Treatment of chronic heart failure in dogs and cats. Dilated cardiomyopathy of Great Danes

Infections caused by sensitive microorganisms: tonsillitis, pneumonia, septic endocarditis, purulent pleurisy, peritonitis, cystitis, sepsis, meningitis, osteomyelitis, urinary and biliary tract infections, wound infections, purulent infections skin, soft tissues, diphtheria, scarlet fever, erysipelas, anthrax, syphilis, gonorrhea, pulmonary actinomycosis, colpitis, ecdocervicitis, endometritis, adnexitis, salpingo-oophoritis, conjunctivitis, blepharitis, dacryocystitis.

Contraindications

The use of the drug is contraindicated in patients with hypersensitivity to beta-lactam antibiotics, bronchial asthma, hay fever, urticaria and other allergic diseases. Epilepsy is a contraindication for endolumbar administration.

Directions for use and doses

The drug is administered intramuscularly, subcutaneously, intravenously (stream and drip), endolumbarally, into the body cavity. The most common route of administration is intramuscular,

Intravenously: for infections moderate severity a single dose of the drug is usually 250,000 - 500,000 units; daily -1,000,000 - 2,000,000 units; for severe infections, up to 10,000,000 - 20,000,000 units per day are administered; with gas gangrene - up to 40,000,000 - 60,000,000 units. The daily dose for children under 1 year of age is 50,000 -100,000 units/kg, over 1 year of age - 50,000 units/kg; if necessary, the daily dose can be increased to 200,000 - 300,000 IU/kg, for lifelong indications - up to 500,000 IU/kg. The frequency of administration of the drug is 4-6 times a day. A solution of Benzylpenicillin-KMP is prepared immediately before use. For intravenous jet administration, a single dose (1,000 LLC - 2,000,000 units) of the drug is dissolved in 5 - 10 ml of sterile water for injection or 0.9% sodium chloride solution and administered slowly over 3-5 minutes. For intravenous drip administration, 2,000,000 - 5,000,000 units of antibiotic are dissolved in 100-200 ml of 0.9% sodium chloride solution or 5% glucose solution and administered at a rate of 60-80 drops per minute. The drug is administered intravenously 1-2 times a day, combined with intramuscular injections.

Intramuscularly: for moderate infections, a single dose of the drug is usually 250,000 - 500,000 units: daily - 1,000,000 - 2,000,000 units; for severe infections, up to 10,000,000 are administered - 20,000,000 units per day; with gas gangrene - up to 40,000,000 - 60,000,000 units. The daily dose for children under 1 year of age is 50,000-100,000 units/kg, over 1 year - 50,000 units/kg; if necessary, the daily dose can be increased to 200,000 units - 300,000 units/kg, for health reasons - up to 500,000 units/kg. The frequency of administration of the drug is 4-6 times a day. For intramuscular injection add 1-3 ml of sterile water for injection or 0.9% sodium chloride solution, or 0.5% novocaine solution to the contents of the bottle. The resulting solution is injected deep into the muscle in the upper outer quadrant of the buttock. Subcutaneously, Benzylpenicillin-KMP is used to inject infiltrates at a concentration of 100,000-200,000 units in 1 ml of 0.25-0.5% novocaine solution.

In the cavity (abdominal, pleural, etc.), a solution of Benzylpenicillin-KMP is administered to adults in a concentration of 10,000 - 20,000 units per 1 ml, for children - 2,000 - 5,000 units per 1 ml. Dissolve in sterile water for injection or 0.9% sodium chloride solution. The duration of treatment is 5-7 days, followed by switching to intramuscular administration.

The drug is administered endolumbarally for purulent diseases of the brain, spinal cord, meninges. Adults are prescribed at a dose of 5,000 - 10,000 units, children - 2,000 - 5,000 units,

Inject slowly - 1 ml per minute 1 time per day. The drug is diluted in sterile water for injection or in 0.9% sodium chloride solution at the rate of 1,000 units per 1 ml. Before injection, 5-10 ml of cerebrospinal fluid is removed from the spinal canal and added to the antibiotic solution in equal proportions. Injections are repeated for 2-3 days, after which they switch to intramuscular administration.

Treatment of patients with syphilis and gonorrhea is carried out according to specially developed regimens.

Depending on the form and severity of the disease, benzylpenicillin-CMP is used from 7-10 days to 2 months or more (sepsis, septic endocarditis, etc.).

Side effect

When administering the drug, it is possible allergic reactions: skin rash, urticaria, fever, chills, headache, joint pain, eoeinophilia, Quincke's edema, interstitial nephritis, impaired myocardial pumping function. IN in rare cases possible development of anaphylactic shock.

Endolumbar administration can cause neurotoxicosis (nausea, vomiting, symptoms of meningism, convulsions).

In weakened patients, newborns, and the elderly, during long-term treatment, superinfection may occur caused by drug-resistant microflora (yeast-like fungi, gram-negative microorganisms).

Overdose

Manifests toxic effect on the central nervous system (more often with endoluminal administration). Convulsions, headache, myalgia, arthralgia occur. In such cases, administration of the drug should be stopped. Treatment is symptomatic.

Interaction with other drugs

The effect of the drug is weakened by drugs that cause bacteriostasis (tetracycline). Probenecid reduces the tubular secretion of benzyl penicillin, thereby increasing the concentration of the latter in the blood plasma, and the elimination half-life increases.

Features of application

Benzylpenicillin-KMP solutions are used immediately after preparation. It is not allowed to add any other drugs to the drug solutions. The use of the drug is possible only in pathological processes caused by microorganisms sensitive to it. When pathogen resistance to the drug appears, it is replaced with other antibiotics. If there is no effect from the use of the drug 3-5 days after the start of treatment, it is necessary to switch to the use of other antibiotics or combine Benzylpenicillin-CMP with other antibiotics or synthetic chemotherapeutic agents. In this case, the possibility of increased side effects should be taken into account. Patients over 60 years of age and pregnant women are not recommended to prescribe large doses (above 10,000,000 units per day). When benzylpenicillin-KMP is dissolved in a novocaine solution, a cloudy solution may form due to the formation of novocaine salt of benzyl penicillin, which is not an obstacle to intramuscular administration of the drug. The drug does not affect the ability to drive a car.

