Arrhythmia Heart Symptoms
Metabolic Arrhythmias
Hypokalemia
Diagnosis
About 98% of potassium in the body is distributed in cells, and in liquid media there is only 2% of potassium. Especially large reserves of potassium are found in muscles and liver. For a day a person loses 1-1.5 mmol / kg of potassium, which is mainly excreted by the kidneys( 90%), and the remaining part( 10%) with sweat and feces. How to use folk remedies for arrhythmia, see here.
Causes of
Causes of
Causes of
Causes of
Incomplete intake of
Transtransfer
Renal loss of
Adrenal loss of
According to a MRFIT study, the use of hydrochlorothiazide at a dose of 50-100 mg / day or chlorthalidone 50 mg / day in patients with hypertension and minimal ECG changes increased the frequency of sudden death. At the same time, other studies have not confirmed this connection. Currently, long-term treatment of hypertension is recommended to be administered at doses of 12.5-25 mg / day.
Assessment of potassium deficiency
Potassium deficiency is assessed by assessing potassium, which is normally 3.5-5.0 mmol / l. However, the level of potassium in the plasma does not fully reflect the content of potassium in the body, especially its intracellular concentration - caligism. For example, with severe hypocaligism, in the case of diabetic ketoacidosis, potassium can be normal due to the release of potassium from the cells. It is shown that with an obvious loss of potassium and a normal level of potassium, potassium deficiency can be up to 200 mmol.
Technical errors, such as the application of a tourniquet in vein puncture or
, prolonged storage of blood, promotes the release of potassium from red blood cells and
to increase potassium.
Clinic
In the case of severe potassium deficiency( hypokalemia <2.5 mmol / l)
, the symptoms shown in the table appear. On the ECG,
increases the amplitude and width of the P wave, a slight increase in the PR interval, the QRS complex widening( +20 msec), an increase in the amplitude of the U wave, a decrease in the T wave and the ST segment, and an extension of the QT interval.
Symptoms of hypokalemia
Arrhythmias
Atrial tachycardia,
VT including bi-directional-spindle,
VF,
AV dissociation,
ventricular and atrial extrasystole.
Cardiac Symptoms
Arterial hypotension,
asystole.
Muscle Symptoms
Muscle weakness,
leg muscle spasm,
weakness of respiratory musculature,
Gastroenterological symptoms
Constipation,
intestinal obstruction( paresis).
Common Symptoms
Weakness,
apathy or irritability,
sensitivity to cold,
thirst.
Treatment of
Despite the unreliability of the determination of potassium in the body for potassium, this indicator is widely used for an approximate assessment of the expressed potassium deficiency.
It is considered that at a potassium level of 3 mmol / l potassium deficiency is about 350 mmol, at a level of 2.5 mmol / l - 470 mmol, and at a level of 2 mmol / l - 700 mmol.
What drugs need to correct the existing lack of potassium?
Potassium content in various preparations.
Potassium preparation Potassium content
Panangin, aspartame 1 mmol in 1 tablet or pellet,
2.5 mmol in 10 ml.
Potassium chloride 13.5 mmol in 1 g of powder,
5.3 mmol in 10 ml of a 4% solution,
10 mmol in 10 ml of a 7.5% solution,
13.2 mmol in 10 ml of a 10% solution.
Potassium-normin 13.5 mmol in 1 tablet( 1 g KCl).
Potassium foamy 15.9 mmol in 1 tablet( 1.18 g KCl).
Note: 1 mmol = 1 meq = 39.1 mg of elemental potassium.1 g = 26.5 mmol.
Note that replenishment of potassium deficiency should not be performed by
on the same day, as this can lead to complications with the introduction of large amounts of potassium chloride in
.If parenteral nutrition is provided, then one should take into account the daily loss of potassium in 80-100 mmol.
Carrying out the infusion of potassium chloride solution, one should remember the local
cauterizing action of the drug with the formation of phlebitis and sclerosing effect. To reduce the side effects, you can warm the solution up to 37%, reduce the concentration, and also inject into different veins. The main danger of treatment with potassium preparations is the ability of a concentrated solution of potassium to cause asystole.
For asymptomatic or low-symptom deficiency of potassium,
is used with a high potassium content.
Arrhythmias sinus node, asystole,
AB blockade( 1-3 degrees),
ventricular tachycardia,
ventricular fibrillation.
Gastroenterological symptoms
Diarrhea,
spastic pain.
Common Symptoms
Weakness, especially in the lower extremities,
anxiety, irritability,
paresthesia.
Treatment of
The cause of hyperkalaemia should be identified and corrected. In addition, for the protection of the heart, specific treatment is needed, urgently needed for potassium> 7 mmol / L or the appearance of electrocardiographic signs. The following emergency drugs are used:
10 units of insulin in 60 ml of 40% glucose IV in 5 minutes. The effect develops in 30-60 minutes and lasts for several hours.
Inhalation of salbutamol through the nebulizer
10 ml of 10% calcium gluconate IV for 2-5 minutes. The effect of the drug develops quickly, so if there is no effect for 5 minutes, then you need to repeat the dose. The duration of the drug is about 1 h.
With the use of cardiac glycosides, the drug is not shown.
Sodium bicarbonate 8.4% 40 ml is administered iv in 5 minutes and, if the ECG changes, repeat the dose in 10-15 minutes. If several drugs are treated, calcium is used before sodium bicarbonate, otherwise convulsions may develop. Possible simultaneous introduction of glucose.
Dialysis
Hypomagniemia
Diagnosis
About 99% of magnesium in the body is distributed in cells. The largest
reserves of magnesium are contained in bones( 50-60%), muscles and soft tissues.
The daily requirement for magnesium in an adult is 12-40 mmol.
Reasons for
Decreased admission
Chronic alcoholism is the main reason.
Fasting. Rich in protein and calcium food. Deficiency of vitamin B6.
