Instructions for Lipril tablets 20 mg blister No. 30
Composition
active ingredient: lisinopril;
1 tablet contains lisinopril (calculated as 100% anhydrous lisinopril) - 20 mg, which corresponds to lisinopril dihydrate - 21.78 mg;
excipients: mannitol (E 421), calcium hydrogen phosphate dihydrate, corn starch, magnesium stearate; iron oxide red (E 172).
Dosage form
Pills.
Main physicochemical properties:
Lipril in a dosage of 20 mg in 1 tablet is a pink, flat-cylindrical tablet with beveled edges and a score. Marbling and inclusions are allowed on the surface of the tablets.
Pharmacotherapeutic group
Angiotensin-converting enzyme (ACE) inhibitors. Lisinopril. ATC code C09A A03.
Pharmacological properties
Pharmacodynamics
Lisinopril is a peptidyl dipeptidase inhibitor. Lisinopril inhibits angiotensin-converting enzyme (ACE), which catalyzes the conversion of angiotensin I to the vasoconstrictor peptide, angiotensin II. Angiotensin II also stimulates the secretion of aldosterone by the adrenal cortex. Inhibition of ACE leads to a decrease in the concentration of angiotensin II in the blood plasma, which leads to a decrease in vasopressor activity and aldosterone secretion, and may also lead to an increase in the concentration of potassium in the blood serum.
Since the mechanism of action in hypertension is through inhibition of the renin-angiotensin-aldosterone system, lisinopril has a hypotensive effect even in hypertensive patients with low renin levels. ACE is identical to kinase II, the enzyme that breaks down bradykinin. The role of increased levels of bradykinin (which has pronounced vasodilating properties) during treatment with lisinopril is not fully understood and requires further study.
Pharmacokinetics
Lisinopril is an orally active, non-sulfhydryl ACE inhibitor.
Absorption
After oral administration of lisinopril, its maximum serum concentration is reached within 7 hours. In patients with acute myocardial infarction, there is a tendency for a slight increase in the time required to reach maximum serum concentration. The average value of absorption of lisinopril is approximately 25% and varies in individual patients depending on the dose taken (5-80 mg) in the range from 6 to 60%. These data are based on the amount of drug determined in the urine. In patients with heart failure, the absolute bioavailability is reduced by approximately 16%. The presence of food in the gastrointestinal tract does not affect the absorption of lisinopril.
Distribution
Lisinopril does not bind to other serum proteins except circulating ACE. Studies in rats indicate that lisinopril does not cross the blood-brain barrier well.
Breeding
Lisinopril is not metabolized and is excreted unchanged in the urine. The effective cumulative half-life of lisinopril after multiple dosing is 12.6 hours. The clearance of lisinopril in healthy volunteers is approximately 50 ml/min. The decline in serum concentrations has a prolonged terminal phase that does not affect drug accumulation. This terminal phase is likely to reflect extensive binding to ACE and is not dose-proportional.
Pharmacokinetics in special patient groups
Liver dysfunction
Impaired liver function in patients with cirrhosis results in reduced absorption of lisinopril (approximately 30%) and increased exposure (approximately 50%) compared to healthy volunteers due to reduced clearance.
Kidney dysfunction
Renal impairment reduces the renal elimination of lisinopril, but this reduction is clinically significant only when the glomerular filtration rate is below 30 ml/min. In mild and moderate renal impairment (creatinine clearance 30-80 ml/min), the mean AUC increased by only 13%, whereas in severe renal impairment (creatinine clearance 5-30 ml/min), a 4.5-fold increase in mean AUC was observed.
Lisinopril can be removed by dialysis. During 4 hours of hemodialysis, plasma concentrations of lisinopril were reduced by an average of 60% with a dialysis clearance of 40-55 ml/min.
Heart failure
Patients with heart failure have a higher exposure to lisinopril compared to healthy volunteers (an increase in AUC of 125% on average), but based on the amount of lisinopril recovered in urine, the apparent reduction in absorption is approximately 16% compared to healthy volunteers.
Elderly patients
In elderly patients, lisinopril plasma concentrations and area under the plasma concentration-time curve are higher (approximately 60% increase) compared to younger patients.
