Digitalis intoxication (poisoning with cardiac glycosides) is a serious complication of the treatment of patients suffering from heart disease and taking drugs of the digitalis group (digoxin).
Lethal doses of cardiac glycosides are usually 10 times or more higher than therapeutic doses. The elderly, patients with impaired function of the thyroid gland, circulatory system and excretion are especially sensitive to them. The toxicity of digitalis group drugs increases in the presence of hypokalemia and hypomagnesemia. Children are more resistant to them.
The duration of the toxicogenic stage correlates with the rate and completeness of absorption of cardiac glycosides in the gastrointestinal tract, the rate of their binding by plasma proteins and excretion. It is quite long-lasting in people with intoxication, poisoned with digitoxin and isolanide, through the hepatic intestinal circulation and significant reabsorption in the kidneys. In particular, digitoxin binds to plasma proteins by 90%, digoxin by 40%, and strophanthin by less than 10%. Every day, the activity of strophanthin in the blood decreases by 40-50%, while digitoxin decreases by 7-10%. Due to the low (3.5%) absorption of strophanthin and digitoxin in the gastrointestinal tract, oral poisoning with them has not been recorded.
Manifestations of acute poisoning with cardiac glycosides do not depend on the route of their entry into the body.
The clinical picture of digitalis intoxication consists of several leading syndromes, in particular:
First of all, dyspeptic manifestations appear in the form of nausea, continuous vomiting with an admixture of bile in the vomit, sometimes blood, diarrhea, signs of dehydration, and abdominal pain. Soon headache, dizziness and visual impairment appear in the form of ring-shaped scotomas, xanthopsia, decreased visual acuity as a result of the development of retrobulbar neuritis. Ataxia, insomnia, agitation, delirium, hallucinations, convulsions, shortness of breath, cyanosis, hypoxia, and decreased diuresis are also characteristic.
On the ECG, along with a decrease in the ST interval and a negative or flattened T wave, the PQ interval lengthens, single atrial P waves fall out. Rhythm and conduction disorders of all types are often observed, especially when acute poisoning with cardiac glycosides was preceded by cardiac disturbances: bradycardia, blockade and etc. Development is very dangerous ventricular extrasystole by type of bigeminy, paroxysmal tachycardia, atrial and ventricular fibrillation. In such cases, death occurs due to cardiac arrest or asphyxia.
Delivery program emergency care at acute intoxication cardiac glycosides involves early detoxification with resuscitation measures and antidotes, interruption of enterohepatic circulation (if poisoning occurs with digitoxin or isolanide), elimination of manifestations of PSCE, arrhythmia, vomiting, agitation and hypoxia, improvement of myocardial contractile function. To do this you need:
A specific antidote for digitalis intoxication with cardiac glycosides, in particular digoxin preparations, are fragments of specific antibodies against digoxin. The essence of their antidote activity lies in binding free digoxin contained in plasma after its absolute or relative overdose, and thus preventing its interaction with myocardial cells. The drug is used in a dose that is molecularly adequate to the amount of digitalis glycoside that is absorbed. (Empirically it has been established that this dose is 800 mg, that is, 20 ampoules of 40 mg each).
Fragments of specific antibodies against digoxin are obtained from specific antibodies that were formed in the body of sheep. Their relationship with digoxin, as well as digitoxin and lantoside, is greater than the relationship of these glycosides with specific receptors (ATPase) in the myocardium. Therefore, these glycosides bind predominantly to fragments of specific antibodies, and not to specific receptors in the myocardium and other tissues. 30 minutes after the administration of the antidote, the content of digoxin or another glycoside in the blood begins to increase, which contributes to intoxication; glycosides associated with protein lose pharmacological activity and are excreted from the body. The dose of the drug is set individually and depends on the amount of glycoside that is absorbed.
Symptoms: 1.Extremely slow heart rate(bradycardia) as a result of the influence on the center of the vagus
nerve, which is replaced by tachycardia, extrasystole, fluttering may occur
ventricles and cardiac arrest.
2. Sharp increase in blood pressure as a result of the direct vasoconstrictor effect of cardiac
glycosides.
3. Decreased diuresis up to anuria due to spasm of the kidney vessels
4. Nausea, vomiting reflexive in nature.
5. Visual impairment(color)
Help: Because poisoning occurs when taking tablet drugs, it is necessary:
rinse the stomach to clean water.
give saline laxatives to remove glycosides from the intestines.
used as antagonists potassium preparations, namely, for mild and moderate poisoning, a 10% KCl solution is prescribed in tablespoons 3 to 4 times a day. For severe poisoning - 0.5% solution of KCl w/w. Among the drugs also prescribed are “Panangin”, “Asparkam”, “Potassium Orotate”, which contain potassium and magnesium aspartate.
You can prescribe the drug “Unithiol” intravenously (ampoules of 5% solution, 5 ml), it promotes the accumulation in the body of the enzyme adenosine triphosphatase (ATPase), which blocks the action of cardiac glycosides.
Prevention poisoning with cardiac glycosides consists in the correct prescription of tablet drugs (according to a decreasing scheme), as well as monitoring of patients by a doctor, who should check the pulse rate and pressure.
The effects and mechanism of action are similar to cardiac glycosides, but the potency of action is significantly superior to herbal preparations, therefore they are used only for acute cardiac weakness, for cardiogenic shock in the form of injections in a hospital setting
DOPAMINE (DOPAMINE)Dopaminum, list “B”, “Dopmin”
By origin, it is a precursor of norepinephrine, which can stimulate α- and β-AR of the cardiovascular system and primarily the heart. It has a pronounced positive systolic (inotropic) effect. Applicable for all types of shock: cardiogenic shock, traumatic, septic, postoperative, hypovolemic, etc.
VWF – 4% solution for injection in ampoules of 5 ml, 2% solution – ampoules of 10 ml. Enter B\B.
DOBUTAMINE,Dobutaminum, list “B”
Its chemical structure is a catecholamine and is closest to dopamine.
It is a pronounced β-Am, stimulating cardiac AR.
Applicable as a cardiotonic when it is necessary to briefly increase the work of the heart
FV – in bottles of 0.25 dry sterile substance for injection, 0.5% solution in ampoules of 50 ml.
The rhythmic work of the heart is ensured by the basic properties of the myocardium: automaticity, excitability, conductivity, contractility. If one or more of these properties is violated, various types of heart rhythm disturbances can develop. The most common types of arrhythmia include:
Extrasystole (interruptions) – premature heart contractions due to the appearance of an additional extraordinary impulse.
Paroxysmal tachycardia is a maximum permissible rapid rhythm, which may be accompanied by interruptions.
Atrial fibrillation is frequent random weak contractions of individual myocardial muscle fibers, i.e. the atria and ventricles can each contract in their own rhythm.
Heart block is the most dangerous look arrhythmia, which begins with erratic contraction of the atria and ventricles, then blockade of impulse transmission from the atria to the ventricles, followed by cardiac arrest.
Drugs of various pharmacological groups have antiarrhythmic properties, these can be cardiac glycosides, anticonvulsants, local anesthetics and coronary dilators.
Classification. Based on the main focus and mechanism of action, all antiarrhythmic drugs are divided into:
Drugs that directly affect the conduction system of the heart, myocardial contractile activity and cardiomyocytes.
Membrane stabilizing agents(sodium channel blockers), which impede the passage of sodium and calcium ions through cell membranes, thereby reducing the excitability and contractility of muscle fibers.