Diarrhea, vomiting, drainage of the stomach.
Malabsorption.
Increased excretion of
Polyuria( diuretics, acute renal failure).
Diabetic ketoacidosis, glucosuria.
Drugs: antibiotics( aminoglycosides, ticarcillin, carbenicillin, amphotericin B), cyclosporine, cardiac glycosides, diuretics( especially looped).
Other causes of
Cirrhosis.
Heart failure.
Diabetes mellitus.
Proton Pump Inhibitors.
Evaluation of magnesium deficiency
To assess the magnesium deficiency in the body, an estimate of the magnesium concentration in the blood plasma is used, which is normally 0.65-1.1 mmol / l. Approximately 25-30% of magnesium is associated with plasma proteins, therefore when hypoalbuminemia the total amount of magnesium in the plasma( magnesium) decreases, and the content of ionized magnesium can not change.
Physiologically the most important is the magnesium fraction not associated with
proteins.
Magnesium level in plasma is not a reliable indicator of magnesium deficiency, since only 1% of magnesium is distributed extracellularly. Therefore, normal magnesium does not exclude the lack of magnesium.
We note that in 40% of the magnesium deficiency is combined with a deficit of potassium.
Clinic
Symptoms that appear only with a pronounced magnesium deficiency,
are shown below. On the ECG, an increase in the PR interval QRS broadening( +20 msec), an increase in the QT interval, a depression of the ST segment and a decrease in the amplitude of the T wave are recorded.
Manifestations of magnesium deficiency
Arrhythmias
Paroxysmal atrial tachycardia with AV blockade,
atrial fibrillation,
,,
monomorphic VT,
polytopic ventricular extrasystole,
ventricular hyging,
digitalis, alcoholic arrhythmia,
resistant arrhythmias.
Cardiac symptoms
Spontaneous angina,
sinus tachycardia, arterial hypertension.
Neuromuscular symptoms
Increased neuromuscular excitability,
skeletal muscle cramps, facial, hand obstetrician, tremor.
Visceral symptoms
Laryngospasm, bronchospasm,
pilorospasm,
spasm of sphincter of Oddi,
of dyskinesia of biliary tract,
nausea, vomiting,
alternation of diarrhea and constipation.
Cerebral symptoms
Depression,
impaired consciousness up to coma,
chronic fatigue syndrome,
eclampsia of pregnant women.
Products rich in potassium( 500 mg per 100 g)
Products
Cocoa powder
Dried potatoes
Dried apricots( dried apricots)
Beans
Dry cow milk
Sea cabbage
Raisins
Parsley
Cream dry
Prunes
Date
Dried Pear
Spinach
Potatoes
Milk Chocolate
Almond Sweet
Halibut
Sorrel
Dried Apples
Also used are table salt substitutes containing 7-14 mmol of potassium per 1 g( Valtek salt, where 30% is chlorineid of potassium), or potassium preparations. The daily dose of additional potassium is usually 30-60 mmol. Powders of potassium chloride should be washed down with a glass of water or fruit juice, since potassium chloride has an irritating effect. In the case of intolerance to oral
preparations, intravenous drip administration is used.
For potassium> 2.5 mmol / l and no change on the ECG, a solution at a concentration of 30 mmol / l is used. To obtain a solution of this concentration, 15 ml of 7.5% potassium chloride should be diluted in 485 ml of 5% glucose. The rate of potassium administration is usually 10 mmol( 330 ml) per hour. Usually, about 60-90 mmol of potassium( 2-3 liters) are administered per day.
With potassium 2.5-2.0 mmol / L, changes in the ECG and the presence of tachyarrhythmia or other symptoms, due to the danger of the condition, more intensive corrective therapy is recommended. Apply solutions of increased potassium concentration - 60 mmol / l. To obtain a solution of this concentration, 30 ml of 7.5% potassium chloride should be diluted in 470 ml of 5% glucose. Concentrated solutions of potassium are introduced only into the peripheral veins to avoid cardiotoxic effect( asystole).The rate of administration of potassium is 40-60 mmol( 660-990 ml) per hour. Continuous monitoring of the ECG and determination of the potassium content in the plasma every 4 hours is required. Typically, 90-150 mmol of potassium( 1.5-2.5 L) are administered per day.
With potassium <2.0 mmol / L or severe arrhythmia( bidirectional-spindle VT, VF), it is recommended to increase the rate of administration of
potassium to 80-100 mmol / h at a solution concentration of 60 mmol / l. However,
in this case will have to inject 1.3-1.7 liters of solution per hour under the control of
CVP, which can be dangerous, especially with left ventricular failure. Apparently, it is possible to increase the concentration of potassium solution to 90 mmol / l and, accordingly, to reduce the infusion to 0.9-1.1 l / h. In case of life threatening, potassium is used at the beginning of treatment as an isotonic solution as a solvent, and not a solution of glucose.
Hyperkalemia
Diagnosis
Reasons
Increased intake
Potassium preparations, potassium salt of penicillin.
Transcellular Transition
Acidosis.
Tissue catabolism( sepsis, trauma, fever, tumor disintegration, hemolysis, gastrointestinal bleeding).Insulin deficiency.
Beta-blockers( with diabetes, hemodialysis).
Decreased elimination
Renal failure.
Drugs( NSAIDs, ACE inhibitors, heparin, cyclosporine, potassium-sparing diuretics).
Addison's disease. Primary hypoaldosteronism. Renal tubular acidosis.
Heart failure.
Pseudohypergalyemia is possible, for example, with blood clotting, leukocytosis( > 70 * 109 / l), thrombocytosis( > 1000 * 109 / L), plugging, haemolysis while taking blood through a thin needle, delayed blood test.
Clinic
Symptoms of hyperkalemia usually appear when the potassium content of the
plasma is> 6.5 mmol / l.