Indication
Essential hypertension; heart failure (symptomatic treatment); acute myocardial infarction (short-term treatment (6 weeks) of patients with stable hemodynamic parameters no later than 24 hours after acute myocardial infarction); treatment of initial nephropathy in patients with type 2 diabetes mellitus with arterial hypertension.
Contraindication
Hypersensitivity to lisinopril, to any of the excipients or to other ACE inhibitors; history of angioedema after taking ACE inhibitors; idiopathic or hereditary angioedema; bilateral renal artery stenosis or stenosis of the artery to a solitary kidney; kidney transplantation; mitral or aortic stenosis, hypertrophic cardiomyopathy with severe haemodynamic compromise; acute myocardial infarction with haemodynamic instability; cardiogenic shock; use of high-flux membranes made of polyacrylonitrile sodium-2-methylallylsulfonate (e.g. AN 69) in dialysis; use with aliskiren-containing medicinal products in patients with diabetes mellitus or with renal impairment (GFR < 60 ml/min/1.73 m2) and serum creatinine > 220 µmol/l; primary hyperaldosteronism; pregnant women or women planning to become pregnant (see "Use during pregnancy or breastfeeding").
Interaction with other medicinal products and other types of interactions
Other antihypertensive drugs: The hypotensive effect of lisinopril may be enhanced. Use with nitroglycerin and other organic nitrates or vasodilators may further reduce blood pressure. Ganglioblockers or adrenergic neurone blockers may be used in combination with lisinopril only under strict supervision.
The combination of lisinopril with aliskiren-containing drugs should be avoided.
Dual blockade of the RAAS through the combined use of ACE inhibitors (including lisinopril), ARBs or aliskiren is associated with a higher frequency of side effects, such as hypotension, hyperkalemia, decreased renal function (including acute renal failure) compared with the use of a single RAAS-blocking drug (see sections "Contraindications", "Special instructions for use").
Diuretics: additive antihypertensive effects have been reported. In patients already taking diuretics, especially those who have recently been prescribed diuretics, the use of lisinopril may occasionally cause an excessive decrease in blood pressure. The risk of symptomatic hypotension can be minimized by discontinuing the diuretic before starting treatment with lisinopril.
Potassium-sparing diuretics, potassium supplements, or potassium-containing salt substitutes: Although serum potassium levels generally remained within normal limits in clinical trials with ACE inhibitors, some patients developed hyperkalemia.
The risk of hyperkalemia is associated with factors such as renal failure, diabetes mellitus, concomitant use of potassium-sparing diuretics (e.g. spironolactone, triamterene, amiloride), potassium-containing food supplements or salt substitutes.
The use of potassium supplements, potassium-sparing diuretics or potassium-containing salt substitutes may lead to significant increases in serum potassium, especially in patients with impaired renal function.
When lisinopril is used with potassium-sparing diuretics, hypokalemia caused by their use may be attenuated.
Cyclosporine, heparin, trimethoprim/co-trimoxazole, lovastatin: increased risk of hyperkalemia when combined with ACE inhibitors.
Lithium preparations: when used with ACE inhibitors, there is a reversible increase in serum lithium concentration and its toxic effects. Concomitant use of thiazide diuretics may increase the risk of lithium intoxication and exacerbate it if it is already caused by concomitant administration of ACE inhibitors. The use of lisinopril simultaneously with lithium is not recommended, but if such a combination is necessary, careful monitoring of serum lithium levels should be carried out.
Nonsteroidal anti-inflammatory drugs (NSAIDs), including acetylsalicylic acid at a dose of ≥ 3 g per day, selective COX-2 inhibitors and non-selective NSAIDs: the hypotensive effect of ACE inhibitors is reduced. Concomitant administration of NSAIDs and ACE inhibitors may lead to impaired renal function, including acute renal failure, especially in elderly patients, in patients with dehydration (including on the background of diuretic therapy), causes an additive effect on increasing serum potassium levels, especially in patients with pre-existing impaired renal function. These effects are usually reversible. Such a combination should be used with caution, especially in cases of impaired renal function, with periodic monitoring of their function.
