- •Ministry of Public Health of Ukraine
- •Basic Symptoms and Syndromes in Diseases of Cardiovascular System.
- •Syndrome of cardiovascular failure
- •Etiology
- •Classification of heart failure
- •Classification of heart failure according n.D. Strazhesko and V.H. Vasilenko
- •Classification of heart failure according to New York Heart Association New York Heart Association Functional Classification (nyha)
- •Clinical features
- •Additional methods of examination
- •Acute heart failure Acute left ventricular failure
- •Cardiac asthma
- •Pulmonary edema
- •Additional methods of examination
- •Acute left atrial heart failure
- •Acute right ventricular heart failure
- •Etiology
- •Clinical features
- •Additional methods of examination
- •Chronic heart failure Chronic left ventricular heart failure
- •Etiology
- •Clinical features
- •Additional methods of examination
- •Chronic left atrial heart failure
- •Chronic right ventricular heart failure Etiology
- •Clinical features
- •Additional methods of examination
- •Syndrome of vascular failure
- •Syndrome of a syncope
- •Clinical features
- •Syndrome of collapse
- •Etiology
- •Clinical features
- •Syndrome of shock
- •Classification according to etiology
- •Clinical features
- •Additional methods of examination
- •Literature
- •Acute rheumatic fever
- •Etiology
- •Pathogenesis
- •Classification
- •The Jones Criteria for Rheumatic Fever, Updated 1992
- •Clinical features
- •Additional methods of examination
- •Literature
- •Contents heart valvular diseases
- •Mitral regurgitation
- •Etiology
- •Disorders of hemodynamics
- •Clinical features
- •Additional methods of examination
- •Mitral stenosis
- •Etiology
- •Disorders of hemodynamics
- •Clinical features
- •Additional methods of examination
- •Literature
- •Contents aortic stenosis
- •Etiology:
- •Disorders of hemodynamics
- •Clinical features
- •Additional methods of examination
- •Aortic regurgitation
- •Etiology
- •Disorders of hemodynamics
- •Clinical features
- •Additional methods of examination
- •Literature
- •Syndrome of the arterial hypertension
- •2. Endocrine hypertension:
- •3. Hemodynamic hypertension:
- •4. Neurogenic hypertension:
- •Clinical features
- •Essential hypertension
- •Etiology
- •Clinical features
- •Additional methods of examination
- •Literature
- •Ischemic heart disease
- •Etiology and pathogenesis
- •Classification of ischemic heart disease (ihd)
- •Stable angina
- •Clinical features
- •Canadian Cardiovascular Society classification of stable angina
- •Additional methods of examination
- •Acute coronary syndrome
- •Clinical features
- •Additional methods of examination
- •Unstable angina
- •Braunwald classification system for unstable angina (ua)
- •Intensity of treatment
- •Myocardial infarction
- •Clinical features
- •Additional methods of examination
- •Optimal time for estimation of myocardial markers of necrosis
- •Dynamic of laboratory markers of myocardial infarction
- •Sudden cardiac death
- •Clinical features
- •Literature
- •Chronic obstructive pulmonary disease (copd)
- •Classification of Chronic Obstructive Pulmonary Disease by Severity
- •Clinical features
- •Additional methods of examination
- •Chronic bronchitis Chronic bronchitis is chronic inflammation of the bronchi and bronchioles. Etiology
- •Pathogenesis. On chronic bronchitis occurs development of classic pathogenetic triad:
- •Clinical features
- •Additional methods of examination
- •Bronchial asthma
- •Etiology
- •Classification
- •Clinical features
- •Additional methods of examination
- •Syndrome of bronchium obstruction (bronchospastic syndrome)
- •Additional methods of examination
- •Syndrome of increased airiness of the pulmonary tissue
- •Additional methods of examination
- •Bronchiectasis
- •Etiology
- •Pathogenesis
- •Clinical features
- •Additional methods of examination
- •Literature
- •Pneumonia
- •Classification
- •Acute lobar pneumonia
- •Additional methods of examination
- •Bronchopneumonia (focal pneumonia)
- •Clinical features
- •Tumors of the lungs
- •Clinical features
- •Literature
- •Pleurisy
- •Dry pleurisy
- •Etiology
- •Pathogenesis
- •Clinical features
- •Additional methods of examination
- •Pleurisy with effusion
- •Etiology
- •Pathogenesis
- •Clinical features
- •Additional methods of examination
- •Syndrome of fluide accumulation in the pleural cavity
- •The main causes of pleural fluid accumulation
- •Classification
- •Clinical features
- •Additional methods of examination
- •Syndrome of air accumulation in the pleural cavity
- •Clinical features
- •Additional methods of examination
- •Respiratory insufficiency