The following sequence of changes is often recorded on the ECG: first, with 5.7-6.5 mmol / l potassium, high and pointed T teeth appear, then a 1-degree AV block can develop. At a potassium of 6.5-7.5 mmol / l, the prongs P, and at the level of 7,0-8,0 the QRS complexes expand and the depression of the ST segment is observed.
The rate of development of symptoms of hyperkalemia may be different.
For example, the first electrocardiographic signs of hyperkalemia to asystole or VF may take several minutes.
Symptoms of hyperkalemia
Driving of transport in arrhythmias
According to available data, medical problems, including arrhythmias,
very rarely lead to transport accidents. Among 3000 accidents when driving personal motor vehicles, only 0.84% was caused by arrhythmias. According to European countries, 0.1% of traffic accidents of commercial transport are associated with medical problems, of which only 10-25% are due to cardiac disorders.
Consider the risk of developing transient disturbances of consciousness during individual arrhythmias and the restriction of access to driving vehicles, on the basis of the recommendations of the AHA / NASPE experts( 1996) and ESC( 1998).
Note that studies to assess cardiac arrhythmias and
conduction in driving are not enough, therefore
most recommendations are based on extrapolation of available data and are empirical.
Ventricular arrhythmias
Ventricular extrasystole and unstable VT without structural
heart lesions are safe and are not a limitation for driving
transport. Heart diseases are excluded after examination( echocardiography, stress test).If there is any doubt about the presence of IHD, especially in men over 36, coronary angiography is indicated. With heart disease, ventricular arrhythmias can increase the risk of sudden death.
Persons with stable VT or VF to driving commercial vehicles
are not allowed. After the successful treatment of resistant VT or VF on the
background of antiarrhythmic treatment, recurrences of ventricular tachyarrhythmias in
occur in the first year in 17% of cases, with the highest incidence of
occurring in the first month, from 2-7 months the frequency of relapses is moderate, and later significantly decreases.
In patients with ICD for several years of observation in 70% of cases, repeated discharges were recorded, of which 10% were accompanied by syncope and 10% pre-fog. Unfortunately, there are no signs predicting the risk of fainting.
Absence of syncope in the first discharge of the ICD also does not guarantee the absence of fainting in subsequent discharges. Since the maximum frequency of relapses falls on the first 6 months after the discharge, driving of personal vehicles during this period is not recommended. There is the same restriction after each discharge of the ICD, regardless of the presence of syncope. Patients are recommended to drive only light vehicles. In the case of long trips, especially on high-speed lines, it is advisable to have an adult partner.
Admission to the transport of patients with ventricular arrhythmias( AHA / NASPE, 1996)
Form VT Personal Commercial
Vehicle transport
Unstable, asymptomatic + +
Unsustainable, symptomatic After 3 months After 6 months
Resistant at 6 months _
Idiopathic, asymptomaticAfter 3 months After 6 months Syndrome & gt;QT asymptomatic + Syndrome & gt;QT Symptom After 6 months?_
Ventricular fibrillation After 6 months?_
Notes: The table indicates the control period of treatment without
symptoms, after which driving is allowed.
Idiopathic fluid is usually asymptomatic and rarely passes into ventricular fibrillation. After the exclusion of heart disease
( hypertrophic cardiomyopathy, right ventricular dysplasia), and the risk of myocardial ischemia during tachycardia( coronary angiography), driving is acceptable.
After eliminating the cause of the acquired syndrome, the extended
rubbed QT( electrolyte disorders, drugs), driving is not restricted. In congenital syndrome, often during the
of physical or emotional stress, VT develops, which can cause fainting or death in
.Treatment is effective in most patients, and the incidence of symptoms is significantly reduced after 40
years. With asymptomatic syndrome of prolonged QT interval or absence of symptoms within 6 months, it is allowed to drive personal vehicles.
Nadzheludochkovye arrhythmias
Among patients with UHT, aimed at EFI, in 25% of the history of
was at least one syncope. A high risk of fainting is observed in young patients, since the AV node can transmit up to 300 pulses per minute, especially when stress occurs while driving a vehicle.
In AF, syncope may be associated not only with a high heart rate, but also a syndrome of bradycardia-tachycardia.
In individuals with AV nodal reciprocal tachycardia, syncope occurs in
33-39% of cases. Very rarely, this tachyarrhythmia is transformed into polymorphic VT or ventricular fibrillation. The effectiveness of
treatment due to spontaneous variability in the frequency of tachycardia is very difficult to assess
.After catheter ablation, the recurrence rate of arrhythmia does not exceed 10%.
Polymorphic atrial tachycardia usually develops in severe lung and heart diseases that impede admission to
driving.
In WPW syndrome, the frequency of syncope is 11-29%, and suddenly
death occurs in 1-8%.After successful catheter ablation of
, the risk of syncope and sudden death is eliminated. The effectiveness of ablation is documented by several daily ECG for 6 months and EFI.Although in the absence of tachyarrhythmia( WPW phenomenon), the risk of sudden death is about 0.1%, it seems reasonable for commercial transport drivers to assess the conductive capacity of the DP, since with a "fast" DP, the first attack of AF can be fatal.
Sinus bradyarrhythmias
Asymptomatic dysfunction of the sinus node with no lesions
of the heart is not a limitation for driving transport.
Symptomatic bradyarrhythmia shows an implantation of ECS, which completely eliminates the symptoms of
.Relapses in symptoms may be due to tachyarrhythmia or the progression of heart disease.
Conductivity disorders
With AB blockade of the 1st degree, especially normalized with a stress test, there are no restrictions. AB blockade of the 2nd degree of type I is also favorable. In the case of AB blockade of the 2nd degree of type II or 3 degree, driving of commercial vehicles is not shown.