A) A group of quinidine and quinidine-like drugs (quinidine sulfate, novocainamide, ajmaline).
B) Local anesthetics (lidocaine)
2 . Means, calcium channel blockers or calcium ion antagonists.
Prevent or reduce the flow of calcium ions into cardiomyocytes and into the conduction system of the heart, thereby reducing myocardial conductivity and contractility (verapamil, nifedipine)
3 .Various means
A) Potassium-containing drugs (potassium orotate, asparkam, panangin)
Potassium supplements are necessary for the heart muscle to contract rhythmically. Potassium ions also act as antagonists of calcium ions.
B) Cardiac glycosides.
Drugs that affect the efferent innervation of the heart (β –Ab: anaprilin, talinolol, atenolol, metaprolol).
Pharmaco-therapeutic effects antiarrhythmic drugs:
Decreased cardiac automaticity.
Inhibition of impulse transmission through the conduction system of the heart.
An increase in the refractory period (diastole), which leads to bradycardia.
Reduced myocardial excitability.
Decreased myocardial contractile activity.
Conclusion: Compared with cardiac glycosides, antiarrhythmic drugs weaken heart contractions. Both cardiac glycosides and antiarrhythmic drugs cause bradycardia.
To the group quinidine And quinidine-like drugs include:
QUINIDINE SULPHATE,Chinidinisulfas, list “B”
Derived from the cinchona alkaloid. White crystalline powder, soluble in water, can slow down the heart, while normalizing heart rhythm. Used to treat extrasystole, atrial fibrillation. May cause a decrease in blood pressure. Contraindicated with cardiac weakness, severe hypotension and angina attacks.
FV – powder, tablets 0.2
NOVOCAINAMIDE,Novocainamidum, list “B”, 1.0
White or creamy crystalline powder, easily soluble in water - salt of novocaine with amide. Can be used for all types of heart rhythm disturbances, as well as for the prevention of arrhythmia before or during heart surgery, and during myocardial infarction. Side effects: headache, nausea, vomiting, insomnia, mental agitation, bitterness in the mouth, there may be allergic reactions. FV – tablets of 0.25, ampoules of 5 ml of 10% solution IM, IV.
AIMALIN,Ajmalinum, list “B”
Rauwolfia serpentine alkaloid, which has a pronounced antiarrhythmic effect. Slightly lowers blood pressure. It is used for extrasystole and paroxysmal tachycardia. Unlike reserpine, obtained from the same plant raw materials, ajmaline does not have a calming and sympatholytic effect.
FV - tablets, 0.05 dragees, ampoules of 2 ml of 2.5% solution, i.m. or i.v. in a 5% glucose solution. Included in the Raunatin tablets (reserpine + ajmaline).
DIFENIN,Dipheninum, list "B"
It is an antiepileptic drug and has pronounced antiarrhythmic activity (blocks sodium channels). Like local anesthetics, it accelerates the repolarization process. Particularly effective for tachyarrhythmias caused by an overdose of cardiac glycosides.
FV – tablets of 0.15; There are injection forms.
LIDOCAINE,Lidocainum,list “B”, “Xycaine”, “Xylocaine”
Used to prevent heart rhythm disturbances during myocardial infarction. Can be used for atrial fibrillation, paroxysmal tachycardia only intramuscularly and intravenously.
FV – ampoules of 2 ml of 10% solution.
TO calcium channel blockers or calcium ion antagonists include:
VERAPAMIL,Verapamilum, list “B”, “Isoptin”
It is used for paroxysmal tachycardia, extrasystole, and can also be used for coronary insufficiency (coronary artery disease - angina). It has a moderate antihypertensive effect and can be used for hypertension occurring against the background of coronary artery disease and cardiac arrhythmia.
FV – tablets of 0.04, ampoules of 2 ml of 0.25% solution for intravenous administration.
NIFEDIPIN,Nifedipinum, list “B”, “Corinfar”, “Kordafen”, “Kordipin”, “Kordaflex”
It is slightly more active than verapamil. Can be used for extrasystole, paroxysmal tachycardia, in the complex treatment of hypertension and for the prevention of angina attacks.
FV – tablets, capsules 0.01, 0.02
Potassium preparations:
POTASSIUM OROTATE,Kaliiorotas
Has a moderate antiarrhythmic effect, i.e. Compared to membrane stabilizers and calcium antagonists, it has a weak antiarrhythmic effect, based on the ability to accumulate potassium ions in the heart muscle. It is used in the form of tablets for the prevention of arrhythmia and for extrasystole.
FV – tablets 0.1; 0.5
More active potassium preparations include
ASPARKAM, PANANGIN
The basis of these drugs is potassium - magnesium osparginate. Panangin is a more complex drug in its composition, therefore it has a more pronounced antiarrhythmic effect.
TO drugs affecting the efferent innervation of the heart, include:
1) Non-selective β–Ab:
Anaprillin (Propranolol), Oxprenalol.
Selective β 1 –Ab:
Talinolol, Metoprolol, Atenolol
Pharmacotherapeutic effect of drugs in this group is associated with their ability to eliminate the influence of efferent nerves on the functioning of the heart. At the same time they provide three main effects:
Antiarrhythmic effect.
Hypotensive effect.
Antianginal effect.
This means that they can be used as antiarrhythmic, antihypertensive and coronary dilators simultaneously.
In the complex treatment of arrhythmias, sedatives, hypnotics, anticonvulsants (diphenin) and tranquilizers are also used.
Antihypertensive (hypotensive) drugs
These are drugs that can lower systemic blood pressure, which means they are used for hypertension (arterial hypertension).
HD is one of the most common diseases. Increased blood pressure may be due to the following factors:
increased excitability of the SDC, which regulates the tone of blood vessels.
change hormonal balance(increased secretion of adrenaline and mineralcorticoids by the adrenal glands; vasopressin by the posterior lobe of the pituitary gland, etc.)
impaired renal function and other factors.
Very often, such changes in the body occur during chronic emotional stress, which can ultimately cause an increase in the tone of the SNS and be the cause of hypertension. An increase in blood pressure makes it difficult for the heart to work, which leads to hypertrophy of the left ventricle of the heart. Hypertension is often complicated by a sharp increase in blood pressure (i.e., a hypertensive crisis occurs), which can lead to cerebrovascular accident and cerebral hemorrhage - a stroke, which in severe cases is fatal. Arterial hypertension contributes to the development of atherosclerosis of blood vessels, angina pectoris, heart failure, visual impairment, and renal dysfunction.
Blood pressure levels are supported:
regulation of the cardiovascular system by CNS
the work of the heart and tone of vascular walls
volume of circulating blood (OTSK)
Thus, pressure numbers can be influenced through the work of the heart, vascular tone, through the state of the central nervous system and through the volume of blood plasma. It follows
Classification of antihypertensive drugs according tomechanism of action:
Antihypertensive drugs with neurotropic action.
Central neurotropic action.
Peripheral neurotropic action.
Antihypertensive drugs with myotropic action (myotropic antispasmodics).
1. Drugs of different structures and uses.
2. Vasodilators.
Inhibitors of angiotensin synthesis or angiotensin-converting enzyme (ACE)).
Calcium channel blockers (calcium ion antagonists).
Antihypertensive drugs affecting water-salt balance(diuretics).