Vladislava Konstantinovna Illarionova - Candidate of Biological Sciences, veterinary cardiologist, head of the Cardiology Department of the Biocontrol clinic

D dilated cardiomyopathy (DCM) is characterized by dilatation of the heart chambers and systole-diastolic myocardial dysfunction. This is one of the most common pathologies hearts in dogs. Theories of the occurrence of this disease are considered, including genetic, nutritional, metabolic, inflammatory, infectious, toxic, etc. One of the breeds most predisposed to this pathology is the Great Dane. The features of the course, diagnosis and treatment of the disease in this breed are analyzed.

Key words: dilated cardiomyopathy, cardiomyopathies, hereditary diseases, Great Danes, echocardiography

Abbreviations: HELL - blood pressure, APF-angiotensin-converting enzyme, WHO- World Health Organization, ICE- disseminated intravascular coagulation, DCM- dilated cardiomyopathy, DNA-deoxyribonucleic acid, IHD - ischemic disease hearts, KDOI- end-diastolic volume index, KMP- cardiomyopathy, KSOI- end-systolic volume index, MT- body weight, OSSN- Society of Heart Failure Specialists, PCR- polymerase chain reaction, RAAS- renin-angiotensin-aldosterone system, RKO- Russian Society of Cardiology, RNMOT- Russian Scientific Medical Society of Therapists, CAC- sympathoadrenal system, SNK- capillary refill rate, chronic renal failure- chronic renal failure, CHF- chronic heart failure, ECG- electrocardiogram, ACC-American College of Cardiology (American College of Cardiology), ANA- American Heart Association (American Heart Association), ESVC-European Society of Veterinary Cardiology (European Society of Veterinary Cardiology).

Classification and etiology of CMP

One of the first definitions of CMP was given by W. Bridgen in 1957 when describing rare diseases of the heart muscle - non-coronarogenic CMP. With this term he designated “myocardial diseases of unknown etiology, not associated with atherosclerosis, tuberculosis and rheumatic heart disease, characterized by the appearance of cardiomegaly of unknown origin and the development of heart failure.” CMP was subsequently divided into three main groups: dilated, hypertrophic and restrictive. To carry out nosological classification, this issue was considered by a special group of WHO experts in 1980 (Report of the WHO/ISFC Task Force, 1980). The approved definition characterized CMP as “diseases of the heart muscle of unknown or unclear etiology.”

In 1995, WHO experts gave a new definition of cardiomyopathy as a myocardial disease accompanied by its dysfunction. At the same time, the classification of CMP was approved, which distinguishes dilated, hypertrophic, restrictive, unclassifiable forms and arrhythmogenic dysplasia of the right ventricle. IN separate group included CMPs with a known etiology and pathogenesis or those that are part of systemic diseases - specific CMPs. This group included ischemic, hypertensive, inflammatory, metabolic, toxic, valvular, postpartum forms and CMP in systemic and neuromuscular diseases.

In 2006, the AHA proposed a new definition of CMP: it is a heterogeneous group of diseases of various etiologies (often genetically determined), accompanied by mechanical and/or electrical dysfunction of the myocardium and (in some cases) disproportionate hypertrophy or dilatation. Myocardial damage in CMP can be primary or secondary (with systemic disease), accompanied by the development of heart failure and ending in the sudden death of the patient. Thus, all CMP were divided into two large groups: ischemic and non-ischemic forms. The non-ischemic form, in turn, is divided into primary and secondary. The primary includes a genetic, acquired or mixed variant of development, the secondary includes all specific CMPs.

In veterinary cardiology, CMP has been considered since 1970. According to the classification, dilated, hypertrophic, restrictive, unclassified forms and arrhythmogenic dysplasia of the right ventricle are distinguished. Specific CMPs are considered within the pathologies that lead to their formation. For example, in the cardiology of dogs and cats, ischemic cardiomyopathy is practically not mentioned, since atherosclerosis in carnivorous animals is extremely rare. However, it can accompany hypercholesterolemia in hypothyroidism and diabetes. The cause of rare myocardial infarctions in dogs and cats is an increased tendency to embolism and thrombus formation against the background of such systemic pathologies as infective endocarditis, acute pancreatitis, terminal stage of chronic renal failure, DIC syndrome, autoimmune hemolytic anemia and long-term treatment with corticosteroids. Myocardial infarction can accompany a number of heart diseases and are associated with non-atherosclerotic narrowing small branches coronary arteries (arteriosclerosis).

There are no alcoholic, postpartum or hypertensive forms in dogs and cats. The toxic form is more often discussed as a complication of antitumor chemotherapy. The main drug for antitumor chemotherapy, characterized by a cardiotoxic effect, is the anthracycline antibiotic doxorubicin. It has both acute and chronic damaging effects on the heart muscle. These effects may occur when the cumulative dose exceeds 160 mg/m2. The animal’s predisposition to the occurrence of these complications plays a role in the development of the toxic effect. If there is already a hidden pathology of the myocardium, then a dose of less than 100 mg/m2 can cause damage.

The inflammatory form of CMP manifests itself as a complication of myocarditis. In people this option the development of DCM has been partially proven, since in 35% of patients with DCM the viral genome is detected in the myocardium (via PCR). In addition, in the majority of patients with myocarditis resulting in DCM, enterovirus envelope protein is detected in the myocardial tissue using immunohistochemistry methods. This confirms the role viral infection in the pathogenesis of DCM. But this connection has not been fully proven, since similar changes are observed in the myocardium of patients with coronary artery disease. In dogs, the relationship between myocarditis and DCM is considered poorly proven. The most common cause of infectious myocarditis in dogs is parvovirus. Cases of mass death of puppies aged 4...8 months as a result of parvovirus myocarditis were described 20...30 years ago. Now this phenomenon is rare. Canine distemper virus can also infect the myocardium, but to a lesser extent compared to parvovirus. Even more rare is the protozoan and bacterial cause development of myocarditis.

