

The NHLBI’s landmark SPRINT study indicated that intensive blood pressure management—lowering systolic blood pressure to less than 120 millimeters of mercury (mm Hg)—can significantly reduce the risk of heart disease, stroke, and death compared to blood pressure targets of less than 140 mm Hg. By contrast, recent observational studies suggest that intensive lowering of diastolic blood pressure might increase the risk of adverse cardiovascular events, including heart attack. To determine whether very low diastolic blood pressure triggered cardiovascular events, researchers analyzed genetic and health data in over 47,000 adult patients enrolled in five study groups worldwide: ARIC, the Framingham Heart Study, the Cardiovascular Health Study, the Multi-Ethnic Study of Atherosclerosis, and the Women’s Health Initiative. The patients had a median age of 60 years and 77% were women. The researchers found no evidence of an increased risk of heart attack when a patient’s diastolic pressure fell to as low as 50 mm Hg. They also found no lower limit of what is considered normal diastolic pressure. As many doctors focus on keeping the bottom blood pressure reading within the 70-90 mm Hg range, the researchers suggest that some patients with high blood pressure may have been undertreated in the past. The study is in agreement with the SPRINT findings indicating that lower blood pressure targets are better for your health, the researchers said. Partly funded by the NHLBI, the new study appeared in Circulation .

Media Coverage

  • New advice for treating high blood pressure
  • New research could change how doctors treat some patients with high blood pressure
  • How Low Can You Go? Diastolic Blood Pressure Standards May Change
  • New Advice For Medics Treating High Blood Pressure
  • Rethinking the ‘J-Curve’: Study Questions Concern Over Too-Low Diastolic BP

Low blood pressure (hypotension)

Low blood pressure is a reading of less than 90/60mmHg. It does not always cause symptoms, but you may need treatment if it does.

Symptoms of low blood pressure

Get your blood pressure checked if you keep getting symptoms like:

  • lightheadedness or dizziness
  • feeling sick
  • blurred vision
  • generally feeling weak

This might mean your blood pressure is too low.

If you get symptoms when you stand up or suddenly change position, you may have a type of low blood pressure called postural hypotension.

Non-urgent advice: See a GP if:

  • you keep getting symptoms of low blood pressure such as dizziness and fainting

How to check your blood pressure

You can check your blood pressure:

  • by asking if a pharmacist can do it
  • by asking a practice nurse or GP to do it
  • at home yourself using a home blood pressure monitor

Low blood pressure is a measurement of less than 90/60mmHg.

Find out about monitoring your blood pressure at home and choosing a monitor from Blood Pressure UK

Understanding your blood pressure reading

If you have a recent blood pressure reading use the NHS Check your blood pressure tool to understand what your reading means. You'll also get information about what to do next.

Important: Regular blood pressure check

If you're 40 to 74 years old, you should have your blood pressure checked at least once every 5 years as part of the NHS Health Check .

Treatment for low blood pressure

If a cause for low blood pressure can be found, a GP will be able to recommend treatment to ease your symptoms.

For example, they may suggest:

  • changing medicines or altering your dose, if this is the cause
  • wearing support stockings – this can improve circulation and increase blood pressure

Medicine to increase blood pressure is rarely needed because simple lifestyle measures or treating the underlying cause is usually effective.

How to ease low blood pressure symptoms yourself

There are things you can do to help with symptoms of low blood pressure.

Do get up slowly from sitting to standing take care when getting out of bed – move slowly from lying to sitting to standing eat small, frequent meals – lying down or sitting still for a while after eating may also help increase the amount of water you drink Don’t

do not sit or stand for long periods

do not bend down or change posture suddenly

do not drink too much alcohol

Causes of low blood pressure

Your blood pressure can vary depending on the time of day.

What you're doing and how you're feeling can also affect it.

There are many possible causes of low blood pressure. It may be low because you're fit and healthy, or you may have inherited it from your parents.

Some people develop low blood pressure as they get older.

It can also be caused by:

  • being pregnant
  • some medical conditions, such as diabetes
  • some medicines

Page last reviewed: 11 July 2023 Next review due: 11 July 2026

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Grounding Patients With Hypertension Improves Blood Pressure: A Case History Series Study

  • PMID: 30982019

Background: Research conducted during the last 15 y has demonstrated that grounding (Earthing) the human body to Earth's surface charge generates multiple beneficial physiological effects. Anecdotal reports include lowering of high blood pressure (BP).

Objective: To test such reports, a pilot case history series was undertaken with hypertensive patients in a single physician cardiology practice.

Intervention: Patients grounded themselves at home for at least 10 h/d for several mo.

Outcome measure: BP was measured at baseline in the clinic, and then, after starting grounding, 3 subsequent times in the clinic again at approximately monthly intervals. Patients were also given a BP monitor and were asked to measure their BP on Mondays, Thursdays, and Saturdays at 8:00 AM and 8:00 PM for 12 wk.

Results: All 10 patient measurements were found to be significantly improved at the end of the trial period, and some, well before the end. Systolic levels decreased during this time, ranging individually from 8.6% to 22.7%, with an average decrease of 14.3%.

Conclusion: This is the first known study measuring the influence of grounding the body on hypertension. The results indicate that grounding appears to be a safe BP-reducing therapy warranting further research.

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Article Contents

Clinical management and treatment decisions, hypertension in black americans, pharmacologic treatment of hypertension in black americans.

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Suzanne Oparil, Case study, American Journal of Hypertension , Volume 11, Issue S8, November 1998, Pages 192S–194S, https://doi.org/10.1016/S0895-7061(98)00195-2

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Ms. C is a 42-year-old black American woman with a 7-year history of hypertension first diagnosed during her last pregnancy. Her family history is positive for hypertension, with her mother dying at 56 years of age from hypertension-related cardiovascular disease (CVD). In addition, both her maternal and paternal grandparents had CVD.

At physician visit one, Ms. C presented with complaints of headache and general weakness. She reported that she has been taking many medications for her hypertension in the past, but stopped taking them because of the side effects. She could not recall the names of the medications. Currently she is taking 100 mg/day atenolol and 12.5 mg/day hydrochlorothiazide (HCTZ), which she admits to taking irregularly because “... they bother me, and I forget to renew my prescription.” Despite this antihypertensive regimen, her blood pressure remains elevated, ranging from 150 to 155/110 to 114 mm Hg. In addition, Ms. C admits that she has found it difficult to exercise, stop smoking, and change her eating habits. Findings from a complete history and physical assessment are unremarkable except for the presence of moderate obesity (5 ft 6 in., 150 lbs), minimal retinopathy, and a 25-year history of smoking approximately one pack of cigarettes per day. Initial laboratory data revealed serum sodium 138 mEq/L (135 to 147 mEq/L); potassium 3.4 mEq/L (3.5 to 5 mEq/L); blood urea nitrogen (BUN) 19 mg/dL (10 to 20 mg/dL); creatinine 0.9 mg/dL (0.35 to 0.93 mg/dL); calcium 9.8 mg/dL (8.8 to 10 mg/dL); total cholesterol 268 mg/dL (< 245 mg/dL); triglycerides 230 mg/dL (< 160 mg/dL); and fasting glucose 105 mg/dL (70 to 110 mg/dL). The patient refused a 24-h urine test.

Taking into account the past history of compliance irregularities and the need to take immediate action to lower this patient’s blood pressure, Ms. C’s pharmacologic regimen was changed to a trial of the angiotensin-converting enzyme (ACE) inhibitor enalapril, 5 mg/day; her HCTZ was discontinued. In addition, recommendations for smoking cessation, weight reduction, and diet modification were reviewed as recommended by the Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VI). 1

After a 3-month trial of this treatment plan with escalation of the enalapril dose to 20 mg/day, the patient’s blood pressure remained uncontrolled. The patient’s medical status was reviewed, without notation of significant changes, and her antihypertensive therapy was modified. The ACE inhibitor was discontinued, and the patient was started on the angiotensin-II receptor blocker (ARB) losartan, 50 mg/day.

After 2 months of therapy with the ARB the patient experienced a modest, yet encouraging, reduction in blood pressure (140/100 mm Hg). Serum electrolyte laboratory values were within normal limits, and the physical assessment remained unchanged. The treatment plan was to continue the ARB and reevaluate the patient in 1 month. At that time, if blood pressure control remained marginal, low-dose HCTZ (12.5 mg/day) was to be added to the regimen.