Contraindications for use
Absolute contraindications:
· intoxication with cardiac glycosides or suspicion of it;
· atrioventricular block II - III degree;
Allergic reactions (rare).
Relative contraindications:
· sick sinus syndrome;
· severe sinus bradycardia (pulse less than 50 per minute);
· atrial fibrillation with a rare rhythm (atrial fibrillation);
· atrioventricular block of the first degree;
· Wolff-Parkinson-White syndrome (impulses due to reduced atrioventricular conduction propagate along an additional path, creating the danger of paroxysmal tachycardia);
· ventricular arrhythmias;
· severe hypertensive heart disease;
· ischemic disease heart (especially after transmural myocardial infarction);
Chronic pulmonary heart disease;
· hypokalemia;
· hypercalcemia;
renal failure;
· serious illnesses lungs ( respiratory failure II - III degrees).
Cardiac glycosides are of no use in left ventricular diastolic dysfunction or conditions with cardiac output greater than 45%. For this reason they are not prescribed to patients hypertrophic cardiomyopathy, mitral and aortic stenosis, constrictive and exudative myocarditis.
At aortic stenosis the exit tract closes asymmetrically hypertrophied interventricular septum, which disrupts the ejection of blood from the left ventricle into the aorta. In this situation, cardiac glycosides, accelerating the formation of obstruction, help reduce cardiac output. With mitral stenosis, cardiac glycosides, increasing the force of contractions of the left ventricle, worsen the conditions of its diastolic filling with blood through the stenotic left atrioventricular opening. In patients, the pressure in the pulmonary artery system increases significantly, and there is a risk of pulmonary edema.
Intoxication with cardiac glycosides varying degrees severity occurs in 5 - 15% of patients; with rapid saturation, its frequency increases to 40 - 50%. Cardiac glycosides have a small breadth of therapeutic action.
Symptoms of intoxication are conventionally divided into cardiac and extracardiac.
Cardiac symptoms
Cardiac disorders are observed in 51 - 90% of cases of intoxication with cardiac glycosides. There are two stages of poisoning - transitional and toxic.
IN transition phase Pulse pressure increases, bradycardia occurs, and atrioventricular conduction slows down. These hemodynamic disturbances are caused by a reflex increase in the tone of the vagus nerve.
IN toxic phase Symptoms of heart failure return, coronary insufficiency and arrhythmias appear:
· ventricular extrasystole of the bi- and trigeminy type;
· polytopic (polymorphic) ventricular extrasystole;
· non-paroxysmal tachycardia from the atrioventricular node;
Paroxysmal atrial tachycardia in combination with atrioventricular block;
· arrest of the sinus node with a replacement rhythm from the atrioventricular node;
Second degree atrioventricular block.
In a toxic dose, cardiac glycosides, blocking Na + , K + -ATPase by 60% or more, cause hypokaligistia - a deficiency of potassium ions in cardiomyocytes. Together with sodium ion retention, hypocalygism reduces sarcolemmal polarization and negative resting potential. This disrupts depolarization and weakens myofibril contractions. Hypocalygistia negatively affects the synthesis of macroergs, glycogen, and protein in myocardial cells, and contributes to the development of intracellular acidosis and extracellular alkalosis. In the blood, the level of potassium ions increases as a result of blockade of Na +, K + -ATPase of skeletal muscles.
In the area of myofibrils, the content of calcium ions increases significantly (sodium/calcium metabolism increases, Ca 2+ removal is impaired due to blockade of calcium-dependent ATPase).
Membrane Na + , K + -ATPase of the heart has unequal sensitivity to cardiac glycosides. They block Na + , K + -ATPase of the conduction system 2.5 times more strongly than the corresponding enzyme of the contractile myocardium. For this reason, heart rhythm disturbances play a leading role in the picture of intoxication. Excessive intake of calcium ions into the cells of the conducting system, as well as the release of norepinephrine from sympathetic endings, are accompanied by the appearance of additional foci of automaticity capable of spontaneous depolarization.
Calcium ions prevent the development of diastole (hypodiastole occurs); by damaging lysosomes, they release enzymes that cause myocardial necrosis.
Weakened systole and impaired diastole worsen the expulsion of blood from the ventricular cavities, which impedes blood flow under the endocardium and aggravates myocardial ischemia.
Cardiac glycosides in toxic doses increase the tone of veins and arteries. An increase in preload and afterload on the heart accelerates the progression of decompensation.
Extracardiac symptoms
Extracardiac symptoms of intoxication with cardiac glycosides - dyspeptic (in 75 - 90% of patients), neurological (30 - 90%), mixed (37%) and rare (thrombocytopenia, allergic vasculitis, gynecomastia, bronchospasm).
Dyspeptic disorders:
· anorexia (decreased appetite) as a result of the accumulation of norepinephrine in the food center of the hypothalamus;
· nausea and vomiting caused by the action of excess dopamine on the trigger zone of the vomiting center;
cramping abdominal pain and diarrhea in the background increased tone vagus nerve;
· intestinal necrosis due to spasm of mesenteric vessels. Neurological manifestations intoxication is caused by blockade of Na +, K + -ATPase of neurons of the central and peripheral nervous system. In this case, the release and circulation of neurotransmitters is disrupted. Victims develop:
Fatigue, headache, muscle weakness;
· fear, delirium, hallucinations, convulsions;
micro- and macropsia, xanthopsia (objects appear yellow or green), loss of visual fields.
Treatment of poisoning
First of all, you need to stop the drug cardiac glycoside and other drugs that increase the level of cardiac glycosides in the blood and sensitivity to them (quinidine, amiodarone). For successful therapy, the concentration of electrolytes in the blood is determined and ECG monitoring is carried out. Physical antagonists are prescribed - 50 - 100 g of activated carbon or 4 - 8 g of cholestyramine, including when cardiac glycosides are administered into a vein, since they are exposed to enterohepatic circulation.
The greatest difficulty is in stopping arrhythmias caused by cardiac glycosides in toxic doses. Antiarrhythmic therapy includes the following measures:
elimination of hypocaligistia and reduction of the binding of cardiac glycosides to Na + , K + -ATPase (when the level of potassium ions in the blood is below 4 mEq/l, potassium preparations are infused into a vein together with its conductors through membranes - panangin or a polarizing mixture);
· elimination of hypercalcemia (complexing agents - sodium citrate, disodium salt of ethylenediaminetetraacetic acid - are injected into the vein);
Prescription of antiarrhythmic drugs that do not reduce atrioventricular conduction and contractility heart (into a vein - lidocaine, diphenine);
· reduction of the arrhythmogenic effect of norepinephrine (into the vein - β - adrenergic blockers);
· reduction of bradycardia and atrioventricular block (under the skin - M-anticholinergic drugs atropine, metacin, itrop);
· chemical inactivation of cardiac glycosides in the blood (into the muscles - the donor of sulfhydryl groups unithiol, into the vein - Fab- fragments of specific antibodies to digoxin and digitoxin);
· electric pulse therapy if drug treatment is ineffective.
Cardiac glycosides, along with many other drugs, are used for heart failure and atrial tachyarrhythmias to reduce the frequency of ventricular contractions. The most commonly prescribed cardiac glycoside is digoxin. Due to the narrow therapeutic window and widespread use, acute and chronic overdose of cardiac glycosides continues to be a frequent and serious complication.