Metabolic diseases of the myocardium include alimentary cardiomyopathy, which develops with a lack or disturbances in the metabolism of certain nutrients. Thus, L-carnitine- and taurine-dependent forms of CMP have been described.

L-carnitine is an amino acid involved in energy metabolism. L-carnitine deficiency has been identified in breeds such as the Boxer, Doberman Pinscher, Great Dane, Irish Wolfhound, Newfoundland and Cocker Spaniel. Dogs of all breeds are deficient in L-carnitine when fed a predominantly vegetarian diet. Complexity clinical definition L-carnitine deficiency is that the concentration of this compound in plasma does not reflect its deficiency in the myocardium. To confirm the carnitine-dependent form of CMP, it is necessary to perform a myocardial biopsy to determine the carnitine concentration.

Taurine is a sulfonic acid involved in lipid metabolism. A lack of taurine in the blood has been described in cocker spaniels with DCM. Replenishment of taurine in such dogs leads to recovery. Low level taurine is determined in dogs with a vegetarian diet and dietary nutrition lamb-rice Cats are very sensitive to taurine deficiency, since they practically do not synthesize it. A diet low in taurine can lead to the development of DCM in cats.

Thus, primary CMP is a diagnosis of exclusion. Primary CMP in animals includes five forms: dilated, hypertrophic, restrictive, unclassified, and arrhythmogenic right ventricular dysplasia. In dogs, DCM and arrhythmogenic dysplasia of the right ventricle are the most common. Canine DCM is called a primary disease of the heart muscle, characterized by ventricular dilatation (eccentric hypertrophy) and myocardial systolic dysfunction. With the development of echocardiography, the diagnostic criteria for DCM became a decrease in global myocardial contractility with a significant increase in the size of the cavities of the left

ventricle and left atrium in the absence of other cardiac anomalies. Definition of specified diagnostic criteria to identify DCM was confirmed in 98% of cases during pathological examination.

Etiology of primary CMP for a long time remained unknown, so they were classified as idiopathic diseases (that is, with an unknown cause). Work in the field of molecular genetics has shown the decisive role of hereditary predisposition in the development of primary CMP. Genetic diseases conditionally divided into two large groups: monogenic and polygenic.

Monogenic are those caused by a mutation (change in the nucleotide sequence) in one gene. Due to this, one protein changes. Inherited heart diseases are caused by mutations in genes encoding three main classes of myocardial proteins: structural, regulatory, and those involved in the generation and conduction of excitation. Primary CMPs are associated with mutations in structural protein genes. DCM develops due to changes in nuclear envelope proteins, contractile proteins, cytoskeletal proteins, tight gap junction proteins and ion channels. Despite the apparent simplicity of monogenic diseases, there are features that determine their bilateral heterogeneity: the same clinical phenotype (disease manifestation) can be caused by different mutations, and vice versa, the same mutation can lead to the development of different clinical phenotypes.

Polygenic diseases arise from the combination of several unfavorable DNA changes (polymorphisms) that only partially affect the function of the encoded proteins. Every polymorphism in small degree changes the functions of the heart muscle, but the combination of such molecular defects can lead to a weakening of the compensatory reserves of the system, especially in combination with other unfavorable factors (for example, the administration of cardiotoxic drugs).

Monogenic diseases can be inherited in a dominant or recessive manner and have five main modes of inheritance:

1. autosomal dominant (one mutant allele is enough to develop the phenotype);
2. autosomal recessive (the disease appears only in homozygous carriers);
3. X-linked recessive ( mutant gene located on the X chromosome and appears in males or females in a homozygous state);
4. X-linked dominant (the mutant gene is located on the X chromosome and also appears in the heterozygous state);
5. mitochondrial (the disease is transmitted by females, since mitochondria are found only in oocytes).

Clinical signs of the disease may appear to varying degrees in patients with the same genetic mutation. This is due to the different expressiveness of the disease, that is, the degree of manifestation of the pathology. Penetrance, that is, the frequency of manifestation of a trait in a certain genotype, also plays a role in the nature of the disease’s manifestation. It is known that penetrance depends on time, since over the years, damage caused by a genetic defect accumulates in the body, and the risk of phenotypic manifestation of the disease increases. Gender can also influence the degree of manifestation of a pathological symptom.

CMP in humans often has a family history, that is, medical analysis of the family tree reveals the hereditary nature of the disease. But only a molecular biological study can confirm the genetic nature of the pathology. It should be taken into account that for this type of diagnosis you need to know the combination of unfavorable variants of several different genes that affect the manifestation and course of the disease. There is still little such data applicable for clinical DNA diagnostics. Therefore very important acquire joint veterinary and medical research aimed at studying the genome of dogs, since different breeds are unique family groups with genetically fixed characteristics and predisposition to certain diseases. Genes responsible for hereditary diseases are easier to identify in purebred dogs, since in such groups of animals inbreeding is carried out, which increases the frequency of genes responsible for a particular pathology. In 2005, work on deciphering the dog's genome was completed. It was revealed that 39 pairs of chromosomes consist of 2.4 billion nucleotides. The DNA samples were obtained from a Boxer dog, which had a high inbreeding rate, making the genome sequencing process easier. But the data obtained on the sequence of nucleotides in a DNA molecule do not provide a complete understanding of their function, since the main part of the genome is not genes, but non-coding regions and tandem turns. This is part of the so-called “junk” DNA, that is, with an unknown function. Deciphering the information encoded in DNA is a painstaking process and involves great technical and ethical difficulties. Therefore, the idea of ​​​​working together with the genome of dogs and humans to determine the genetic basis of similar diseases quickly found supporters. Started in 2007 international project LUPA PROJECT (LUPA project, WP2 Cardiovascular disorders. //www. eurolupa.org), the goal of which was to identify gene mutations in dogs with pathologies common to humans. Dogs of the Doberman Pinscher, Great Dane, Irish Wolfhound, New Foundland and Boxer breeds were selected for the DCM study. The project is not yet completed, but has been identified a whole series DNA regions that need further study.

