Trandate (labetalol) dosing, indications, interactions, adverse effects, and more

Apo-Labetalol – Uses, Side Effects, Interactions

How does this medication work? What will it do for me?

Labetalol belongs to a class of medications called beta-blockers. It is used to treat high blood pressure. It helps to decrease blood pressure by reducing the workload on the heart and by opening the blood vessels.

Labetalol may be used alone, but is often used in combination with additional high blood pressure medications called diuretics (water pills). The injectable form of labetalol is used for emergency treatment of severe high blood pressure.

This medication may be available under multiple brand names and/or in several different forms. Any specific brand name of this medication may not be available in all of the forms or approved for all of the conditions discussed here. As well, some forms of this medication may not be used for all of the conditions discussed here.

Your doctor may have suggested this medication for conditions other than those listed in these drug information articles. If you have not discussed this with your doctor or are not sure why you are being given this medication, speak to your doctor. Do not stop using this medication without consulting your doctor.

Do not give this medication to anyone else, even if they have the same symptoms as you do. It can be harmful for people to use this medication if their doctor has not prescribed it.

What form(s) does this medication come in?

Apo labetalol is available as tablets in strengths of 100 mg and 200 mg..

How should I use this medication?

The recommended starting dose of labetalol is 100 mg by mouth twice daily after food. Your doctor may adjust the dose of the medication once or twice a week according to your needs and response to the medication. The usual maintenance dose ranges from 200 mg to 400 mg by mouth twice daily. The maximum recommended dose is 600 mg by mouth twice daily.

Many things can affect the dose of a medication that a person needs, such as body weight, other medical conditions, and other medications. If your doctor has recommended a dose different from the ones listed here, do not change the way that you are taking the medication without consulting your doctor.

It is important to take this medication exactly as prescribed by your doctor. If you miss a dose, take it as soon as possible and continue with your regular schedule. If it is within 8 hours of your next dose, skip the missed dose and continue on with your regular dosing schedule. Do not take a double dose to make up for a missed one. If you are not sure what to do after missing a dose, contact your doctor or pharmacist for advice.

Do not stop taking this medication suddenly without checking with your doctor first. Stopping the medication suddenly after you have been taking it for a while may cause unpleasant and potentially harmful effects.

Do not dispose of medications in wastewater (e.g. down the sink or in the toilet) or in household garbage. Ask your pharmacist how to dispose of medications that are no longer needed or have expired.

Who should NOT take this medication?

Do not take this medication if you:

• are allergic to labetalol or any ingredients of the medication
• are experiencing cardiogenic shock with very low blood pressure
• have a severely slow heart rate
• have asthma or a history of obstructive airway disease such as emphysema or chronic bronchitis
• have serious heart block
• have uncontrolled congestive heart failure
• have severely decreased blood flow in your feet and your legs (peripheral artery disease)

What side effects are possible with this medication?

Many medications can cause side effects. A side effect is an unwanted response to a medication when it is taken in normal doses. Side effects can be mild or severe, temporary or permanent.

The side effects listed below are not experienced by everyone who takes this medication. If you are concerned about side effects, discuss the risks and benefits of this medication with your doctor.

The following side effects have been reported by at least 1% of people taking this medication. Many of these side effects can be managed, and some may go away on their own over time.

Contact your doctor if you experience these side effects and they are severe or bothersome. Your pharmacist may be able to advise you on managing side effects.

• dizziness
• headache
• nausea
• unusual tiredness
• vomiting

Although most of these side effects listed below don’t happen very often, they could lead to serious problems if you do not seek medical attention.

Check with your doctor as soon as possible if any of the following side effects occur:

• breathing difficulty or wheezing
• dizziness or lightheadedness when getting up from a lying down or sitting position
• joint or muscle pain
• signs of heart problems (e.g., fast, irregular heartbeat or pulse, chest pain, sudden weight gain, difficulty breathing, leg swelling)
• signs of liver problems (e.g., nausea, vomiting, diarrhea, loss of appetite, weight loss, yellowing of the skin or whites of the eyes, dark urine, pale stools)
• slow heartbeat (especially less than 50 beats per minute)

Stop taking the medication and seek immediate medical attention if any of the following occur:

• signs of a serious allergic reaction (e.g., abdominal cramps, difficulty breathing, nausea and vomiting, or swelling of the face and throat)

Some people may experience side effects other than those listed. Check with your doctor if you notice any symptom that worries you while you are taking this medication.

Are there any other precautions or warnings for this medication?

Before you begin using a medication, be sure to inform your doctor of any medical conditions or allergies you may have, any medications you are taking, whether you are pregnant or breast-feeding, and any other significant facts about your health. These factors may affect how you should use this medication.

Breathing conditions: In general, people who have asthma and certain other breathing problems should avoid taking a beta-blocker such as labetalol, as this group of medications can cause breathing difficulty. If you have breathing problems and your doctor has prescribed labetalol for you, it may be at a lower dose, and your doctor will monitor you regularly while you are taking this medication. If you have breathing problems, discuss with your doctor how this medication may affect your medical condition, how your medical condition may affect the dosing and effectiveness of this medication, and whether any special monitoring is needed.

Diabetes: The signs of low blood sugar may not be as noticeable when taking labetalol. If you have diabetes and take insulin or other medications that work by reducing the blood sugar, discuss with your doctor how this medication may affect your medical condition, how your medical condition may affect the dosing and effectiveness of this medication, and whether any special monitoring is needed.

Dizziness: Move slowly when moving from a lying down or sitting position to a standing position as dizziness may occur, especially when this medication is first being started.

Dry eyes: Dry eyes have been reported with the use of this medication.

Heart disease: Beta-blockers, such as labetalol, can worsen existing heart failure. It is important to take labetalol exactly as prescribed by your doctor to decrease the chance of this happening. If you have a history of heart disease, discuss with your doctor how this medication may affect your medical condition, how your medical condition may affect the dosing and effectiveness of this medication, and whether any special monitoring is needed.

Hyperthyroidism (high level of thyroid hormones): Labetalol may reduce the symptoms of hyperthyroidism and give a false impression of improvement. Stopping labetalol suddenly could cause hyperthyroidism to become worse. If you have a history of thyroid disease, discuss with your doctor how this medication may affect your medical condition, how your medical condition may affect the dosing and effectiveness of this medication, and whether any special monitoring is needed.

Liver function: Liver disease or reduced liver function may cause this medication to build up in the body, causing side effects. If you have liver problems, discuss with your doctor how this medication may affect your medical condition, how your medical condition may affect the dosing and effectiveness of this medication, and whether any special monitoring is needed. Your doctor may want to test your liver function regularly with blood tests while you are taking this medication.

Rarely, liver injury has been reported with the use of this medication. If you experience symptoms of liver problems such as fatigue, feeling unwell, loss of appetite, nausea, yellowing of the skin or whites of the eyes, dark urine, pale stools, abdominal pain or swelling, and itchy skin, contact your doctor immediately.

Pheochromocytoma: Although labetalol is used to treat the high blood pressure that is a symptom of pheochromocytoma (a tumour of the adrenal gland), it has been known to worsen the symptoms it is supposed to be treating. If you have a pheochromocytoma, discuss with your doctor how this medication may affect your medical condition, how your medical condition may affect the dosing and effectiveness of this medication, and whether any special monitoring is needed.

Severe allergies: If you have allergies severe enough to cause anaphylaxis (a severe allergic reaction where swelling of the face, lips, and throat make it difficult to breathe), discuss with your doctor what to do if you have an allergic reaction. Labetalol, like other beta-blockers, may make it more difficult to treat severe allergic reactions with epinephrine.

Skin conditions: Various skin rashes have been reported with the use of this medication.

Stopping the medication: This medication should not be stopped suddenly. People with heart disease who stop taking this medication abruptly may experience serious effects, such as severe worsening of angina, heart attack, or abnormal heart rhythms. If you have heart disease, do not stop taking this medication without checking with your doctor first. When this medication needs to be stopped, it should be done gradually, under the supervision of your doctor.

Surgery: If you are scheduled for surgery, inform all health care professionals involved in your care that you are taking labetalol.

Pregnancy: Labetalol should not be used during pregnancy unless the benefits outweigh the risk. If you become pregnant while taking this medication, contact your doctor immediately.

Breast-feeding: This medication passes into breast milk. If you are a breast-feeding mother and are taking labetalol, it may affect your baby. Talk to your doctor about whether you should continue breast-feeding.

Children: The safety and effectiveness of using this medication have not been established for children.

Seniors: Seniors may be more sensitive to the side effects of labetalol and may require lower doses.

What other drugs could interact with this medication?

There may be an interaction between labetalol and any of the following:

• aldesleukin
• aliskiren
• alpha agonists (e.g., clonidine, methyldopa)
• alpha blockers (e.g., alfuzosin, doxazosin, tamsulosin)
• alpha/beta agonists (e.g., epinephrine, norepinephrine)
• amiodarone
• amifostine
• amphetamines (e.g., dextroamphetamine, lisdexamphetamine)
• angiotensin converting enzyme inhibitors (ACEIs; captopril, enalapril, ramipril)
• angiotensin receptor blockers (ARBs; e.g., candasartan, irbesartan, losartan)
• antipsychotics (e.g., chlorpromazine, clozapine, haloperidol, olanzapine, quetiapine, risperidone)
• barbiturates (e.g., butalbital, pentobarbital phenobarbital)
• beta-adrenergic blockers (e.g., atenolol, propranolol, sotalol)
• beta-2 agonists (e.g., formoterol, salbutamol, salmeterol)
• brimonidine
• calcium channel blockers (e.g., amlodipine, diltiazem, nifedipine, verapamil)
• ceritinib
• chloroquine
• clonidine
• digoxin
• dipyridamole
• disopyramide
• diuretics (water pills; e.g., furosemide, hydrochlorothiazide, triamterene)
• donepezil
• dronedarone
• duloxetine
• ergot alkaloids (e.g., ergotamine, dihydroergotamine)
• fentanyl
• fingolimod
• galantamine
• grass pollen allergen extract
• guanfacine
• hydroxychloroquine
• insulin
• lacosamide
• lanreotide
• levodopa
• methylphenidate
• minoxidil
• nitrates (e.g., nitroglycerin, isosorbide dinitrate, isosorbide mononitrate)
• non-steroidal anti-inflammatory medications (NSAIDs; e.g., diclofenac, ibuprofen, naproxen)
• obinutuzumab
• octreotide
• pasireotide
• pentoxifylline
• phosphodiesterase-5 inhibitors (e.g., sildenafil, tadalafil, vardenafil)
• pilocarpine
• pramipexole
• propafenone
• quinine
• rasagiline
• regorafenib
• rifabutin
• rifampin
• rivastigmine
• ropinirole
• selegiline
• sufentanil
• sulfonylureas (e.g., gliclazide, glyburide, tolbutamide)
• theophyllines (e.g., aminophylline, oxtriphylline, theophylline)
• tizanidine
• tofacitinib
• tolcapone

If you are taking any of these medications, speak with your doctor or pharmacist. Depending on your specific circumstances, your doctor may want you to:

• stop taking one of the medications,
• change one of the medications to another,
• change how you are taking one or both of the medications, or
• leave everything as is.

An interaction between two medications does not always mean that you must stop taking one of them. Speak to your doctor about how any drug interactions are being managed or should be managed.

Medications other than those listed above may interact with this medication. Tell your doctor or prescriber about all prescription, over-the-counter (non-prescription), and herbal medications you are taking. Also tell them about any supplements you take. Since caffeine, alcohol, the nicotine from cigarettes, or street drugs can affect the action of many medications, you should let your prescriber know if you use them.

All material copyright MediResource Inc. 1996 – 2021. Terms and conditions of use. The contents herein are for informational purposes only. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Source: www.medbroadcast.com/drug/getdrug/Apo-Labetalol

Trandate Tablets – NPS MedicineWise

What is in this leaflet

This leaflet answers some common questions about TRANDATE tablets. It does not contain all the available information. It does not take the place of talking to your doctor or pharmacist.

All medicines have risks and benefits. Your doctor has weighed the risks of you taking TRANDATE against the benefits he or she expects it will have.

If you have any concerns about taking this medicine, ask your doctor or pharmacist.

Keep this leaflet with the medicine.

You may need to read it again.

What TRANDATE is used for

The name of your medicine is TRANDATE. The active ingredient is called labetalol hydrochloride.

Labetalol hydrochloride belongs to a group of medicines called the beta-blockers. The beta-blockers are used for the treatment of high blood pressure (hypertension).

TRANDATE is used for the treatment of all degrees of hypertension. Hypertension is a condition marked by high blood pressure.