- •Literature
- •Syndrom of functional dyspepsia
- •Classification
- •Clinical features
- •Chronic gastritis
- •Etiology
- •Classification
- •Clinical features
- •Additional methods of examination
- •Peptic ulcer disease (Gastric and Duodenal Ulcer)
- •Etiology
- •Pathogenesis
- •Cinical features
- •Additional methods of examination
- •Complications
- •Irritable bowel syndrome
- •Clinical features
- •Literature
- •Syndrome of bile ducts dyskinesia (dysfunctional bile tract disorders)
- •Classification
- •Clinical features
- •Additional methods of examination
- •Chronic cholecystitis
- •Clinical features
- •Additional methods of examination
- •Cholangitis
- •Etiology
- •Pathogenesis
- •Classification
- •Clinical features
- •Additional methods of examination
- •Jaundice
- •Etiology
- •Pathogenesis
- •Additional methods of examination
- •Literature
- •Classification
- •II. Classification by grade or by stage:
- •Pathological anatomy
- •Clinical features
- •Additional methods of examination
- •Etiology
- •Clinical features
- •Additional methods of examination
- •Syndrome of portal hypertension
- •Classification
- •Hepatic insufficiency
- •Literature
- •Glomerulonephritis
- •Classification
- •Etiology
- •Acute glomerulonephritis
- •Clinical features
- •Additional methods of examination
- •Chronic glomerulonephritis (nephritic form)
- •Clinical features
- •Additional methods of examination
- •Chronic glomerulonephritis (hypertensive form)
- •Clinical features
- •Additional methods of examination
- •Chronic glomerulonephritis (mixed form).
- •Clinical features
- •Additional methods of examination
- •Chronic glomerulonephritis (latent form)
- •Clinical features
- •Additional methods of examination
- •Pyelonephritis
- •Pathogenesis
- •Infectious agents may be transmitted by contact, hematogenous or lymphatic ways in obligatory presence of urodynamic abnormalities. Acute pyelonephritis
- •Clinical features
- •Additional methods of examination
- •Chronic pyelonephritis
- •Clinical features
- •Additional methods of examination
- •Syndrom of chronic renal failure
- •Etiology
- •Pathogenesis
- •Classification of chronic renal diseases (nkf, usa)
- •Clinical features
- •Additional methods of examination
- •Literature
- •Syndrome of anemia
- •Classification
- •Iron deficiency anemia
- •Etiology
- •Vitamin b12 deficiency anemia
- •Hemolytic anemia
- •Classification of hemolytic anemias
- •Additional methods of examination
- •Complete Blood Count (cbc)
- •Normal wbc count
- •Complete Blood Count (cbc)
- •Literature
- •The main methods of laboratory diagnostics of hemorrhagic syndromes
- •Tests for plasma factors involved in coagulation and fibrinolisis
- •Hemorrhagic syndrome
- •Etiology
- •Pathogenesis
- •Clinical feature
- •Additional methods of examination
- •Hemophilia b (Christinas' disease)
- •Clinical feature
- •Additional methods of examination
- •Additional methods of examination
- •Literature
- •Eucosis (Hemoblastosis)
- •Classification of hemoblastosis
- •Acute myeloblastic leukemia
- •Etiology
- •Pathogenesis
- •Clinical features
- •Additional methods of examination
- •Chronic myelocytic leukemia
- •Etiology
- •Pathogenesis
- •Clinical features
- •Additional methods of examination
- •Chronic lymphocytic leukemia
- •Etiology
- •Pathogenesis
- •Clinical features
- •Additional methods of examination
- •Literature
- •Diabetes mellitus
- •Etiological classification of glycemia disorders
- •Classification according to clinical feature
- •Etiology and pathogenesis of insulin dependent diabetes mellitus
- •Etiology and pathogenesis of insulin nondependent diabetes mellitus
- •Clinical features
- •Comparative clinical features of iddm and niddm
- •Hypoglycemia
- •Clinical features
- •Diabetic ketoacidosis
- •Clinical feature
- •Objective examination
- •Additional methods of examination
- •Hyperosmolar non-ketotic coma
- •Clinical features
- •Additional methods of examination
- •Additional methods of examination dm
- •Hyperthyridism
- •Etiology
- •Pathogenesis
- •Clinical feature
- •Additional methods of examination
- •Hypothyroidism
- •Etiology
- •Pathogenesis
- •Clinical features
- •Additional methods of examination
- •Literature
- •Contens
Additional methods of examination
Clinical blood analysis - leukocytosis with mild nuclear shift to the left occurs in a few hours after onset of chest pain, reached the peak at 2-4 days and normalized in a week. The degree of leukocytosis depends on amount of damaged myocardial tissue. Accelerated ESR is observed at 2-3 days from onset of chest pain, reached maximal level till 2 week and normalized at 3-4 weeks.