Hypertension remains a significant health problem in the United States (US) despite recent advances in antihypertensive therapy. The role of hypertension as a risk factor for cardiovascular morbidity and mortality is well established. 2–7 The age-adjusted prevalence of hypertension in non-Hispanic black Americans is approximately 40% higher than in non-Hispanic whites. 8 Black Americans have an earlier onset of hypertension and greater incidence of stage 3 hypertension than whites, thereby raising the risk for hypertension-related target organ damage. 1 , 8 For example, hypertensive black Americans have a 320% greater incidence of hypertension-related end-stage renal disease (ESRD), 80% higher stroke mortality rate, and 50% higher CVD mortality rate, compared with that of the general population. 1 , 9 In addition, aging is associated with increases in the prevalence and severity of hypertension. 8

Research findings suggest that risk factors for coronary heart disease (CHD) and stroke, particularly the role of blood pressure, may be different for black American and white individuals. 10–12 Some studies indicate that effective treatment of hypertension in black Americans results in a decrease in the incidence of CVD to a level that is similar to that of nonblack American hypertensives. 13 , 14

Data also reveal differences between black American and white individuals in responsiveness to antihypertensive therapy. For instance, studies have shown that diuretics 15 , 16 and the calcium channel blocker diltiazem 16 , 17 are effective in lowering blood pressure in black American patients, whereas β-adrenergic receptor blockers and ACE inhibitors appear less effective. 15 , 16 In addition, recent studies indicate that ARB may also be effective in this patient population.

Angiotensin-II receptor blockers are a relatively new class of agents that are approved for the treatment of hypertension. Currently, four ARB have been approved by the US Food and Drug Administration (FDA): eprosartan, irbesartan, losartan, and valsartan. Recently, a 528-patient, 26-week study compared the efficacy of eprosartan (200 to 300 mg/twice daily) versus enalapril (5 to 20 mg/daily) in patients with essential hypertension (baseline sitting diastolic blood pressure [DBP] 95 to 114 mm Hg). After 3 to 5 weeks of placebo, patients were randomized to receive either eprosartan or enalapril. After 12 weeks of therapy within the titration phase, patients were supplemented with HCTZ as needed. In a prospectively defined subset analysis, black American patients in the eprosartan group (n = 21) achieved comparable reductions in DBP (−13.3 mm Hg with eprosartan; −12.4 mm Hg with enalapril) and greater reductions in systolic blood pressure (SBP) (−23.1 with eprosartan; −13.2 with enalapril), compared with black American patients in the enalapril group (n = 19) ( Fig. 1 ). 18 Additional trials enrolling more patients are clearly necessary, but this early experience with an ARB in black American patients is encouraging.

Efficacy of the angiotensin II receptor blocker eprosartan in black American with mild to moderate hypertension (baseline sitting DBP 95 to 114 mm Hg) in a 26-week study. Eprosartan, 200 to 300 mg twice daily (n = 21, solid bar), enalapril 5 to 20 mg daily (n = 19, diagonal bar). †10 of 21 eprosartan patients and seven of 19 enalapril patients also received HCTZ. Adapted from data in Levine: Subgroup analysis of black hypertensive patients treated with eprosartan or enalapril: results of a 26-week study, in Programs and abstracts from the 1st International Symposium on Angiotensin-II Antagonism, September 28–October 1, 1997, London, UK.

Figure 1.

Approximately 30% of all deaths in hypertensive black American men and 20% of all deaths in hypertensive black American women are attributable to high blood pressure. Black Americans develop high blood pressure at an earlier age, and hypertension is more severe in every decade of life, compared with whites. As a result, black Americans have a 1.3 times greater rate of nonfatal stroke, a 1.8 times greater rate of fatal stroke, a 1.5 times greater rate of heart disease deaths, and a 5 times greater rate of ESRD when compared with whites. 19 Therefore, there is a need for aggressive antihypertensive treatment in this group. Newer, better tolerated antihypertensive drugs, which have the advantages of fewer adverse effects combined with greater antihypertensive efficacy, may be of great benefit to this patient population.

1. Joint National Committee : The Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure . Arch Intern Med 1997 ; 24 157 : 2413 – 2446 .

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2. Veterans Administration Cooperative Study Group on Antihypertensive Agents : Effects of treatment on morbidity in hypertension: Results in patients with diastolic blood pressures averaging 115 through 129 mm Hg . JAMA 1967 ; 202 : 116 – 122 .

3. Veterans Administration Cooperative Study Group on Antihypertensive Agents : Effects of treatment on morbidity in hypertension: II. Results in patients with diastolic blood pressures averaging 90 through 114 mm Hg . JAMA 1970 ; 213 : 1143 – 1152 .

4. Pooling Project Research Group : Relationship of blood pressure, serum cholesterol, smoking habit, relative weight and ECG abnormalities to the incidence of major coronary events: Final report of the pooling project . J Chronic Dis 1978 ; 31 : 201 – 306 .

5. Hypertension Detection and Follow-Up Program Cooperative Group : Five-year findings of the hypertension detection and follow-up program: I. Reduction in mortality of persons with high blood pressure, including mild hypertension . JAMA 1979 ; 242 : 2562 – 2577 .

6. Kannel WB , Dawber TR , McGee DL : Perspectives on systolic hypertension: The Framingham Study . Circulation 1980 ; 61 : 1179 – 1182 .

7. Hypertension Detection and Follow-Up Program Cooperative Group : The effect of treatment on mortality in “mild” hypertension: Results of the Hypertension Detection and Follow-Up Program . N Engl J Med 1982 ; 307 : 976 – 980 .

8. Burt VL , Whelton P , Roccella EJ et al.  : Prevalence of hypertension in the US adult population: Results from the third National Health and Nutrition Examination Survey, 1988–1991 . Hypertension 1995 ; 25 : 305 – 313 .

9. Klag MJ , Whelton PK , Randall BL et al.  : End-stage renal disease in African-American and white men: 16-year MRFIT findings . JAMA 1997 ; 277 : 1293 – 1298 .

10. Neaton JD , Kuller LH , Wentworth D et al.  : Total and cardiovascular mortality in relation to cigarette smoking, serum cholesterol concentration, and diastolic blood pressure among black and white males followed up for five years . Am Heart J 1984 ; 3 : 759 – 769 .

11. Gillum RF , Grant CT : Coronary heart disease in black populations II: Risk factors . Heart J 1982 ; 104 : 852 – 864 .

12. M’Buyamba-Kabangu JR , Amery A , Lijnen P : Differences between black and white persons in blood pressure and related biological variables . J Hum Hypertens 1994 ; 8 : 163 – 170 .

13. Hypertension Detection and Follow-up Program Cooperative Group : Five-year findings of the Hypertension Detection and Follow-up Program: mortality by race-sex and blood pressure level: a further analysis . J Community Health 1984 ; 9 : 314 – 327 .

14. Ooi WL , Budner NS , Cohen H et al.  : Impact of race on treatment response and cardiovascular disease among hypertensives . Hypertension 1989 ; 14 : 227 – 234 .

15. Weinberger MH : Racial differences in antihypertensive therapy: evidence and implications . Cardiovasc Drugs Ther 1990 ; 4 ( suppl 2 ): 379 – 392 .

16. Materson BJ , Reda DJ , Cushman WC et al.  : Single-drug therapy for hypertension in men: A comparison of six antihypertensive agents with placebo . N Engl J Med 1993 ; 328 : 914 – 921 .

17. Materson BJ , Reda DJ , Cushman WC for the Department of Veterans Affairs Cooperative Study Group on Antihypertensive Agents : Department of Veterans Affairs single-drug therapy of hypertension study: Revised figures and new data . Am J Hypertens 1995 ; 8 : 189 – 192 .

18. Levine B : Subgroup analysis of black hypertensive patients treated with eprosartan or enalapril: results of a 26-week study , in Programs and abstracts from the first International Symposium on Angiotensin-II Antagonism , September 28 – October 1 , 1997 , London, UK .

19. American Heart Association: 1997 Heart and Stroke Statistical Update . American Heart Association , Dallas , 1997 .

  • hypertension
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Acute Effects of Exercise on Blood Pressure: A Meta-Analytic Investigation

Elizabeth carpio-rivera.

1 School of Physical Education and Sports, University of Costa Rica - Costa Rica

José Moncada-Jiménez

2 Human Movement Sciences Research Center (CIMOHU), University of Costa Rica - Costa Rica

Walter Salazar-Rojas

Andrea solera-herrera.

Author contributions

No potential conflict of interest relevant to this article was reported.