Incomplete BNPGs and their branches are not contraindications to the driving of transport. Complete BNPG in case of normal results of
echocardiography, stress test and Holter monitoring ECG
also does not limit the driving of commercial vehicles. In the case of
, complete BLNGP requires coronary angiography in addition.
Note that the pathology of the conducting system reflects the presence of local or widespread myocardial damage, which predisposes to the appearance of ventricular tachyarrhythmias, often causing syncope.
Neurogenic syncope
Neurogenic( 37%) predominate among syncope when driving a vehicle, and arrhythmogenic syncope( 12%) is less common.
Neurogenic syncope most often has a mixed development mechanism, including bradycardia and vasodilation. The complexity of the assessment is due to the pronounced variability of the disorder. On the one hand, many people have a single short-term faint in their life, and, on the other hand, frequent fainting occurs despite aggressive treatment.
The tactics of treatment are affected by the severity of syncope: weak and rare fainting with harbingers that occur only in a vertical position, or frequent and prolonged without precursors, arising in any position.
In the case of carotid sinus syndrome during the 3-year period of
, after implantation of ECS, the frequency of syncope was 9% compared to 57% of
without implantation of ECS.
Arrhythmias in pregnancy
Pregnancy is accompanied by an increase in the arrhythmia frequency both with
structural heart disease, and without it. Often, atrial and ventricular extrasystoles are recorded, which, even at high frequency and polymorphic nature, usually do not affect the state of the mother
and fetus. The frequency of paroxysmal atrial and ventricular tachycardias is described.
In most cases, tachyarrhythmias( paroxysmal atrioventricular and atrial), bradyarrhythmias( sinoatrial block, pacemaker migration atrial, atrial or AV rhythm) and extrasystoles are not accompanied by hemodynamic disorders and do not require treatment.
During normal pregnancy, dizziness, fainting and palpitations are common, but these symptoms are rarely associated with
cardiac rhythm and conduction disorders.
If there are frequent uncontrolled episodes of arrhythmia with hemodynamic disorders, pregnancy is not indicated.
Pregnancy makes high demands on the safety of medicines for the fetus. During the period of the laying of the fetal organs( the first 3-8 weeks), the use of drugs is possible only for vital indications. As a rule, new drugs with insufficient experience of use in women during pregnancy are not used. When treating antiarrhythmic drugs should monitor the ECG and cardiac activity of the mother and fetus.
Treatment of tachyarrhythmias
Emergency relief of tachycardia is indicated only with severe
hemodynamic disorders. Especially dangerous is arterial hypotension, which can worsen the blood supply of the fetus and in the case of bradycardia in the fetus, a cardioversion, either medicamental or electrical, is necessary.
It should be noted the safety of EIT in all periods of pregnancy. In
the same time, although the discharge energy reaching the fetus is negligible, monitor monitoring of the fetus is necessary.
Note that the short-term use of antiarrhythmic drugs for tachycardia during pregnancy is much safer than long-term preventive therapy.
Beta-blockers are safe, but the ability of
to strengthen uterine contractility should be considered. To exclude the development of a newborn bradycardia, hypotension, hypoglycemia and neonatal asphyxia
, it is necessary to stop treatment with beta-blockers 48-72 hours before the birth of the child. If this is not possible, then for 48-72 h
after the birth of the child, constant monitoring of heart rate, blood pressure, respiratory function, and newborn glycemia is necessary. Verapamil is widely used in obstetric practice as a tocolytic.
Quinidine is well studied in pregnant women, therefore it is
that this drug is recommended for arresting AF( ACC /AHA/ ESC, 2001).
However, it should be noted that large doses of the drug may increase
uterine contractility.
For tachycardia, lidocaine, procainamide, flecainide and amiodarone can also be used.
Preventive maintenance of tachyarrhythmias
First of all it is necessary to try to eliminate provoking and causal factors of arrhythmias: drugs( beta-agonists), thyroid gland diseases, smoking, alcohol, caffeine-containing drinks, electrolyte imbalance.
For the evaluation of drug safety during pregnancy, the FDA
committee has developed a special classification.
Risk Categories for Pregnancy( FDA)
Class B Drugs:
Lidocaine, Morazine
Class C: Verapamil, digoxin, disopyramide, diltiazem, ibutilide, mexiletine, metoprolol, procainamide, propafenone, propranolol, sotalol, toxainide, flecainide, quinidine,esmolol
Class D: Amiodarone, atenolol, phenytoin
Beta-adrenoblockers( bisoprolol, metoprolol) are quite safe. Non-selective beta-blockers( propranolol, nadolol, timolol) can cause fetal growth retardation, and in later terms are safe and widely used.
Quinidine increases uterine contractility only in toxic doses of
or with the initiation of spontaneous uterine contractions. In the usual
therapeutic maintenance doses, it is safe. Prokainamid with
prolonged admission causes a lupus syndrome, so it is rarely used. Experience with the use of disopyramide is inadequate and there are reports of increased uterine contractility when taken in normal doses.
The effect on the fetus of 1C class drugs and mexiletine has been little studied.
Amiodarone penetrates partially through the placenta and the concentration of the drug is about 20% of the maternal. With long-term treatment with
9% of newborns are diagnosed with neonatal hypothyroidism and goiter. Therefore, the
drug is prescribed only for severe tachyarrhythmias in the case of ineffectiveness of other drugs.
Sotalol perfectly penetrates the placenta and accumulates in the amniotic fluid. This pharmacokinetics allows the use of this
drug for the treatment of tachycardia( flutter, supraventricular tachycardia) in the fetus. Sotalol does not seem to delay the development of the fetus.
Radiofrequency catheter ablation, widely used for the prevention of many tachyarrhythmias, is undesirable during pregnancy due to the danger of ionizing radiation.
Treatment of bradyarrhythmias
In the case of symptomatic bradycardia( AB blockade of 2-3 degrees, bifascicular blockade) during pregnancy, temporary or permanent cardiostimulation is indicated.