Gold preparations: Nitritoid reactions (symptoms of vasodilation, including flushing, nausea, dizziness, hypotension, which can be very severe) after injection of gold (e.g. sodium aurothiomalate) have been reported more frequently in patients treated with ACE inhibitors.
Tricyclic antidepressants, antipsychotics and anesthetics: possible increase in arterial hypotension.
Sympathomimetics: the hypotensive effect of ACE inhibitors may be reduced.
Hypoglycemic drugs (insulins, oral hypoglycemic agents): possible increase in the blood glucose-lowering effect with the risk of hypoglycemia. The likelihood of such an effect is particularly high during the first weeks of combined treatment, as well as in cases of impaired renal function.
Estrogens, corticosteroids: possible reduction in the antihypertensive effect of ACE inhibitors due to fluid retention in the body.
Agents that suppress bone marrow function: increased risk of neutropenia and/or agranulocytosis.
Cytostatics, immunosuppressants, corticosteroids, procainamide: when used simultaneously with lisinopril, leukopenia may develop.
Allopurinol: increased risk of leukopenia and hypersensitivity reactions, especially in patients with impaired renal function.
Tissue plasminogen activators, immunosuppressants such as mTOR inhibitors (e.g. temsirolimus, sirolimus, everolimus): possible increased risk of angioedema.
Antacids: The bioavailability of lisinopril may be reduced, therefore Lisinopril should be taken 1-2 hours before or 1-2 hours after taking an antacid.
Lisinopril can be administered concomitantly with acetylsalicylic acid (in doses used in cardiology), thrombolytics, β-blockers and/or nitrates.
Alcohol potentiates the hypotensive effect of ACE inhibitors.
Application features
Symptomatic hypotension
Symptomatic hypotension is uncommon in patients with uncomplicated hypertension. In hypertensive patients taking lisinopril, hypotension is more likely to occur in cases of volume depletion, such as those resulting from diuretic therapy, dietary salt restriction, dialysis, diarrhoea or vomiting, or severe renin-dependent hypertension. Symptomatic hypotension has been reported in patients with heart failure with or without associated renal insufficiency. It has been more common in patients with more severe heart failure who are receiving high doses of loop diuretics, have hyponatraemia or have functional renal insufficiency.
In patients at increased risk of symptomatic hypotension, initiation of therapy and dose adjustment should be carried out under close medical supervision. Similar monitoring is also necessary for patients with ischemic heart disease or cerebrovascular disease, in whom excessive reduction in pressure could lead to myocardial infarction or stroke.
In case of arterial hypotension, the patient should be placed on his back and, if necessary, intravenous infusion of saline solution should be given. Transient arterial hypotension during administration of the drug is not a contraindication for its further use after normalization of blood pressure and restoration of BCC.
In some patients with heart failure and normal or low blood pressure, the drug may further reduce systemic blood pressure. This effect is expected and is not usually a reason for discontinuation of treatment. If hypotension becomes symptomatic, it may be necessary to reduce the dose or discontinue lisinopril.
Arterial hypotension in acute myocardial infarction
In patients with acute myocardial infarction, treatment with lisinopril should not be initiated if there is a risk of further serious haemodynamic deterioration after vasodilator therapy. This applies to patients with a systolic blood pressure of 100 mm Hg or lower or patients in cardiogenic shock. If the systolic blood pressure is 120 mm Hg or lower, the dose should be reduced during the first 3 days after the infarction. If the systolic blood pressure is 100 mm Hg or lower, the maintenance dose should be reduced to 5 mg or temporarily to 2.5 mg. If hypotension persists (systolic blood pressure less than 90 mm Hg for more than 1 hour), lisinopril should be discontinued.
Aortic and/or mitral valve stenosis/hypertrophic cardiomyopathy.
As with other ACE inhibitors, lisinopril is not recommended for use in patients with mitral valve stenosis and left ventricular outflow obstruction (e.g., aortic stenosis or hypertrophic cardiomyopathy).
Kidney dysfunction
In patients with renal insufficiency (creatinine clearance < 80 ml/min), the initial dose of lisinopril should be adjusted according to creatinine clearance (see Table 1) and subsequently according to blood pressure. In such patients, serum potassium and creatinine levels should be monitored periodically.