Hypertension affects 25% of the world's population and is considered a risk factor for cardiovascular disorders and other diseases. The aim of this study was to examine the evidence regarding the acute effect of exercise on blood pressure (BP) using meta-analytic measures. Sixty-five studies were compared using effect sizes (ES), and heterogeneity and Z tests to determine whether the ES were different from zero. The mean corrected global ES for exercise conditions were -0.56 (-4.80 mmHg) for systolic BP (sBP) and -0.44 (-3.19 mmHg) for diastolic BP (dBP; z ≠ 0 for all; p < 0.05). The reduction in BP was significant regardless of the participant's initial BP level, gender, physical activity level, antihypertensive drug intake, type of BP measurement, time of day in which the BP was measured, type of exercise performed, and exercise training program (p < 0.05 for all). ANOVA tests revealed that BP reductions were greater if participants were males, not receiving antihypertensive medication, physically active, and if the exercise performed was jogging. A significant inverse correlation was found between age and BP ES, body mass index (BMI) and sBP ES, duration of the exercise's session and sBP ES, and between the number of sets performed in the resistance exercise program and sBP ES (p < 0.05). Regardless of the characteristics of the participants and exercise, there was a reduction in BP in the hours following an exercise session. However, the hypotensive effect was greater when the exercise was performed as a preventive strategy in those physically active and without antihypertensive medication.

Introduction

Exercise training has been shown to reduce blood pressure (BP). 1 - 9 However, studies reporting a reduction in BP resulting from chronic exercise might disregard an acute effect following the exercise session ( i.e. , post-exercise hypotension [PEH]) that is lost over time. 4 Although the mean reductions in ambulatory systolic BP (sBP) and diastolic BP (dBP) monitoring over 24 hours are 3.2 mmHg and 1.8 mm Hg, respectively, 10 the magnitude of the reduction is greater during the first few hours after the exercise, to the point that some subjects with hypertension achieve normal BP values.

The PEH response is measured by comparing BP values after an exercise with the values in a control day in which the exercise is not performed, or by comparing BP values before and after an exercise session. 5 However, findings in the literature are contradictory, not only regarding the conclusion of whether an acute exercise elicits a reduction in BP, but also about the magnitude and duration of the PEH response. These contradictions may be partially explained by the characteristics of the samples ( i.e. , hypertensives versus normotensives), 10 - 18 use of antihypertensive medication, 16 , 17 training status, 19 - 23 participants' age, 24 - 27 and characteristics of the measurement performed. This relates to whether the BP was measured at rest or by ambulatory monitoring, 5 since the latter is more effective in distinguishing the "white coat syndrome" (a transient elevation in BP when the measurements are performed in a laboratory or in the clinic). 28 , 29 Finally, other confounding factors include the duration of the measurement 5 and characteristics of the exercise, such as type ( i.e. , aerobic or resistance), 30 , 31 intensity, 8 , 32 - 35 duration of the session, 7 , 36 , 37 muscles involved, 7 whether the exercise is performed intermittently or continuously, 38 and the time of day when it is performed. 39 , 40

Given this plethora of ambivalent variables, the purpose of this meta-analysis was to determine the effect of acute exercise on the BP response and examine the role of moderator variables.

Search strategy . A systematic search was conducted from August 8, 2012, to March 9, 2013, on the databases MEDLINE (Ovid), SciELO, SPORTDiscus, Google Scholar, ProQuest, SpringerLink, and PubMed. The following keywords were used alone and in combination: "acute effect of exercise", "blood pressure", "hypertension", "post-exercise hypotension", and "physical activity". We performed a hand search of the reference lists of the retrieved studies to detect manuscripts not found by the search in the electronic engines mentioned above.

Inclusion criteria . Studies were included in this meta-analysis if they: 1) were published in English, 2) reported the effect of exercise on BP in the minutes or hours following the training session, 3) reported the mean and standard deviation (SD) or standard error values of the BP in the experimental and control groups before and after the exercise, 4) included only humans, and 5) performed BP readings at rest or ambulatory measurements in the hours that followed the exercise session.

Exclusion criteria . Studies were excluded from this meta-analysis if their data: 1) were used to publish other manuscripts, to prevent their results from being included more than once in our database ( i.e. , studies using the same dataset were taken into consideration only once), and 2) resulted from an interaction between exercise and medication or intervention to evaluate possible physiological mechanisms that might explain the occurrence of PEH.

Variable coding . The coded moderator variables included the characteristics related to the following: 1) studies (number of participants, study quality, experimental condition or group); 2) participants (BP level, gender, medication status, age, body mass index [BMI], physical activity level, maximum oxygen uptake [VO 2 max]); 3) BP measurement (type, duration and time of day when it was performed); and 4) exercise (type, training protocol, training mode, intensity, rest between sets or intervals, and number of exercises, sets, and repetitions). The quality of the studies was determined using the Jadad scale, 41 in which the quality according to the total score is categorized as low when < 3 points, moderate when 3 points, and high when > 3 points. Multiple effect sizes (ES) for the same study were computed for trials with a repeated measures design including multiple interventions. Likewise, the ES was computed for the intervention or control groups when the information was available.

Statistical analysis . The following analyses were computed for each dependent variable (sBP and dBP). To calculate the ES, we followed the procedures described elsewhere. 42 , 43 First, the ES was computed separately for the experimental and control conditions with the following formula: 43 , 44 ES = (Mean post-test - Mean pre-test ) / SD pre-test . Second, the ES was corrected taking into consideration the sample size using the following formula: 44 ES corrected = ES x 1 - (3 / 4 x m - 9) . Once the global corrected ES was obtained, we determined the possibility of a "file-drawer effect" using the following formula: 45 K 0 = K (d 1 - d 2 ) / d 2 ; where K 0 is the number of studies theoretically required to reduce the computed global ES to a non-significant ES, K is the number of meta-analyzed studies, d 1 is the global ES, and d 2 is the non-significant global ES, in this case, 0.20. 46 The Z test was used to determine whether the ES were significantly different from zero. 43 Statistical heterogeneity among the studies was assessed using Cochran's Q test, and the I 2 index. 42 One-way ANOVA was used to determine the global experimental ES and ES differences in the control conditions. 44 One-way ANOVA for independent groups and Pearson's correlation were computed on the nominal and continuous moderator variables, respectively, when heterogeneity was found in the global ES. Tukey's post-hoc analyses were computed when significant F ratios were obtained. Analyses were performed using the software SPSS, version 20.0 (IBM Corporation, New York, USA). Significance was set a priori at p < 0.05.

Sixty-five studies (denoted by * in the reference list) out of 216 initial citations were included in the meta-analysis ( Chart 1 ). The studies enrolled 1408 participants (931 males, 455 females, 22 with undisclosed gender), with a mean age of 36.1 ± 15.1 years, BMI of 25.9 ± 2.6 kg/m 2 and VO 2 max of 33.1 ± 10.2 mL x min -1 x kg -1 . Of these participants, 466 engaged in studies with a repeated measures design including experimental and control conditions; 309 participated in studies with a repeated measures design including only experimental conditions; 429 participated in studies with an independent measures design including only experimental groups; 204 participated in studies with an independent measures design in which 117 exercised; and 87 were controls. From this sample, 1101 ES were computed.

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Study selection flow diagram.

All the obtained ES were included in the subsequent analysis given the lack of statistically significant differences in the quality of the moderator variable of the study for sBP ( F = 1.91, p = 0.11) and dBP ( F = 0.40, p = 0.81). Table 1 shows that, in contrast to the experimental condition, the corrected ES in the control condition were not different from zero. However, Cochran's Q test indicated that data from both experimental and control conditions were heterogeneous. Figure 1 shows the overall corrected ES for the experimental and control conditions for the dependent variables sBP and dBP. One-way ANOVA showed significant differences between control and experimental conditions regarding sBP and dBP (p ≤ 0.01 for all). Assessment of a file drawer effect determined that for global effects to be no longer significant, 122 significant unpublished studies were needed for sBP and 165 studies for dBP. In the control condition, while the Z score showed ES = 0, the Cochran's Q test found heterogeneity explained by the sBP ( F = 13.90) and dBP ( F = 5.37). Further analysis showed that the BP increased when measured later on during the day (p ≤ 0.01 for both). The experimental conditions not only showed heterogeneity in the obtained ES but also global ES ≠ 0 in sBP and dBP ( Table 1 ).

Global corrected ES, Z scores, Q statistic and I2 index heterogeneity tests, and post-session blood pressure change (Δ mmHg)

Experimental condition or groupVariableES ± SD (mmHg)
ControlsBP0.05 ± 0.56-0.13186.87 95.180.53
dBP0.21 ± 1.101.81329.84 97.270.26
ExperimentalsBP-0.56 ± 0.90-20.21 1452.57 99.38-4.80
dBP-0.44 ± 1.14-15.91 751.47 98.80-3.19

ES: effect size; SD: standard deviation; Z: Z score; Q: Cochran Q test; I2: heterogeneity percentage; Δ: post-test minus pre-test change in blood pressure; sBP: systolic blood pressure; dBP: diastolic blood pressure; Z: Z score ≠ 0, p < 0.05;

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Global effect size of systolic and diastolic blood pressure. ES: effect size; sBP: systolic blood pressure; dBP: diastolic blood pressure; z: ES ≠ 0, p < 0.05; p < 0.05 between a and b, c and d. Open bars represent the experimental condition, and black bars represent the control condition.