Women with an artificial pacemaker are usually well tolerated. Preference should be given to ECS working in the "demand" mode and with an adaptively changing frequency of stimulation. Apparently, the EKS with isotopic energy sources are quite safe, the radiation level of which is lower than the natural radioactivity.
Arrhythmias in athletes
Heart rhythm and conduction disorders occur in sports-
menus often. When evaluating and predicting an athlete's arrhythmia, an important sign is that the risk of sudden death and symptoms( presyncope, syncope),
, can lead to severe trauma.
Analysis of 1866 sudden deaths in athletes in the period 1980-2006
in the United States showed that the main cause was cardiovascular disease( 56%, including hypertrophic cardio-
myopathy 36%, congenital coronary artery anomalies 17%).
Arrhythmias in myocardial infarction
Patients with acute myocardial infarction often develop
cardiac rhythm and conduction disorders, which can go through a few chastov-days as the myocardium stabilizes.
The most commonly detected accelerated ventricular rhythm, ventricular
extrasystole and tachycardia, atrial fibrillation, as well as dysfunction of the sinus node and AV blockade.
Treatment of
Despite the unreliability of the magnesium level in magnesium, the latter is widely used to estimate the pronounced magnesium deficiency( & lt; 0.5 mmol / l).Hypomagnesemia is recorded only when there is a pronounced magnesium deficiency in the body. Therefore, in the case of a clear cause of magnesium loss and symptoms presumably associated with magnesium deficiency, treatment is usually initiated despite normal magnesium.
Among medicines, we note the low magnesium content of
in the widely distributed preparations of panangin and asparcomb.
Magnesium content in various preparations
Magnesium preparation Magnesium content
Panangin 0.5 mmol( 12 mg) in 1 tablet, dragees,
Asparks 1.4 mmol( 34 mg) in 10 ml.
Magnesium sulfate 8 mmol in 1 g of powder,
20 mmol in 10 ml of 25% solution.
MAG-OX 10 mmol( 240 mg) in 1 tablet.
Uro-mag 3.5 mmol( 84 mg) in 1 tablet.
Magne B6 2 mmol in 1 tablet.
Note: 1 mmol = 2 meq = 24 mg of elemental magnesium
If there is an asymptomatic or low-symptom deficiency of magnesium,
then use oral agents, for example magnesium oxide or chloride, at a dose of 10 mmol( 240 mg), preferably 1-2 times. Simultaneously, it is useful to assign fixing means.
Products containing magnesium rich
Products rich in magnesium( > 100 mg per 100 g)
Products
Halva tahini
Watermelon
Parsley
Egg powder
Halva Sunflower
Sea cabbage
Almond sweet
Oat flakes
Groats buckwheat
Oat groats
Dry milk
Apricots without pits( dried apricots)
Beans
Prunes
Groats millet
It should be remembered that in case of renal insufficiency, the magnesium dose should be reduced approximately 2 times.
Among the risk factors for cardiac arrhythmias and conduction are the following:
Necrosis / myocardial ischemia.
Left ventricular dysfunction.
Stress, hyperkatecholamineemia.
Vagotonia.
Electrolyte disturbances.
For cardiac rhythm and conduction disorders in conditions of decreased coronary blood supply, frequent intensification of myocardial ischemia
, increased left ventricular dysfunction and heart failure, arterial hypotension, and the emergence of psychoemotional stress and fear of death are characteristic.
Atrial fibrillation
AF occurs in 13-15% of patients with myocardial infarction and develops more often with ST-segment elevation on the ECG and in the elderly. Patients with AF
are more likely to have right coronary artery occlusion, especially with
left ventricular failure.
With this arrhythmia, hospital mortality increases by 79%, total mortality in the long-term period increases by 46%, and the risk of stroke increases 2.3 times.
Secondary AF, developed in the acute period of myocardial infarction, in the
may not subsequently recur.
In the absence of serious hemodynamic disorders, it is possible to limit the heart rate control with beta-blockers. If there are
indications for cardioversion, especially in severe cases, then EIT is preferable. For drug-induced cardioversion, amiodarone, sotalol, and, less desirably, procainamide and propafenone are used.
Usually with myocardial infarction, active antithrombotic therapy is performed, which reduces the risk of thromboembolism and cardioversion
, if necessary, without preparation.
When the AF is preserved, warfarin( INR 2.0-2.5) is shown together with aspirin and clopidogrel for 3-6 months, then warfarin plus aspirin or clopidogrel, and after 12 months, one warfarin with an INR level of 2.0-3,0.
Long-term use of warfarin in patients after myocardial infarction
with AF reduced by 29% relative and by 7% absolute annual mortality. This situation is considered in more detail in the treatment of atrial fibrillation.
Accelerated idioventricular rhythm
Accelerated idioventricular rhythm occurs in 20-60% of patients with myocardial infarction, often with reperfusion of the myocardium and usually
is associated with abnormal automatism of Purkinje fibers.
The accelerated idioventricular rhythm is manifested by monomorphic
wide QRS complexes with heart rate of 60-120 per min, duration of
usually up to several minutes, and usually is not accompanied by symptoms. It is important to note that this VT can also be well tolerated by patients.
Unlike full AV, atrial blockades are excited with the usual
frequency, which is usually lower than the frequency of ventricular excitation.
With VT, the frequency of ventricular excitation is usually higher than 120 and hemodynamics is disturbed.
Patients with this arrhythmia are diagnosed with a slower and less
ST segment resolution, worse coronary artery passageway and
with a greater myocardial risk area.
It is important to note that the accelerated idioventricular rhythm does not increase the risk of VT / FF and does not require antiarrhythmic therapy. Moreover, in
, communications with reduced automatism of the sinus node of antiarrhythmics can cause
to become asystolic.