In the elderly, the risk of overdose with cardiac glycosides is especially high, which may be due to both age-related impairments in absorption and elimination, and the interaction of cardiac glycosides with other chronically taken drugs. An overdose of cardiac glycosides can also be caused by eating certain plants and animals. Cardiac glycosides are found in common oleander (Nerium oleander), yellow oleander (Thevetia peruviana), foxglove (Digitalis spp.), lily of the valley (Convallaria majalis), hempweed (Apocynum cannabinum), sea onion (Urginea maritima) and the dried secretion of the aga toad (Bufo Marinus).
Pharmacokinetics
The effects of cardiac glycosides depend on the average serum concentration of the drug, which, in turn, is determined by the rates of absorption, distribution and excretion. Digoxin has a biphasic distribution, so high serum concentrations of the drug measured within 6 hours after dosing (during the distribution phase when drug concentrations in tissues increase) may be misleading. In the second phase (elimination phase), T1/2 is approximately 36 hours.
Taking loop diuretics and ion exchange resins that bind potassium, as well as insufficient dietary potassium intake and diarrhea, can cause hypokalemia, which enhances the effects of cardiac glycosides and causes cardiac arrhythmias at lower serum concentrations of these drugs. Taking antibiotics, especially macrolides, can suppress the metabolism of digoxin.
Glycoside intoxication manifests itself equally in children and adults. In acute and chronic glycoside intoxication, the nature of the symptoms is different.
Extracardiac manifestations
Acute glycoside intoxication
The asymptomatic period after taking cardiac glycosides lasts from several minutes to several hours, then the first symptoms appear, usually nausea, vomiting and in the abdomen. Central manifestations include drowsiness, drowsiness and weakness, not associated with hemodynamic disturbances.
Chronic glycoside intoxication
Chronic overdose of cardiac glycosides is often difficult to diagnose due to its gradual development and variety of manifestations. The symptoms are the same as for acute glycoside intoxication, but they are often less pronounced. Gastrointestinal disturbances, confusion, disorientation, drowsiness, visual disturbances (eg, rainbow rings around luminous objects), hallucinations and, rarely, epileptic seizures may occur.
Electrolyte disturbances
In acute glycoside intoxication, hyperkalemia has important prognostic significance: potassium levels are more correlated with the likelihood of death than early changes in the ECG and serum concentrations of glycosides. But hyperkalemia is only an indicator of the severity of intoxication, and not the direct cause of complications and death, so simple correction of potassium levels does not increase survival.
Cardiac manifestations
With an overdose of glycosides, almost any type of tachyarrhythmia with high AV conduction is possible, with the exception of supraventricular tachyarrhythmias. The first and most common cardiac arrhythmia is usually ventricular extrasystoles. Although there are no arrhythmias pathognomonic for glycoside toxicity, this condition is suspected in cases of bidirectional ventricular tachycardia, atrial tachycardia with high-degree AV block.
Acute overdose of cardiac glycosides
IN early period acute overdose of cardiac glycosides, increased parasympathetic effects on the sinus and AV nodes causes bradyarrhythmias, which can be treated with atropine.
Chronic overdose of cardiac glycosides
Bradyarrhythmias developing in late period acute glycoside intoxication and chronic glycoside intoxication are caused by the direct effect of cardiac glycosides on the heart. These arrhythmias, as a rule, practically do not respond to the administration of atropine. Ventricular tachyarrhythmias occur during chronic glycoside intoxication or in the late period of acute glycoside intoxication more often than in the early period of acute glycoside intoxication.
Determination of serum digoxin concentration has great value for the management of patients with overdose of cardiac glycosides. Typically, clinical symptoms appear when the serum concentration of digoxin (measured no earlier than 6 hours after its administration) exceeds 2 ng/ml (therapeutic range - 0.5-2 ng/ml). An elevated digoxin concentration alone does not warrant a diagnosis of glycoside intoxication: the patient's condition, the time interval between taking the last dose of the drug and taking a blood sample, electrolyte disturbances (especially hyper- or hypokalemia, hypomagnesemia, hypercalcemia, hypernatremia and alkalosis), the presence of hypothyroidism and hypoxemia, as well as the use of catecholamines, calcium antagonists, quinidine, amiodarone and diuretics.
Most tests for digoxin give a positive reaction with other cardiac glycosides. Detection of such glycosides is important, but the clinical significance of measuring their serum concentrations has not yet been established. Some cardiac glycosides are not detected by the digoxin reaction, so negative results do not exclude glycoside intoxication.
There are ways to measure both total and free digoxin. It is usually sufficient to determine the serum concentration of total digoxin, which correlates well with the concentration of digoxin in the heart. However, after the use of antidigoxin, which almost completely remains in the vascular bed (volume of distribution 0.4 l/kg), the serum concentration of total digoxin increases sharply, as cardiac glycosides exit the tissues into the bloodstream, bind to antidigoxin and remain in the blood. In this case, only the determination of free digoxin is of clinical significance.
Endogenous digoxin-like immunoreactive factor
Sometimes positive reaction Digoxin occurs in people who have not received cardiac glycosides. This is due to the presence of the so-called endogenous digoxin-like immunoreactive factor, structurally and functionally similar to cardiac glycosides. This factor appears in cases where it is necessary to increase the strength of heart contractions or when kidney function is reduced - in particular, in newborns, pregnant women, in patients with renal failure, liver disease or hypothermia.
In case of acute glycoside intoxication, they begin with general supportive measures, withdrawal of cardiac glycosides, preventing their further entry and absorption into the gastrointestinal tract. Next, ECG monitoring is established, serum concentrations of electrolytes and digoxin are determined, antidigoxin is prescribed and arrhythmias, electrolyte disturbances and other complications are eliminated.
Prevention of absorption into the gastrointestinal tract
Artificial vomiting and gastric lavage are usually ineffective. Most cardiac glycosides participate in the enteric circulation, so delayed or repeated administration of activated charcoal may help reduce their serum concentrations, especially if an antidote is not available. With long-term use of cardiac glycosides, measures to prevent their absorption in the gastrointestinal tract are ineffective.
Specific treatment
Antidigoxin
The use of this drug is part of the standard treatment plan for cardiac glycoside overdose. Despite the high cost of antidigoxin, the benefit in reducing the risk of complications, costly intensive care unit stays, and repeated determinations of serum potassium and digoxin concentrations is significantly greater.
Drug treatment of arrhythmias
For hemodynamically significant supraventricular bradyarrhythmias or high-degree AV block, atropine is administered intravenously: adults 0.5 mg, children 0.02 mg/kg, but not less than 0.1 mg. For ventricular arrhythmias and the inability to immediately administer antidigoxin, phenytoin and lidocaine are prescribed in normal doses.
Pacing and electrical cardioversion
External cardiac pacing may in some cases be useful in cases of persistent bradyarrhythmia. Endocardial pacing is contraindicated because it can cause fatal ventricular arrhythmias. Electrical cardioversion is used only for severe, life-threatening arrhythmias. Electrical cardioversion is rarely necessary when antidigoxin is available.