The results of the experimental condition on the two dependent variables are presented next.

Systolic Blood Pressure. Table 2 shows the corrected mean sBP ES at different levels of the moderator variables. Results regarding the characteristics of the sample showed a significant decrease in sBP regardless of the initial BP levels, gender, antihypertensive drug intake, and physical activity level. However, post-hoc analyses detected a significantly larger ES in males ( F = 5.58, p = 0.001, Figure 2b ), and non-medicated ( F = 8.76, p = 0.001, Figure 2c ) and physically active subjects ( F = 4.42, p = 0.002, Figure 2d ). Results regarding the exercise characteristics showed that the sBP decreased significantly regardless of the exercise modality. Results were consistent for aerobic exercises such as running, jogging, walking, cycling, or a combination of these, as well as for conventional or circuit resistance training exercise. Nevertheless, reductions in sBP were significantly greater for jogging exercise compared with circuit resistance training exercise ( F = 2.73, p < 0.01, Figure 2e ). Significant sBP reductions were also found regardless of whether the exercise was performed continuously, intermittently, or increasingly. However, largest reductions occurred when the intensity increased during the exercise session ( F = 5.50, p = 0.004, Figure 2f ). Significant correlations were found for sBP ( Table 3 ). Because in most cases the post-exercise BP decreased, the ES were negative, and therefore, the direction ( i.e. , sign) of the correlations opposed to those commonly reported. For example, the higher the age of the participants, the lower the decrease in sBP ( r = 0.21, p = 0.001, Figure 3a , Table 3 ). In addition, higher BMI values were associated with a lower decrease in sBP ( r = 0.26, p = 0.001, Figure 3b ). Also, the longer the duration of the exercise session the greater the reduction in sBP ( r = -0.19, p = 0.01, Figure 3c ), and the lower number of resistance exercises performed, the higher the decrease in sBP ( r = 0.21, p = 0.001, Figure 3d ). Finally, the greater the number of sets of resistance exercises, the greater the reduction in sBP ( r = -0.47, p = 0.001, Figure 3e ).

Mean corrected sBP ES, Z scores, F-ratio, significance level, and post-exercise score change by moderator variable in the experimental group

Moderator variableCoding scheme Mean corrected ES ± SD p (mmHg)
Sample characteristics    0.740.48 
•Normotensive249-0.54 ± 0.89-15.5   -3.75
•Prehypertensive23-0.78 ± 1.17-4.4   -5.80
•Hypertensive72-0.54 ± 0.81-13.1   -8.13
   5.580.004 
•Males213-0.68 ± 0.94-20.5   -4.95
•Females40-0.27 ± 0.60-4.44   -3.98
•Mixed91-0.40 ± 0.84-6.95   -4.81
   8.760.001 
•Medicated
•Nonmedicated
•Unreported
58
250
36
-0.27 ± 0.50
-0.68 ± 0.97
-0.18 ± 0.57
-6.19
-19.4
-2.71
  -4.90
-5.08
-2.74
   4.420.002 
•Sedentary107-0.46 ± 0.79-11.2   -5.05
•Active192-0.71 ± 0.98-19.9   -5.45
•Athletes20-0.27 ± 0.66-2.58   -1.64
•Mixed13-0.03 ± 0.360.35  -0.75
•Unreported12-0.06 ± 0.47-1.02  -1.89
Measurement features    0.550.46 
•Resting306-0.56 ± 0.92-18.1   -4.81
•Ambulatory40-0.46 ± 0.66-8.71   -4.31
   2.200.11 
•Morning101-0.71 ± 1.16-17.6   -4.58
•Afternoon9-0.74 ± 1.05-4.9   -5.11
•Unreported234-0.49 ± 0.74-11.7   -4.89
Exercise characteristics    0.970.38 
•Aerobic148-0.62 ± 0.87-16.1   -6.22
•Resistance training175-0.49 ± 0.95-11.5   -3.36
•Concurrent20-0.69 ± 0.52-7.7   -7.33
   2.730.01 
•Conventional (RT)127-0.55 ± 1.04-10.4   -3.24
•Circuit (RT)48-0.34 ± 0.64-4.99   -3.7
•Running (AT)6-1.39 ± 1.05-6.16   -8.53
•Jogging (AT)20-1.08 ± 1.02-8.86   -8.7
•Walking (AT)9-0.53 ± 0.27-6.52   -7.81
•Bicycling (AT)114-0.50 ± 0.82-11.2   -5.45
•Mixed20-0.69 ± 0.52-7.7   -7.33
   5.500.004 
•Constant277-0.50 ± 0.91-16.5   -4.00
•Intermittent42-0.67 ± 0.44-10.7   -7.12
•Incremental23-1.12 ± 1.16-8.03   -10.87
   0.240.87 
•12 min163-0.54 ± 0.96-12.6   -3.86
•35 min22-0.52 ± 0.65-4.14   -5.09
•Unreported12-0.45 ± 0.66-3.66   -4.75

BP: blood pressure; sBP: systolic blood pressure; ES: effect size; RT: resistance training; AT: aerobic training; Mode: both AT and RT are included;

Pearson’s correlation of mean sBP and dBP, corrected ES, and moderator variables according to the coding scheme

Characteristics of the moderator variableCoding schemeBPr =p ≤
Participants•AgesBP0.210.001
dBP0.120.03
•WeightsBP0.0070.24
dBP-0.060.37
•Body mass indexsBP0.260.001
dBP0.090.14
•VO2maxsBP-0.030.70
dBP-0.040.61
Measurement•Measurement durationsBP0.080.15
dBP-0.070.21
Exercise•Exercise intensity estimated from the VO maxsBP-0.160.11
dBP0.040.72
•Exercise intensity estimated from the HRRsBP0.110.56
dBP-0.100.57
•Exercise intensity estimated from the HRmaxsBP-0.190.58
dBP-0.470.14
•Exercise intensity estimated from the anaerobic thresholdsBP0.330.17
dBP0.350.15
•Exercise intensity estimated from 1RMsBP-0.050.51
dBP-0.040.58
•Duration of the exercise sessionsBP-0.190.01
dBP-0.080.32
•Number of RT exercisessBP0.300.001
dBP-0.200.006
•Number of setssBP-0.470.001
dBP-0.020.75
•Number of repetitionssBP0.140.05
dBP0.070.37

VO 2 max: maximal oxygen consumption; HRR: heart rate reserve; HRmax: maximal heart rate; 1RM: one repetition maximum; RT: resistance training; BP: blood pressure; sBP: systolic blood pressure; dBP: diastolic blood pressure.

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Corrected systolic blood pressure effect size by categorical variables. Normotens.: normotensive; Prehypertens.: prehypertensive; Hypertens.: hypertensive; BP: blood pressure; sBP: systolic blood pressure; z: ES ≠ 0, p < 0.05; *: different from others, p < 0.05; a and b: different between each other, p < 0.05; Conv.: Conventional resistance training; Circ.: Circuit resistance training; Run: running; Jog: jogging; Walk: walking; Cycl.: bicycling; Conc.: Concurrent training.

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Correlation between corrected systolic blood pressure (sBP), effect sizes, and continuous variables. Note: sBP: systolic blood pressure; BMI: body mass index.

Diastolic Blood Pressure. Table 4 shows the corrected mean dBP ES at different levels of the moderator variables. Results regarding the characteristics of the subjects showed a significant decrease in dBP regardless of the initial BP level, gender, antihypertensive drug intake, and physical activity level. However, post-hoc analyses detected a significantly larger ES in non-medicated samples ( F = 4.26, p < 0.02). This finding is consistent with the sBP response depicted in Figure 2c . Results regarding the exercise characteristics showed that the dBP decreased significantly regardless of the exercise modality. Most of the results were consistent for aerobic exercises such as jogging, cycling, and a combination of these, as well as for conventional or circuit resistance training exercise. However, as depicted in Table 4 , the largest reductions in dBP occurred when jogging was the exercise mode ( F = 4.09, p < 0.001). Interestingly, dBP ES were not different from zero when the participants walked. Significant correlations were found for dBP ( Table 4 ). Also, the higher the age of the participants, the lower the reduction in dBP ( r = 0.12, p = 0.03), and the greater the number of resistance exercises performed, the higher the decrease in dBP ( r = -0.20, p = 0.006).