TRANDATE is used to lower high blood pressure. It works by changing the body’s response to some nerve impulses. Therefore, it widens the blood vessels in the body, causing the blood pressure to fall.

Your doctor may have prescribed this medicine for another condition.

Ask your doctor if you have any questions about why TRANDATE has been prescribed for you.

TRANDATE tablets are only available with a doctor’s prescription.

Before you take it

When you must not take it

Do not take TRANDATE if you are allergic to:

• labetalol hydrochloride or any other agents used to treat hypertension
• any of the ingredients listed at the end of this leaflet.

Some of the symptoms of an allergic reaction to TRANDATE may include red, itchy skin rashes, difficulty in breathing, swelling of the face, lips, mouth or throat, faintness or shortness of breath.

Do not use TRANDATE after the expiry date (EXP.) printed on the pack.

Do not take it if the packaging is torn or shows signs of tampering.

Before you start to take it

You must tell your doctor if:

• you are allergic to any other medicines or any foods, dyes or preservatives
• you are pregnant or intend to become pregnant.
  TRANDATE is rated in Australia as a Category C drug for the use in pregnancy. TRANDATE should not be taken early in pregnancy.
  If it is necessary for you to take TRANDATE later in your pregnancy, your doctor will discuss the risks and benefits of taking it.
• you are breast-feeding or intend to breast-feed.
  TRANDATE is able to pass into breast milk. There is a possibility that the breast-fed baby may be affected. Therefore, do not take it if you are breast-feeding or plan to breast-feed.

Tell your doctor if you have or have had any other medical conditions/ health problems, especially the following:

• breathing problems such as asthma
• any other heart problems
• allergic disorders including hay fever
• diabetes
• kidney problems
• liver problems such as jaundice
• an overactive thyroid gland
• any blood vessel disorders causing poor circulation in the arms and legs
• phaechromocytoma, which is a rare tumour of the adrenal gland
• certain types of angina such as Prinzmetal angina or variant angina
• shock or severe low blood pressure

If you have not told your doctor about any of the above, tell them before you start to take any TRANDATE.

Taking other medicines

Tell your doctor if you are taking any other medicines, including medicines that you buy without a prescription from a pharmacy, supermarket or health food shop.

SOME of these medicines may interfere with TRANDATE. These include:

• medicines used to treat angina or an irregular heart beat
• other medicines used to treat high blood pressure such as verapamil, clonidine and methyldopa
• fluid tablets, also called diuretics
• some medicines used during surgery and emergency situations such as anaesthetics
• cimetidine, a medicine commonly used to treat stomach ulcers
• some medicines used to treat depression
• guanethidine, a medicine used to treat certain heart conditions
• insulin or other medicines used to treat diabetes
• some medicines used to treat fever, pain and inflammation such as paracetamol and aspirin (NSAIDs)

The above medicines either reduce the effectiveness of TRANDATE, reduce its own effectiveness and/or react with TRANDATE resulting in untoward or sometimes dangerous side effects.

This list is not exhaustive. Your doctor or pharmacist has more information on medicines to be careful with or to avoid while taking TRANDATE.

Tell your doctor or pharmacist that you are taking TRANDATE before you start to take any other medicine.

How to take it

Your doctor will tell you how much TRANDATE to take and when to take it.

Take it exactly as directed by your doctor.

How much to take

The dose of TRANDATE may vary from patient to patient. Your doctor will decide on the right dose for you.

Adults:
The usual starting dose is 100 to 200 mg twice daily. Your doctor may change this dose depending on how you respond to TRANDATE.

Elderly patients may need smaller doses.

Do not change your dose of TRANDATE unless your doctor tells you to do so.

This medicine is not recommended for use in children.

How to take it

Swallow TRANDATE tablets with a glass of water.

When to take it

It is best to take your TRANDATE tablets immediately after meals.

How long to take it

To properly control your blood pressure, TRANDATE must be taken every day.

Continue taking TRANDATE as long as your doctor recommends it.

If you forget to take it

If it is almost time for your next dose, skip the dose you missed and take your next dose when you are meant to.

Otherwise, take your dose as soon as you remember, and then go back to taking it as you would normally.

Do not take a double dose to make up for the dose that you missed.

This may increase the chance of you getting an unwanted side effect. If you are unsure about whether to take your next dose, speak to your doctor or pharmacist.

If you have trouble remembering when to take your medicine, ask your pharmacist for some hints.

If you take too much (Overdose)

Immediately telephone your doctor or Poisons Information Centre (telephone 13 11 26) for advice, or go to casualty at your nearest hospital, if you think that you or anyone else may have taken too much TRANDATE. Do this even if there are no signs of discomfort or poisoning. Also, report any other medicine or alcohol which has been taken. You may need urgent medical attention.

Keep telephone numbers for these places handy.

If you take too much TRANDATE you may have the following symptoms: nausea, vomiting, dizziness, light-headedness, faintness, and a very slow heart beat.

While you are using it

Things you must do

Immediately stop taking TRANDATE if a skin rash or any other allergic reaction occurs.

If you become pregnant while taking TRANDATE, tell your doctor immediately.

If you are being treated for diabetes, make sure you check your blood sugar level regularly.

TRANDATE may affect how well your diabetes is being controlled. It may also cover up some of the symptoms of low blood sugar such as fast heart beat.

This medicine may also make low blood sugar last longer. Your doctor may need to change your dose of diabetic medicines, including insulin.

If you have to have any medical tests, tell your doctor you are taking TRANDATE.

It may affect the results of some tests.

Tell your doctor if you do not feel TRANDATE is helping your condition.

Visit your doctor regularly.

Your doctor needs to check your progress and see whether you need to stop taking TRANDATE.

Always discuss with your doctor any problems or difficulties during or after taking TRANDATE.

Things you must not do

Do not take any other medicines while you are taking TRANDATE, without first talking to your doctor.

Do not stop taking TRANDATE without first checking with your doctor.

Your doctor may want you to gradually reduce the amount of TRANDATE you are taking before stopping completely. This may help reduce the possibility of heart complications occurring.

Do not give this medicine to anyone else, even if his or her symptoms seem similar to yours.

Things to be careful of

Do not drive or operate machinery until you know how TRANDATE affects you.

TRANDATE may cause dizziness, light-headedness or drowsiness in some people.

Try to get up slowly when you are getting up from a sitting or lying position, as you may feel dizzy, light-headed, or faint.

If you continue to feel unwell, please contact your doctor.

Make sure you drink a lot of water while you are taking TRANDATE.

If you do not drink enough water, you may begin to feel faint, light-headed, or sick. This is because your blood pressure is dropping suddenly. If you continue to feel unwell, please contact your doctor.

Side effects

Tell your doctor or pharmacist as soon as possible if you do not feel well while you are taking TRANDATE.

This medicine helps most people with the medical condition listed in the beginning of this leaflet, but it may have unwanted side effects in some people.

All medicines have side effects. Sometimes they are serious, most of the time they are not. You may need medical treatment if you get some of the side effects.

Ask your doctor or pharmacist any questions you may have.

Tell your doctor if you notice any of the following and they worry you:

• Dizziness
• Light-headedness
• Headache
• Tiredness
• Lack of energy
• Depressed mood
• Blurred vision
• Dry, red or sore eyes
• Muscle cramps
• Unusual movements including tremor
• Tingling of the skin, especially the scalp
• Fever or chills
• Nausea (feeling sick)
• Upset stomach
• Vomiting
• Swelling of the ankles
• Problems with sexual function
• Blocked nose
• Increased sweating

Tell your doctor or pharmacist immediately if you notice any of the following:

• Feeling generally unwell, sometimes yellowing of the skin and/or eyes (jaundice)
• Slow or irregular heart beat
• Skin rashes which include redness, itching or hives
• Difficulty passing urine or unable to pass urine

If any of the following occur, tell your doctor immediately or go to casualty at your nearest hospital:

• Chest tightness, wheezing or shortness of breath
• Swelling of the face, lips, mouth, tongue or throat which may cause difficulty in swallowing or breathing

Some people may get other side effects while taking TRANDATE.

Check with your doctor as soon as possible if you have any problems while taking TRANDATE, even if you do not think the problems are connected with this medicine or are not listed in this leaflet.

After using it

Storage

Keep your tablets in the bottle they were provided in until it is time to take them.

Keep it where children cannot reach it.

A locked cupboard at least one and a half metres above the floor is a good place to store medicines.

Keep your medicine in a cool dry place where the temperature stays below 25°C and protect from light.

Do not store it, or any other medicines in a bathroom or near a sink.

Do not leave it in the car or on windowsills.

Heat and dampness can destroy some medicines.

Do not take TRANDATE if the tablets do not look quite right.

Disposal

If your doctor tells you to stop taking this medicine OR it has passed its expiry date, ask your pharmacist what to do with any left over.

Product description

What it looks like

TRANDATE tablets (oral) come in 2 strengths:

• 100 mg, orange, film-coated, biconvex tablets embossed “TRANDATE 100” on one face, in bottles of 100.
• 200 mg, orange, film-coated, biconvex tablets embossed “TRANDATE 200” on one face, in bottles of 100.

Ingredients

Active ingredient:

Other ingredients:

• Lactose
• Starch – maize
• Starch – pregelatinised maize
• Magnesium stearate
• Methyl hydroxybenzoate
• Propyl hydroxybenzoate
• Pharmacoat 606
• Opaspray M-1-3499D

TRANDATE is gluten and sucrose free, however contains lactose.

Buy Labetalol 100mg Generic @ $0.45 per Tablet

Labetalol is used to treat hypertension (high blood pressure). Lowering high blood pressure helps prevent strokes, heart attacks, and kidney problems. It belongs to a group of drugs called beta-blockers. By blocking the action of certain natural chemicals such as epinephrine in your body, Labetalol lowers blood pressure, heart rate, and strain on the heart. This medicine may also be used to treat other conditions as determined by your doctor.

The dosage of Labetalol prescribed to each patient will vary. Always follow your physician’s instructions and/or the directions on the prescription drug label.

Labetalol can be taken with or without food.

What if you miss a dose of Labetalol?

If your physician has instructed or directed you to take Labetalol medication in a regular schedule and you have missed a dose of this medicine, take it as soon as you remember. However, if it is almost time for your next dose, then skip the missed dose and go back to your regular dosing schedule. Do not double the doses unless otherwise directed.

What if you overdose on Labetalol?

Any medication taken in excess can have serious consequences. If you suspect an overdose of Labetalol, seek medical attention immediately.

It may be noted that drugs other than those listed above may also interact with Labetalol.

Usually drug interactions occur when it is taken with another drug or with food. Before you take a medication for a particular ailment, you should inform the health expert about intake of any other medications including non-prescription medications, over-the-counter medicines that may increase the effect of Labetalol, and dietary supplements like vitamins, minerals and herbal, so that the doctor can warn you of any possible drug interactions.

Labetalol can interact with diabetes medication, heart medication, and asthma medication.

Do let your doctor know if you smoke, consume alcohol or caffeinated drinks, or use illegal drugs as these may interfere with the action of your medication. Make sure to inform your doctor of any medical conditions you may have, or any family history of medical problems. Do not start or stop using any medicine without consulting your doctor.

Like other medicines, Labetalol can cause some side effects. If they do occur, the side effects of Labetalol are most likely to be minor and temporary. However, some may be serious and may require the individual to inform the doctor or visit the nearest hospital immediately.

It is pertinent to note that side effects of Labetalol cannot be anticipated. If any side effects of Labetalol develop or change in intensity, the doctor should be informed as soon as possible.

Labetalol can cause side effects such as dizziness, tiredness, impotence, anxiety, and nervousness. This is not a complete list of all side effects. Do concur with your doctor and follow his directions completely when you are taking Labetalol.

Is it possible for me to take Labetalol with other drugs?

Should certain beverages, foods and other products be avoided when I take Labetalol?

What are the possible drug interactions of Labetalol?

How will Labetalol work in my body?

How should Labetalol be taken?

How to reduce the risk of Labetalol drug interactions and side effects?

Note

The health and medical information provided here is intended to supplement and not substitute for the expertise and judgment of your physician, pharmacists or other health care professional. It should not be understood to indicate that the use of Labetalol is safe, appropriate or effective for you. Always consult your health care professional before using this, or any other, drug.

Properties of labetalol, a combined α-and β-blocking agent, relevant to the treatment of myocardial ischemia

(PDF) Labetalol: A Chapter Review

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Toxicity

Supportive care and close monitoring are the staples of treatment for an overdose of beta-blockers with the addition of

glucagon for severe refractory hypotension and bradycardia.