Characteristics of DCM

Classification. DCM is accompanied by the development of heart failure. To systematize the nature of changes at various stages of the pathological process, various classifications of CHF are introduced into cardiological practice. In medical and veterinary cardiology, there are several classifications of heart failure, each of which has its own pros and cons. At the moment, in veterinary cardiology, the modified AHA/ACC classification is most often used, according to which heart failure is divided into 4 stages, designated by the letters: A, B, C and D.

Stage A: animals without structural changes in the heart, but at risk of developing cardiac pathology (for example, Maine Coon cats, British Shorthairs, Boxer dogs, Doberman Pinscher, Great Dane, etc.).

Stage B: animals with heart pathology, but without clinical manifestations. This stage is divided into two substages:

• substage B1 - animals with minimal signs of structural and geometric changes (remodeling) of the left ventricle;
• substage B2 - animals with more pronounced signs of cardiac remodeling.

Stage C: animals with structural changes in the heart and signs of heart failure.

Stage D: animals with clinical signs of heart failure refractory to standard therapy.

Clinical signs and pathogenesis. Manifestations of the disease may vary by breed. Great Dane DCM is characterized by the rapid occurrence of rhythm disturbances in the form of atrial fibrillation ( atrial fibrillation), which sometimes serves as the first pathological

a sign that is already followed by structural changes in the heart. The disease has a rather long asymptomatic stage, so it is rarely diagnosed at the initial stage. The development of the disease leads to the formation of CHF, which is a syndrome in which the structure and function of the heart is impaired. In this case, the heart is not able to satisfy the body's oxygen needs at normal filling pressure. When the pumping function of the heart decreases, compensatory mechanisms are mobilized in the body, which allows maintaining cardiac output at a sufficient level. Main role SAS, RAAS and myocardial natriuretic peptides play in this process. The synchronous interaction of these systems allows the heart to be in a state of adaptation to the emerging pathological conditions. However, the activation of neurohormones plays a dual role. Short-term mobilization of protective forces allows you to compensate for lost functions. Permanent hyperproduction of neurohormones leads to pathological changes in vital organs and ends in a “failure” of adaptation. From this moment on, a period of decompensation begins with the appearance of characteristic clinical signs.

The clinical picture often develops quickly - within a few days. General weakness, exercise intolerance, lethargy, tachypnea, shortness of breath and cough appear. As the disease progresses, anorexia, decreased body weight, ascites, hydrothorax and fainting occur. Clinical signs may be expressed to varying degrees and appear at different times. Great Danes with isolated atrial fibrillation may remain asymptomatic for a long time. However, an increase in heart rate with this arrhythmia provokes over time the development of the tachycardic form of DCM.

Histological and pathological features. DCM in dogs is divided into two histological types. The first type is degenerative with fatty infiltration and the second type is with the formation of weakened and wavy myofibrils. DCM of Great Danes is characterized by the second histological type. It consists of the formation of thin, weakened and wavy myofibrils, swelling of the intercellular space and the development of minimal subendocardial myocardial fibrosis.

DCM of Great Danes is accompanied by an increase in myocardial mass due to eccentric hypertrophy. Predominant dilatation of the left or all four chambers of the heart, thinning of the walls, smoothness of the papillary muscles, and pale, soft myocardium are revealed. The fibrous rings of the atrioventricular valves are stretched. Minimal myocardial fibrosis is detected. The coronary arteries do not undergo changes.

Physical examination. On examination, pale mucous membranes and increased SNK are revealed as a result of decreased cardiac output with increased sympathetic tone and peripheral vasoconstriction. Hypothermia or cold extremities are often noted. The apex beat of the heart is diffuse, reduced in strength. Pulse on femoral arteries frequent with reduced filling and tension. With concomitant atrial fibrillation, a pulse deficit is determined, in which not every heartbeat accompanied by a pulse wave. With severe myocardial dysfunction, an alternating pulse occurs with different amplitudes of pulse waves. Signs of left ventricular failure are tachypnea (more than 30 respiratory movements at rest), expiratory shortness of breath. A dog with this type of breathing breathes frequently using the abdominal muscles as it exhales. When right ventricular failure occurs, swelling of the jugular veins or hepatojugular reflux, ascites, hydrothorax, and hydropericardium appear. When auscultating the lungs, dry and moist rales and bronchial breathing are heard. On auscultation of the heart, the sounds are slightly muffled, a third heart sound and a weak murmur of relative atrioventricular valve insufficiency (usually not exceeding 3/6 volume*) may occur. With severe heart failure, sinus tachycardia develops with disappearance sinus arrhythmia. With DCM, a wide variety of rhythm and conduction disturbances can occur. In Great Danes, atrial fibrillation and ventricular arrhythmias are the most commonly reported.

Laboratory tests. At biochemical analysis blood most often reveal an increase in urea and creatinine, which reflects prerenal azotemia, an increase in the activity of liver enzymes as a result of portal hypertension. With severe heart failure, hypoproteinemia, hyperkalemia and hyponatremia appear. Assessment of natriuretic hormone levels provides valuable information about the presence and severity of heart failure. An increase in the content of NT-pro BNP (terminal fragment of brain natriuretic peptide) serves as a reliable marker of CHF, as it provides information on the severity of heart failure, helps to conduct screening studies in populations of predisposed animals, and has prognostic value. In addition, the high level of NT-pro BNP allows you to deliver differential diagnosis with accompanying respiratory pathology. Natriuretic hormones are species-specific, that is, analyzed using medical test systems

is not possible because it is necessary to study the canine peptide. Veterinary test systems existing on the world market are not yet available in Russia. IN given time The development of domestic methods for studying the level of NT-pro BNP in dogs is underway. Chest X-ray. This method has expert value for determining signs of venous stasis, pulmonary edema and pleural effusion. With venous pulmonary stagnation, the expansion of the lobar pulmonary vein to the cranial lobe of the lung and the strengthening of the vascular pattern of the lungs due to the pulmonary veins are determined. With interstitial pulmonary edema, the interstitial pattern of the lungs intensifies; with alveolar edema, “cotton wool” shading appears in the roots and in the caudal lobes of the lungs (often with a picture of air bronchograms). Less commonly, cardiogenic alveolar edema spreads to other parts of the lungs. With the development of right-sided heart failure,

In addition, dilation of the caudal vena cava, signs of hydrothorax, ascites and hepatomegaly are noted. Detection of cardiomegaly indicates significant changes in the heart. As a rule, an increase in the size of the left chambers of the heart is detected first, and as the disease progresses, the heart becomes rounded shape due to dilatation of all chambers.