Mean corrected dBP ES, Z score, F ratio, significance level, and post-exercise score change by moderator variable in the experimental group

Characteristics of the moderator variableCoding scheme Mean corrected ES ± SD p Δ (mmHg)
Sample    1.80.17 
•Normotensive249-0.44 ± 0.97-13.9   -3.07
•Prehypertensive20-0.85 ± 3,16-4.08   -5.28
•Hypertensive67-0.30 ± 0.44-6.72   -3.02
   0.410.67 
•Male207-0.48 ± 1.38-12.2   -3.4
•Female40-0.34 ± 0.59-4.75   -2.85
•Mixed89-0.38 ± 0.61-9.20   -2.85
   4.260.02 
•Medicated58-0.20 ± 0.43-4.54   -1.79
•Nonmedicated242-0.55 ± 1.31-15.7   -3.87
•Unreported36-0.08 ± 0.38-1.04  -0.88
   0.870.49 
•Sedentary105-0.48 ± 1.49-8.09   -3.25
•Active186-0.47 ± 1.03-12.9   -3.49
•Athletes20-0.35 ± 0.32-3.70   -2.72
•Mixed13-0.25 ± 0.36-4.46   -2.36
•Unreported12-0.10 ± 0.630.14  0.22
BP measurement    1.470.23 
•Resting296-0.47 ± 1.21-15.3   -3.36
•Ambulatory40-0.23 ± 0.37-4.64   -1.92
   1.030.36 
•Morning99-0.31 ± 0.55-10.5   -1.97
•Afternoon9-0.29 ± 0.68-1.89  -1.33
•Unreported228-0.50 ± 1.33-11.91  -3.79
Exercise    0.810.45 
•Aerobic141-0.53 ± 1.61-10.2   -3.80
•Resistance training175-0.38 ± 0.64-11.4   -2.73
•Concurrent20-0.29 ± 0.34-4.51   -2.93
   4.090.001 
•Conventional (RT)127-0.43 ± 0.67-10.8   -2.84
•Circuit (RT)48-0.27 ± 0.54-3.77   -2.43
•Running (AT)6-0.77 ± 0.99-4.00   -3.90
•Jogging (AT)18-1.66 ± 3.20-7.80   -10.83
•Walking (AT)7-0.19 ± 0.49-0.45  -0.84
•Bicycling (AT)107-0.36 ± 1.20-6.79   -2.82
•Mixed20-0.29 ± 0.34-4.51   -2.93
   0.440.64 
•Constant277-0.46 ± 1.24-14.1   -3.24
•Intermittent39-0.28 ± 0.30-4.63   -2.55
•Incremental17-0.47 ± 0.56-6.07   -4.29
   0.540.66 
•12 min163-0.35 ± 0.58-11.1   -2.67
•35 min20-0.39 ± 0.67-2.83   -3.14
•Unreported11-0.54 ± 0.74-4.35   -2.65

BP: blood pressure; dBP: diastolic blood pressure; ES: efect size; RT: resistance training; AT: aerobic training; Mode: both, AT and RT are included;

The purpose of this meta-analysis was to determine the effectiveness of acute exercise interventions on the BP response. Although initially we intended to find the intensity, duration, and type of exercise that best reduced BP, we found that regardless of the participant, measurement features, and exercise characteristics, there was a reduction in BP in the hours that followed an exercise session. The reductions in BP following an exercise session were demonstrated by the corrected ES significantly different from zero in the experimental conditions. Significant ES were found for sBP (-0.56 or -4.8 mm Hg) and dBP (-0.44 or -3.2 mm Hg). The ES for the controls conditions were equal to zero.

The magnitude of the ES is considered moderate when between 0.41 and 0.70. 46 From a clinical perspective, epidemiological studies indicate that a decrease of 2 mmHg in the sBP is likely to reduce the mortality associated with stroke by 6% and coronary heart disease by 4%, whereas a reduction of 5 mmHg is likely to reduce the risk of these diseases by 14% and 9%, respectively. 1 , 47 Therefore, the reductions of 3 to 4 mmHg found in this meta-analysis confirm the importance of acute exercise as a non-pharmacological treatment of hypertension.

The fact that the ES in the control condition was not different from zero indicates that there was no contamination by extraneous variables in this set of studies. The heterogeneity of the data from the control condition might have been partially explained by the significant differences between measurements taken in the afternoon as opposed to the morning. This finding suggests a confounding effect of the circadian rhythm in hemodynamic variables, given the reductions in BP, heart rate, cardiac output, and stroke volume as the night approaches. 48 Other aspects may also influence this response, for instance, the fact that the BP measurement in the control condition was affected by exercise performed in the previous 48 hours. 49 Therefore, both factors must be considered in the design of future research protocols.

In the case of the corrected ES arising from the experimental condition, it is noteworthy that although all participants benefited from exercise to lower the sBP, males achieved greater reductions than females. This finding is consistent with those of other studies 50 that have suggested that females have a lower support of the autonomic tone necessary to regulate BP, as well as a lower effectiveness of the components that regulate the baroreflex. However, the same authors reported as a limitation of the study a failure to standardize the time of the menstrual cycle in the group of studied females. Evidence suggests that the different phases of the menstrual cycle are involved in the regulation of the autonomic nervous system. 51 While we computed 213 ES for males, we computed only 40 ES for females. Researchers have apparently neglected the female population, probably due to a fear that the menstrual cycle might confound the findings due to its involvement in BP regulation. Although the PEH can be reached at any point during the menstrual cycle in normotensive women, it is greater if the woman exercises during the early follicular phase. 52 However, further investigation is required on this topic to determine potential physiological mechanisms responsible for PEH, for instance, whether an interaction exists between gender, age, and arterial stiffness. 53

Based on speculations from previous findings, 10 we expected to find a greater PEH in hypertensive subjects than in prehypertensive and normotensive ones. However, the level of the participants' BP had no influence on the findings of the present study. This difference might be explained by the inclusion of non-medicated hypertensive and normotensive subjects in the study by Pescatello and Kulikowich; 10 therefore, given a higher initial BP there was also a greater change in post-exercise BP when determined by ambulatory measurement. Although the PEH was significant in normotensive, prehypertensive, and hypertensive patients in the present study, there were no differences between these categories. Moreover, there were significantly greater changes in non-medicated participants compared with medicated ones. This finding might be explained by the interaction between medication intake and exercise intervention. 5 Another feasible explanation for our findings opposing those by others 10 might have been that some participants were classified as "medicated hypertensive", and therefore, BP values were close to or within the normal range. If this explanation holds true, the "baseline" law 8 , 10 , 54 also seems to apply in the present study. In other words, since BP values were close to normal even in hypertensive subjects ( i.e. , baseline), it is harder to achieve a lower BP following an exercise session. Therefore, these speculations deserve to be investigated with further post-meta-analytical studies, since the physiological mechanisms potentially explaining these findings are largely unknown.

Physically active individuals achieved higher BP decreases after the exercise session. This was observed even though the PEH occurred independently from the level of physical activity of the participants. This seems to support the theory proposed by some authors 55 who observed that some physiological mechanisms that chronically reduce BP also play a role in the onset of PEH. For example, exercise training has been shown to cause a systemic adaptation of the arterial wall in healthy individuals, 56 which might translate to better arterial vessel compliance that may facilitate the decrease in peripheral resistance following an exercise session.

We observed in this study an inverse association between age and PEH. Increasing age decreases the magnitude of PEH. As a person ages, there is an increase in arterial stiffness that results from progressive destruction of the elastic fibers, a decrease in capillary density, and an increase in arteriolar wall thickness. These structural and functional changes, in turn, increase vascular resistance and limit the response to vasodilator agents released during exercise. 57 Similarly, if the VO 2 max is greatest when the person is young and active, then the relationship between a higher VO 2 max and a greater decrease in sBP could also be explained by the aforementioned physiological mechanisms.

The finding that a lower BMI was associated with a greater reduction in sBP is in line with evidence showing that adipose tissue accumulation, especially in the abdominal area, is linked to several mechanisms leading to hypertension, including sympathetic overactivity, endothelial dysfunction, arterial stiffness, and inflammation. 55 , 58 , 59 The implications of these findings are significant, given that a large proportion of the world population is hypertensive and obese; therefore, maintaining a normal BMI could lead in many cases to a greater hypotensive effect following an exercise session. 60

More than a decade ago, the American College of Sports Medicine (ACSM), 3 recommended that resistance exercise should be accompanied by aerobic exercise. Recent studies attempted to determine whether resistance exercise alone could produce the same hypotensive effect than aerobic exercise. 31 , 61 - 62 Motivated by the increase in the number of these studies, we decided to meta-analyze the type of exercise as a moderator variable. We found that both aerobic and resistance exercises alone were able to induce a hypotensive effect.