Glucagon provides several important clinical effects when used for beta-blocker overdose. It provides an increase in

HR and improves both myocardial contractility as well as atrioventricular conduction. Its MOA seems to be

independent of the beta-adrenergic binding site allowing it to be effective. The recommended initial dose of glucagon

for the purpose of reversing severe symptomatic beta-blockade is 50 mcg/kg IV as a loading dose, followed by an

infusion of 1 to 15 mg per hour IV, titrated to clinical response and improvement.[8]

Enhancing Healthcare Team Outcomes

As labetalol is typically used for the treatment of acute hypertension, whether that be an emergency or urgency, an

interprofessional team approach and effective communication are essential for quality patient care. In the

emergency department, swift intake and triaging by the nurse or medical technician to identify a patient with the

dangerously elevated blood pressure and quickly, but effectively to convey the critical information to a physician or

provider is necessary. If hospital admission is warranted, communicating the crucial details of the patient’s

presentation, medical history, and the treatment and current medical workup that have been completed are important,

so time and resources are not wasted on repeating tests and exams.

Questions

To access free multiple choice questions on this topic, click here.

References

Peacock WF, Hilleman DE, Levy PD, Rhoney DH, Varon J. A systematic review of nicardipine vs labetalol for

the management of hypertensive crises. Am J Emerg Med. 2012 Jul;30(6):981-93. [PubMed: 21908132]

Muzzi DA, Black S, Losasso TJ, Cucchiara RF. Labetalol and esmolol in the control of hypertension after

intracranial surgery. Anesth. Analg. 1990 Jan;70(1):68-71. [PubMed: 1967515]

Elatrous S, Nouira S, Ouanes Besbes L, Marghli S, Boussarssar M, Sakkouhi M, Abroug F. Short-term treatment

of severe hypertension of pregnancy: prospective comparison of nicardipine and labetalol. Intensive Care Med.

2002 Sep;28(9):1281-6. [PubMed: 12209278]

Duley L, Henderson-Smart DJ, Meher S. Drugs for treatment of very high blood pressure during pregnancy.

Cochrane Database Syst Rev. 2006 Jul 19;(3):CD001449. [PubMed: 16855969]

Baum T, Sybertz EJ. Pharmacology of labetalol in experimental animals. Am. J. Med. 1983 Oct 17;75(4A):15-23.

[PubMed: 6314811]

Facchini E, Degiovanni A, Cavallino C, Lupi A, Rognoni A, Bongo AS. Beta-Blockers and Nitrates:

Pharmacotherapy and Indications. Cardiovasc Hematol Agents Med Chem. 2015;13(1):25-30. [PubMed:

25544116]

Morales DR, Jackson C, Lipworth BJ, Donnan PT, Guthrie B. Adverse respiratory effect of acute β-blocker

exposure in asthma: a systematic review and meta-analysis of randomized controlled trials. Chest. 2014

Apr;145(4):779-786. [PubMed: 24202435]

Bailey B. Glucagon in beta-blocker and calcium channel blocker overdoses: a systematic review. J. Toxicol. Clin.

Toxicol. 2003;41(5):595-602. [PubMed: 14514004]

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Labetalol – Uses, Side Effects, Substitutes, Composition And More

Labetalol helps in the treatment of hypertension, commonly known as high blood pressure. The drug may either be prescribed on its own or in combination with other drugs. Labetalol may also be prescribed for the treatment of other health issues as per your doctor’s discretion. The drug works as an adrenergic receptor blocker, which effectively blocks alpha as well as beta receptors present in the body.

Doctors do not recommend the drug to those patients who are allergic to any substance that is present in it. Patients suffering from heart blockage, asthma, breathing problems or irregular heart beat are not prescribed Labetalol as their condition may worsen.

The drug is mostly administered in the form of an injection either at the doctor’s clinic or at the hospital. You can also learn to administer the drug yourself at home. In order to do so, ensure that your doctor teaches you how to administer the injection and use the drug the correct way. Labetalol should not be used if the liquid has turned cloudy or the vial is damaged. The drug as well as the needles and syringes should be kept away from kids and pets. Also make sure that you do not reuse a syringe or needle that you have already opened. Make sure that you dispose them properly.

One of the side effects of Labetalol is dizziness. To avoid any accident as a result of dizzy spells or fainant stay in bed after you receive your dose. You can return back to your daily activities about 3 hours after taking the dosage. Ensure that you move slowly as well.

Some other side effects of Labetalol are nausea, development of excess acid in the stomach, headache, heartburn, indigestion, rashes, foul taste in the mouth, weakness, pain or discomfort and belching.

Information given here is based on the salt content of the medicine. Uses and effects of the medicine may vary from person to person. It is advisable to consult a Cardiologist before using this medicine.

Memorial Sloan Kettering Cancer Center

This document, provided by Lexicomp ^® , contains all the information you need to know about the drug, including the indications, route of administration, side effects and when you should contact your healthcare provider.

Trade names: Canada

APO-Labetalol; RIVA-Labetalol; Trandate

What is this drug used for?

• Used to treat high blood pressure.

What do I need to tell my doctor BEFORE taking this drug?

• If you are allergic to this drug, any of its ingredients, other drugs, foods or substances. Tell your doctor about your allergy and how it manifested itself.
• For low blood pressure.
• If you have any of the following health problems: bronchial asthma or other lung disease or breathing problems that cause shortness of breath or wheezing, heart failure (weakened heart), certain types of heart rhythm disturbances called heart block or weakness syndrome sinus node, or bradycardia.
• If you are taking any of these drugs: diltiazem or verapamil.

This list of drugs and diseases that may be adversely associated with this drug is not exhaustive.

Tell your doctor and pharmacist about all the medicines you take (both prescription and over-the-counter, natural products and vitamins) and your health problems. You need to make sure that this drug is safe for your medical condition and in combination with other drugs you are already taking.Do not start or stop taking any drug or change the dosage without your doctor’s approval.

What do I need to know or do while taking this drug?

• Tell all healthcare providers that you are taking this drug. These are doctors, nurses, pharmacists and dentists.
• Avoid driving or other activities that require increased attention until you see how this drug affects you.
• To reduce the risk of dizziness or loss of consciousness, get up slowly from a lying or sitting position. Use caution when going up and down stairs.
• Measure blood pressure and heart rate as directed by your doctor.
• Perform blood tests as directed by your doctor. Please consult your doctor.
• This drug may interfere with some laboratory tests.Tell all healthcare providers and laboratory staff that you are taking this drug.
• This drug may mask signs of low blood sugar. Consult your doctor.
• If you have high blood sugar (diabetes), your blood sugar should be checked regularly.
• Do not stop taking this drug suddenly. If you stop taking this drug abruptly, your chest pain may worsen and, in some cases, even a heart attack.The risk may be increased with certain types of heart disease. To avoid side effects, this drug should be stopped gradually as directed by your doctor. Call your doctor right away if you experience or worsen chest pain or other heart problems.
• If you have had a very severe allergic reaction, consult your doctor. If you come into contact with the agent that caused the allergy, there is a risk of an even more severe reaction.Talk to your doctor if you are using epinephrine to treat very severe allergic reactions. Epinephrine may not work well while you are taking this drug.
• If you are having cataract surgery or any other eye procedure, talk to your doctor.
• Talk to your doctor before taking an over-the-counter drug that can increase blood pressure. These drugs include medicines for coughs and colds, diet pills, stimulants, nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen or naproxen, and some naturally occurring drugs.
• If you are 60 years of age or older, use this drug with caution. You may have more side effects.
• This drug may affect the characteristics of semen. It is not known if this can affect the ability to conceive.
• Tell your doctor if you are pregnant, planning to become pregnant, or breastfeeding. The benefits and risks for you and your child will need to be discussed.

What side effects should I report to my doctor immediately?

WARNING. In rare cases, some people with this drug can have serious and sometimes deadly side effects. Call your doctor or get medical help right away if you have any of the following signs or symptoms, which may be associated with serious side effects:

• Signs of an allergic reaction such as rash, hives, itching, reddened and swollen skin with blisters or scaling, possibly associated with fever, wheezing or wheezing, tightness in the chest or throat, difficulty breathing, swallowing or speaking, unusual hoarseness, swelling in the mouth, face, lips, tongue, or throat.
• Severe dizziness or fainting.
• Bradycardia.
• Unusual burning, numbness, or tingling sensations.
• Inability to achieve or maintain an erection.
• There have been cases of heart failure and worsening of previous heart failure while taking this drug. Talk to your doctor if you have a heart condition. If you experience shortness of breath, a sudden increase in body weight, an irregular heartbeat, swelling of the hands and feet, or if these symptoms worsen, consult a doctor immediately.
• Liver problems have rarely happened with this drug. Sometimes these cases were fatal. Call your doctor right away if you have signs of liver problems such as dark urine, tiredness, lack of appetite, nausea or abdominal pain, discolored stools, vomiting, yellowing of the skin or eyes.

What are some other side effects of this drug?

Any medicine can have side effects.However, many people have little or no side effects. Call your doctor or get medical help if these or any other side effects bother you or do not go away:

• Feeling dizzy, tired, or weak.
• Nausea.
• Tingling of the scalp.
• stuffy nose.

This list of potential side effects is not exhaustive. If you have any questions about side effects, please contact your doctor.Talk to your doctor about side effects.

You can report side effects to the National Health Office.

You can report side effects to the FDA at 1-800-332-1088. You can also report side effects at https://www.fda.gov/medwatch.

What is the best way to take this drug?

Use this drug as directed by your healthcare practitioner. Read all the information provided to you.Follow all instructions strictly.

Pills:

• Continue taking this drug as directed by your doctor or other healthcare professional, even if you feel well.

Injection:

• For intravenous infusion.

What should I do if a dose of a drug is missed?

Pills:

• Take the missed dose as soon as you can.
• If it’s time to take your next dose, do not take the missed dose and then return to your normal drug schedule.
• Do not take 2 doses at the same time or an additional dose.

Injection:

• Call your doctor for further instructions.

How do I store and / or discard this drug?

Pills:

• Store at room temperature in a dry place.Do not store in the bathroom.

Injection:

• If you need to store this drug at home, ask your doctor, nurse, or pharmacist for information about how it is stored.

All forms of issue:

• Store all medicines in a safe place. Keep all medicines out of the reach of children and pets.
• Dispose of unused or expired drugs.Do not empty into toilet or drain unless directed to do so. If you have any questions about the disposal of your medicinal products, consult your pharmacist. Your area may have drug recycling programs.

General information on medicinal products

• If your health does not improve or even worsens, see your doctor.
• You should not give your medicine to anyone and take other people’s medicines.
• Some medicines may have different patient information sheets. If you have questions about this drug, talk with your doctor, nurse, pharmacist, or other healthcare professional.
• Some medicines may come with other patient information sheets. Check with your pharmacist. If you have questions about this drug, talk with your doctor, nurse, pharmacist, or other healthcare professional.
• If you think an overdose has occurred, call a Poison Control Center immediately or seek medical attention. Be prepared to tell or show which drug you took, how much and when it happened.

Use of information by the consumer and limitation of liability

This information should not be used to make decisions about taking this or any other drug. Only the attending physician has the necessary knowledge and experience to make decisions about which drugs are appropriate for a particular patient.This information does not guarantee that the drug is safe, effective, or approved for the treatment of any disease or specific patient. Here are only brief general information about this drug. It does NOT contain all available information on the possible use of the drug with instructions for use, warnings, precautions, information about interactions, side effects and risks that may be associated with this drug. This information should not be construed as a treatment guide and does not replace information provided to you by your healthcare professional.For complete information on the possible risks and benefits of taking this drug, consult your doctor. Use of this information is governed by the Lexicomp End User License Agreement available at https://www.wolterskluwer.com/en/solutions/lexicomp/about/eula.

Copyright

© UpToDate, Inc. and its affiliates and / or licensors, 2021. All rights reserved.

The use of b-blocker bisoprolol in cardiological practice | Teplova N.V., Teplova N.N.

After the description in 1948 by the famous pathophysiologist A. Ahlquist of two types of adrenergic receptors (a and b), the development of drugs that actively affect these formations began, which led to the creation of a large number of very diverse drugs. With regard to the group of b-blockers (BAB), research proceeded in two main directions – the development of drugs with greater b1-selectivity, as well as the synthesis of drugs with prolonged action.Meanwhile, it was noted that BABs (regardless of whether they have a higher or lower selectivity) also have a peripheral vasoconstrictor effect, which narrowed the area of ​​their application.