Ventricular tachyarrhythmias
When monitoring ECG in patients with acute myocardial infarction
, VT occurs in 45-60% of cases, mainly in the first 48 hours. Development or maintenance of a stable VT after 48 hours from the onset of myocardial infarction leads to an increased risk of death from VF.In this case, according to the GISSI-3 study, lethality increased more than 6-fold within 6 weeks.
The vast majority of VT / FF appears in the first 48 hours after the onset of
pain and does not increase the risk of sudden death in the future. In
, at the same time, stable VT and VF after 48 h are prone to relapse and are associated with increased lethality. In the
MERLIN-TIMI study 36, an unstable VT after 48 hours in patients with myocardial infarction
without ST elevation increased the annual risk of sudden cardiac
death by 2.2-2.8 times.
Fears of reperfusion ventricular arrhythmias are greatly exaggerated and reperfusion rather reduces the risk of ventricular tachyarrhythmias than
raises them.
It is interesting that early reperfusion, on the one hand, retains more viable myocardium and reduces scar size, and on the other hand,
increases heart rate in the development of VT due to a decrease in the length of the return excitation around the anatomical obstruction. In connection with the increased risk of sudden arrhythmic death, patients with myocardial infarction before discharge from the hospital should conduct Holter monitoring and stress test.
Recovery of sinus rhythm. With stable monomorphic
VT without hemodynamic disturbances, intravenous
administration of 150 mg of amiodarone can be used for 10 min and repeat 150 mg after 10-30 minutes up to 8 times. Perhaps the use of procainamide, and which lidocaine is significantly inferior. If the treatment is ineffective, signs of myocardial ischemia or severe
hemodynamic disorders, an
( monophasic) electric discharge in 100-200-300-360 Joules is needed.
In the case of a life-threatening polymorphic VT, an electrical cardioversion with a discharge of 200-300-360 J is immediately performed.
For refractory resistant and polymorphic VT including "electric storm", urgent revascularization is shown, suppression of sympathicotonia by
with beta-blockers( propranolol 0.1 g / kg, metoprolol 5
mg iv iv 3 times every 2 min) or blockade of stellateganglion, intra-aortic balloon counterpulsation. It is also advisable to administer potassium and magnesium preparations to the level of 4.0-4.5 mmol / l and 2.0 mmol / l, respectively. For example, recommend to enter 5 mg of magnesium( 20 ml of 25% solution for 4 hours).
In the case of brady-dependent forms of tachyarrhythmias,
may be useful as a temporary pacemaker to suppress tachyarrhythmia with a higher frequency of an artificial pacemaker.
Treatment of
Treatment of hyperthyroidism
In hyperthyroid OP without thyroid function suppression, no significant effect should be expected from antiarrhythmic therapy. In cases where the euthyroid condition was achieved, 62% of patients had sinus rhythm restored after 8-10 weeks. After 3 months recovery of sinus rhythm is unlikely.
Treatment with thyrostatics( thiamazole, metimazole, propylthiouracil)
is carried out for a long time( 12-18 months) with a high relapse rate within a year after discontinuation of treatment( up to 60-70%).For example, prescribe
thiamazole at a dose of 30 mg / day. After achieving euthyroidism( by 4-8 weeks), gradually reducing the dose by 5 mg per week pass to a maintenance dose of 5-10 mg / day. Control of treatment is performed by evaluating the thyroid-stimulating hormone and free thyroxine every 3 months.
Thyroid resection may be complicated by hyperparathyroidism,
by a laryngeal nerve damage( about 1%), relapse of hyperthyroidism( about 10%), therefore it is used only in special cases( squeezing goitre, uncontrolled amiodarone hyperthyroidism, side effects of drug treatment in pregnant women).
Safer radical treatment with radioactive iodine with
followed by replacement therapy with levothyroxine. Such treatment for
can be performed at Botkin Hospital in Moscow, North-West Regional Endocrinology Center in St. Petersburg, Omsk
Regional Hospital, City Hospital 13 Nizhny Novgorod, Sanatorium "Chigota" in Serbia.
Treatment of AF
Since it is not advisable to restore sinus rhythm, beta-blockers( atenolol, metoprolol, propranolol) are used for heart rate control with gradual cancellation. It should be noted that in hyperthyroidism, the clearance of drugs metabolized in the liver( carvedilol, propranolol, metoprolol) is increased, and a dose increase may be required. As far as achieving euthyroidism, it is necessary to reduce the dose of medications accordingly. It should be noted that in 37% of cases with thyrotoxicosis the level of alanine transaminase increases, and in 64% the level of alkaline phosphatase testifying to cholestasis. Possible development of hepatitis, including fulminant.
If beta-blockers can not be prescribed, then antagonists of
calcium( verapamil, diltiazem) are used. With hyperthyroidism, digoxin resistance increases and the risk of side effects increases.
Although reliable data on the association of thyrotoxicosis with an increased risk of
thromboembolism is currently not available, in Russian and international
recommendations, it is advisable to prescribe oral anticoagulants, at least until the euthyroid status is achieved.
At the same time, in later ACCP recommendations( 2008), the appointment of oral anticoagulants is based on a system of criteria for high risk of thromboembolism CHADS2, including thyrotoxicosis.
If the doctor decided to prescribe warfarin, then it is important to consider that in patients with hyperthyroidism the choice of oral anticoagulant dose is more difficult. For example, the clearance of K-dependent clotting factors may increase and, accordingly, the risk of bleeding increases.
In the case of planning AF treatment using radiofrequency catheter
thermal ablation, it is first necessary to achieve euthyroidism and perform
treatment while maintaining AF not earlier than 6 months later.
Amiodarone-induced thyroid defeats
In patients taking amiodarone,
thyroid dysfunction often develops( up to 34%)( Fuks A. G., et al., 2004).The frequency of complications depends on the dose of the drug and the consumption of iodine in a given population.