Electrocardiography. Electrocardiography reveals signs of left ventricular hypertrophy - high R waves and widened QRS complexes, left atrium - widened R waves. In case of hypertrophy or hemodynamic overload

of the right ventricle, deep S waves are recorded in the precordial leads (V4 and V2) and right-sided displacement electrical axis hearts; with hypertrophy of the right atrium, high, pointed P waves. With subendocardial myocardial ischemia, depression of the S–T segment occurs. When pleural and/or pericardial effusion appears, the amplitude of the electrocardiogram waves decreases. Conduction disorders may develop (at various levels of the conduction system). The most characteristic rhythm disorder in Great Danes is atrial fibrillation, which is characterized by an irregular rhythm with the appearance of low-amplitude f waves instead of P waves. At severe stages of the disease, ventricular extrasystoles which can develop into ventricular tachycardia.

24-hour Holter ECG monitoring. Holter ECG monitoring is a non-invasive method of recording ECG throughout the day. An ECG is recorded in several chest leads, which are attached to the skin using Velcro electrodes. For monitoring, a portable recorder is used, which continuously records the ECG. After this, computer processing and analysis of the obtained data is carried out. This study indispensable for identifying episodes of rhythm and conduction disturbances. It is used when animals are suspected of having threatening arrhythmias (especially in risk-group breeds such as Doberman Pinscher, Boxer and Great Dane), if the animal has episodes of loss of consciousness, to determine indications for antiarrhythmic therapy and assess its effectiveness.

Tonometry. Blood pressure in dogs is measured by direct and indirect methods. The direct method is invasive, which gives the most accurate results, but involves catheterization of the artery. It is used in the operating room. Indirect methods include oscillometry and the Doppler method. The oscillometric method is based on electronic processing of the vibration of the sound wave created in the cuff by the pulse wave. When air is deflated from the cuff, systolic, diastolic and mean blood pressure are automatically determined. Doppler tonometry is based on a change in the frequency of a sound wave when reflected from a moving object, that is, blood. The device's sensor simultaneously emits and receives ultraviolet sound waves with a frequency of 8...10 MHz. The device converts the signal received from the artery into audible sound waves when the blood pressure and pressure in the cuff coincide. This method gives accurate results of systolic blood pressure, but does not accurately measure diastolic and mean blood pressure. Tonometry is performed in dogs with DCM to diagnose hyper- or hypotension during the initial study and during treatment.

Echocardiography. Echocardiography is used to evaluate the structure and function of the heart. This is an expert method for diagnosing DCM and excluding other pathologies that lead to changes in the geometry of the heart cavities (for example, birth defects hearts). The ESVC proposed a scoring system for making the echocardiographic diagnosis of DCM. This system is indicative, so care must be taken in its use when studying certain breeds. To make a diagnosis of DCM, you need to score 6 points. Each major criterion is worth 3 points, each small criterion is worth 1 point.

Large criteria include:

1. an increase in the size of the left ventricle (systolic and diastolic sizes exceed the 95% confidence interval for breed or BW);
2. increase in left ventricular sphericity (sphericity index< 1,65)
3. decrease in shortening fraction value< 20…25 % (в зависимости от породных особенностей);
4. reduction in ejection fraction< 40 % (по методу Simpson).

Small criteria include:

1. the presence of arrhythmia in boxers and Doberman pinschers;
2. atrial fibrillation;
3. increase in septal separation value from point E (EPSS) > 7.7 mm;
4. the value of the shortening fraction is more than 20...25%, but less than 30% (depending on the breed characteristics);
5. an increase in the size of the left or both atria.

For echocardiographic diagnosis of DCM of Great Danes, there are separate breed criteria:

1. an increase in the size of the left ventricle by more than 60 mm in diastole and more than 49 mm in systole;
2. DPI exceeds 100 ml/m2;
3. KSOI exceeds 30 ml/m2;
4. increase in septal separation value from point E (EPSS) > 12 mm;
5. change in diastolic filling (E/A ratio less than 1).

In case of insufficient points for making a confident diagnosis of DCM, dynamic observation is carried out with control echocardiographic studies after 3...6 months.

Treatment. Treatment of DCM depends on the stage of CHF and the presence of various rhythm and conduction disorders. The national recommendations of OSHF, RKO, RNMOT for the diagnosis and treatment of CHF (in the fourth revision, 2013) formulate 6 tasks to which the doctor’s efforts should be directed: preventing the development of symptoms of CHF; elimination of symptoms of CHF; slowing the progression of the disease by protecting the heart and other target organs (brain, kidneys, blood vessels); improving the patient's quality of life; reduction in the number of hospitalizations; improved prognosis.

All of these tasks can be extrapolated to veterinary cardiology. There are several ways to achieve your goals:

√ diet, the purpose of which is to reduce sodium intake, control weight (extreme conditions - obesity and cachexia can be an additional aggravating factor in the course of the disease);

√ mode physical activity. Moderate physical activity is recommended for DCM, with the exception of cases of acute decompensation of CHF with indications for hospitalization and life-threatening arrhythmias. Physical activity accompanied by high emotional activity, as well as long trips, are not recommended.

√ owner’s interest in treatment and good contact with the attending physician. It is very important for the doctor to convince the animal owner of the need to treat and monitor the condition of the sick animal, which implies constant contact with the attending physician and conducting routine examinations and studies;

√ drug therapy. The principles of drug treatment of DCM are based on a complex effect on all parts of the pathogenesis of CHF, including blockade of neurohumoral mechanisms of the development of heart failure, inotropic support, control of fluid accumulation and rhythm and conduction disturbances. At the same time, the medicinal effect is based on evidence-based medicine, that is, drugs that have proven their effectiveness and safety in large studies are recommended for treatment. Only in the absence of such studies are small studies and expert opinions taken into account. In medicine, there are three degrees of evidence of effectiveness therapeutic effects: A, B and C.