In patients with heart failure, hypotension caused by the use of ACE inhibitors may lead to a further decline in renal function with the possible subsequent development of reversible (after drug withdrawal) acute renal failure.
Some hypertensive patients without overt signs of renovascular disease may experience slight transient increases in serum urea and creatinine, particularly when lisinopril is used concomitantly with diuretics. This is more likely in patients with pre-existing renal impairment. This condition may require dose reduction and/or discontinuation of the diuretic and/or lisinopril.
In acute myocardial infarction, treatment with lisinopril is not indicated in patients with evidence of renal dysfunction (creatinine (CK) concentration greater than 177 μmol/l and/or proteinuria greater than 500 mg/day). If renal dysfunction develops during lisinopril therapy (CK greater than 265 μmol/l or this indicator is twice the value before treatment), the physician should consider discontinuing the drug.
There is no experience in the use of the drug in patients with a recent kidney transplant, therefore the drug should not be used in this group of patients.
Hypersensitivity/angioedema
Angioedema of the face, extremities, lips, tongue, vocal cords and/or larynx has been reported in isolated cases in patients treated with ACE inhibitors, including lisinopril. Angioedema may occur at any time during treatment. In such cases, lisinopril should be discontinued immediately, appropriate treatment should be given and the patient should be observed until symptoms resolve.
Even in cases where swelling is limited to the tongue and there are no signs of respiratory distress, patients may require prolonged observation, as treatment with antihistamines and corticosteroids may be insufficient.
Very rarely, fatalities have been reported as a result of angioedema of the larynx or tongue. If the swelling extends to the tongue, vocal cords or larynx, airway obstruction may occur, especially in patients who have previously undergone respiratory surgery. In such cases, emergency treatment (adrenaline (epinephrine) administration and/or maintenance of a patent airway) should be initiated immediately. The patient should be kept under close medical supervision until complete and sustained resolution of symptoms.
Patients with a history of angioedema unrelated to ACE inhibitor therapy may be at increased risk of developing angioedema when treated with ACE inhibitors.
Anaphylactoid reactions during hemodialysis
Patients dialyzed with high-flux membranes (e.g. AN 69) and treated concomitantly with ACE inhibitors are at risk of anaphylactoid reactions. It is recommended that these patients use a different type of dialysis membrane or a different class of antihypertensive drug.
Anaphylactoid reactions during low-density lipoprotein (LDL) apheresis
Rarely, life-threatening anaphylactoid reactions may occur during LDL apheresis with dextran sulfate in patients receiving ACE inhibitors. Such reactions can be avoided by temporarily withholding ACE inhibitor therapy prior to each apheresis.
Anaphylactoid reactions during desensitization therapy
Patients receiving ACE inhibitors during desensitization therapy with allergens (e.g., hymenoptera venom) have developed prolonged anaphylactoid reactions. These reactions can be avoided by withholding ACE inhibitors during desensitization, but accidental re-administration of ACE inhibitors has provoked the development of anaphylactoid reactions.
Liver dysfunction
Very rarely, the use of ACE inhibitors has been associated with a syndrome that begins with cholestatic jaundice or hepatitis and progresses to fulminant hepatic necrosis, sometimes with fatal outcome. The mechanism of this syndrome is unknown. If patients taking ACE inhibitors develop jaundice or significantly increase the activity of liver enzymes in the blood serum, the drug should be discontinued and the patient should be kept under medical supervision until the symptoms disappear.
Neutropenia/agranulocytosis
Neutropenia/agranulocytosis, thrombocytopenia and anemia have been reported in patients receiving ACE inhibitors. Neutropenia is rare in patients with normal renal function and in the absence of other complicating factors. Neutropenia and agranulocytosis are reversible upon discontinuation of ACE inhibitors.
Lisinopril should be used with particular caution in patients with diffuse connective tissue diseases, in treatment with immunosuppressants, allopurinol or procainamide, as well as in the combination of these complicating factors, especially in the presence of pre-existing renal impairment.
Some of these patients have developed serious infections, sometimes unresponsive to intensive antibiotic therapy. When using lisinopril in such patients, periodic monitoring of white blood cell counts is recommended and patients should be advised to report any signs of infection to their physician.