In this study, we found jogging to be the exercise modality that elicits the greater magnitude of sBP and dBP changes. Other findings were that walking does not reduce the dBP; that the longer the duration of the exercise session, the greater the sBP reduction; and that incremental exercise protocols produced the highest reductions in sBP. These findings seem to agree with a previous report 63 that associated the PEH with the total exercise workload and not with the intensity at which the exercise was performed. However, these findings should be confirmed in future studies, because the results could have been masked by BMI, age, and physical activity level of the participants included in the different studies. This might be partially explained by a tendency to use walking as the exercise intervention if participants are overweight, elderly, or sedentary; 64 , 65 and jogging if the subjects are not obese, younger, or physically active. 22

Post meta-analytical studies assessing resistance training programs are needed, since reductions in dBP were found with a greater number of resistance exercises, although these exercises also led to a minor decrease in sBP. Because of the contradictory findings, it is likely that future studies may manipulate these variables to determine whether several resistance exercise sets reflect an increased workload and, therefore, a greater PEH, 63 , 66 or if the design of the program should require several resting periods between exercises to dampen the BP elevation that normally occurs during resistance exercise 67 in order to facilitate the onset of the PEH.

One implication arising from this meta-analysis affects the prescription of exercise. It is necessary to determine whether the PEH is greater as the exercise workload increases, 63 , 68 and whether it varies in females according to the menstrual cycle phase. 52 Other questions that remain to be answered include the duration of the PEH when the individual is performing daily living activities ( i.e. , outpatient phase), 5 , 10 and what is the role played by genetics in triggering the PEH response. 69 , 70

In conclusion, regardless of the characteristics of the sample and exercise, the BP reduced in the hours following an acute exercise session. However, the reduction was greater if the exercise was performed as a preventive strategy and in physically active individuals who were not yet medicated.

Sources of Funding

There were no external funding sources for this study.

Study Association

This study is not associated with any thesis or dissertation work.

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  • Published: 06 September 2024

Home blood pressure measurement and hypertension control according to the length of antihypertensive treatment among employees

  • Yukako Tatsumi 1 , 2 ,
  • Azusa Shima 2 , 3 ,
  • Michihiro Satoh 4 , 5 ,
  • Ayumi Morino 2 , 3 ,
  • Yuichiro Kawatsu 3 ,
  • Kei Asayama 1 ,
  • Naomi Miyamatsu 2 &
  • Takayoshi Ohkubo 1  

Hypertension Research ( 2024 ) Cite this article

Metrics details

This study aimed to investigate the association between the frequency of home blood pressure (HBP) measurement and hypertension control in a middle-aged working population. This study included 627 employees aged 40 years or older who underwent health check-ups for 2 consecutive years from 2019 to 2022 and had blood pressure (BP) ≥ 140/90 mmHg at the health check-up in the first year. The participants were stratified by the length of antihypertensive treatment (within 1 year, >1 year) using data in the first and second years, and were classified by the frequency of HBP measurement (<6 times/week, almost every day) using data in the second year. In each treatment length, logistic regression analyses were used to estimate multivariable adjusted odds ratios (ORs) of controlled hypertension (BP at health check-ups <140/90 mmHg in the second year) in those who measured HBP almost every day compared with those who measured HBP < 6 times/week. The ORs (95% confidence intervals) were 1.56 (0.94–2.73) in those within 1 year of starting treatment and 0.74 (0.44–1.22) in those with more than 1 year of starting treatment. In participants with BP ≥ 160/100 mmHg in the first year, the corresponding ORs were 1.94 (1.04–3.64) and 0.41 (0.13–1.23), respectively. In conclusion, in individuals within 1 year of starting treatment, those who measure HBP almost every day tend to have good control of hypertension. In particular, in those who have BP ≥ 160/100 mmHg before starting antihypertensive medication, measuring HBP almost every day is associated with good control of hypertension.

case study on low blood pressure

Among those within 1 year of starting the treatment (Group1) especially in those with blood pressure ≥160/100 mmHg, the frequency of home blood pressure measurement was associated with hypertension control. It was not associated among those with more than 1 year of starting the treatment (Group 2).

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Acknowledgements

We thank all members of Heiwado Health Insurance Society and Heiwado Occupational Health Care Office, especially Ms. Atsuko Kawamura for her careful coordination of the staff who administered the health check-ups and Mr. Shinobu Takada for his contribution to collecting the data. This study was supported by Grants-in-Aid for Scientific Research from the Japan Society for the Promotion of Science (21K17313 and 21K19670).

This study was supported by Grants-in-Aid for Scientific Research from the Japan Society for the Promotion of Science (21K17313, 21K19670, and 22H03358).

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Department of Hygiene and Public Health, Teikyo University School of Medicine, Tokyo, Japan

Yukako Tatsumi, Kei Asayama & Takayoshi Ohkubo

Department of Clinical Nursing, Shiga University of Medical Science, Shiga, Japan

Yukako Tatsumi, Azusa Shima, Ayumi Morino & Naomi Miyamatsu

Occupational Health Care Office, HEIWADO CO., LTD., Shiga, Japan

Azusa Shima, Ayumi Morino & Yuichiro Kawatsu

Division of Public Health, Hygiene and Epidemiology, Faculty of Medicine, Tohoku Medical and Pharmaceutical University, Sendai, Japan

Michihiro Satoh

Department of Pharmacy, Tohoku Medical and Pharmaceutical University Hospital, Sendai, Japan

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Correspondence to Yukako Tatsumi .

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Three of the authors (AS, AM, and YK) are health professionals of the retail company whose employees are insured by the Employees’ Health Insurance Society. They provided the data for the present study. The other authors do not have any conflict of interest to disclose.

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Tatsumi, Y., Shima, A., Satoh, M. et al. Home blood pressure measurement and hypertension control according to the length of antihypertensive treatment among employees. Hypertens Res (2024). https://doi.org/10.1038/s41440-024-01863-9

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DOI : https://doi.org/10.1038/s41440-024-01863-9

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case study on low blood pressure

SciTechDaily

Study Confirms: New 3-in-1 Low-Dose Blood Pressure Pill Vastly Superior for Hypertension Treatment

Cardiology Heart Pills Concept Art

Over 80% of patients achieved control within a month, sustained at six months.

New triple-drug combination therapy GMRx2 has proven more effective than standard hypertension treatments, significantly lowering blood pressure in patients with uncontrolled hypertension. This could drastically reduce cardiovascular event risks and improve global health outcomes, especially in low- and middle-income countries.

New Hypertension Treatment Research

According to new research, a treatment plan based on a novel combination of low doses of three anti-hypertensive drugs in a single pill – known as GMRx2 – was superior to a high-quality standard care treatment plan at lowering blood pressure in patients with uncontrolled hypertension. [1]

Results of the ‘deliVERy of Optimal blood pressure coNtrol in afrICA (VERONICA)-Nigeria’ trial, led by The George Institute for Global Health, were presented today at the European Society of Cardiology Congress 2024 and simultaneously published in the Journal of the American Medical Association (JAMA) .

Comparing GMRx2 to Standard Care

The GMRx2 treatment plan involved a once-daily pill containing telmisartan, amlodipine, and indapamide at a quarter, half, or standard doses. The standard care treatment plan recommended by the Nigerian Ministry of Health began with monotherapy, followed by dual and triple combination therapy, and was typical of hypertension guidelines for many countries. [2]

After 6 months of treatment, home systolic blood pressure was 31mmHg lower in the GMRx2 group compared to 26 mmHg lower with standard care – the 5.8 mmHg difference was highly clinically and statistically significant. Existing evidence shows that with every 5 mmHg reduction in systolic blood pressure, there is a 10% reduction in major cardiovascular events such as stroke, heart attack, and heart failure. [3]

After just one month, 81% of participants in the GMRx2 group achieved clinic-measured blood pressure control versus 55% with standard care. This improvement was sustained at six months with 82% achieving control, compared with 72% under standard care. The tolerability of both treatment plans was good, with no withdrawals due to adverse events.

High Effectiveness in Diverse Populations

Prof Dike Ojji, Head of the Cardiovascular Research Unit at the University of Abuja, Nigeria and study principal investigator said, “The triple pill still produced clinically meaningful reductions in blood pressure compared to standard care, even when standard care closely followed current guidelines and involved more clinic visits.”