Modern cardiology cannot be imagined without drugs of the BAB group, of which more than 20 names are currently known. For more than 30 years of use, b-adrenergic receptor blockers have taken a strong position in the pharmacotherapy of cardiovascular diseases.
Modern treatment with b-adrenergic receptor blockers is undergoing a certain evolution.Since their introduction in the 60s of the XX century, a large number of compounds of this class with high selectivity to b-adrenergic receptors have been synthesized into clinical practice, which made it possible to successfully use them as antianginal and antihypertensive agents. It is known that b-blockers give a good therapeutic effect in persons who have had myocardial infarction, with the presence of chronic circulatory failure and ventricular arrhythmias, significantly reducing the frequency of repeated myocardial infarctions, life-threatening tachycardias and sudden cardiac death.b-blockers of a new generation with high cardioselectivity to b1-receptors have advantages over the first generation drugs, including a longer half-life, high bioavailability, a lower likelihood of developing complications such as bronchospastic syndrome in chronic obstructive pulmonary diseases, vasoconstriction in peripheral atherosclerosis, violation of glyconeogenesis in patients with diabetes mellitus associated with a high degree of b2-adrenergic receptor blockade.
The main mechanism of action of BABs is that they are competitive antagonists of catecholamines, that is, norepinephrine (the main mediator of the sympathetic nervous system) and adrenaline (the main hormone of the adrenal medulla) in relation to b-adrenergic receptors. BABs are heterogeneous in their pharmacological effects, and the drugs of this class are united by the presence of competitive antagonism in relation to b1-adrenergic receptors. They differ from each other in the ability to simultaneously block b2-adrenergic receptors (non-selective BAB) and the presence or absence of their own (internal) sympathomimetic activity, that is, the ability to stimulate b-adrenergic receptors along with the blockade.Some of the newer BABs possess competitive antagonism against b-adrenergic receptors. Non-selective BAB equally affect both types of b-adrenergic receptors. Selective blockade of b1-adrenergic receptors is a relative and dose-dependent property, that is, as the dose of selective BAB increases, the ratio of blocked b1- and b2-adrenergic receptors decreases. Non-selective BABs include: propranolol, nadolol, sotalol, carvedilol, oxprenalol, timolol, labetalol and others. The b1-selective BAB subgroup includes: atenolol, metoprolol, nebivolol, bisoprolol, talinolol, esmolol and others.BABs with intrinsic sympathomimetic activity do not significantly affect resting heart rate, this property was regarded as an advantage of this subgroup of BABs, however, experience has shown that drugs with their own sympathomimetic activity (pindolol, oxprenalol, talinolol) do not reduce the risk of cardiovascular death. Probably, it is the negative chronotropic effect of BAB that improves the prognosis of patients with myocardial infarction. Some BABs (labetalol, pindolol, celiprolol, carvedilol, etc.)) have vasodilating properties. In addition to the main ones, there are also secondary pharmacological effects of BAB, among them the following are described – inhibition of renin secretion by the juxtaglomerular apparatus of the kidneys, inhibition of the formation of angiotensin II in the vascular wall, rearrangement of the baroreceptor mechanisms of the aortic arch and carotid sinus to another level of systemic blood pressure, stimulation of the endothelial formation of the prostacyclin walls, increased secretion of atrial natriuretic factor in response to exercise.It is possible that some of these processes form the antihypertensive effect of BAB. In addition, it should be noted such effects as increased gastrointestinal motility, relaxation of the sphincter of the bladder, a decrease in the secretion of the lacrimal glands, and others.
Pharmacokinetic differences in BAB are largely determined by their solubility in fats and water. Fat-soluble (lipophilic) BABs (metoprolol, oxprenalol, carvedilol, timolol and others) are rapidly and almost completely absorbed in the gastrointestinal tract, metabolized in the liver and well penetrate the biological membranes, the blood-brain barrier.These mechanisms require a reduction in doses or frequency of administration of lipophilic BAB in patients with reduced hepatic blood flow (patients with chronic heart failure (CHF), liver cirrhosis, in the elderly). It should also be borne in mind that drugs that reduce (cimetidine, chlorpromazine) or increase (barbiturates, rifampicin, smoking, alcohol) the activity of liver microsomal enzymes, respectively, slow down or accelerate the elimination of lipophilic BAB. It is known that an increase in the tone of the vagus nerve under the influence of lipophilic BABs penetrating the blood-brain barrier plays a major role in the formation of their antifibrillatory effect.On the contrary, it is the penetration of lipophilic BABs through the blood-brain barrier that explains the increased frequency of side effects from the central nervous system (general weakness, drowsiness, insomnia, hallucinations, depression). Lipophilic BAB usually have a short half-life and should be prescribed 2-3 times a day. In recent years, prolonged forms of lipophilic BABs, administered once a day, have been created. Water-soluble (hydrophilic) BABs (atenolol, sotalol, nadolol), unlike lipophilic ones, have a longer half-elimination period, penetrate the blood-brain barrier worse, biological membranes, are partially and unevenly absorbed in the gastrointestinal tract, are poorly metabolized in the liver and are excreted mainly by the kidneys, therefore, when renal failure, dose adjustment is necessary.
Some BABs dissolve in both fats and water (bisoprolol, acebutalol, pindolol and others). Fat- and water-soluble BABs have two elimination pathways – hepatic metabolism and renal excretion. The balanced clearance of these BAB explains the low probability of their interaction with other drugs and the safety of use in patients with moderate hepatic or renal insufficiency.
BABs are successfully used for the treatment of arterial hypertension, all forms of coronary heart disease (stable and unstable angina pectoris, myocardial infarction), various cardiac arrhythmias, hypertrophic cardiomyopathy, CHF, and are also used for secondary prevention after myocardial infarction and surgical myocardial revascularization.
A new step towards the optimization of anti-ischemic and antihypertensive therapy is the use of long-acting b-blockers, which allow maintaining a stable concentration of the drug in the blood at rest and during exercise for 24 hours after a single dose.
Clinical practice has gained experience in the successful use of a new long-acting cardioselective b1-adrenergic blocker bisoprolol (Bidop drug, pharmaceutical company Gedeon Richter) in the treatment of cardiovascular diseases.
Bisoprolol (Bidop) is a highly selective b1-blocker. The results of numerous studies have shown that the affinity of bisoprolol for b1-adrenergic receptors is 100 times higher than for b2-adrenergic receptors, a high degree of selectivity of the action of this drug in relation to b1-adrenergic receptors has been proven using an in vitro model on preparations of various tissues, including tissues of human organs as well as in vivo. Research results indicate that bisoprolol is a highly selective b1-blocker that does not have intrinsic sympathomimetic activity.Today it is the drug with the highest cardioselectivity index – 1:75. Its hemodynamic effect consists in a decrease in the heart rate at rest and during exercise, in a decrease in cardiac output and a slight (usually in the first days of treatment) increase in the total peripheral vascular resistance. On the other hand, at the therapeutically recommended doses (5 and 10 mg), the drug practically does not show antagonistic activity against b2-adrenergic receptors and therefore does not cause metabolic effects mediated by the blockade of b-adrenergic receptors, such as hyperglycemia or hyperlipidemia.This selectivity of action on b1-adrenergic receptors turns out to be clinically significant in the following cases: in patients with diabetes mellitus, the use of bisoprolol avoids hypoglycemia, in patients with vascular diseases, the use of bisoprolol avoids blockade of b2-adrenergic receptors, in which the vasodilating effect of endogenous adrenaline is inhibited, resulting in increased vasoconstriction mediated by a-adrenergic receptors.
The pharmacokinetics of bisoprolol (Bidop) differs from the pharmacokinetics of other selective b-blockers and is characterized by two positive properties: the presence of a long half-life, which makes it possible to prescribe this drug once a day, and a balanced clearance, which makes it possible to use this drug in the treatment of patients with concomitant dysfunction liver and kidney.
Drug treatment of patients with impaired liver or kidney function is very often difficult due to the fact that the metabolism of the drug used depends on the state of these organs. In bisoprolol (Bidop), more than 50% of the original substance is excreted in the urine, the remaining 50% are metabolized, and inactive metabolites are excreted in the urine. Only in the case of severe renal dysfunction and in patients with anuria, the half-life of the drug can more than double. Due to the unique balanced total clearance, it is possible to take bisoprolol (Bidop) once a day for all patients who need it, even in the presence of severe renal and / or liver dysfunction.A daily dose of 10 mg should not be exceeded in end-stage chronic renal or hepatic failure. Due to the 10-12-hour half-life, which does not change with impaired renal or hepatic function, a single dose of the drug should not be corrected in such patients.
In the treatment of arterial hypertension (AH), BABs are widely used along with thiazide diuretics, angiotensin-converting enzyme inhibitors, calcium antagonists, both as monotherapy and in combination with drugs of these classes.The main limitations in the use of BAB in the treatment of hypertension are associated with fears of the development of negative metabolic effects (increased insulin resistance, proatherogenic changes in the lipid spectrum of the blood), worsening of the course of concomitant COPD, and peripheral arterial disease. The best choice, especially for patients with comorbidities, are b1-selective BABs, since the risk of developing undesirable effects is minimal. For the treatment of hypertension, the use of long-acting drugs is preferable.
In comparative studies using outpatient 24-hour blood pressure monitoring, it was found that the effectiveness of bisoprolol within 24 hours is higher than that of other drugs prescribed once a day (for example, atenolol or the calcium antagonist nitrendipine). It was also found that a decrease in blood pressure during the day and a decrease in left ventricular hypertrophy are more pronounced when taking bisoprolol than when using second-generation angiotensin-converting enzyme inhibitors.
The use of BAB, especially bisoprolol (Bidop), improves the prognosis of coronary heart disease. The use of bisoprolol showed that in patients with ischemic heart disease, treatment is accompanied by a significant decrease in mortality, as well as an improvement in the general condition of patients. Bisoprolol (Bidop) improves exercise tolerance to a greater extent than atenolol and metoprolol, has a dose-dependent effect on exercise tolerance, improves quality of life and has few side effects.In the absence of contraindications, BAB is recommended to be prescribed to all patients who have had myocardial infarction, however, therapists and cardiologists do not use these drugs unjustifiably because of fear of the development of side effects of therapy. The results of a number of large epidemiological studies carried out in city hospitals and hospitals have shown that only 21 to 34% of patients with myocardial infarction receive BAB therapy. For the prevention of ischemic heart disease, it is considered preferable to prescribe b1-selective BABs without intrinsic sympathomimetic activity, including in patients with relative contraindications to their use or an increased risk of side effects of therapy.
It has been proven that in patients with coronary heart disease, drugs in this group not only reduce the severity of symptoms, but also improve the prognosis. The results of recent studies of bisoprolol have shown that in patients with stable angina pectoris, the number and duration of transient episodes of ischemia (both painful and painless) can be significantly reduced. In a comparative study of the sustained-release form of nifedipine and bisoprolol, it was found that the latter reduced the total “ischemic load” to a much greater extent than nifedipine.According to preliminary data from one of the prospective studies, a decrease in the total “ischemic load” is accompanied by an improved prognosis in patients with coronary heart disease. Thus, bisoprolol (Bidop) is the drug of choice in the treatment of patients with coronary heart disease.
The results of numerous clinical studies demonstrate the high efficiency of BAB (especially bisoprolol) in the treatment of supraventricular and ventricular arrhythmias, as well as in the correction of heart rate in patients with sinus tachycardia and atrial fibrillation.The most important BAB acquired in connection with their ability to prevent the development of life-threatening ventricular arrhythmias in patients with a high risk of sudden death (myocardial infarction, hypertension, CHF). A meta-analysis of the results of treatment of this category of patients showed that the use of BAB leads to a decrease in the risk of death from cardiovascular causes by 30-50%.
BABs are the drugs of choice in the treatment of hypertrophic cardiomyopathy. In the obstructive form of hypertrophic cardiomyopathy, drugs with vasodilating properties and internal sympathomimetic activity are not indicated.To prevent the occurrence of life-threatening ventricular arrhythmias (the main cause of death in patients with hypertrophic cardiomyopathy), large doses of drugs are prescribed for a long time.
Bisoprolol (Bidop) has good tolerance, as well as high selectivity to b1-receptors in the entire therapeutic dose range and during the entire period of its use. The undoubted advantages of bisoprolol include its high efficiency with long-term therapy, compatibility with other drugs, which is especially important for elderly patients.
Bisoprolol (Bidop) does not affect the metabolism of fats and glucose, and its bioavailability is about 90%. Bisoprolol (Bidop) is excreted from blood plasma through two equally active pathways: 50% metabolism to inactive metabolites, 50% excretion of unchanged substance through the kidneys. Bidop is a special registered form of bisoprolol 5, 10 mg for the treatment of patients with diseases of the cardiovascular system.
Thus, when choosing a drug for the complex treatment of patients with cardiovascular diseases from the point of view of efficacy and safety, at present, preference should be given to cardioselective b-blockers, and first of all to bisoprolol.