Dual blockade of the renin-angiotensin-aldosterone system (RAAS)
The concomitant use of ACE inhibitors (including lisinopril), angiotensin II receptor blockers (ARBs) or aliskiren increases the risk of hypotension, hyperkalemia and decreased renal function (including acute renal failure). Therefore, dual blockade of the RAAS by the combined use of ACE inhibitors with ARBs or aliskiren is not recommended.
If dual RAAS blockade is considered absolutely necessary, it should only be done under close specialist supervision and with frequent, careful monitoring of kidney function, blood electrolyte levels (especially potassium), and blood pressure.
ACE inhibitors and ARBs should not be used concomitantly in patients with diabetic nephropathy.
Angioedema has been reported more frequently in black patients treated with ACE inhibitors than in non-black patients. As with other ACE inhibitors, the antihypertensive effect of lisinopril is less pronounced in black patients than in non-black patients, possibly because of a higher prevalence of low-renin states in black patients with hypertension.
Cough
Treatment with ACE inhibitors may cause a nonproductive persistent cough that resolves after discontinuation of the drug. Cough caused by ACE inhibitors should be differentiated from cough in other diseases.
Surgical interventions/anesthesia
During major surgery or during anesthesia with drugs that cause hypotension, lisinopril may block the formation of angiotensin II due to compensatory renin release. In the event of hypotension that can be explained by this mechanism, it should be corrected by increasing the BCC.
Hyperkalemia
Some patients have experienced increases in serum potassium while taking ACE inhibitors, including lisinopril. Risk factors for the development of hyperkalemia include renal insufficiency, diabetes mellitus, concomitant use of potassium-sparing diuretics (e.g. spironolactone, triamterene or amiloride), potassium supplements or potassium-containing salt substitutes, or other drugs that may increase serum potassium (e.g. heparin, trimethoprim/sulfamethoxazole, also known as co-trimoxazole). If the use of these drugs during treatment with ACE inhibitors is considered necessary, regular monitoring of serum potassium and renal function is recommended.
Monitoring of blood electrolytes is particularly important in patients receiving potassium-sparing diuretics and ACE inhibitors or ARBs for heart failure. The lowest effective doses of potassium-sparing diuretics and ACE inhibitors/ARBs should also be used in such cases. In the event of hyperkalemia, consideration should be given to interrupting or discontinuing treatment.
Diabetes mellitus
Patients taking oral antidiabetic agents or insulin should have close glycemic control, especially during the first month of treatment with ACE inhibitors.
Primary hyperaldosteronism
In patients suffering from primary aldosteronism, ACE inhibitors are ineffective, so the drug should not be used in this group of patients.
Lithium
The concomitant use of lithium and lisinopril is generally not recommended.
Ability to influence reaction speed when driving vehicles or other mechanisms
During treatment with the drug, adverse reactions from the nervous system (dizziness, confusion, drowsiness) may occur, especially at the beginning of treatment, therefore, when using the drug, you should refrain from driving or using other mechanisms until your individual reaction to the drug is established.
Use during pregnancy or breastfeeding
ACE inhibitor drugs are contraindicated for use in pregnant women or women planning to become pregnant.
Epidemiological data on the risk of teratogenicity when ACE inhibitors are used during the first trimester of pregnancy are mixed; however, a small increase in risk cannot be excluded. Data on the effects of ACE inhibitor therapy during the second and third trimesters indicate fetotoxicity (renal impairment, oligohydramnios, skull hypoplasia) and neonatal toxicity (renal failure, hypotension, hyperkalemia).
When planning pregnancy, an alternative antihypertensive treatment with a drug with an established safety profile for use during pregnancy should be chosen.
If pregnancy is diagnosed during treatment with ACE inhibitors, the use of the drug should be stopped immediately and, if necessary, replaced with other drugs approved for use in pregnancy. In this case, ultrasound monitoring of renal function and fetal skull is recommended.
Newborns whose mothers have taken ACE inhibitors should be closely observed for the possibility of developing hypotension, oliguria, and hyperkalemia.