“In low-income countries, fewer than one in four treated people achieve blood pressure control and in high-income settings, it is only between 50% and 70%,” added Prof Ojji, “so to see rates of over 80% in just one month is impressive.”

Potential Global Impact on Cardiovascular Health

It is estimated that over a billion adults live with hypertension worldwide, with two-thirds living in low- and middle-income countries. 4 High blood pressure is the leading risk factor for mortality, accounting for 10.8 million deaths a year. [4,5] It is hoped this new treatment could have a big impact on reducing rates of cardiovascular disease , particularly in countries with the highest burden.

GMRx2 is the leading drug candidate of George Medicines, a late-stage, biopharmaceutical company addressing significant unmet need in the treatment of cardiometabolic disease, established to commercialise the research of The George Institute for Global Health. Earlier this month, GMRx2 was submitted to the US Food and Drug Administration (FDA) for the treatment of hypertension.

Positive Outcomes in Additional GMRx2 Trials

Phase III data from two additional GMRx2 trials were also presented at the congress, showing good tolerability and clinically relevant blood pressure reductions compared to placebo and dual combination therapy. [6,7]

Prof Anthony Rodgers, Senior Professorial Fellow at The George Institute and Chief Medical Officer at George Medicines said, “Our mission is to develop sustainable solutions that can improve the health of millions of people worldwide and alleviate strain on health systems. There is a global goal to reach 80% blood pressure control among those treated, but no country has yet achieved this. With the VERONICA trial, we’ve shown the potential of this novel strategy to reach this ambitious target.”

“There has been little innovation in this field, so it’s rewarding to see many years of research by The George Institute culminate in a novel treatment using established medicines to address an unmet need,” he added.

The VERONICA trial is funded by the Australian National Health and Medical Research Council.

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case study on low blood pressure

1. Introduction

2. materials and methods, 2.1. study design, 2.2. patients, 2.3. dietary advice, 2.4. questionnaires, 2.4.1. study questionnaire, 2.4.2. rome iv questionnaire, 2.4.3. irritable bowel syndrome-severity scoring system, 2.4.4. visual analog scale for irritable bowel syndrome, 2.5. statistical analyses, 3.1. basal characteristics, 3.2. gastrointestinal and extraintestinal symptoms, 3.3. anthropometric data, 3.4. follow-up, 3.5. safety outcomes, 4. discussion, 5. conclusions, supplementary materials, author contributions, institutional review board statement, informed consent statement, data availability statement, acknowledgments, conflicts of interest.

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Click here to enlarge figure

ParametersSSRD
N = 77
Low FODMAP
N = 78
p-Value
41.0 (29.5–53.0)43.0 (33.8–56.0)0.227
15 (19.5)/62 (80.5)10 (12.8)/68 (87.2)0.283
71.5 (63.6–82.8)68.6 (63.0–83.4)0.389
)25.1 (22.6–28.4)24.7 (22.1–27.6)0.479
16 (7–27)20 (10–30)0.261
0.585
Primary school5 (6.5)2 (2.6)
Secondary school10 (13.0)13 (16.7)
Education after secondary school20 (26.0)17 (21.8)
Examination at university42 (54.5)46 (59.0)
0.963
Working full time48 (62.3)46 (59.0)
Working 99–51%6 (7.8)9 (11.5)
Working 50%1 (1.3)1 (1.3)
Studying10 (13.0)10 (12.8)
Sick leave3 (3.9)2 (2.6)
Unemployment3 (3.9)2 (2.6)
Retirement6 (7.8)8 (10.3)
0.837
Living alone16 (20.8)14 (17.9)
Living together55 (71.4)56 (71.8)
Other6 (7.8)8 (10.3)
0.086
Never42 (54.5)43 (55.1)
Former26 (33.8)28 (35.9)
Present un regular2 (2.6)6 (7.7)
Present regular7 (9.1)1 (1.3)
1.000
Missing 1
<134 (44.2)33 (42.3)
1–428 (36.4)29 (37.2)
5–913 (16.9)13 (16.7)
10–141 (1.3)2 (2.6)
≥151 (1.3)0
0.475
Missing 1
No time10 (13.0)8 (10.4)
<30 min11 (14.3)14 (18.2)
30–60 min16 (20.8)14 (18.2
60–90 min8 (10.4)16 (20.8)
90–120 min8 (10.4)8 (10.4)
>120 min24 (31.2)17 (22.1)
SSRD
N = 77
Low FODMAP
N = 78
p-Value *
VAS-IBS (mm)Valuep-ValueDifferenceValuep-ValueDifference
5 (1–13)
Baseline47 (28–64)--50 (32–65)--0.368
2 weeks17 (8–30)<0.001−27 (−47–(−9))22 (13–40)<0.001−19 (−36–(−3))0.252
4 weeks16 (0–31)<0.001−24 (−44–(−9))13 (0–27)<0.001−30 (−53–(−8))0.425
6 months32 (19–63)0.003−6 (−28–3)30 (16–54)<0.001−16 (−38–4)0.270
3 (0–10)
Baseline53 (19–73)--37 (4–74)--0.245
2 weeks15 (4–48)<0.001−14 (−51–0)10 (0–37)<0.001−14 (−38–0)0.793
4 weeks17 (3–39)<0.001−8 (−48–2)8 (0–24)<0.001−16 (−53–0)0.633
6 months31 (8–68)<0.001−12 (−39–0)11 (3–44)0.008−8 (−30–7)0.457
6 (2–16)
Baseline53 (6–72)--54 (10–76)--0.439
2 weeks16 (2–50)<0.001−12 (−36–2)20 (0–68)0.02−6 (−28–4)0.510
4 weeks16 (2–43)<0.001−8 (−46–0)21 (0–55)<0.001−13 (−33–0)0.815
6 months22 (0–61)0.121−3 (−24–12)42 (2–70)0.022−4 (−32–3)0.528

10 (2–23)
Baseline73 (58–88)--73 (54–86)--0.677
2 weeks34 (18–53)<0.001−37 (−53–(−9))23 (13–50)<0.001−39 (−56–(−16))0.469
4 weeks24 (10–54)<0.001−43 (−63–(−11)19 (8–50)<0.001−44 (−61–(−25))0.359
6 months62 (30–75)0.002−15 (−38–14)56 (33–70)<0.001−18 (−33–(−3))0.416

2 (0–4)
Baseline13 (2–34)--13 (1–36)--0.957
2 weeks6 (0–12)<0.001−7 (−20–0)4 (0–12)<0.001−7 (−22–0)0.773
4 weeks3 (0–12)<0.001−6 (−15–0)0 (0–11)<0.001−7 (−21–0)0.743
6 months8 (1–21)0.002−4 (−14–1)5 (0–21)0.009−2 (−17–1)0.892

2 (0–14)
Baseline74 (57–84)--70 (54–84)--0.694
2 weeks29 (15–60)<0.001−36 (−52–(−11))30 (17–60)<0.001−28 (−50–(−15))0.688
4 weeks24 (12–62)<0.001−30 (−60–(−10))22 (10–50)<0.001−33 (−53–(−18))0.593
6 months40 (23–76)<0.001−12 (−45–0)48 (24–68)<0.001−26 (−43–(−2))0.492