Markers of myocardial infarction are plasma enzymes, which are normally concentrated within cardiac cells. During the necrosis of cardiomyocytes their membranes destroyed and the enzymes released at first at microcirculation and later at systemic circulation. Thus myocardial infarction causes a detectable rise in the plasma enzymes which serve as laboratory markers of necrosis: creatine kinase, lactate dehydrogenase, aspartate aminotransferase, troponin T and I, myoglobin. Optimal time for estimation of myocardial markers of necrosis depicted at table.
Optimal time for estimation of myocardial markers of necrosis
Markers |
Optimal time for estimation of myocardial markers of necrosis |
Myoglobin |
In 1-2 hours after chest pain |
Creatine kinase |
Every 12 hours 3 time |
Creatine kinase MB |
In 60-90 minutes after chest pain, every 12 hours 3 time |
Lactate dehydrogenase |
In 24 hours after chest pain, one time |
Troponin T |
In 12 hours after chest pain, one time |
Troponin I |
In 12 hours after chest pain, one time |
Baseline and peak elevation of markers of myocardial damage is different. Dynamic of laboratory markers of myocardial infarction is depicted at table
Dynamic of laboratory markers of myocardial infarction
Markers |
Norma |
Time from onset of myocardial infarction | ||
|
|
Baseline elevation hours |
Peak elevation hours |
Normalization days |
Creatine kinase MB |
0-4 ME/L |
3-6 |
12-24 |
1,5-3 |
Lactate dehydrogenase |
15-30% |
12-24 |
24-72 |
7-14 |
Aspartate aminotransferase |
28-125 mmol/l |
8-12 |
24-48 |
3-5 |
Troponin T, I |
Less 0,1 mkg/1 |
3-12 |
12-48 |
3-16 |
Myoglobin |
20-66 mkg/1 |
1-4 |
6-7 |
1 |
ECG: one of the most significant uses of a 12 lead ECG is to aid in determining whether a myocardial infarction has occurred.
The usual first finding in an infarction is elevation of the ST-segment, which occurs some hours after infarction. Hours to days later the T-wave inverts, diminution of the size of the R-wave and the Q-wave becomes deep and wide. The height of the R-wave is directly proportional to the amount of living tissue that escapes death. In case of full thickness myocardial infarction the R-wave is disappeared. Days to weeks later the ST-segment returns to near normal isoilectric line position. Weeks to moths later the T-wave becomes upright again, but Q-wave may remain abnormal. As the infarction heals the Q-wave may remain as the only sign of an old coronary occlusion. Since a deep and wide Q-wave is often indicate of an old infarction. The Q-wave may considered abnormal if it is over 0,03 second wide and if it is greater in depth than one fourth the height of the R-wave.
Echo-CG: two-dimensional echocardiography may assess the cardiac structures, pericardium and ascending aorta, allows identification of regional wall motion abnormalities, valvular abnormalities, global left and right ventricular function and detecting important complications such as cardiac rupture, ventricular septal defect, mitral regurgitation and pericardial effusion.
Radioisotope scintigraphy by technetium-99m-pyrophosphate. Scintigraphy is generally used for the diagnosis of myocardial infarction in patients hospitalized late after the onset of symptoms in which cardiac enzymes are no longer elevated or are unreliable. Imaging is optimal 2-7 days after myocardial infarction. Focal increases in technetium pyrophosphate uptake are generally diagnostic of infarction. This technique is highly sensitive (>90 %) in detecting large transmural infarctien but is less reliable in the detection of small non-Q-wave myocardial infarction.
Radionuclide ventriculography allows to reveal right and left ventricular ejection fraction and assessment of regional wall motion abnormalities. Because radionuclide ventriculography provides less information regarding the cardiac structures, echocardiography is generally preferred in the initial evaluation of patients with myocardial infarction