Because no information is available regarding the use of lisinopril during breastfeeding, lisinopril is not recommended for use in nursing mothers. Alternative antihypertensive treatments with better established safety profiles during breastfeeding are preferable, especially while nursing a newborn or preterm infant.
Method of administration and doses
The drug should be taken once a day in the morning, preferably at the same time, with sufficient water. Lipril can be used regardless of meals.
The dose and course of treatment are determined by the doctor individually depending on the severity of the disease, the state of kidney function and concomitant therapy.
Essential hypertension
Initial dose. The recommended initial dose is 10 mg per day. In patients with an overactive renin-angiotensin-aldosterone system (in particular, with renovascular hypertension, excessive electrolyte depletion and/or dehydration, cardiac decompensation or severe arterial hypertension), an excessive decrease in blood pressure may occur after taking the initial dose. Therefore, at the beginning of treatment, such patients should be under medical supervision, the recommended initial dose is 2.5-5 mg.
Maintenance dose. The usual effective maintenance dose is 20 mg once daily. If the desired therapeutic effect is not achieved after 2-4 weeks of use of the prescribed dose, the dose may be increased. The maximum daily dose should not exceed 80 mg.
Patients taking diuretics
In patients receiving diuretic therapy, symptomatic arterial hypotension may occur after taking the first dose of the drug. Diuretic treatment should be discontinued 2-3 days before starting Lipril. If diuretics cannot be discontinued, the initial dose of Lipril should not exceed 5 mg per day. Renal function and serum potassium should be monitored. The subsequent dosage regimen should be established in accordance with blood pressure indicators. If necessary, diuretic treatment can be resumed.
Patients with renal insufficiency
For patients with renal insufficiency, the initial dose should be set depending on the creatinine clearance value (see Table 1).
Table 1
Dose adjustment in renal failure
| Creatinine clearance (ml/min) | Starting dose (mg/day) |
| < 10 (including patients on hemodialysis) | 2.5* |
| 10-30 | 2.5-5 |
| 31-80 | 5-10 |
*The dose and/or dosing regimen should be established based on blood pressure values.
The dose may be increased to no more than 40 mg per day under blood pressure control.
Heart failure
In patients with symptomatic heart failure, lisinopril can be used as an adjunct to therapy with diuretics, digitalis, or β-blockers.
The initial dose, which should be taken under medical supervision to determine the initial effect on blood pressure, is 2.5 mg per day. The dose of the drug should be increased by no more than 10 mg, at intervals of at least 2 weeks and up to a maximum dose of 35 mg per day.
When adjusting the dose, the clinical response of the individual patient should be taken into account.
In patients at high risk of developing symptomatic hypotension (e.g., those with electrolyte depletion with or without hyponatremia, hypovolemia, or those receiving intensive diuretic therapy), the above conditions should be corrected before starting treatment. Treatment with lisinopril should be carried out under the control of renal function and serum potassium levels.
Acute myocardial infarction
Patients should receive concomitant standard therapy with thrombolytic drugs, acetylsalicylic acid, and β-blockers. Lisinopril is compatible with intravenous or transdermal nitroglycerin.
Lisinopril therapy should be initiated within 24 hours of the onset of symptoms of myocardial infarction according to the following regimen: initial dose is 5 mg, the next dose (after 24 hours) is 5 mg, then (after 48 hours) is 10 mg. Thereafter, the maintenance dose is 10 mg per day. Patients with low systolic blood pressure (120 mm Hg or lower) should be given 2.5 mg at the beginning of treatment or in the first 3 days after myocardial infarction.
In renal insufficiency (creatinine clearance < 80 ml/min), the initial dose of Lipril should be adjusted according to the patient's creatinine clearance (see Table 1).
The maintenance dose is 10 mg once daily. If hypotension occurs (systolic blood pressure less than or equal to 100 mm Hg), the maintenance dose of 5 mg should be temporarily reduced to 2.5 mg. If prolonged hypotension occurs (systolic blood pressure less than 90 mm Hg for more than 1 hour), treatment should be discontinued.
The duration of treatment is 6 weeks, after which the patient's condition must be re-evaluated. The appearance of symptoms of heart failure does not exclude further use of the drug.