Amiodarone reduces the peripheral conversion of thyroxine to triiodothyronine, leading even to euthyroidism to an increase in thyroxine and
levels in reducing triiodothyronine at a normal level of thyroid-stimulating hormone( the phenomenon of euthyroid hyperthyroxinemia).In addition, taking
amiodarone can cause a transient decrease or increase in thyroid-stimulating hormone, as well as a slight increase in the level of free thyroxin.
Thyrotoxicosis
Thyrotoxicosis in the EMIAT study was recorded in 1.6% of cases of
receiving amiodarone at a dose of 200 mg / day. At the same time, in regions with low
iodine consumption, the frequency of amiodarone thyrotoxicosis reaches
10-12% versus 1.7% in regions with high iodine intake. Often the complication is manifested by relapse AF, with tachycardia usually not observed. Experts recommend to monitor the function of the thyroid every 4 to 6 weeks in the treatment of amiodarone.
A large amount of iodine( 75 mg in a tablet at a requirement of 100-200 μg / day) and chemical similarity of amiodarone with thyroxine contribute to the appearance of persistent strengthening of thyroid function, up to the development of true thyrotoxicosis.
Diagnosis of
When diagnosing amiodarone-induced thyrotoxicosis,
should take into account that a small decrease in thyroid-stimulating hormone and an elevated free thyroxine can not be reliable diagnostic
signs, but should focus on increasing triiodothyronine.
Part of the cases of amiodarone-induced thyrotoxicosis is associated with
by the effect of excess iodine and more often develops against a background of nodular goiter or
of latent diffuse toxic goiter in areas with low consumption of iodine( type 1).Excess iodine causes an uncontrolled synthesis of
hormones by the thyroid gland( iodine-based phenomenon).In these cases
in Doppler ultrasound is determined by hypervascularization, normal
or increased uptake of radioactive iodine( > 5% per day), antibodies to thyroid peroxidase can be determined.
In other patients, amiodarone-induced thyrotoxicosis develops
due to inflammation of the thyroid gland usually on the background of the
of the normal thyroid gland. In these cases hypovas- sis
is determined for sonography, very low absorption of radioactive
iodine( & lt; 2% per day) and histological signs of destructive thyroiditis
( type 2).Antibodies to thyroid peroxidase are absent. Often, the lesion of the thyroid gland has features 1 and 2 types.
Treatment of
In 50% of cases after amiodarone cancellation,
is recovered. For type 1, thionamides may help, possibly in combination with per-
potassium chlorate. Often, the treatment of amiodarone-induced
thyrotoxicosis with thyrostatics is very difficult and often non-
is possible.
Type 2 corticosteroids are effective( eg, prednisolone 30-40 mg / day with a gradual dose reduction for 2-3 months), sometimes plasmapheresis. If it is impossible to distinguish the type of disease, combined treatment with prednisolone and thyreostatics is used. If even combined treatment( thiamazole + potassium perchlorate + corticosteroids) does not help, then in severe cases, including when continuing treatment with amiodarone, it is necessary to carry out a thyroectomy. The latter should be done earlier, before the development of severe consequences.
Increased iodine content in the body after taking amiodarone
does not allow the most effective treatment with radioactive
iodine.
Hypothyroidism
Amiodarone-induced hypothyroidism more often develops in areas of
with high iodine intake. At the heart of the disease is the Volf-
Chaikova effect, which is characterized by a decrease in the synthesis of thyroid hormones
with a high content of iodides.
Diagnosis is based not so much on the increase of thyrotropic hormone
on, which can be normal within 3 months after the withdrawal of
amiodarone, but on the reduction of free thyroxin.
The subclinical form of hypothyroidism with
is significantly more likely to increase the thyroid-stimulating hormone and normal levels of thyroxin
and triiodothyronine.
Treatment is initiated with discontinuation of amiodarone, if possible. Usually, in patients without the original autoimmune thyroiditis, thyroid function usually normalizes within 2-4 months.
If continuation of treatment with amiodarone is necessary due to a dangerous
arrhythmia, then levothyroxine is prescribed, the doses of which may be higher than the
of conventional ones.
The choice of a dose of levothyroxine is based on maintaining a high norm-
of a small level of free thyroxin or even slightly above normal. In
, unlike other types of hypothyroidism, do not try to normalize the thyrotropic hormone level, since high
doses of levothyroxine( ~ 250 μg / day) are often required with the development of hyperthyroidism.
For the purpose of prevention of resistant VT, it is recommended, first of all, to perform angiography and percutaneous coronary intervention, and, if necessary, coronary bypass and aneurysmectomy.
For drug prevention of resistant VT use amiodarone, which reduces the risk of sudden death, especially in combination with
beta-blockers. At the same time, the overall mortality rate does not decrease, and with
cardiac insufficiency III-IV F, the drug may be dangerous. Apparently, sotalol is also quite effective. Beta-blockers are not able to effectively prevent stable VT.
In the case of heart failure in patients after myocardial infarction
, the risk of sudden cardiac death increased 3.2-fold for
five years of follow-up. Therefore, in patients with left ventricular dysfunction( FV & lt; 30-35%) and heart failure after 40 days, implantation of a cardioverter-defibrillator is advisable( ACC /AHA/ HRS, 2008).
With frequent bouts of VT without hemodynamic disorders, radiofrequency catheter ablation reduces the frequency of recurrence of tachycardia.
Unstable VTs usually do not cause hemodynamic disorders of
and do not require treatment. For prophylaxis, beta-blockers
( atenolol 100 mg 1 time, metoprolol 100 mg 2 times) are used. In the case of left ventricular dysfunction( PV <40%), the ACE inhibitor is shown. In controlled trials of
, the use of first-class drugs in patients after myocardial infarction
was associated with an increase in mortality, so these drugs are not indicated.