Correction electrolyte disturbances
Potassium
Hypokalemia, which most often occurs while taking diuretics, can enhance the cardiotoxic effect of cardiac glycosides. Correction of hypokalemia is sometimes sufficient to eliminate the tachyarrhythmia for a day. Glycoside intoxication itself, on the contrary, causes hyperkalemia: In acute overdose of glycosides, antidigoxin is indicated if the potassium level exceeds 5.0 mEq/L. If hyperkalemia is accompanied characteristic changes on the ECG, and there is no opportunity to immediately administer antidigoxin, you need to try to reduce the potassium level by IV administration of insulin, glucose, sodium bicarbonate and oral administration of an ion exchange resin that binds potassium - sodium polystyrene sulfonate. Calcium chloride has good effect in most patients with hyperkalemia, but in the case of glycoside intoxication, the use of calcium salts can be extremely dangerous, since in such patients the intracellular concentration of calcium is already increased.
Magnesium
In case of heart failure and overdose of glycosides, hypomagnesemia is sometimes observed due to long-term use of diuretics. It can lead to persistent hypokalemia that is not corrected by potassium administration, so such patients are given magnesium sulfate (in addition, magnesium sulfate can eliminate extrasystole, although this is only a temporary measure used before starting treatment with antidigoxin). Magnesium sulfate is often prescribed at a dose of 2 g IV over 20 minutes for adults and at a dose of 25-50 mg/kg, but not more than 2 g, for children. After normalization of the condition, severe hypomagnesemia may require administration of magnesium sulfate at a rate of 1-2 g/hour for adults, and for children at a rate of 25-50 mg/kg/hour, but not more than 2 g/hour.
Extracorporeal detoxification
Forced diuresis, hemosorption and hemodialysis do not accelerate the elimination of digoxin due to the large volume of distribution.
The article was prepared and edited by: surgeonThe greatest sensitivity to drugs in this group is observed among elderly people, as well as patients with diseases of the excretory and circulatory systems, and the thyroid gland.
The toxicity of cardiac glycosides increases in the case of hypomagnesemia and hypokalemia.
The development of acute intoxication with cardiac glycosides is possible regardless of the route of their entry into the body. human body(orally or by injection).
Digitalis intoxication most often occurs while taking Digoxin, since it is the most used medication among cardiac glycosides. Digitoxin and Celanide are used much less frequently, and only in a hospital setting.
The drugs in this group have a fairly narrow “therapeutic window”, i.e. even a minimal overdose can provoke very serious consequences, cause severe poisoning with possible death. Symptoms of poisoning occur even when the therapeutic dose is doubled, and increasing this dose by 5-10 times creates a danger of death.
Digitalis drugs have accumulative properties. They bind to plasma proteins and then remain in the bloodstream for a long time.
When intoxicated with these drugs, a powerful imbalance of electrolytes occurs in the heart cells. They accumulate calcium and sodium, but the amount of potassium is significantly reduced. Such transformations lead to an increase in the strength of heart contractions. At the same time, Digoxin reduces the speed of impulses passing through the conduction system of the heart. These changes lead to the development of digitalis intoxication.
The first signs of intoxication with digitalis preparations are detected on the ECG, when there is still no clinical evidence of poisoning. An electrocardiogram demonstrates a variety of heart rhythm disturbances:
Other changes are also observed, but only qualified doctors can detect them. If you don't start helping early stage intoxication, clinical symptoms will begin to appear.
There are several groups of clinical signs.
The acute form of poisoning is characterized by the rapid (several minutes or hours after consuming Digoxin) development of a pronounced clinical picture. In this case, the patient’s condition sharply worsens, which is accompanied by convulsions, falling blood pressure and cardiac arrest.
In case of Digoxin intoxication, it is important to provide first aid in a timely manner and begin treatment. As for therapy, it consists of a corresponding number of important activities:
Prevention of poisoning with digitalis drugs consists of careful selection of the dose of the drug. Take glycosides only as prescribed by a doctor!
The course of treatment should be accompanied by constant monitoring of ECG dynamics, as well as the level of blood electrolytes (monitoring the concentration of potassium is most important).
The patient must inform the cardiologist about the medications he is taking for treatment concomitant diseases(antibiotics, diuretics, antiarrhythmics, etc.).
Be sure to include potassium-rich foods in your diet (dried apricots, prunes, raisins, potatoes in their skins).
Thus, it is a very dangerous and insidious phenomenon. If timely assistance is not provided and therapy is not started, a person may die due to cardiac arrest.
Of greatest toxicological interest are cardiac glycosides and preparations from various types digitalis - digitoxin, gitoxin, celanide, lantoside, digalen-neo and others, as well as glycosides from oleander that are related to them in their pharmacological properties. Absorbed at different rates from the stomach and intestines: preparations of digitalis purpurea slowly, woolly (celanide) - quickly.
In the blood they are adsorbed by blood plasma proteins and excreted slowly (cumulated) by the kidneys.
Poisoning with digitalis and its preparations can occur either as a result of an overdose or with prolonged use due to the ability of this group of cardiac glycosidoses to accumulate in the body, as well as due to increased sensitivity to them.
The lethal dose of foxglove leaves and sea onion bulbs is 2-4 g, digitoxin - 2-4 mg; for other digitalis-like drugs it is 20-50 times more than the maintenance dose.
Pathogenesis and symptoms of poisoning. In the pathogenesis of poisoning with cardiac glycosides of the digitalis group, the deterioration of heart function is important when direct action toxic doses of these drugs, as well as a direct effect on the central nervous system, in particular, a stimulating effect on the centers of the vagus nerve. As a result of a sharp deterioration in atrioventricular conduction and increased excitability, significant disturbances in heart rhythm may occur: extrasystole, bigeminy, partial or complete atrioventricular block with symptoms of atrial fibrillation, tachysystole and paroxysmal tachycardia of ventricular origin. The effect on the central nervous system, in particular stimulation of the vomiting center, causes anorexia, nausea, and vomiting. Less commonly observed are neuropsychiatric disorders associated with hypoxic changes and the effect of drugs on the activity of the cerebral cortex ( motor excitement, delirium, convulsions, loss of consciousness). The inhibition of diuresis observed during the period of poisoning is associated with a central dysfunction of the vagus nerve and with spasm of the renal vessels.
Symptoms of acute poisoning with cardiac glycosides: anorexia, nausea, persistent vomiting, hiccups, colicky pain in the epigastric region and abdomen, diarrhea with delayed diuresis. The pulse is sharply slow and irregular. Rhythm disorders - from individual extrasystoles, bigeminy to ventricular fibrillation, ventricular paroxysmal tachycardia (with complete atrioventricular block). Characteristic changes on the ECG are prolongation of the PQ interval, displacement of the ST segment under the isoelectric line. Vision may be impaired: xanthopsia, diplopia, photophobia, etc. The pupils are dilated (less often constricted), exophthalmos and paresis of the eye muscles are observed.
Headache, weakness, drowsiness are noted; in severe poisoning - delirium, shortness of breath, cyanosis, coma, convulsions, decreased blood pressure, ventricular fibrillation, cardiac arrest in diastole.
Symptoms of irritation digestive system(colic, vomiting, diarrhea) are clearly manifested in case of poisoning with oleander and its preparations.
First aid and treatment for poisoning with cardiac glycosides. Gastric lavage through a tube with a suspension of activated carbon (20-30 g in 1 liter of water) or a 0.2-0.5% tannin solution, followed by the administration of a saline laxative and a cleansing enema. Emetics are contraindicated in case of poisoning with digitalis preparations and their analogues. The toxic effect of cardiac glycosides on the myocardium (arrhythmias, cardiogenic collapse) is stopped by potassium chloride. At normal function kidneys, the latter is prescribed (in the absence of vomiting) orally 0.5 g (dissolved in water) every 15 minutes or in the form of a 0.3% solution of potassium chloride (in 5% glucose solution) slowly intravenously - until the ECG shows there will be no noticeable improvement or the potassium content in the blood will not increase to 5 mmol/l.