Literature
1. Ageev F.T. Use of β-blockers after myocardial infarction. // Rus. Honey. Journal. – 1999. – No. 5 – p. 733-736.
2. Arutyunov GP, Rylova AK, B-blockers in clinical practice. // Journal of Heart Failure. – 2001.– vol. 2, no. 2 – pp. 92–94.
3. Arutyunov G.P. B blockers and heart failure. // Journal of Heart Failure. – 2002.– v. 3, No. 1 (11) – pp. 27–28.
4. Karpov Yu.A., Shubina A.T. The use of β-blockers in the treatment of patients with arterial hypertension: new opportunities and prospects.// Russian medical journal. – 2005. – T. 13. – No. 19 (243). – S. 1265-1269.
5. Cleophas M., Noschese P., D * Amato G., Matera M.G. The pharmacologic treatment of incomplicated arterial hypertension in patients with airway dysfunction. Chest. – 2002.– 12 (1) – 230–241.
6. Edes I., Gasior Z., Wita K. Effects of nebivolol on left ventricular function in elderly patients with chronic heart failure: results of the ENECA study. Eur J Heart Fail. – 2005: 7: 631-9.

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Labetalol hydrochloride and breastfeeding. Is Labetalol Hydrochloride compatible with breastfeeding?

Is Labetalol Hydrochloride compatible with breastfeeding? Do we have alternatives for Labetalol Hydrochloride?

August 29, 2018 (Very Low Risk)

Labetalol is a non-cardioselective beta-blocker used in the treatment of hypertension, chronic stable angina pectoris, sympathetic hyperactivity syndrome associated with severe tetanus, blood pressure control in patients with pheochromocytoma, in pregnant women with preeclampsia and the production of controlled hypotension during anesthesia to reduce bleeding from surgery.
Administration is given orally twice daily or intravenously for the emergency treatment of hypertension.

Despite the lack of high protein binding (Riant 1986), other pharmacokinetic properties (moderate lipid solubility and high volume of distribution) probably explain that labetalol is excreted from breast milk in clinically insignificant amounts (Hale 2019, Anderson 2018, FDA 2010 , Atkinson 1990 y 1988, Lunell 1985, Michael 1979).

In addition, its low oral bioavailability makes it difficult to transfer to infant plasma through breast milk, except in premature infants and in the immediate neonatal period, during which intestinal permeability may be increased.

No problems were observed in infants whose mothers received labetalol while breastfeeding (Briggs 2017, AEMPS 2001, Michael 1979). Plasma levels in infants whose mothers received labetalol were very low (Lunell 1985, Michael 1979).

It is not known which case of asymptomatic bradycardia is reported in a 26-week gestational preterm infant and 640 g birth weight whose mother was taking 600 mg of labetalol daily. He received 0.1 mg / kg / day of labetalol through milk, which is 1% of the maternal dose and 0.8% of the pediatric dose (Mirpuri 2008).

Oral labetalol does not affect prolactin secretion (Barbieri 1982).
Labetalol during pregnancy or childbirth, but not during lactation, has been associated with neonatal hypoglycemia (Munshi 1992). The use of labetalol for the treatment of hypertension during pregnancy has been associated with Raynaud’s phenomenon of nipples and nipples during breastfeeding. Discontinuation of labetalol eliminated nipple pain (McGuinness 2013).

Some authors do not consider beta-blockers to be the drugs of choice for the treatment of hypertension, unless another indication exists at the same time, such as the prevention of migraine or angina pectoris (Anderson 2018).

Several medical societies, experts and expert consensus consider the use of this medication safe or likely safe during breastfeeding (Hale 2019 p 418, Briggs 2017, Serrano 2014, Davanzo 2014, Rowe 2013, Podymow 2011, Ghanem 2008).
The American Academy of Pediatrics considers labetalol to be a drug generally compatible with breastfeeding (AAP 2001).

The protective role of breastfeeding against maternal hypertension has been proven (Park 2018).

Hypertensive crises: diagnosis and treatment. Consensus of the Ukrainian Association of Cardiologists and the Ukrainian Stroke Association (Part 2). Features of blood pressure correction in complicated hypertensive crises depending on the target organ damage

Dear Colleagues!

We propose to consider a document that has the character of an agreement (consensus) of experts on an extremely urgent problem of modern medicine – hypertensive crises.Its importance is determined not only by the high prevalence of arterial hypertension among the population of Ukraine and numerous cases of destabilization of the course, but also by the high frequency of complications with injuries of target organs. Many of these complications develop suddenly and pose a threat to life (acute disorders of the coronary and cerebral circulation, dissection of the aortic walls, etc.), others are delayed and lead to progressive organ dysfunction. Therefore, the problem of timely diagnosis and treatment of hypertensive crises is especially relevant for specialists in various fields, and not only for cardiologists.This became the basis for the creation of a document with the participation of a committee of experts from various medical specialties, who for the first time jointly consider the problem of an acute increase in blood pressure from the position of a cardiologist, neuropathologist, anesthesiologist, ananimatologist, obstetrician gynecologist. Taking into account modern ideas about the pathophysiological patterns of the formation of a hypertensive crisis in various clinical situations, approaches to lowering blood pressure may differ and have different prognostic significance.Thus, the presented first attempt at a multidisciplinary approach to the problem of hypertensive crises is not final and requires further development with the participation of a larger number of specialists.

I would like to express my gratitude to everyone who took an active part in the preparation and comprehensive discussion of this document.

Parkhomenko A.N., Doctor of Medical Sciences, Professor, Corresponding Member of the National Academy of Medical Sciences of Ukraine, Chairman of the Working Group on Emergency Cardiology of the Association of Cardiologists of Ukraine, Head of the Department of Resuscitation and Intensive Therapy of the National Scientific Center “Institute of Cardiology named afteracad. N. D. Strazhesko “NAMS of Ukraine

Acute coronary syndrome

Often in a patient with ACS and elevated blood pressure, it is very difficult to determine whether this increase is primary (the cause of ACS) or developed in response to acute coronary circulation disorder. But approaches to blood pressure control in most cases are the same and are determined by the blood pressure level at the time of assessment and before the development of ACS, the presence of complications of ACS (acute heart failure, mechanical complications, etc.) and lesions of other target organs.

Specific antihypertensive therapy should be started when SBP increases> 160 mm Hg. and / or DBP> 100 mm Hg. The goal of therapy is to reduce mean blood pressure by 20–30% within an hour [105]. Thrombolytic therapy is possible only if the blood pressure is <185/110 mm Hg. [58]. The drugs of choice for controlling blood pressure in patients with ACS are nitroglycerin and adrenergic blockers.

Nitroglycerin reduces the hemodynamic load on the heart (mainly preload), reduces its oxygen demand and energy costs, dilates the coronary vessels, which, in addition to lowering blood pressure, provides an additional clinical effect in acute myocardial ischemia and makes nitroglycerin the drug of choice in these patients.At the same time, before prescribing nitro drugs in a patient, it is necessary to find out the possibility of taking 5-phosphodiesterase inhibitors. The use of nitrates against the background of drugs of this group can cause the development of significant hypotension, therefore, within 24 (sildenafil) – 48 (tadalafil) hours from the last dose of 5phosphodiesterase inhibitors, the use of nitro drugs is contraindicated [106].

An alternative to nitroglycerin can be adrenergic blockers. There is no consensus regarding the possibility of early intravenous administration of drugs in this group to patients with acute myocardial infarction.Several studies have shown a decrease in patient mortality [107, 108], a decrease in the size of myocardial infarction [109-111], prevention of cardiac arrhythmias, and a decrease in the number of reinfarctions with early intravenous administration of adrenergic blockers [112]. The highest efficacy was observed in patients without ST segment elevation [113].

However, according to the results of the largest study COMMIT (45,852 patients), intravenous administration of metoprolol (especially in the first 24 hours) in patients with ACS with ST-segment elevation (apart from preventing reinfarctions and cardiac arrhythmias) significantly increased the risk of cardiogenic shock [114].

Therefore, to date, in patients with ACS only with a significant increase in blood pressure and the development of tachyarrhythmias, the use of intravenous adrenergic blockers is indicated [115].

Contraindications for the appointment of adrenergic blockers are moderate or severe heart failure and pulmonary edema, bradycardia (<60 cardiac contractions per minute), signs of impaired peripheral circulation, blockade of 2-3 degrees, or obstructive pulmonary disease.

ACE inhibitors are recommended for all patients with acute myocardial infarction in the absence of contraindications from the very first day of the disease [116-118].At the same time, intravenous administration of enalapril to these patients in the CONSENSUS II study was accompanied by an increase in mortality, which was more likely associated with the development of hypotension [119]. Therefore, the appointment of intravenous ACE inhibitors in patients with ACS (including for the treatment of GC) is contraindicated. Urapidil can be used as an alternative to adrenergic blockers and nitrates in ACS [120].

Acute pulmonary edema

Elevated BP levels (SBP> 140 mm Hg) are observed in approximately 50% of patients with acute pulmonary edema (AR).Art.). In some patients, such a hypertensive reaction is not primary, but develops in response to shortness of breath, agitation and / or angina pectoris. Therefore, such patients need to establish oxygen therapy, calm down and provide adequate pain relief. The drug of choice in this case is morphine, which also has some other beneficial effects in patients with OOL. The goal of further treatment of this category of patients is to reduce pre and afterload and ensure sufficient diuresis. Lowering blood pressure can reduce the heart’s need for oxygen and increase cardiac output.With OOL, blood pressure must be reduced urgently and quickly. The drugs of choice are nitroglycerin and sodium nitroprusside, which are used against the background of diuretic therapy [58, 121]. Schemes of drug administration are presented in table. 5.

One non-randomized, open-label study demonstrated the advantage of using high doses of nitroglycerin (repeated bolus injections of 2 mg every 3 minutes) to lower blood pressure over a standard regimen (intravenous infusion) in patients with OOL on a background of HA (ABP ≥ 160 mm Hg.Art. or mean blood pressure ≥ 120 mm Hg) [122].

The intensive care group was characterized by a significantly lower incidence of admissions to the intensive care unit (37.9% versus 80.0%), intubation (13.8 versus 26.7%) and an increase in troponin levels (17.2 versus 28.9%). … One (3.4%) patient in the active treatment group developed symptomatic hypotension; in the standard therapy group, such cases were not recorded. Therefore, such a scheme for the use of nitroglycerin can be used only after careful weighing of the possible benefits and risks and requires further confirmation.

An alternative to nitrovasodilators for lowering blood pressure in patients with OOL can be the use of urapidil. This drug, unlike other vasodilators, does not cause the development of reflex tachycardia [62], which is especially important in patients with acute heart failure. In the NITURA study, the use of urapidil (against the background of oxygen therapy, morphine and diuretics) in patients with HA complicated by OOL was accompanied by a significant decrease in blood pressure and a more significant improvement in respiratory and metabolic parameters than with the use of nitroglycerin [123].

Acute aortic dissection

Aortic dissection (RAo) is a cardiac emergency characterized by damage to the middle layer of the aorta (media) in the form of separation, followed by penetration and spread of blood along the aortic wall. In most cases (90% of patients), the penetration of blood into the aortic wall occurs as a result of damage to its inner layer (intima) directly or due to penetration of an atherosclerotic ulcer [124], but primary hematoma formation in the middle layer of the aorta as a result of bleeding from the vasa vasorum is also possible. [125, 126].

The prognosis of patients with RAo is extremely unfavorable – up to 40% of patients die instantly, then mortality is about 1% of patients during each subsequent hour and 5–20% during or immediately after surgery [127–129].

Therefore, in RAo, timely diagnosis and rapid initiation of therapy are extremely important. Treatment approaches for acute thoracic aortic dissection depend on its anatomical location. According to the Stanford classification, two types of RAo are distinguished: type A – covers all dissections that affect the ascending aorta, and type B – all dissections without affecting the ascending aorta [124].

Changes in blood pressure are very common in this category of patients. According to the IRAD registry, 71% of patients with type B dissection and 36% of patients with type A dissection have a SBP greater than 150 mmHg. [130, 131]. In contrast, about 20% of patients on hospitalization have persistent hypotension or symptoms of shock [228]. It is this category of patients that is characterized by a poor prognosis [132].

Partial occlusion of the main branches of the aorta (including the subclavian arteries) due to dissection may cause falsely low blood pressure readings.Therefore, measurements must be taken on both arms and both legs of the patient.

The basis of the initial stage of management of patients with RA is the prevention of further stratification by reducing hemodynamic stress and the simultaneous identification of patients requiring surgical or endovascular intervention.