Grade A implies absolutely proven effect of the drug in at least two large controlled studies. Grade B lower, suggests the participation of the drug in one large study and the receipt of conflicting results, which requires additional research. Lowest with Level of evidence C- this is the participation of the drug in small studies with empirical results, or confirmation by expert opinion.

The main classes of drugs for the treatment of DCM: ACE inhibitors, mineralcorticoid receptor antagonists, diuretics, positive inotropes, beta blockers and antiarrhythmics.

ACE inhibitors They are considered first-line drugs in the treatment of CHF. This class of drugs is involved in the deactivation of stress hormonal systems - the RAAS and SAS, which leads to breaking the vicious circle of CHF formation. Several drugs of this class are used in veterinary cardiology. One of the most studied is benazepril (Fortecor).

Mineralcorticoid receptor antagonists reduce the effect of secondary aldosteronism in CHF, which stimulates hormonal imbalance with water and sodium retention and potassium loss and the development of myocardial fibrosis. Main representative of this class drugs is spironolvactone (veroshpiron), which has proven effective in the treatment of CHF in dogs.

Diuretics- essential medications for the development of signs of fluid retention in the body. For a long time he has been the leader in the treatment of CHF in medical and veterinary cardiology. loop diuretic furosemide IN lately A more effective and safe diuretic of the same class, torasemide, occupies a stable position in the treatment of humans and animals. Paradoxically, there is no sufficient evidence base for the use of diuretics for the treatment of edema syndrome, since these studies are not possible for reasons of patient safety.

Positive inotropes enhance myocardial contractility. This class includes several groups. In veterinary cardiology, cardiac glycosides, for example, digoxin, and calcium sensitizers - pimobendan (vetmedin) are used. The use of digoxin is indicated for the treatment of atrial fibrillation. Pimobendan, which also has vasodilating properties, has taken a strong position in veterinary cardiology due to its proven effectiveness and safety.

ᵦ - adrenergic blockers are complex neurohormonal modulators that block hyperactivation of the SAS. In medical cardiology, four drugs of this class (bisoprolol, delayed release metoprolol succinate, carvedilol and nebivolol) have proven their effectiveness and safety. Despite attempts to extrapolate the findings of these studies to veterinary cardiology, a sufficient evidence base for the use of these drugs has not been obtained.

B i b l i o g r a p h i a

1. Ames, M.K. Effect of furosemide and high-dosage pimobendan administration on the reninangiotensin-aldosterone system in dogs / M.K. Ames, C.E. Atkins, A.C. Lantis, S.R. Werre // Am J Vet Res. - 2013 Aug. - V. 74. -N. 8. - R. 1084–90.
2. Dukes-McEwan, J. Proposed guidelines for the diagnosis of canine idiopathic dilated cardiomyopathy. ESVC Taskforce for Canine Dilated Cardiomyopathy / J. Dukes-McEwan, M. Borgarelli, A. Tidholm, A.C. Vollmar, J. Haggstrom // J Vet Cardiol. - 2003 Nov. - V. 5. - N. 2.-R. 7–19.
3. Esposito, C.T. Spironolactone improves the arrhythmogenic substrate in heart failure by preventing ventricular electrical activation delays associated with myocardial interstitial fibrosis and inflammation / C.T. Esposito, S. Varahan, D. Jeyaraj, Y. Lu, B. Stambler // J Cardiovasc Electrophysiol. - 2013 Jul. - V. 24. - N. 7. - R. 806–812.
4. Oyama, M.A. Decreased triadin and increased calstabin2 expression in Great Danes with dilated cardiomyopathy / M.A. Oyama, S.V. Chittur, C.A. Reynolds // J Vet Intern Med. - 2009 Sep-Oct. - V. 23. - N. 5. - R. 1014–1019.
5. Higgins, R. Canine distemper virus-associated cardiac necrosis in the dog / S. Krakowka, A.E. Metzler, A. Koestner // Veterinary Pathology. - 1981. - N. 18. - P. 472–486.
6. Haggstrom, J. Longitudinal Analysis of Quality of Life, Clinical, Radiographic, Echocardiographic, and Laboratory Variables in Dogs with Myxomatous Mitral Valve Disease Receiving Pimobendan or Benazepril: The QUEST Study / J. Haggstrom, A. Boswood et al. // J Vet Intern Med. - 2013 Sep. - N. 6.
7. Kittleson, M.D. Efficacy of spironolactone on survival in dogs with naturally occurring mitral regurgitation caused by myxomatous mitral valve disease / M.D. Kittleson, J.D. Bonagura // J Vet Intern Med. - 2010 Nov-Dec. - V. 24. -N. 6. - P. 1245–1246.
8. Lefebvre, H.P. Safety of spironolactone in dogs with chronic heart failure because of degenerative valvular disease: a population-based, longitudinal study / H.P. Lefebvre, E. Ollivier, C.E. Atkins, B. Combes, D. Concordet, V. Kaltsatos, L. Baduel // J Vet Intern Med. - 2013 Sep-Oct. - V. 27. - N. 5. - P. 1083–1091.
9. Knee, B.W. Evidence for the role of myocarditis in the pathophysiology of dilated cardiomyopathy. In: Proceedings of the 11th ACVIM Forum/ B.W. Knee // Washington DC, 1993 - P. 565–567.
10. Liu, L. Effect of benazepril on atrial cytoskeleton remodeling in the canine atrial fibrillation models / L. Liu, X. Qu, et al. //

SUMMARY

V.K. Illarionova
Veterinary Clinic "Biocontrol" (Moscow)
Dilated Cardiomyopathy in Great Dane Dogs. Dilated cardiomyopathy (DCM), characterized by chamber dilatation and myocardial systolic and diastolic dysfunction, is one of the most common heart diseases in dogs. Several theories genetically concerning, nutritional, metabolic, inflammatory, infectious, or drug or toxin induced myocardial disease have been discussed. Dilated cardiomyopathy (DCM) is a common cardiac disease of Great Dane dogs. The disease is characterized by progressive loss of myocardial systolic function, eccentric dilation, atrial fibrillation, and congestive heart failure. DCM carries a poor prognosis in dogs. The treatment of dogs with congestive heart failure caused by DCM include several components.