5 (2–15)
Baseline39 (15–65)--45 (16–59)--0.708
2 weeks24 (11–42)<0.001−7 (−26–0)27 (8–46)0.021−4 (−25–5)0.339
4 weeks20 (5–32)<0.001−12 (−29–(−2)18 (2–34)<0.001−13 (−32–1)0.788
6 months22 (11–50)0.009−6 (−20–4)26 (8–39)0.043−2 (−30–7)0.911
Baseline301 (233–348)--300 (238–360)--0.845
2 weeks136 (87–223)<0.001−138 (−212–(−82))151 (100–232)<0.001−110 (−188–(−68))0.310
4 weeks119 (66–230)<0.001−146 (−240–(−88))116 (63–176)<0.001−153 (−231–(−90))0.585
6 months204 (146–234)<0.001−55 (−130–4)220 (144–301)<0.001−93 (−181–(−20))0.069
SSRDp-Value *Low FODMAPp-Value *p-Value **
N = 77 N = 78 0.078
IBS-C14 (18.2) 12 (15.4)
IBS-D29 (37.7) 15 (19.2)
IBS-M22 (28.6) 32 (41.0)
IBS-U2 (2.6) 5 (6.4)
FBD10 (13.0) 14 (17.9)
0.621
IBS-C8 (10.4) 10 (12.8)
IBS-D8 (10.4) 7 (9.0)
IBS-M14 (18.2) 9 (11.5)
IBS-U0 2 (2.6)
FBD23 (29.9) 25 (32.1)
Healthy19 (24.7) 19 (24.4)
Missing5 (6.5)<0.0016 (7.7)<0.001
0.198
IBS-C6 (7.8) 11 (14.1)
IBS-D8 (10.4) 6 (7.7)
IBS-M12 (15.6) 9 (11.5)
IBS-U1 (1.3) 3 (3.8)
FBD23 (29.9) 13 (16.7)
Healthy3 (3.9) 7 (9.0)
Missing24 (31.2)<0.00129 (37.2)0.046
SSRD
N = 77
Low FODMAP
N = 78
p-Value *
Extraintestinal IBS-SSSValuep-ValueDifferenceValuep-ValueDifference
Baseline10 (2–26)--6 (0–22)--0.267
2 weeks4 (0–12)0.002−3 (−13–3)3 (0–13)0.005−2 (−11–0)0.951
4 weeks2 (0–13)<0.001−4 (−16–1)0 (0–9)<0.001−3 (−12–0)0.629
6 months4 (0–14)0.074−2 (−13–4)2 (0–18)0.053−1 (−10–0)0.940
Baseline33 (10–66)--27 (9–58)--0.737
2 weeks14 (5–36)<0.001−5 (−30–2)15 (2–47)<0.001−6 (−22–0)0.993
4 weeks14 (2–32)<0.001−9 (−27–2)12 (0–35)<0.001−9 (−31–0)0.855
6 months24 (10–55)0.185−1 (−21–8)20 (4–50)0.001−4 (−21–2)0.324
Baseline20 (4–50)--28 (4–65)--0.395
2 weeks6 (0–29)<0.001−6 (−21–0)14 (0–39)<0.001−2 (−26–2)0.409
4 weeks6 (0–30)<0.001−7 (−22–0)4 (0–35)<0.001−7 (−32–0)0.998
6 months23 (4–58)0.157−4 (−18–8)24 (4–70)0.6750 (−14–12)0.501
Baseline57 (30–81)--74 (48–84)--0.055
2 weeks33 (16–68)<0.001−14 (−27–0)47 (19–70)<0.001−12 (−32–0)0.660
4 weeks27 (9–56)<0.001−18 (−32–(−2))37 (14–60)<0.001−19 (−38–(−3))0.712
6 months49 (18–68)0.004−7 (−20–4)48 (19–69)<0.001−13 (−27–0)0.128
Baseline72 (48–85)--75 (52–87)--0.621
2 weeks24 (10–66)<0.001−21 (−51––(−6))37 (14–66)<0.001−23 (−44–(−6))0.804
4 weeks14 (6–40)<0.001−41 (−67–(−6))21 (8–45)<0.001−41 (−59–(−19))0.878
6 months47 (20–68)<0.001−13 (−33–(−2))48 (22–70)<0.001−15 (−37–(−2))0.599
Baseline20 (7–50)--20 (2–60)--0.678
2 weeks5 (0–18)<0.001−12 (−27–0)7 (0–35)<0.001−6 (−30–0)0.274
4 weeks4 (0–20)<0.001−12 (−28–0)3 (0–26)<0.001−10 (−30–0)0.945
6 months11 (4–26)0.002−6 (−20–2)21 (2–54)0.013−3 (−18–2)0.727
Baseline14 (2–64)--22 (4–64)--0.491
2 weeks7 (0–24)<0.001−7 (−24–0)7 (0–33)<0.001−8 (−29–0)0.598
4 weeks4 (0–23)<0.001−6 (−34–0)3 (0–22)<0.001−13 (−44–0)0.290
6 months18 (0–44)0.003−7 (−22–1)16 (0–53)0.003−7 (−19–0)0.975
Baseline2 (0–9)--0 (0–18)--0.995
2 weeks1 (0–15)0.2810 (−4–2)0 (0–10)0.0360 (−3–0)0.776
4 weeks0 (0–7)0.0240 (−4–0)0 (0–5)0.0050 (−4–0)0.564
6 months2 (0–12)0.7740 (−2–2)0 (0–14)0.5730 (−2–2)0.682
Baseline25 (5–56)--30 (4–72)--0.506
2 weeks11 (0–46)0.002−5 (−20–1)18 (0–57)0.014−1 (−20–4)0.616
4 weeks13 (0–30)<0.001−10 (−27–0)12 (0–39)<0.001−3 (−35–1)0.699
6 months23 (5–53)0.032−3 (−17–4)19 (4–70)0.084−2 (−18–7)0.755
Baseline160 (110–208)--172 (120–242)--0.268
2 weeks96 (50–154)<0.001−60 (−89–(−20))115 (55–156)<0.001−54 (−82–(−30))0.852
4 weeks91 (28–140)<0.001−72 (−112–(−41))77 (44–136)<0.001−83 (−118–(−44))0.408
6 months127 (71–191)<0.001−44 (−75–2)133 (78–214)<0.001−36 (−59–(−10))0.977
SSRD
N = 77
Low FODMAP
N = 78
p-Value *
VariablesValuep-ValueDifferenceValuep-ValueDifference
(kg)
Baseline71.5 (63.6–82.8)--68.6 (63–83.4)--0.513
4 weeks70 (63.2–81)<0.001−1.6 (−2.4–(−0.4))67.8 (62.5–82.7)<0.001−0.8 (−1.6–(−0.1))0.006
6 months74.1 (66.6–85.7)0.516−0.2 (−1.4–1.2)68.6 (62.8–80.8)0.079−0.3 (−1.6–0.6)0.438
(kg/m )
Baseline25.14 (22.64–28.45)--24.68 (22.13–27.64)--0.538
4 weeks24.8 (21.97–27.6)<0.001−0.55 (−0.86–(−0.15))24.63 (22–27.32)<0.001−0.26 (−0.56–(−0.03))0.005
6 months25.95 (22.66–28.57)0.504−0.07 (−0.53–0.44)25.08 (22.05–26.76)0.089−0.11 (−0.54–0.23)0.526
(cm)
Baseline88 (76–97)--86 (79–94.8)--0.831
4 weeks86 (75–94)<0.001−2 (−4–0)85 (79–93)<0.001−2 (−3–1)0.981
6 months89 (77.5–97)0.022−1 (−4–1)85.5 (80–93.5)0.038−1 (−3–1)0.758
(mmHg)
Baseline125 (114–139) 126 (116–139) 0.657
4 weeks123 (114–135)0.097−2 (−10–6)124 (113–135)0.024−3 (−8–3)0.762
6 months127 (116–138)0.588−1 (−7–6)126 (117–136)0.138−3 (−12–8)0.399
(mmHg)
Baseline81 (72–88) 81 (74–90) 0.403
4 weeks78 (70–84)0.006−3 (−6–3)80 (73–85)<0.001−4 (−8–2)0.225
6 months80 (76–86)0.575−2 (−6–5)80 (72–86)0.044−1 (−10–3)0.190
(mm)
Baseline66 (40–85)--60 (29–80)--0.384
4 weeks34 (17–67)<0.001−15 (−41–0)41 (22–69)0.001−8 (−23–5)0.050
6 months53 (31–72)0.058−7 (−23–10)48 (28–72)0.246−2 (−10–8)0.448

(mm)
Baseline74 (52–93)--77 (68–86)--0.833
4 weeks83 (69–93)0.1074 (−12–24)80 (62–90)0.6881 (−10–12)0.261
6 months77 (69–90)0.4730 (−12–16)72 (62–87)0.464−2 (−13–16)0.275
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Roth, B.; Nseir, M.; Jeppsson, H.; D’Amato, M.; Sundquist, K.; Ohlsson, B. A Starch- and Sucrose-Reduced Diet Has Similar Efficiency as Low FODMAP in IBS—A Randomized Non-Inferiority Study. Nutrients 2024 , 16 , 3039. https://doi.org/10.3390/nu16173039

Roth B, Nseir M, Jeppsson H, D’Amato M, Sundquist K, Ohlsson B. A Starch- and Sucrose-Reduced Diet Has Similar Efficiency as Low FODMAP in IBS—A Randomized Non-Inferiority Study. Nutrients . 2024; 16(17):3039. https://doi.org/10.3390/nu16173039

Roth, Bodil, Mohamed Nseir, Håkan Jeppsson, Mauro D’Amato, Kristina Sundquist, and Bodil Ohlsson. 2024. "A Starch- and Sucrose-Reduced Diet Has Similar Efficiency as Low FODMAP in IBS—A Randomized Non-Inferiority Study" Nutrients 16, no. 17: 3039. https://doi.org/10.3390/nu16173039

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