To solve the first question, it is necessary to remember that the dissemination of the dissection is caused not only by the level of blood pressure, but also by the parameters of the LV work, namely, the rate of its contraction (dP / dt) and heart rate.Therefore, adrenergic blockers (esmolol, labetalol, metoprolol or propranolol), which affect all of these components of pathogenesis, are the drugs of choice for the treatment of patients with RAo. The goal of therapy is to reduce the heart rate to less than 60 per minute and maintain the SBP level within 100–120 mm Hg. [133].

In patients with relative contraindications for the use of adrenergic blockers (asthma, HF, chronic obstructive pulmonary disease, etc.), the drug of choice may be esmolol, which is characterized by a very short half-life.In case of intolerance to adrenoblockers, an acceptable alternative may be the use of nondihydropyridine calcium antagonists (verapamil, diltiazem). However, a decrease in heart rate in patients with significant aortic regurgitation should be carried out very carefully, since it can provoke the development of acute heart failure.

The use of adrenergic blockers in most cases does not allow adequate control of blood pressure; therefore, the use of vasodilators is recommended [130, 134, 135].

In a study [136], the prescription of 4 different antihypertensive drugs was required to target blood pressure reduction in patients with RAo.For this, intravenous administration of sodium nitroprusside, nitroglycerin, nicardipine, and a number of other antihypertensive agents can be used [124]. However, it must be remembered that the appointment of vasodilators before adrenergic blockers is very dangerous and can provoke the development of reflex tachycardia and increased heart rate, which are risk factors for further stratification [229].

Adequate analgesia against the background of intravenous administration of opiates can significantly increase the effectiveness of antihypertensive therapy, primarily by reducing sympathetic activation.

In all patients with aortic dissection, consultation with a cardiac surgeon is required to determine the need for surgical treatment [124]. In the absence of severe comorbidities, surgery is indicated for all patients with type A dissection [137].

Patients with type B RAo require intensive drug therapy. In this case, the operation is performed only if it is impossible to stabilize the patient’s condition (progression of dissection, insufficient perfusion syndrome, hemodynamic instability, etc.) [130, 138–141].

After stabilization of the condition due to surgery and intravenous antihypertensive therapy, most patients with RAo should be prescribed long-term antihypertensive therapy. This therapy, in addition to an adrenergic blocker, should include an ACE inhibitor or an angiotensin receptor blocker, the use of which can reduce further dilatation of the aorta [124].

Acute hypertensive encephalopathy

Acute hypertensive encephalopathy (AHE) is an emergency condition caused by acute cerebral edema against the background of GC and characterized by the development of neurological (mainly cerebral) symptoms in the form of impaired consciousness, headache, epileptic seizures, and meningeal syndrome.The OGE occupies an intermediate position between uncomplicated GC and acute stroke and is diagnosed only if the latter is not confirmed.

OGE, as a rule, develops in patients with a long history of hypertension. Impaired autoregulation of cerebral blood flow in these patients leads to an increase in the permeability of the blood-brain barrier in response to a significant increase in blood pressure [142].

In this case, conditions arise for the filtration of blood plasma to the tissues of the brain and the development of its vasogenic edema.Deterioration of the rheological properties of blood due to a decrease in its liquid part and compression of the microvasculature by edematous tissues lead to the appearance of areas of cerebral ischemia. Further damage and necrosis of arterioles against the background of increased blood pressure is the cause of their paretic expansion and increased cerebral edema, which determines the clinical picture of the disease [143].

The main clinical symptom of OGE is headache. In most cases, the headache is accompanied by nausea, vomiting, vestibular (dizziness, instability, feeling of swaying) and / or visual (photopsia, loss of visual fields) disorders, convulsive syndrome.Unlike a stroke, stable focal neurological symptoms are not observed, but it is possible to develop passing diffuse small focal symptoms (numbness or paresthesia of the extremities, tongue, lips, weakness in the extremities, etc.) due to focal cerebral ischemia. The severity of a patient’s condition with AGE is determined by the level of impairment of consciousness, which can vary from insignificant (weakness, confusion) to coma development [144, 145].

OGE is a diagnosis that is established by excluding other possible causes for the occurrence of neurological symptoms (primarily ischemic and hemorrhagic strokes, subarachnoid bleeding, neoplasms, etc.).etc.). It is very important to quickly and correctly diagnose OGE, since the approaches to lowering blood pressure in various neurological emergencies are different. Therefore, in addition to the obligatory examination by a neurologist and an ophthalmologist [146], these patients are recommended to perform magnetic resonance imaging (better) or computed tomography as early as possible. Signs of cerebral edema in the absence of focal lesions, trauma, or hemorrhage confirm the diagnosis of OGE [147].

The mechanisms of autoregulation provide a relatively constant level of cerebral blood flow under conditions of significant fluctuations in the parameters of central hemodynamics (Fig.2). Morphofunctional rearrangement of cerebral arteries in patients with persistent hypertension leads to a shift in the autoregulation curve to the right. This allows, on the one hand, to adapt to significant increases in blood pressure without significant changes in the level of cerebral blood flow, on the other hand, leads to ischemia in the case of a rapid or significant decrease in blood pressure [29, 142].

Therefore, in patients with OGE (especially with a long-term hypertensive history), a balanced approach to the degree and rate of blood pressure decrease is recommended.It is believed that a decrease in mean blood pressure by 25% within 8 hours or DBP to 100–110 mm Hg. it is safe enough and allows you to return to the limits of autoregulation [148].

Pharmacological drugs for lowering blood pressure in patients with OGE should not have side effects from the central nervous system. Urapidil, labetalol are used. It is not recommended to use nifedipine, nitroprusside and hydralazine. Nitroprusside can be prescribed only in case of ineffectiveness of other drugs, as well as with DBP above 140 mm Hg.Art. [148].

The drugs of choice for the treatment of cerebral edema are saluretics (furosemide, torasemide). Unlike osmodiuretics, these drugs do not lead to the formation of a delayed increase in ICP due to hyperosmolarity. If these methods of therapy are ineffective, barbiturates and decompression surgery are used.

Ischemic stroke

In the majority of patients with acute ischemic stroke (AIS), a significant increase in blood pressure is observed in the first hours of the disease, followed by its involuntary decrease over the next few days [149, 150].

An increase in blood pressure may be due to a stress response to the development of cerebrovascular accident, nausea, pain, pre-AH, response to hypoxia or increased ICP [151, 152].

In the mechanisms of the development of an acute hypertensive reaction with impaired cerebral circulation, impaired baroreflex also plays a significant role [153]. The dependence of the course of AIS on the level of blood pressure is not fully understood. Some studies have confirmed the relationship between an increase in baseline blood pressure and an unfavorable course of the disease [154, 155]; in some, such a relationship was not revealed.This indicated that the increase in blood pressure in acute ischemic stroke is projective and is aimed at maintaining adequate intracerebral blood flow, especially in the peri-infarction zone [156-158].

According to other studies, this dependence was U-shaped, i.e. complications were more often observed in patients with very high and low blood pressure levels [159-161]. Thus, in a study by L.G. Stead et al. observed an increase in mortality among patients with SBP <155 mm Hg. and> 220 mm Hg.Art. and a DBP level <70 mm Hg. and> 105 mm Hg [162]. The relationship between an unfavorable prognosis and an increase in pulse blood pressure has also been shown [163].

Theoretically, the reasons for lowering blood pressure in patients with acute ischemic stroke are the ability to reduce cerebral edema, prevent hemorrhagic transformation, and prevent further vascular damage. An immediate decrease in blood pressure is also necessary in case of damage to other target organs or the development of hypertensive encephalopathy [152, 164].On the other hand, an active decrease in blood pressure can lead to a worsening of neurological symptoms due to a decrease in perfusion of ischemic brain regions that form around the main focus [165, 166]. The optimal blood pressure level in patients with a history of hypertension is 180-190 / 105 mm Hg, without hypertension – 160/90 mm Hg.

Most of the studies that tested the effectiveness of early active blood pressure lowering in patients with acute ischemic stroke have been unsuccessful. Moreover, the negative consequences of a rapid decrease in blood pressure in this category of patients did not depend on whether specific antihypertensive drugs were used for this.Thus, J. Oliveira Filho et al. demonstrated a decrease in blood pressure by an average of 28% during the first day of acute stroke, regardless of the use of antihypertensive drugs, while a decrease in blood pressure by every 10% led to an almost twofold increase in the number of early complications [167].

In a study by J. Castillo et al. deterioration of neurological symptoms, an increase in the size of the lesion and the number of adverse events, taking into account death, were associated with a decrease in both SBP and DBP by more than 20 mm Hg.Art. [161].

In the randomized multicenter study INWEST, the adverse effect of nimodipine in acute ischemic stroke was associated precisely with a decrease in blood pressure while taking it [168, 169].

At the same time, when using other drugs (ACE inhibitor and adrenergic blocker) in the CHHIPS study, a decrease in blood pressure in patients with acute ischemic stroke did not lead to a deterioration in treatment results and even reduced mortality. 179 patients with BP ≥ 160 mm Hg up to 36 hours from the onset of symptoms of acute ischemic stroke, lisinopril, labetalol, or placebo were started.Doses of the drugs were increased until the target SBP values ​​of 145–150 mm Hg were achieved. or its decrease by 15 mm Hg. As a result of treatment, the SBP level was significantly lower in the active group than in the control group, both after 24 hours and after 2 weeks. from the moment of randomization. There were no differences between groups in the incidence of serious side effects during the follow-up period, worsening neurological symptoms in the first 72 hours, and death / disability after 2 weeks. from the start of treatment.There was a tendency towards a decrease in the incidence of death from all causes after 3 months. observations in the active treatment group (9.7% versus 20.0%, P = 0.05) [170].

In the COSSACS study (n = 763), it was proved that the continuation of antihypertensive therapy in the acute phase of acute ischemic stroke leads to a significant decrease in blood pressure, but does not reduce the likelihood of death / disability after 2 weeks. observation, and also does not affect the number of serious side effects and major cardiovascular events within 6 months.[171].

Reducing the incidence of death and adverse vascular events after acute stroke was demonstrated in the ACCESS study using the angiotensin II receptor blocker candesartan. Candesartan was administered from the first day of the acute stroke with a gradual increase in dose at SBP> 160 mm Hg. or DBP> 100 mm Hg, and on the 7th day, if necessary, other antihypertensive agents were added. At very high BP levels, urgent intravenous BP correction was used.However, the positive effects of candesartan were not observed during the first months of treatment, and a significant divergence of the curves began only after 1 year [172].

In the recently published multicenter placebo-controlled study SCAST (n = 2029) in patients with acute ischemic stroke and BP> 140 mmHg. also did not reveal a positive effect of early (within the first 7 days) administration of candesartan on the development of major cardiovascular events (death / nonfatal MI / stroke) within 6 months.observation. The functional state of patients taking candesartan according to the modified Rankin scale after 6 months. was assessed as worse than in the control group (P = 0.048, although in this study the differences were considered significant at P <0.025) [173].

When analyzing the results of 37 studies (total 9008 patients), in which the efficacy of 13 different antihypertensive drugs was tested, did not reveal statistically significant advantages of early antihypertensive therapy in patients with acute ischemic stroke compared with the control group.In the active treatment group, the dependence of adverse events on changes in blood pressure was U-shaped or J-shaped – both a significant decrease and any increase in blood pressure were associated with a deterioration in treatment results. The best results in the active treatment group were observed with a fairly moderate (from 8.1 to 14.6 mm Hg) decrease in SBP [174].

Research results are rather ambiguous, but most of them indicate the safety of a moderate approach to lowering blood pressure in patients with acute ischemic stroke and high blood pressure.At the same time, the levels of blood pressure, which require urgent treatment, have not been quite clearly established, as well as the rate and limit for its reduction have not been determined. To date, increased blood pressure in patients with acute ischemic stroke is corrected, taking into account the possibility of thrombolytic therapy. For patients who are planning to receive a tissue plasminogen activator, an urgent decrease in blood pressure is recommended when the SBP increases> 185 mm Hg. and / or DBP> 110 mm Hg, since exceeding these levels is a contraindication for the administration of a thrombolytic drug.In the rest of the patients, the limit for immediate treatment was defined as SBP> 220 mm Hg. and DBP> 120 mm Hg. [175].

A decrease in blood pressure must be carried out very carefully in order to prevent an increase in neurological symptoms due to a deterioration in intracerebral hemodynamics. It is considered advisable to reduce the mean blood pressure by 15–25% during the first day [98, 175].

The choice of an antihypertensive drug depends on the speed and duration (in case of worsening neurological symptoms against the background of a decrease in blood pressure) of its action, on possible side effects and the effect on intracerebral circulation.