General information

The drug is a sterile liquid dark brown. Precipitation is allowed.

Compound

1.0 cm3 of the drug contains 20.0 mg of iron, 4.5 mg of iodine, 1.0 mg of selenium, 2.0 mg of zinc, 0.08 mg of manganese, 0.040 mg of cobalt.

Indications for use

The drug is used to prevent diseases in cattle and pigs caused by a deficiency of its constituent bioelements; treatment of calves suffering from enzootic goiter, iron deficiency anemia, white muscle disease, toxic liver dystrophy; to improve the reproductive function of cows and sows, as well as to prevent birth and postpartum pathology; to increase the viability of newborn young animals and for the morphofunctional activation of its endocrine glands, including the thyroid gland.

Procedure for using the drug

The drug is administered to cattle subcutaneously or intramuscularly: heifers and cows once 20-55 days before calving at a dose of 15.0-20.0 cm³ per animal, for calves the therapeutic dose is 1.5 cm3 per 10 kg of animal weight (but not more than 10.0 cm3 per head). The drug is administered to pigs intramuscularly: for main sows the drug is prescribed 10-20 days before farrowing in a dose of 2.0-3.0 cm³ on the stomach, and for replacement gilts 1.0-1.5 cm³ per injection 10-14 days before the expected insemination . For mature pigs, the dose of the drug should not exceed 3.5 cm³. The drug is recommended for piglets at a dose of 0.5 cm³. If additional treatment of animals is necessary, CMP is used in the same doses, but not earlier than 15 days after the first administration of the drug.

Pharmacological properties

The pharmacological properties of the drug are due to complex impact components included in its composition. Iron in the body of animals is associated primarily with proteins, which transport, bind, reserve oxygen and play an important role in the processes of tissue respiration. Affects growth and development, the state of erythropoiesis, metabolism, resistance to diseases and adverse environmental factors. Iodine is an essential component of thyroid hormones, which regulate the level of basal metabolism, thermoregulation, growth energy, and the activity of the central nervous system, cardiovascular system, gastrointestinal tract, hematopoiesis and immunity. Zinc affects the activity of many farmers and hormones that regulate growth and development, basal metabolism, the function of the gonads, adrenal glands and thymus, the condition of the skin and the antioxidant and immune status of the animal body. Selenium is part of a number of specific proteins in the body that regulate the permeability of cell membranes, ensure the motility and viability of germ cells, and protect lipids cellular structures from overoxidation, increase the activity of immunocompetent cells, and also promotes the metabolism of many vitamins and the normal functioning of the thyroid gland. Methionine is necessary for normal height and development of young animals, ensuring nitrogen metabolism in adult animals, synthesis of choline, creatine, adrenaline, other biologically active compounds, functioning of muscles, liver, kidneys, pancreas, as well as neutralization of toxins. Manganese is part of the enzymes pyruvate carboxylase and ornithinase, is necessary for the synthesis of glycans of cartilage tissue, red blood cells and the formation of hemoglobin, promotes hematopoiesis, the absorption of fat and protein, the synthesis of vitamin C in the body, affects the action of vitamins B, E, C and minerals(iron, calcium, phosphorus). In interaction with copper and cobalt, it normalizes the processes of fertilization and reproduction. Cobalt stimulates erythropoiesis, improves the use of iron in hematopoiesis, is necessary for the synthesis of hemoglobin, the formation of vitamin B12, and promotes better absorption of vitamins A, E and C by the body. Together with iodine, it enhances the synthesis and accumulation of vitamin B12 in the body. With a lack of cobalt, the absorption of calcium and phosphorus decreases, anemia develops, and the growth of young animals is delayed.

Side effects

The veterinary drug CMP does not cause complications in animals and side effects. A day before mass treatments of livestock, it is necessary to test tolerance on 3-5 animals by administering the drug in recommended doses. If there are no adverse reactions, the drug is administered to the remaining animals. Contraindications A contraindication to the use of the drug is the treatment of animals within the last 15 days with preparations containing selenium, iodine, and cobalt. Meat, after administering the drug to animals, can be used for food after 3, and liver and kidneys - 7 days, milk - without restrictions. In case of forced slaughter earlier than the specified dates, the meat is used to feed carnivores, and the internal organs are disposed of.

Package

The drug is produced in glass bottles of 100, 200 and 400 cm3.

Shelf life and storage conditions

Store in a place protected from light at a temperature from + 5 to +25 ° C. Shelf life is 2 years from the date of manufacture, subject to storage and transportation rules.

Description:

Instructions for use of the veterinary drug "KMP"
1. General information

1.1. KMP (KMR)
1.2. CMP is a complex compound of iron, iodine, magnesium, selenium and methionine. I cm of the drug contains, mg: Fe-15.0; J- 6.7; Mg -6.0; Se - 0.34.
1.3. The drug is a dark brown liquid, the presence of sediment is allowed.
1.4. KMP are produced in 100, 200, 250 and 400 cm in glass bottles. Store according to list B in a place protected from light at a temperature from +2 to +25°C. Shelf life: 2 years.
2. Pharmacological properties

2.1. CMP activates hematopoietic processes, redox and enzymatic reactions of the body, normalizes metabolism, replenishing the deficiency of iron, iodine, magnesium and selenium, increases the reproductive capacity of animals, as well as their growth energy and resistance to diseases. The drug is excreted from the body primarily through urine.
H. Procedure for using the drug