If renal function is reduced, it is necessary to first determine the potassium content in the blood serum before administering potassium chloride. Maximum dose potassium chloride on the first day after poisoning - 4 g; in the next day - 2g. 20 ml of a 10% tetash-calc solution with 300 ml of a 5% glucose solution is injected intravenously.
To reduce the toxic effect of cardiac glycosides, unithiol (5 ml of a 5% solution 4 times a day intramuscularly) and EDTA disodium salt (2-4 g in a 5% glucose solution intravenously by drip for 3-4 hours) are also used.
Apply anaprilin (10-30 mg 3 times a day), novocaine-amide - orally 0.5-1 g every 2 hours (up to 4 g in total) or intramuscularly 5-10 ml of a 10% solution 3-4 times a day. day, as well as quinidine sulfate - 0.2 g orally 3-4 times a day, novocaine - intravenously 2-5 ml of 0.25% solution 2-3 times a day. Severe bradycardia, nausea, and vomiting are stopped by repeated administration of atropine sulfate (0.5-1 ml of 0.1% solution under the skin).
To combat dehydration, parenteral fluid administration (isotonic sodium chloride solution, 5% glucose solution) is recommended. To eliminate hypoxia, oxygen inhalation is used. The phenomena of excitement are stopped with barbiturates. In the case of cardiogenic collapse, vasoconstrictors (epinephrine hydrochloride, norepinephrine hydrotartrate) can cause ventricular fibrillation and are therefore contraindicated. When treating acute poisoning with cardiac glycosides, strict bed rest is necessary.
Treatment of acute poisoning, 1982
More articles about acute poisoning:
Cardiac glycosides are cardiological drugs of plant origin, one of the main groups of drugs in the complex therapy of acute and chronic heart failure. These include Digoxin, Digitoxin, Strophanthin, Korglykon, Celanide.
Plant substrates for cardiac glycosides are foxglove, spring adonis, lily of the valley, jaundice, strophanthus, etc.
The main effect of this group of drugs is cardiotonic, which is manifested by an increase in the force of heart contraction. In addition, negative chronotropic (decrease in heart rate) and negative dromotropic (slowdown in conduction speed) are characteristic. nerve impulses on heart tissue) effect.
When used in therapeutic doses, cardiac glycosides reduce tachycardia, eliminate shortness of breath and edema accompanying heart failure, and help improve peripheral circulation.
A dangerous undesirable effect when taking glycosides in subtoxic or toxic doses is their ability to increase the excitability of cardiac structures, thereby provoking cardiac arrhythmias.
Main side effect cardiac glycosides is glycosidic, or digitalis, intoxication - a life-threatening condition.
Poisoning with cardiac glycosides is common: according to various sources, from 15 to 24% of patients receiving drugs are exposed to it to one degree or another. This is due to the characteristics of absorption, distribution of glycosides in the systemic circulation and their excretion.
Therapeutic latitude (the interval between the minimum dose that causes a therapeutic effect and the minimum dose that causes side effects) for this group of products is extremely small, which significantly limits their use, despite their effectiveness.
The lethal dose is only 5-10 times higher than the dose that causes a therapeutic effect, and the first symptoms of intoxication appear when the therapeutic dose is doubled.
The development of acute glycoside intoxication is possible in several cases.
Poisoning in persons receiving a therapeutic dose of the drug:
However, more often acute poisoning occurs when the drug is taken incorrectly:
Symptoms of acute poisoning with cardiac glycosides can be divided into 3 groups: dyspeptic, neurological and cardiac disorders.
Manifestations from the gastrointestinal tract are associated with irritating effect glycosides on the mucous membrane of the stomach and intestines:
Neurological disorders manifest themselves:
A characteristic manifestation of acute glycoside intoxication is specific visual impairment: a yellow or yellow-green glow around objects (xanthopsia), which intensifies when looking at a light source, decreased visual acuity, perception of objects in a reduced or enlarged form, photophobia, loss of visual fields.
Symptoms of acute poisoning with cardiac glycosides from the cardiovascular system are the most dangerous and are usually manifested by disturbances in heart rhythm and conduction:
Most often, cardiac symptoms precede dyspeptic and neurological ones.
If glycoside intoxication occurs during injection with the drug, its administration should be stopped immediately.
Acute poisoning with cardiac glycosides requires immediate measures:
Gastric lavage in case of acute poisoning with cardiac glycosides is not recommended, since it may lead to an increase in parasympathetic tone and thereby aggravate the condition of the victim.
Since glycoside intoxication is a serious, life-threatening condition, medical attention is required in all cases.
An emergency medical team must be called if symptoms from at least one of the systems (digestive, nervous, cardiovascular) appear while taking medications.
In a hospital setting, the victim will be provided with qualified assistance:
The main consequences of poisoning with cardiac glycosides are rhythm and conduction disturbances, which can lead to the death of the victim:
Glycoside intoxication is a condition of acute or chronic poisoning with digitalis group drugs used to treat heart diseases. Cardiac glycosides are substances isolated from the foxglove plant (in Latin - Digitális), they are used to treat chronic heart failure. As a rule, this is the drug Digoxin most often prescribed to heart patients, or Digitoxin or Celanide prescribed in the hospital.
The essence of intoxication is that the electrolyte balance is disrupted in the heart cells and excessive amounts of calcium and sodium accumulate, but the potassium content sharply decreases. As a result, heart contractions increase. In addition, the conduction system of the heart is also disrupted, and impulses arise in those parts of the heart muscle where this is not provided for during normal functioning, and in general, the conduction of impulses in the heart slows down.
Often this serious complication occurs due to an overdose of cardiac glycosides (they have very strict therapeutic “limits” and exceed required dose too easy). Also, intoxication with cardiac glycosides can occur even with normal concentrations of drugs in the blood due to a decrease in the body’s tolerance to drugs, which manifests itself for a number of reasons:
In addition to heart patients, people who ineptly use medicinal plants or people attempting suicide are at risk of digitalis intoxication. However, it should be noted that the lethal dose of cardiac glycosides is an order of magnitude higher than the therapeutic dose, therefore, an error in taking medications in most cases leads to poisoning, but not to death.
The phenomenon of intoxication with cardiac glycosides is quite common; this condition occurs in 5 to 25% of patients constantly taking digitalis (digitalis) or other cardiac glycosides.
To provide timely and correct assistance, it is very important to establish in time what we are actually dealing with. To do this, it is important to know the clinical picture of digitalis intoxication - what it is, how it manifests itself and what the main syndromes are. There are several of them:
It is important to remember that the stronger the degree of intoxication, the more pronounced the symptoms, and the faster they appear (within minutes or hours after taking the drug). In this case, the condition quickly worsens, so help should be immediate. This condition requires the use of antidotes and resuscitation measures.
In any case, if digitalis intoxication occurs, treatment should only be prescribed by a doctor and should be carried out in a hospital setting.
The action of the digoxin antidote is to bind free digoxin in the body and stop its interaction with myocardial cells. Antidotes are fragments of antibodies against digoxin in an amount adequate to the dose of the glycoside that is absorbed into the blood (the formula for calculating the dose is always included in the instructions for the antidote drug). Half an hour after receiving the antidote, the glycoside content in the body increases, it combines with protein, loses its activity and is excreted from the body.
