Most often, a marked decrease in blood pressure occurs with a decrease in the volume of circulating blood (BCC), caused by diuretic therapy, a decrease in salt intake, dialysis, diarrhea, or vomiting.
In patients with CHF with simultaneous renal failure or without it, a marked decrease in blood pressure is possible.
Patients with IHD, cerebrovascular insufficiency, in whom a sharp decrease in blood pressure can lead to myocardial infarction or stroke, the drug should be administered only under strict medical supervision.
Transient arterial hypotension is not a contraindication for taking the next dose of the drug.
When using the drug in some patients with CHF, but with normal or low blood pressure, there may be a decrease in blood pressure, which is usually not a reason for stopping treatment.
In CHF, severe arterial hypotension can lead to impaired renal function.
In some cases, in the presence of CHF with normal or low blood pressure, the drug can also cause an additional decrease in blood pressure. This effect is not a contraindication for further administration of the drug.
In patients with bilateral renal artery stenosis or stenosis of the single kidney artery, in the treatment of ACE inhibitors, in some cases an increase in the concentration of urea nitrogen in plasma and serum creatinine was observed. These changes were almost always reversible and disappeared after the withdrawal of the ACE inhibitor. These complications are especially characteristic for patients with existing renal dysfunction. If the patient has renovascular hypertension, then the risk of severe arterial hypotension and renal failure increases.In this category of patients, treatment should begin with smaller doses of the drug under medical supervision.
Since the simultaneous use of diuretics is an additional risk factor for the development of arterial hypotension, they should be canceled and during the first week to monitor the function of the kidneys.
An increase in the concentration of urea nitrogen in blood plasma and serum creatinine was also noted in patients with hypertension without concomitant renal impairment, especially with the simultaneous use of lisinopril and diuretics. These changes were mild, and the rates returned to normal after withdrawal of lisinopril or a diuretic.
In patients with acute myocardial infarction, drug therapy should not be started if there are signs of impaired renal function, such as an increase in plasma creatinine levels above 177 μmol / L and / or proteinuria above 500 mg / day. If the renal dysfunction develops against the background of taking the drug (the creatinine concentration in the blood plasma is above 265 μmol / L or doubled relative to the values before the start of therapy), then it is necessary to consider the possibility of drug cancellation.
Treatment with lisinopril in acute myocardial infarction is performed against the background of standard therapy (thrombolytics, acetylsalicylic acid (as an antiplatelet agent), beta-blockers). Lisinopril can be used with a solution of nitroglycerin for intravenous administration or with the use of nitroglycerin sublingually.
It is not recommended to use lisinopril in patients who underwent acute myocardial infarction if systolic blood pressure does not exceed 100 mm Hg.
When using drugs that lower blood pressure in patients with extensive surgery or during general anesthesia, lisinopril can block the formation of angiotensin II, secondary to the compensatory release of renin. Before surgery (including dental surgery) should stop taking the drug for 24 hours and inform the surgeon / anesthesiologist about the use of an ACE inhibitor.
It is assumed that the simultaneous administration of ACE inhibitors and insulin, as well as hypoglycemic drugs for oral administration may lead to the development of hypoglycemia.The greatest risk of development is observed during the first weeks of combination therapy, as well as in patients with impaired renal function.
Patients with diabetes require careful monitoring of glycemia, especially during the first month of therapy with an ACE inhibitor.
Before beginning treatment, it is necessary to compensate for the loss of fluid and salts. In patients with risk factors for symptomatic arterial hypertension (patients who follow a diet with limited intake of salt with or without hyponatremia, patients with hypovolaemia or who receive diuretic therapy), it should be possible to adjust the condition data as far as possible before starting treatment with lisinopril.
Risk factors for the development of hyperkalemia include chronic renal failure, diabetes mellitus, and simultaneous use of potassium-sparing diuretics (spironolactone, eplerenone, triamterene, or amiloride), potassium or salt substitutes containing potassium ions, and the use of drugs that are associated with an increase in potassium levels in the blood plasma (eg, heparin). Periodic monitoring of the potassium content in blood plasma is recommended.
Angioedema of the face, extremities, lips, tongue, mucous membranes, epiglottis and / or larynx was noted with the use of ACE inhibitors, including preparations containing lisinopril. This side effect can occur at any stage of therapy. In such cases, it is necessary to urgently cancel the use of the drug and prescribe adequate therapy. The patient should be under the supervision of a physician until the symptoms of the edema are completely regressed. It should be borne in mind that even in cases where there is only swelling of the tongue, the patient should be under the supervision of a doctor, since therapy with antihistamine and corticosteroid drugs may not be sufficient.
Patients who have previously undergone surgical intervention on the respiratory organs have a higher risk of developing angioedema of the larynx or tongue.
Patients who underwent angioedema, not associated with the administration of ACE inhibitors, are at greater risk of developing such a complication with the administration of ACE inhibitors. It should be borne in mind that the use of ACE inhibitors in patients of the Negroid race leads to a higher risk of developing angioedema.The effectiveness of ACE inhibitors in reducing blood pressure in patients of the Negroid race is lower than in representatives of other races. This effect is probably associated with a marked predominance of low-grade status in patients of the Negroid race with arterial hypertension.
In patients taking ACE inhibitors during the desensitization procedure for venom of Hymenoptera, extremely rare, life-threatening anaphylactoid reactions can develop. This can be avoided by temporarily discontinuing treatment with an ACE inhibitor before each desensitization procedure.
Dry cough that occurs with the use of ACE inhibitors is unproductive, persistent and occurs after discontinuation of treatment. In the differential diagnosis of cough, its possible association with ACE inhibitors should be considered.
The safety and efficacy of lisinopril in children is not established.
Very rarely there were cases of the development of the syndrome, which began with the development of cholestatic jaundice, progressed to fulminant necrosis and in some cases resulted in death. The mechanism of development of this syndrome is not clear. Application of the drug lisinopril patients with signs of jaundice development or a significant increase in the activity of "liver" transaminases should be discarded and appropriate monitoring of laboratory indicators and patient condition should be carried out.
There have been cases of development of neutropenia / agranulocytosis, thrombocytopenia and anemia in patients receiving ACE inhibitors. Such cases are quite rare in patients with normal renal function. Neutropenia and agranulocytosis disappear after the withdrawal of ACE inhibitors.
Lizinopril should be used with extreme caution in patients with systemic connective tissue diseases receiving immunosuppressive therapy, treatment with allopurinol or procainamide, or these risk factors are present simultaneously, especially in patients with impaired renal function. In such patients, in some cases, infectious diseases resistant to antibiotic therapy can develop. In the case of the drug in such patients, regular monitoring of blood leukocytes should be carried out.
If any symptoms of infection (eg, sore throat, fever) appear, the patient should consult a doctor immediately, as they may be a manifestation of neutropenia.
In rare cases, against the background of therapy with ACE inhibitors, angioedema develops in the intestine. Thus, patients have a pain in the abdomen as an isolated symptom or in combination with nausea and vomiting in some cases without prior angioneurotic edema of the face and at normal levels of C1-esterase. The diagnosis is established by means of computed tomography of the abdominal cavity, ultrasound examination or in surgical intervention. Symptoms disappeared after discontinuation of ACE inhibitors. Therefore, patients with abdominal pain receiving ACE inhibitors should take into account the possibility of developing angioedema of the intestine during differential diagnosis.