To date, in order to lower blood pressure in patients with acute ischemic stroke, the use of labetalol, urapidil is recommended. Given the absence of a negative effect on intracerebral circulation in general and on blood circulation in the peri-infarction zone with acute ischemic stroke, urapidil is recommended by the European Stroke Organization for the correction of blood pressure in acute cerebrovascular accident.

Antihypertensive therapy regimens are presented in table. 7. At the same time, in order to prevent the development of a hypotensive reaction, it is necessary to strictly adhere to the recommended protocols for the regimen of drug administration and to strictly control the blood pressure level [176].

Sodium nitroprusside and nifedipine increase the ICP level and disrupt the autoregulation of intracerebral circulation [50–52], therefore, the use of these drugs in acute ischemic stroke is contraindicated.

Nitroprusside can be used only as a “last resort” in case of ineffectiveness of other antihypertensive drugs and DBP above 140 mm Hg. if a rapid decrease in blood pressure is necessary (for example, concomitant pulmonary edema or aortic dissection). If the patient receives antihypertensive therapy before the stroke, he continues to take it in the acute period of stroke.Patients with untreated hypertension from the second week of the disease should take combined antihypertensive drugs.

Hemorrhagic stroke

In patients with hemorrhagic stroke, the prognosis of the disease is primarily determined by the volume of intracranial hematoma (ICH), which increases during the first hours (especially the first 3 hours) and significantly slows down or stops after 1 day [177, 178].

ICH volume directly correlates with the degree of SBP increase (≥ 160 mm Hg).Art.) [179], which is observed in 46-75% of patients with intracranial bleeding (ICH) [180-182].

Stress-induced activation of the neuroendocrine system (sympathetic nervous system, renin-angiotensin-aldosterone mechanism, glucocorticoid system) and increased ICP are considered potential pathophysiological mechanisms of increased blood pressure. Hypertension can theoretically contribute to a hydrostatic increase in hematoma and perihematoma edema, as well as increase the likelihood of rebleeding [194].

According to the results of meta-analysis, an increase in SBP from 140 to 150 mm Hg. in the first 12 hours after the development of ICH, it was accompanied by an almost twofold increase in the risk of death or by limitation of legal capacity [154, 183].

Unfortunately, today there are few data on the effect of lowering blood pressure on the size of ICG. On the contrary, theoretically there is a threat that an active decrease in blood pressure may impair the perfusion of the brain and cause its ischemic damage. Therefore, the American Heart Association / American Stroke Association guidelines in 2007a fairly moderate approach to the correction of blood pressure in patients with ICH was fixed (Table 8) [184].

This approach was based primarily on expert opinion and the results of small clinical trials. However, in a number of experimental and clinical studies, no zones of hypoperfusion or disorders of cerebral blood flow autoregulation around ICH were found, which could cause ischemic brain damage [180, 185–189].

Several nonrandomized clinical trials have also confirmed the safety of early BP reduction or even shown an improvement in the clinical course of the disease in patients with ICH.In a study by S. Koch et al. compared standard (mean blood pressure 110–130 mm Hg) and intensive (mean blood pressure <110 mm Hg) antihypertensive therapy in patients with ICH, who were randomized in the first 8 hours (mean 3.2 ± 2, 2 hours) from the moment the symptoms of the disease appear. The mean blood pressure was maintained with standard drugs according to routine clinical practice (labetalol, nicardipine, or sodium nitroprusside) for 48 hours. On average, the required blood pressure level was reached after 87.1 ± 59.6 and 163.5 ± 163.8 minutes in the groups of standard and intensive therapy, respectively.After 90 days, there were no differences between the groups in the frequency of early deterioration of neurological symptoms, hematoma size and peri-hematoma edema, and clinical follow-up results [190].

A. Qureshi et al. evaluated the tolerance and safety of intensive antihypertensive therapy (hydralazine and labetalol) in 27 patients with ICH. Kept the CAP below 160 mm Hg. and DBP less than 90 mm Hg. within at least 24 hours from the development of the disease. Worsening of neurological symptoms was observed in 2 (7.4%) patients, an increase in ICH size – in 2 (9.1%) of 22 patients who underwent repeated computed tomography.The authors concluded that the early use of intensive pharmacotherapy for acute increases in blood pressure in patients with ICH is possible [191].

In February 2010, the results of the ATASN study were published, in which patients were divided into three groups depending on the target levels of systolic blood pressure: 170-200, 140-170 and 110-140 mm Hg. The study included patients with symptoms of spontaneous ICH within 6 hours from the development of the disease and a blood pressure of 170 mm Hg. The reduction and maintenance of target blood pressure levels for 18-24 hours was achieved by intravenous infusion of nicardipine according to the standard scheme.Of 774 selected patients, only 60 patients were randomized – 18, 20, and 22 patients, respectively, into groups 1, 2 and 3. The target SBP levels were achieved in all patients of the 1st and 2nd groups and in 13 (59.1%) patients of the 3rd group. Worsening of neurological symptoms during the first 24 hours was observed in 1 (6%), 2 (10%) and 4 (18%) patients, and the development of serious side effects within 72 hours – in 0; 1 (5%) and 3 (14%) patients of the 1st, 2nd and 3rd groups. After 3 months. follow-up, 3 (17%), 2 (10%) and 5 (23%) patients died, respectively.The incidence of undesirable side effects was less than expected before the start of the study; therefore, the authors concluded that the intensive approach to lowering blood pressure in patients with ICH is safe [192].

The research results served as the basis for a new project – ATASNII. Its goal is to determine the possibility of preventing death and limiting legal capacity after 90 days by intensive antihypertensive therapy with nicardipine in the first 24 hours after the development of the disease. The study includes patients with VChK within 3 hours from the onset of the first neurological symptoms and a SBP level of 180–240 mm Hg.Art. The target SBP in the intensive care group is 140 mm Hg, in the control group – 180 mm Hg. Patient enrollment began in 2010, and the planned number of participants is about 1300 [193].

The INTERACT study recruited patients with spontaneous ICH within 6 hours of the onset of symptoms and an elevated SBP level (150–220 mm Hg). Subsequently, the patients were divided into the groups of standard (SBP ≤ 180 mm Hg) and active control of blood pressure (decrease in SBP ≤ 140 mm Hg within 1 hour after the start of therapy and maintaining this level for a week).To lower blood pressure, the drugs most used in the clinic were used according to the standard scheme (urapidil and / or furosemide in more than 80% of patients from the intensive treatment group). In 2008, the results of the first phase of the study were published (203 patients in the intensive group and 201 patients in the standard therapy group). One hour after randomization, the mean SBP in the standard control group was 167 mm Hg, in the intensive control group – 153 mm Hg. (P <0.0001), average SBP from 1 to 24 hours - 157 and 146 mm Hg, respectively.Art. (P <0.0001). After 24 hours of treatment in the group of intensive blood pressure control, a 22.6% smaller increase in the size of ICH was noted (P = 0.06), as well as a significantly lower percentage of patients with a significant (> 33% or 12.5 ml) increase in the size of ICH (P = 0.05). The incidence of adverse events and death during 90 days of observation did not differ significantly. The results obtained allowed the authors to conclude that an early intensive decrease in blood pressure in patients with ICH is achievable, well tolerated and, probably, leads to a decrease in the increase in ICH [76].

Thus, today, recommendations for a moderate decrease in blood pressure in patients with spontaneous ICP, taking into account the level of ICP, remain valid. At the same time, taking into account the data of previous studies, in patients with VChK and SBP 150–220 mm Hg. acute decrease in blood pressure to 140 mm Hg. can be considered safe. It is this position that is reflected in the new 2010 American Heart Association / American Stroke Association guidelines [194].

Subarachnoid hemorrhage

Subarachnoid hemorrhage (SAH) of non-traumatic genesis is a fairly frequent pathological process (up to 5% of all strokes), which consists in the ingress of blood into the subarachnoid space due to rupture of a saccular aneurysm or arteriovenous malformation.The main treatment for this disease is surgical (or invasive). The goal of drug therapy is to prevent and treat cerebral edema, re-hemorrhage and angiospasm. Therefore, blood pressure control is a very important component of drug therapy. Although today there is no unambiguous data on whether adequate blood pressure control affects the likelihood of re-hemorrhage, most studies confirm the development of this complication in patients with elevated blood pressure levels and significant changes in blood pressure [195, 196].In these studies, the development of rebleeding was associated with a SBP level of more than 150–160 mm Hg.

At the present stage, the goal of antihypertensive therapy in patients with SAH in the preoperative period is to maintain SBP below 140 mm Hg. and DBP below 90 mm Hg. [197, 198].

To achieve target blood pressure levels, long-term infusion of nicardipine, labetalol or esmolol is used. The use of sodium nitroprusside should be avoided due to the potential for increased ICP and toxicity in case of prolonged use [199].

In contrast, urapidil does not affect the ICP level and allows reliable and safe blood pressure control in these patients [200].

After SAH, spasm of the arteries of the base of the brain is recorded in 30–70% of patients, which leads to a significant deterioration in distal cerebral blood flow. As a rule, signs of vasospasm are observed on the 3rd-5th day, reach a maximum on the 5-14th day and disappear by the end of the 2nd-4th week [201, 202].

In about half of patients, the deterioration of intracerebral hemodynamics due to vasospasm leads to the emergence of a new neurological deficit, which may pass or lead to the development of cerebral infarction [203, 204].

To prevent and treat cerebral vasospasm, SAH surgery should be performed as soon as possible. From the first hours after the development of SAH, all patients should take nimodipine (60 mg 4 times a day). There are currently no data on the effectiveness of other calcium antagonists [199, 205].

Treatment of cerebrovascular accidents due to cerebral vasospasm consists of an increase in circulating blood volume (hurervolemia), hemodilution (haemodilution) and an increase in blood pressure (hypertension) – rule 3h [199].

In some patients during this period, a spontaneous increase in blood pressure is observed, which in most cases has a compensatory character and is aimed at maintaining the proper level of cerebral circulation [206].

Therefore, in patients with SAH in the postoperative period (the cause of rebleeding has been eliminated), antihypertensive therapy is not performed if the SBP level is up to 200 mm Hg. [198].

Eclampsia and preeclampsia

Hypertension complicates the course of pregnancy in about 12% of women and is the cause of maternal death in 18% of cases [207].

Therapy of preeclampsia / eclampsia is quite complex and consists in the control of fluid exchange, prevention of seizures and normalization of blood pressure [208-210].

Treatment of hypertension is not pathogenic, but necessary for the mother and fetus. Lowering blood pressure is necessary to prevent the development of hypertensive encephalopathy and cerebral hemorrhage. One should strive to bring blood pressure to a safe level (140/90–150/100 mm Hg, not lower!), Which ensures the maintenance of adequate cerebral and placental blood flow.A rapid and sharp drop in blood pressure can worsen the condition of the mother and fetus.

Antihypertensive therapy is carried out with an increase in SBP of more than 160 mm Hg. and / or DBP more than 105 mm Hg. [211, 212]. It is necessary to reduce and maintain blood pressure at an optimal level, which will, on the one hand, prevent the development of HF, heart failure and infarction / placental abruption, on the other hand, it will not lead to deterioration of cerebral and / or placental circulation [213].

It is believed that the optimal SBP level is 140–160 mm Hg.Art., DBP – 90-105 mm Hg. A rather narrow range of target blood pressure levels in combination with the instability of its parameters, which is a characteristic feature of patients with preeclampsia / eclampsia, necessitates constant monitoring of such patients in intensive care units. The use of large doses of magnesium also requires hourly monitoring of urine output and the level of deep tendon reflexes. There is no ideal drug for controlling blood pressure in patients with preeclampsia / eclampsia. Traditionally, hydralazine is used for this purpose.This drug slightly penetrates the placental barrier and does not lead to a deterioration in placental circulation. In most cases, it is well tolerated, but it can lead to the development of side effects (headache, nausea, vomiting, reflex tachycardia), which are difficult to distinguish from exacerbation of preeclampsia. The drug is also characterized by a delayed, unpredictable and prolonged hypotensive effect, which significantly limits its use [214].

Hydralazine: 20 mg (1 ml) of the drug is dissolved in 20 ml of 0.9% sodium chloride solution, 5 ml (5 mg of hydralazine) is slowly injected intravenously every 10 minutes until the DBP drops to a safe level (90-100 mm Hg).Art.). If necessary, repeat the introduction of hydralazine 5-10 mg hourly or 12.5 mg intramuscularly every 2 hours.

Labetalol may also be used to lower blood pressure in pregnant women [215-218]. It is a water-soluble drug, so it hardly penetrates the placental barrier. A direct comparison of the use of labetalol and hydralazine in a randomized clinical trial did not reveal significant differences in the incidence of hypotension in mothers, while hydralazine therapy was more often accompanied by tachycardia.Neonates also did not differ in the main indicators, except for blood pressure and bradycardia, the frequency of which was significantly higher with labetalol. In this study, both drugs were found to be acceptable for the treatment of severe hypertension during pregnancy [230].