Since the antidote is obtained by the synthesis of antibodies formed in the body of sheep, in people who have previously received drugs containing sheep or chicken egg white, can be observed allergic reaction.
The treatment regimen is as follows:
If you are forced to take cardiac glycosides for the treatment of chronic heart failure, in no case exceed the dosage and pay attention to the slightest negative changes in your condition listed in the list of symptoms of intoxication with cardiac glycosides. Even a slight increase in dose can lead to dire consequences and even death, and it should also be taken into account that cardiac glycosides tend to accumulate in the body.
If you are engaged in herbalism and are a fan of herbal medicine, it is important to remember that poisoning with cardiac glycosides can occur mainly when using digitalis as a medicinal plant (poisoning with plants such as oleander and lily of the valley can also have a similar effect). It is important to know that currently any independent use of foxglove as a medicinal plant is prohibited. As a medicinal plant, digitalis was used to treat the heart, as well as to reduce swelling and increase urination. It has been known for at least 4 thousand years; it has been popular in Europe for centuries, but due to frequent cases of poisoning, it was periodically banned. But in the 18th century, digitalis glycoside was discovered in Great Britain, but it was used extremely carefully due to the difficulty of finding a safe but effective dose (overdose occurs extremely easily due to its high toxicity). In a word, foxglove is a classic illustration of the immortal saying of Paracelsus: “Everything is poison and everything is medicine, it’s just a matter of dose.”
Digitalis intoxication (poisoning with cardiac glycosides) is a serious complication of the treatment of patients suffering from heart disease and taking drugs of the digitalis group (digoxin).
Lethal doses of cardiac glycosides are usually 10 times or more higher than therapeutic doses. The elderly, patients with impaired function of the thyroid gland, circulatory system and excretion are especially sensitive to them. The toxicity of digitalis group drugs increases in the presence of hypokalemia and hypomagnesemia. Children are more resistant to them.
The duration of the toxicogenic stage correlates with the rate and completeness of absorption of cardiac glycosides in the gastrointestinal tract, the rate of their binding by plasma proteins and excretion. It is quite long-lasting in people with intoxication, poisoned with digitoxin and isolanide, through the hepatic intestinal circulation and significant reabsorption in the kidneys. In particular, digitoxin binds to plasma proteins by 90%, digoxin by 40%, and strophanthin by less than 10%. Every day, the activity in the blood of strophanthin decreases by 40-50%, while digitoxin decreases by 7-10%. Due to the low (3.5%) absorption of strophanthin and digitoxin in the gastrointestinal tract, oral poisoning with them has not been recorded.
Manifestations of acute poisoning with cardiac glycosides do not depend on the route of their entry into the body.
The clinical picture of digitalis intoxication consists of several leading syndromes, in particular:
First of all, dyspeptic manifestations appear in the form of nausea, continuous vomiting with an admixture of bile in the vomit, sometimes blood, diarrhea, signs of dehydration, and abdominal pain. Soon headache, dizziness and visual impairment appear in the form of ring-shaped scotomas, xanthopsia, decreased visual acuity as a result of the development of retrobulbar neuritis. Ataxia, insomnia, agitation, delirium, hallucinations, convulsions, shortness of breath, cyanosis, hypoxia, and decreased diuresis are also characteristic.
On the ECG, along with a decrease in the ST interval and a negative or flattened T wave, the PQ interval lengthens, single atrial P waves fall out. Rhythm and conduction disorders of all types are often observed, especially when acute poisoning with cardiac glycosides was preceded by cardiac disturbances: bradycardia, blockade and etc.. The development of ventricular extrasystole such as bigeminy, paroxysmal tachycardia, atrial and ventricular fibrillation is very dangerous. In such cases, death occurs due to cardiac arrest or asphyxia.
The emergency care program for acute intoxication with cardiac glycosides provides for early detoxification with resuscitation measures and antidotes, interruption of enterohepatic circulation (if poisoning occurs with digitoxin or isolanide), elimination of manifestations of PSCE, arrhythmia, vomiting, agitation and hypoxia, improvement of myocardial contractile function. To do this you need:
A specific antidote for digitalis intoxication with cardiac glycosides, in particular digoxin preparations, are fragments of specific antibodies against digoxin. The essence of their antidote activity lies in binding free digoxin contained in plasma after its absolute or relative overdose, and thus preventing its interaction with myocardial cells. The drug is used in a dose that is molecularly adequate to the amount of digitalis glycoside that is absorbed. (Empirically it has been established that this dose is 800 mg, that is, 20 ampoules of 40 mg each).
Fragments of specific antibodies against digoxin are obtained from specific antibodies that were formed in the body of sheep. Their relationship with digoxin, as well as digitoxin and lantoside, is greater than the relationship of these glycosides with specific receptors (ATPase) in the myocardium. Therefore, these glycosides bind predominantly to fragments of specific antibodies, and not to specific receptors in the myocardium and other tissues. 30 minutes after the administration of the antidote, the content of digoxin or another glycoside in the blood begins to increase, which contributes to intoxication; glycosides combined with protein lose their pharmacological activity and are excreted from the body. The dose of the drug is set individually and depends on the amount of glycoside that is absorbed.
The dose is calculated according to the instructions attached to the pharmaceutical product.
An undesirable complication when using the digitalis antidote may be an allergic reaction in sensitized patients who have previously been administered drugs containing sheep protein or protein chicken egg. So we have the following drugs: Digibind - capsules of 40 mg of lyophilized fragment of the antibody against digitoxin; digitalis antidote BM - ampoules of 80 mg of antibody fragment against digoxin (dry substance).
The vagomimetic effect of cardiac glycosides (bradycardia, vomiting) should be eliminated with atropine sulfate - 0.5-1 milliliter of 0.1% solution. In the presence of arrhythmias resulting from digitalis intoxication with cardiac glycosides, use diphenin or a polarizing mixture (100 ml of 10% glucose + 0.5 g of potassium chloride + 2 units of insulin + mg of cocarboxylase). Riboxin is used to improve cardiac activity.
Dehydration of the body is eliminated by administering infusion solutions: 5% glucose with insulin, convulsions - anticonvulsants (sodium hydroxybutyrate, sibazone, aminazine). Vitamin therapy and oxygen therapy are indicated.
In the absence positive results it is advisable to carry out hemosorption, and when severe poisoning digoxin or strophanthin - hemodialysis, introduce specific antibodies.
Cardiac glycosides belong to a group of drugs necessary for the treatment of heart failure. A course or single use of these medications ensures effective heart function, positively affecting the condition and functioning of the myocardium.
Intoxication with cardiac glycosides is explained by certain characteristics of these drugs, which contribute to the accumulation of the drug in the body and can cause serious pathological changes.
Cardiac glycosides are prescribed according to strict indications. In this group there are drugs that have an immediate therapeutic effect, and they are used to relieve acute conditions.
Other types of cardiac glycosides are prescribed for long-term treatment, during which adjustment of their dose must be carried out constantly.
Glycoside toxicity most often occurs in patients using these drugs to treat heart disease. This condition develops less frequently in people taking the drug for the purpose of suicide; even less often, an overdose occurs when accidentally consuming plants containing glycosides.