Arrhythmias and Thyroid Diseases
An increase in thyroid function in 5-15% of cases is accompanied by cardiac rhythm disturbances, usually in the form of AF.About 3-5% of cases of AF are associated with hyperthyroidism, with 75% of these subclinical variants with a normal level of thyroxine, triiodothyronine and a reduced level of the thyroid-stimulating hormone
.In the Rotterdam epidemiological study, it was shown that even levels of thyroid-stimulating hormone and thyroxine at the upper limit of the norm are associated with an increase in the risk of AF by 62-94%.
In 15-25% of cases, hyperthyroidism manifests itself in a persistent AF, which is often preceded by relapses of this tachyarrhythmia.
For elderly AF, often the only manifestation of hyperthyroidism, in contrast to the young( 35% vs 2%), therefore in all cases of this tachyarrhythmia in the elderly should evaluate the possibility of hyperthyroid origin, even in the absence of clinical signs of thyrotoxicosis. In some cases, patients with thyrotoxicosis may develop irreversible changes in the myocardium, and then the
AF becomes permanent.
Despite contradictory data, the increase of
risk of ischemic stroke in patients with thyrotoxic AF
can not be ruled out. Thromboembolism often appears in the first month of the disease.
Along with AF, hyperthyroidism can be manifested by strengthening the existing
ventricular tachyarrhythmia.
Reasons for
Toxic diffuse goiter( Graves' disease).
Toxic multinodular goiter.
Toxic adenoma.
Thyroiditis( subacute, postpartum, lymphocyte, drug).
Iodine-induced hyperthyroidism( amiodarone, contrast agents).
Hyperthyroidism caused by thyroid hormones. Pituitary adenoma.
Metastatic thyroid cancer.
Diagnosis
Clinical and laboratory signs of thyrotoxicosis are presented in the table.
Table
Diagnosis of thyrotoxicosis
Subjective manifestations
Sweating,
anxiety,
heart palpitations,
increased fatigue,
sleep disorder,
weakness of proximal muscles( if squatting, it is difficult to get up),
exercise dyspnea,
hyperdefection,diarrhea.
Objective manifestations
Tremor of the hands, tongue,
exophthalmos,
lag in the eyelids,
weight loss with preserved appetite,
hot and moist palms,
edema of the legs,
tachycardia, atrial fibrillation,
goiter( diffuse, nodular).
The choice of a dose of levothyroxine is based on maintaining a high normal level of free thyroxin or even slightly above normal. Unlike other types of hypothyroidism, you should not try to normalize the level of thyroid-stimulating hormone, as it often requires high doses of levothyroxine( ~ 250 mcg / day) with the development of hyperthyroidism.
Arrhythmias in the elderly and the elderly
Atrial fibrillation
About 70% of all AF occurs at ages 65-85 at a close frequency in men and women. Increased arrhythmia is associated with risk factors for arrhythmia, such as left ventricular dysfunction and heart failure, arterial hypertension, coronary artery disease.
AF is an independent risk factor for mortality. In persons of older age groups, a constant form of AF is much more frequent( 58-67%).
With age, the proportion of AF increases among causes of strokes and, accordingly, the need for anticoagulant therapy. It is no coincidence that the criteria for selecting CHADS2 anticoagulants include age> 75 years and closely associated age-related diseases with strategies for managing patients with AF - rhythm control with antiarrhythmic drugs and control of heart rate with medication blockade AV conduction - showed close results. In the elderly and the elderly, the presence of heart disease, the propensity for persistent
, the increased risk of side effects of drugs, in
, in most cases, prefer HR control with adequate anticoagulant therapy. For example, treatment with amiodarone in elderly patients is associated with an increase in the frequency of implantation of ECS by 2.1 times.
The increased risk of the side effects of drugs, the difficulty in choosing a dose, reduced adherence explain the fact of receiving adequate treatment in the elderly and the elderly in less than half the cases.
It is important to note that despite the increased risk of hemorrhagic
complications in elderly people, warfarin reduces mortality and significantly
is superior to aspirin as a means of preventing thromboembolic complications and should be appointed if
is available to monitor INR monthly. Moreover, the incidence of aspirin side effects is significantly higher( 33% vs 6%, p = 0.002) than in warfarin among patients older than 80 years.
When planning treatment with oral anticoagulants, one should also evaluate the incidence of falls in elderly patients.
When planning invasive treatment of AF with the help of radiofrequency catheter ablation, an increased risk of complications in the elderly and a decrease in the effectiveness of treatment should be considered.
Ventricular arrhythmias
Ventricular arrhythmias occur in the elderly and elderly enough
often, especially with cardiovascular disease and Holter monitoring. According to epidemiological studies, more than 80% of sudden cardiac deaths develop in people older than 65 years.
It is important to know that complicated ventricular extrasystoles and unstable VT in patients without heart disease do not affect the risk of coronary heart disease, sudden death and total mortality, and in asymptomatic cases of treatment is not required.
In the presence of heart disease( IHD, left ventricular dysfunction, heart failure), ventricular arrhythmias( complex extrasystoles, resistant and unstable VT), revealed in Holter monitoring, are an indicator of an increased risk of coronary events and sudden death. In this regard, active treatment of the underlying disease, including beta-blockers, is necessary. The latter in the elderly with IHD reduce the frequency of arrhythmia, sudden and general mortality. If necessary,
can be prescribed sotalol or amiodarone.
In most studies on primary prevention of sudden
death using ICD, the results were independent of age. For example, in patients after myocardial infarction with left ventricular dysfunction, a reduction in mortality after implantation of a cardioverter-defibrillator after the age of 75 was similar to that in patients less than 65 years old( -68%).
However, in a recent ICD study did not bring significant benefits to patients after 80 years.
Hospital mortality after implantation of cardioverter-defibrillators increased after 80 years, and no special randomized trials were conducted in this group.