Labetalol is used initially intravenously 10 mg, after 10 minutes in the absence of an adequate response (DBP above 110 mm Hg) – an additional 20 mg. Blood pressure is monitored every 10 minutes, and if DBP remains above 110 mm Hg.Art., enter 40 mg, and then 80 mg of labetalol (up to a maximum of 300 mg).

In the absence of labetalol, nifedipine 5-10 mg sublingually may be used. If the effect is not observed, then after 10 minutes it is necessary to give another 5 mg under the tongue. It should be remembered that against the background of the administration of magnesium sulfate, nifedipine can lead to the rapid development of hypotension.

Urapidil. The initial dose of urapidil is 6.5 mg, after 5 minutes, if there is no adequate response, an additional 2.5 mg. Blood pressure is monitored every 10 minutes.In the future, continue the infusion of urapidil at a rate of 2-4 mg / h until blood pressure stabilizes or until the end of labor.

Urapidil and dihydralazine were equally effective in lowering blood pressure in pregnant women with preeclampsia. However, the hemodynamic effects of urapidil were more predictable and the drug is better tolerated [78, 79].

In another study, the use of urapidil was associated with a significantly lower effect on hemodynamic parameters of the newborn than intravenous dihydralazine [80].

Urapidil is recommended for emergency care of patients with hypertension during pregnancy (European Society of Cardiology, 2011).

Magnesium sulfate is used as an anticonvulsant with a simultaneous antihypertensive effect, which is the drug of choice for the prevention and treatment of seizures that occur in hospitalized women due to insufficient treatment of severe preeclampsia. Magnesia therapy is started from the moment of hospitalization if DBP is> 105 mm Hg.Art. The starting dose – 4 g of dry matter (16 ml of 25% magnesium sulfate solution) – is injected with a syringe very slowly over 15 minutes (in case of eclampsia – within 5 minutes). Supportive therapy is usually started with a dose of 1 g dry matter of magnesium sulfate per hour.

The use of ACE inhibitors and sodium nitroprusside in pregnant women is contraindicated.

Hypertensive crisis due to hypersympathicotonia

Most often, this type of HA is caused by the use of sympathomimetic agents, such as cocaine or amphetamines, less often observed in patients with pheochromocytoma, as well as with the simultaneous administration of monoamine oxidase inhibitors and foods containing tyramine (hard cheeses, alcoholic beverages, protein mixtures).The development of hypersympathicotonia is also possible in patients who abruptly stopped taking clonidine or adrenoblockers.

When treating such GCs, adrenergic blockers should not be used, at least as first-line drugs. The blockade of adrenergic receptors can increase the level of catecholamines in the blood plasma and enhance the activation of adrenergic receptors. The consequence of this activation is spasm of the coronary arteries with the development of acute myocardial ischemia, a progressive increase in blood pressure and an increase in mortality [92, 219, 220].

Even for labetalol, which for a long time was theoretically considered as an ideal drug for the treatment of this category of patients, there is no confirmation of its effectiveness in clinical practice due to the suppressive blockade of adrenoreceptors [221-225]. The drugs of choice for the treatment of such patients are peripheral adrenergic blockers (in Ukraine only urapidil) or nitroglycerin / nitroprusside in combination with diazepam. It is possible to use verapamil [226].

Perioperative hypertension

Perioperative hypertension occurs in approximately 25% of patients with concomitant hypertension.Given the significant prevalence of hypertension (about 12 million patients were registered in Ukraine in 2009), the problem of preoperative preparation, intraoperative and postoperative management of these patients becomes very urgent due to the high risk of cardiovascular complications and death against the background of changes in blood pressure. A separate problem is also the increased risk of hemorrhagic complications.

Perioperative increase in blood pressure is more often observed during induction of anesthesia intraoperatively – due to stimulation of the sympathetic nervous system in response to pain; in the early post-anesthetic period – as a result of pain, hypothermia, hypoxia or fluid overload during surgery; 24–48 hours after surgery – in response to the redistribution of fluid from the extravascular space into the vessels.Postoperative increase in blood pressure may also be due to the withdrawal of antihypertensive therapy. More often, blood pressure increases during operations on the carotid arteries, abdominal aorta, peripheral arteries, abdominal or thoracic organs. Increased DBP> 110 mm Hg is a preoperative marker for the development of cardiovascular events during and immediately after surgery. Thus, all patients taking antihypertensive therapy should continue to do so immediately prior to surgery, including the morning before surgery.

Preoperative hypertension

In most cases, preoperative hypertension meets the criteria for uncomplicated HA. An increase in blood pressure does not lead to damage to the target organs, but only poses a potential threat to the patient. In addition, in most cases, there is sufficient time before surgery to adequately reduce blood pressure. However, the very fact of preoperative hypertension (SBP> 180 mm Hg or DBP> 110 mm Hg) in men is associated with an increased risk of death by more than 3-4 times after non-cardiac surgery.Therefore, planned operations should be postponed until adequate blood pressure control. A significant increase in blood pressure in patients before urgent surgery without direct damage to the target organs is also considered as uncomplicated HA. In this case, blood pressure must be lowered immediately before the operation, preferably with short-acting drugs, which will prevent the occurrence of bleeding and damage to vital organs during and after the operation.

Particular attention should be paid to patients taking clonidine for blood pressure control.Sudden withdrawal of the drug can lead to a rebound syndrome with the development of GC, as in pheochromocytoma, especially in patients taking adrenergic blockers. Therefore, before performing a planned intervention, it is necessary to gradually transfer the patient to other antihypertensive drugs or to use clonidine before an emergency operation. In the case of the development of rebound syndrome, intramuscular administration of clonidine is used.

In peripheral vascular bypass grafting, coronary artery bypass grafting, carotid artery endarterectomy, intracerebral tumor resection and arterial aneurysm removal operations, it is especially important to control blood pressure during the intervention to prevent complications, therefore, the preoperative preparation of this category of patients should be carried out very carefully.

Preoperative GC in patients with acute aortic dissection, hypertension of pregnant women and pheochromocytoma is considered as complicated. These conditions require an active reduction in blood pressure before the intervention and during the operation according to the principles recommended for such nosologies.

Intra and postoperative hypertension

An acute increase in SBP or mean blood pressure by 20% or more during surgery is considered as complicated by GC. Most often, HA occurs during operations on the heart, great vessels (carotid artery, aorta), kidneys, head and neck, neurosurgical interventions and operations associated with injuries (burns, head trauma), but it is also possible with any surgical intervention under general or local anesthesia.

Basically, drugs for anesthesia cause a decrease in blood pressure, but some (for example, ketamine) can dramatically destabilize hemodynamics and provoke intraoperative hypertension, especially with monotherapy.

Inadequate general anesthesia is often the cause of intraoperative hypertension. In such cases, the elimination of hypertension involves, first of all, a reassessment of the depth of general anesthesia, if necessary, deepening of anesthesia, and then the use of antihypertensive drugs.

A common cause of intraoperative hypertension is the use of vasoconstrictors (epinephrine hydrochloride) alone (mucosal application) or together with local anesthetics (infiltration or conduction anesthesia). This situation is typical for dental, otolaryngological, ophthalmic, endoscopic surgical interventions. Moreover, similar cases of intraoperative hypertension are recorded when not a ready-made form of local anesthetic is used, but a mixture of local anesthetic and adrenaline hydrochloride ex tempore is prepared.With careful monitoring of blood pressure, the increase in DBP can reach 45–70%. As a result, even after one intraoperative episode of GC, patients may develop acute hypertensive encephalopathy, the clinical signs of which are delayed awakening, psychomotor agitation, convulsive readiness, nausea and / or vomiting, severe headache, manifestations of ataxia. Intraoperative GCs, as a rule, increase the volume of surgical blood loss.

Postoperative hypertension is defined as an increase in SBP ≥ 190 mm Hg.Art. and / or DBP ≥ 100 mm Hg based on the results of two consecutive measurements. The development of hypertension, which is a fairly frequent event in the early postoperative period, is associated with an increase in the tone of the sympathetic nervous system and an increase in vascular resistance. The main reasons for the destabilization of blood pressure are postoperative pain, psychoemotional reactions, skipping a dose of an antihypertensive drug or their combination before surgery, etc. The increase in blood pressure, as a rule, begins about 10–20 minutes after the intervention and lasts up to 4–6 hours.If treatment is not carried out adequately and in a timely manner, the risk of bleeding, cerebrovascular events, or myocardial infarction increases sharply. The prevalence of postoperative hypertension varies from 4 to 35%, depending on the patient population and the type of surgery. The highest risk is noted in patients with operations on the heart and great vessels.

Perioperative hypertension treatment

The best result is the prevention of perioperative hypertension. In most patients, an increase in blood pressure during or after surgery occurs in response to a violation of a long-term regimen of antihypertensive therapy.Therefore, it is recommended to transfer the patient to long-acting medications before the intervention (at least a few days before), take the last dose of the antihypertensive agent in the morning before the operation, and after it, resume the usual therapy as soon as possible.

Preoperative hypertension before emergency surgery is treated according to the principle of therapy for uncomplicated GC. At the same time, it is optimal to use short-acting antihypertensive drugs and those that do not have a negative pharmacological interaction with drugs for anesthesia.

The presence of elevated blood pressure in patients who are scheduled for elective surgery requires a more careful selection of therapy, preferably with the use of long-acting drugs. In patients with a history of hypertension, the level of DBP is within 110 mm Hg. is not a reason for delaying surgery.

During and immediately after surgery, the blood pressure level is recommended to be maintained within 20% of the preoperative one. In the treatment of intra- and postoperative hypertension, there is no generally accepted opinion regarding the rate of decrease and target blood pressure levels (especially in non-cardiological patients).The decision about the type of therapy is often made at the patient’s bedside by the anesthesiologist and surgeon, taking into account the baseline blood pressure levels, comorbidity and the possible risk of complications. In most cases, the goal of therapy is to reduce mean blood pressure by no more than 25% using parenteral antihypertensive drugs. In the first 30-60 minutes of therapy, it is necessary to achieve a decrease in DBP by 10-15%, or about 110 mm Hg. Against the background of a decrease in blood pressure, it is recommended to carry out moderate infusion therapy with saline solutions to replenish the circulating blood volume, restore perfusion and prevent a rapid decrease in blood pressure and hypoperfusion of vital organs (primarily the brain and kidneys).It is recommended to return to the initial blood pressure level in 24–48 hours.

A more proactive approach is recommended in cardiac patients. In this case, antihypertensive therapy should be started at BP> 140/90 mm Hg. or the level of average blood pressure 105 mm Hg. and higher.

Pain and anxiety also contribute to an increase in blood pressure, so they must be overcome before starting antihypertensive therapy. It is also necessary to eliminate such possible causes of an increase in blood pressure in the postoperative period, such as hypothermia with chills, hypoxemia, hypercapnia, bladder overflow.

The use of urapidil, labetalol and esmolol has been proven to stabilize blood pressure in the event of perioperative complicated HA. The benefits of using a particular antihypertensive drug in various categories of surgical patients have been tested in many clinical trials. However, it should be noted that against the background of the action of propofol, these drugs can excessively reduce blood pressure, therefore, their use requires more careful monitoring of blood pressure.

One of the drugs that has successfully proven itself in the treatment of perioperative hypertension is the selective adrenoblocker urapidil.In addition to the blockade of peripheral adrenergic receptors, urapidil interacts with serotonin 5HT1Areceptors of the vasomotor center of the medulla oblongata, due to which the correction of blood pressure against the background of its use does not cause the development of reflex tachycardia. The effect of urapidil on blood pressure and other hemodynamic parameters in cardiac surgery patients with perioperative hypertension has been studied in a number of studies. The antihypertensive efficacy of urapidil is the same as that of sodium nitroprusside and phentolamine, and better than that of nitroglycerin.Urapidil has also been successfully used in a number of studies for the treatment of perioperative hypertension in general surgical practice.

Results

This document is an interdisciplinary consensus on the diagnosis and treatment of hypertensive crises. It is consistent in nature and corresponds to the modern concepts of various specialists in the diagnosis and treatment of these conditions. The authors hope that it will resonate with both general practitioners and relevant professionals.The first sign of acceptance and recognition of the practical significance of this document should be considered its support by the Association of Cardiologists of Ukraine – it was agreed and approved during the National Congress of Cardiologists of Ukraine in September 2011. Further implementation of the practical aspects of the developed document will depend on the efforts of specialists in specialties related to cardiology and its acceptance by general practitioners

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