Intoxication with glycosides occurs when the dosage of these drugs is exceeded. A lethal outcome can occur if a single dose is 5-10 times higher than the prescribed therapeutic dose.
Sensitivity to cardiac glycosides increases in certain diseases and conditions of the body; this group of provoking factors includes:
When prescribing cardiac glycosides, the doctor must carefully examine the medical history and only then select the required dosage.
Intoxication with cardiac glycosides may begin to develop several weeks after the first dose. A glycoside such as digoxin, used for treatment in old age, tends to accumulate in the body. Therefore, its dose after treatment for several days should be adjusted downwards.
In older people, overdose often occurs due to their memory problems and therefore taking glycosides in old age should be controlled by relatives.
Glycoside intoxication is manifested by a decrease in the number of heart contractions, extrasystole, and damage to the gastrointestinal tract, which is expressed by nausea and vomiting.
Symptoms of intoxication consist of gastrointensive, psychoneurological, cardiovascular syndrome, and visual impairment is also added. Acute poisoning with cardiac glycosides can be suspected if the following symptoms are recorded:
Acute poisoning affects the appearance visual changes. You may notice a decrease in vision, the appearance of yellow and green spots when looking at an object. The patient is worried, he experiences cyanosis of the nasolabial triangle and lips, hypoxia, shortness of breath, and in severe cases, convulsions and coma.
Intoxication with glycosides can also be detected after an ECG. On the cardiogram, the PQ interval lengthens, a negative or flattened T wave is revealed, and conduction and rhythm disorders are noticeable.
The development of ventricular extrasystole and atrial fibrillation is considered dangerous. Death from an overdose of glycosides occurs due to cardiac arrest or asphyxia.
If symptoms of intoxication with cardiac glycosides are recorded, then it is necessary to act according to the following scheme:
In case of acute poisoning, early detoxification should be aimed at reducing the concentration of the drug in the stomach, for this purpose the following is carried out:
Treatment in a hospital includes the following activities:
After all resuscitation measures have been carried out and the patient’s condition has been stabilized with positive dynamics on the ECG, he must be monitored medically for several days. A favorable prognosis is given if the patient’s condition returns to normal within 24 hours after poisoning.
Overdose of cardiac glycosides
Mortality from cardiovascular diseases is quite high today. That's why cardiac drugs, are generally widely available and many are sold without a prescription. A fairly significant part of this group consists of digitalis drugs, which are prescribed for heart failure.
These substances, used for weak heart function, are among the vital medicines that are primarily needed by older people.
However, only the correct dosage of the drug will provide a good therapeutic effect.
Used for weak heart function
The process of drug absorption is quite complex; even a slight deviation from the prescribed dose can play a cruel joke: instead of the desired improvement in the condition, the patient experiences glycoside intoxication.
Glycosidic substances can restore balance minerals in the heart muscle for its normal functioning. They cope well with heart failure, weakness of the heart muscle, bradycardia and tachycardia.
However, only the exact dose will help the patient feel much better. An overdose of cardiac glycosides can occur even with an insignificant excess of a substance that has the ability to accumulate. That is why the first symptoms of an overdose of cardiac glycosides may occur a day or two after increasing the dose used.
Poisoning with cardiac glycosides affects the functioning of the following systems of the human body:
Glycoside intoxication weak degree may slightly worsen the patient's condition. If it was an extraordinary pill that a person took out of simple forgetfulness, then intoxication with cardiac glycosides may resemble food poisoning.
Emergency care for glycoside intoxication with cardiac drugs is necessary if the following symptoms occur:
Give the patient activated charcoal and plenty of fluids
Poisoning with cardiac glycosides in small doses can cause nausea and vomiting. If it was a one-time thing excess intake, then the symptoms of malaise will subside within a few hours. In a day the person will feel much better.
If you notice signs of an overdose in yourself or a close relative, you should calm him down, give him activated charcoal and provide him with plenty of fluids.
Poisoning with cardiac glycosides causes a serious burden on the nervous system. Specific sign is the appearance of color visual hallucinations (primary colors – yellow and green).
Hand tremors and convulsions may occur.
When intoxicated with such substances, the general condition of a person worsens, confusion, dizziness and an acute lack of fresh air occur.
Glycosidic substances and excretory functions
An excess of such substances in the body affects the liver and kidneys. A distinctive feature of the manifestation of these substances in the body can be considered a lack of appetite and a sharp decrease in urine output, up to its complete absence.
In case of overdose, bradycardia occurs
The paradoxical effect of substances is that their excess leads to sharp deterioration the symptoms for which the medicine was used. The victim appears:
Anyone with heart problems, as well as close relatives of these people, need to know about first aid in case of an overdose of the drugs they are taking. After all, digitalis intoxication, the treatment of which requires constant monitoring by specialists, can negate the long regressive period of the disease.
Most often, hospital treatment is necessary, because an ECG in case of an overdose of cardiac glycosides may be required quite often.
If cardiac drug poisoning is suspected, you should stop taking the next dose and take activated charcoal according to your weight.
It is necessary to rinse the stomach
When the drug has been used for a long time and there is a suspicion that several tablets were taken at once, you should rinse the stomach by drinking several glasses of water in one gulp and then pressing on the root of the tongue.
It is important to ensure good air access and complete rest, unfasten tight clothing and put the victim to bed.
The cardiac glycoside antidote is administered in a hospital setting. This may be a drug based on antibodies to digoxin, obtained from sheep serum or chicken protein. IN medical practice Several substances with similar properties are used, but choosing the most effective one can only be qualified specialist in a hospital setting.
At home, the emergency team will perform additional gastric lavage using a special tube. Through an additional tube, about a glass of oil can be injected into the stomach to stop the spread of digoxin throughout the body.
Depending on the condition of the victim and the data on the cardiogram, the emergency team analyzes whether the this type assistance, and what next steps are needed. Thus, they come to a decision about the need for hospitalization.
An antidote is administered in the hospital
In case of intoxication with cardiac glycosides caused by a dose twice the therapeutic dose, treatment is carried out in a hospital setting. It is important to remember that if you take five times more of the drug than necessary, a person can die.
Therefore, the use of these substances by persons who have memory problems should be carried out under the supervision of relatives. In cases of accidental overdose, it is necessary urgent help specialists.
In a hospital setting, all available methods are used to alleviate the victim’s condition. After the antidote has been administered, positive dynamics should be observed within an hour. It can be clearly traced if special cardiac equipment is used.
If the body tolerated the introduction of the antidote well, then the consequences are corrected and painful condition person.
Since the digitalis drugs used disrupt the balance of essential microelements in the heart muscle, additional injections of potassium or magnesium electrolytes may be required.
Glucose deficiency may occur, then a saline solution with glucose is administered by drip. This combination is useful for almost any type of poisoning.
Further treatment is carried out under the strict supervision of specialists, who, with the help of laboratory observations, must restore the disturbed balance.
The positive effect of digitalis substances on the cardiovascular system has been known for a long time. To improve heart function, foxglove was used, the Latin name of which is “digitalis”.
However, an overdose of this drug could be very dangerous, so in order to have healthy heart and feel good, it is important to follow the recommendations prescribed by your doctor.
If your health worsens, you should immediately contact a medical facility, and not prescribe without permission. additional medications. Timely medical assistance will help avoid further unpleasant consequences.
With the correct actions of doctors, the human body is able to recover in a few days. After this, the main cardiac treatment will be adjusted.