3.1. CMP is used for the prevention of diseases caused by deficiency of iodine, selenium, magnesium, iron, treatment of calves and piglets with enzootic goiter, white muscle disease, toxic liver dystrophy, iron deficiency anemia, hypomagpyemia, as well as to increase the nonspecific resistance of the body of young animals, reproductive abilities of females, prevention of postpartum diseases, treatment and prevention of subclinical mastitis in cows.
3.2. The drug is administered to animals subcutaneously or intramuscularly: heifers and cows once a day lactation period and 25-45 days before calving at a dose of 15-20 cm", for calves the therapeutic dose is 2.5 cm" per 10 kg of live weight (but not more than 10 cm per head), prophylactic - 1.5 cm per 10 kg of live weight masses; For main sows, KMP is prescribed 8-12 days before weaning of piglets and 20-25 days before farrowing at a dose of 10-12 cm per injection, and for replacement gilts - 7-14 days before the expected insemination (covering) and 20-25 days before farrowing in a dose of 8-10 cm; in order to prevent anemia, the drug is injected into suckling piglets twice - on days 3-5 and 10-15 of life at the rate of 1.5 cm7 kg of live weight. For older young animals, the drug is prescribed at the rate of. 0.5 cm" per 1 kg of live weight (but not more than 5 cm per head). If necessary, additional treatment of animals. CMP is administered in the same doses, but not earlier than 10 days after the first prescription of the drug.
3.3. In recommended doses, CMP does not cause complications or side effects in animals. However, a day before mass treatments of livestock, it is necessary to test tolerance on 5-10 animals.
3.4. A contraindication to the use of the drug is the treatment of animals within the last 10 days with preparations containing selenium, iron, iodine.
3.5. After using the drug on animals, meat can be used for food after 3 days, liver and kidneys - 7 days, milk - without restriction.

4. Personal prevention measures

4.1. When working with the drug, generally accepted personal hygiene measures and safety regulations should be observed.

10 pcs. - contour cell packaging (4) - cardboard packs.

Pharmacological action

Antibiotic wide range actions. The mechanism of action is associated with a violation of the synthesis of microbial proteins. Has a bacteriostatic effect. Active against gram-positive bacteria: Staphylococcus spp., Streptococcus spp.; gram-negative bacteria: Neisseria gonorrhoeae, Neisseria meningitidis, Escherichia coli, Haemophilus influenzae, Salmonella spp., Shigella spp., Klebsiella spp., Serratia spp., Yersinia spp., Proteus spp., Rickettsia spp.; also active against Spirochaetaceae and some large viruses.

Chloramphenicol is active against strains resistant to penicillin and sulfonamides.

Resistance of microorganisms to chloramphenicol develops relatively slowly.

Pharmacokinetics

After oral administration, it is quickly and completely absorbed from the gastrointestinal tract. Bioavailability is 80%. Quickly distributed in the body. Protein binding is 50-60%. Metabolized in the liver. T1/2 is 1.5-3.5 hours. It is excreted in the urine, small amounts in feces and bile.

Indications

For oral administration: infectious and inflammatory diseases caused by microorganisms sensitive to chloramphenicol, including: paratyphoid fever, dysentery, brucellosis, tularemia, whooping cough, typhus and other rickettsioses; trachoma, pneumonia, meningitis, sepsis, osteomyelitis.

For external use: purulent skin lesions, boils that do not heal for a long time, second and third degree burns, cracked nipples in nursing women.

For local use in ophthalmology: inflammatory eye diseases.

Contraindications

Blood diseases, severe liver dysfunction, deficiency of the enzyme glucose-6-phosphate dehydrogenase, skin diseases (psoriasis, eczema, fungal diseases); pregnancy, lactation, children up to 4 weeks of age (newborns), hypersensitivity to chloramphenicol, thiamphenicol, azidamphenicol.

Dosage

Individual. When taken orally, the dose for adults is 500 mg 3-4 times a day. Single doses for children under 3 years old - 15 mg/kg, 3-8 years old - 150-200 mg; over 8 years old - 200-400 mg; frequency of use - 3-4 times/day. The course of treatment is 7-10 days.

For external use, apply to gauze pads or directly to the affected area. Apply a regular bandage on top, possibly with parchment or compress paper. Dressings are performed depending on the indications after 1-3 days, sometimes after 4-5 days.

Used locally in ophthalmology as part of combination drugs in accordance with indications.

Side effects

From the hematopoietic system: thrombocytopenia, leukopenia, agranulocytosis, aplastic anemia.

From the outside digestive system: nausea, vomiting, diarrhea, flatulence.

From the central nervous system and peripheral nervous system: peripheral neuritis, neuritis optic nerve, headache, depression, confusion, delirium, visual and auditory hallucinations.

Allergic reactions: skin rash, urticaria, angioedema.

Local reactions: irritating effect (for external or local use).

Drug interactions

With the simultaneous use of chloramphenicol with oral hypoglycemic drugs, an increase in the hypoglycemic effect is observed due to the suppression of the metabolism of these drugs in the liver and an increase in their concentration in the blood plasma.

When used simultaneously with drugs that inhibit bone marrow hematopoiesis, there is an increased inhibitory effect on the bone marrow.

When used simultaneously with clindamycin, lincomycin, a mutual weakening of the effect is observed due to the fact that chloramphenicol can displace these drugs from the bound state or prevent their binding to the 50S subunit of bacterial ribosomes.

When used simultaneously with penicillins, chloramphenicol counteracts the bactericidal effect of penicillin.

Chloramphenicol suppresses the cytochrome P450 enzyme system, therefore, when used simultaneously with phenytoin, warfarin, there is a weakening of the metabolism of these drugs, a slower elimination and an increase in their concentration in the blood plasma.

Special instructions

Use with caution in patients who have previously received treatment with cytotoxic drugs or radiation therapy.

At simultaneous administration alcohol, a disulfiram-like reaction may develop (skin hyperemia, tachycardia, nausea, vomiting, reflex cough, convulsions).

During treatment, systematic monitoring of peripheral blood patterns is necessary.

Pregnancy and lactation

Chloramphenicol is contraindicated for use during pregnancy and lactation (breastfeeding).

Use in childhood

Chloramphenicol is not used in newborns, because the development of “gray syndrome” is possible (flatulence, nausea, hypothermia, gray-blue skin color, progressive cyanosis, dyspnea, cardiovascular failure).

For liver dysfunction

Contraindicated in cases of severe liver dysfunction.