Nephropathy in diabetes mellitus
In the treatment of hypertension in patients with type 2 diabetes mellitus and incipient nephropathy, the dose of the drug is 10 mg once a day. If necessary, the dose can be increased to 20 mg per day to achieve diastolic blood pressure below 90 mm Hg in the sitting position.
In renal insufficiency (creatinine clearance < 80 ml/min), the initial dose of the drug should be adjusted depending on the patient's creatinine clearance (see Table 1).
Elderly patients
No differences in efficacy or safety have been identified based on patient age. The starting dose of lisinopril for elderly patients with reduced renal function should be based on the data in Table 1. Thereafter, the dose should be adjusted according to blood pressure.
Children
The efficacy and safety of lisinopril in children have not been established, so the drug should not be used in this age group.
Overdose
Symptoms: hypotension, circulatory shock, fluid and electrolyte imbalance, renal failure, hyperventilation, tachycardia, palpitations, bradycardia, dizziness, restlessness and cough.
Treatment: symptomatic, intravenous administration of saline is recommended. In case of arterial hypotension, the patient should be placed in bed (legs should be raised). Angiotensin II infusion and/or intravenous administration of catecholamines are possible. If the drug was taken recently, then induction of vomiting, gastric lavage, administration of enterosorbents and sodium sulfate are recommended for its removal. Lisinopril can be removed from the body by hemodialysis, while the use of polyacrylonitrile metal sulfonate high-flux membranes (for example, AN 69) should be avoided.
Pacemaker therapy is indicated for the treatment of persistent bradycardia. Vital signs, serum electrolytes, and creatinine should be monitored continuously.
In the event of angioedema, adequate emergency therapy is necessary (adrenaline (0.3-0.5 ml of adrenaline solution (1:1000) transdermally), glucocorticosteroids, antihistamines, ensuring airway patency by intubation or laryngotomy).
Adverse reactions
Blood and lymphatic system: decreased hemoglobin and hematocrit levels, bone marrow suppression, anemia, thrombocytopenia, leukopenia, neutropenia, agranulocytosis, hemolytic anemia, lymphadenopathy, autoimmune diseases.
Nervous system: dizziness, headache, mood changes, paresthesia, vertigo, taste disturbances, sleep disturbances, confusion, smell disturbances, balance disorders, disorientation, tinnitus, decreased visual acuity, symptoms of depression, syncope, hallucinations.
Cardiovascular system: hypotension (especially after the first dose in patients with sodium deficiency, dehydration, heart failure), orthostatic effects (including hypotension), myocardial infarction or cerebrovascular stroke, possibly secondary to excessive hypotension in high-risk patients; palpitations, tachycardia, Raynaud's phenomenon. When using lisinopril in patients with acute myocardial infarction, AV block of II-III degrees, severe hypotension and/or impaired renal function, in rare cases - cardiogenic shock are possible, especially in the first 24 hours.
Musculoskeletal system: muscle spasms have been reported.
Respiratory, thoracic and mediastinal disorders: cough, rhinitis, bronchitis, dyspnoea, bronchospasm, sinusitis, allergic alveolitis/eosinophilic pneumonia. Upper respiratory tract infections have been reported.
Digestive tract and hepatobiliary system: diarrhea, constipation, vomiting, nausea, abdominal pain, dyspepsia, dry mouth, glossitis, decreased appetite, pancreatitis, intestinal angioedema, hepatocellular or cholestatic hepatitis, jaundice, hepatic failure.
Skin and subcutaneous tissue: rash, pruritus, urticaria, alopecia, psoriasis, hypersensitivity reactions/angioedema: angioedema of the face, extremities, lips, tongue, vocal cords and/or larynx, hyperhidrosis, pemphigus, toxic epidermal necrolysis, Stevens-Johnson syndrome, erythema multiforme, cutaneous pseudolymphoma.
A complex reaction has been reported, including one or more of the following symptoms: fever, vasculitis, myalgia, arthralgia/arthritis, positive antinuclear antibody test, increased erythrocyte sedimentation rate (ESR), eosinophilia and leukocytosis, rash, photosensitivity reactions or other dermatological manifestations.
Urinary system
