Instructions for practical classes on the subject \"Internal medicine\" icon

Instructions for practical classes on the subject "Internal medicine"




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Ministry of Education, Science, Youth and Sports of Ukraine

Sumy State University

Medical Institute


3512 Methodological instructions

for practical classes

on the subject “Internal medicine”

for the students of speciality “Medical practice”


Module 3

MODERN PRACTICE OF INTERNAL MEDICINE


Module 4

EMERGENCIES IN INTERNAL MEDICINE CLINIC


Sumy

Sumy State University

2013

Methodological instructions for practical classes on the subject “Internal medicine”. Module 3. Modern practice of internal medicine. Module 4. Emergencies in internal medicine clinic / compilers: G. A. Fadeeva, V. G. Psareva, L. N. Prystupa, V. F. Orlovskyi, V. V. Laba, N. M. Kyrychenko, O. S. Pogorelova, O. V. Orlovskyi, Y. O. Ataman, N. O. Murenets. – Sumy : Sumy State University, 2013. – 91 p.


Department of internal medicine of postgraduate education

Module 3

^ MODERN PRACTICE OF INTERNAL MEDICINE


Semantic module 1. Management of patients in cardiology clinic


1. MANAGEMENT OF PATIENS WITH ARTERIAL HYPERTENSION (AH)


Time frame – 6 hours.

Professional motivation. Individuals with a systolic BP of 120 to 139 mm Hg or a diastolic BP of 80 to 89 mm Hg should be considered as prehypertensive and require health-promoting lifestyle modifications to prevent cardiovascular disease. The prevalence of hypertension increases with age and most individuals with hypertension are diagnosed with primary (essential) hypertension. Hypertension occurs in 10–20% of persons aged 25 to 45 years and 30–40% of persons aged 55 to 74 years. Although it is a “silent” disease, these patients usually have no specific symptoms, hypertension is posed as a major risk factor for coronary artery disease (heart attack), cerebrovascular disease (stroke), and renal disease (kidney failure). It is the second most common reason for office visits to physicians in the United States. Analysis of the Framingham study data suggested that individuals aged 40 to 69 years have an increasing risk of stroke or coronary artery disease mortality with every 20 mm Hg increment in systolic blood pressure. On the other hand, a recent Cochrane review revealed that aiming for blood pressure targets lower than 140/90 mm Hg is not beneficial, as it is not proven that this approach will reduce heart attack and stroke.

There are 2 categories of hypertension. Over 90% of all cases of high blood pressure are called “essential hypertension”, which has no specific identifiable cause but is due to the body inability to regulate the blood pressure within the normal range – SBP 120–140 mm Hg / DBP 60–85 mm Hg. Onset is usually between ages 30 and 50 years. Essential hypertension is treated with medication, diet, and fluid restriction and is not curable. “Secondary hypertension”, on the other hand, is high blood pressure that has an identifiable cause, occurs in a wide age range, is severe, and is abrupt in onset. Secondary hypertension is potentially curable because it is most commonly caused by stenosis of the renal arteries. Less often, secondary hypertension can be caused by tumours of the adrenal gland that secrete hormones acting to increase the blood pressure.

^ Place of carrying out: class-room, wards of the cardiology department, ward of the emergency, department of functional diagnostics.

Study objective: to be able to put provisional diagnosis and assign management.

Basic level:

1. Mechanism of blood pressure regulation.

2. To be able to collect complaints, case history, carry out objective examination. Methods of blood pressure measurement.

3. To interpret instrumental and laboratory data in patients with arterial hypertension.

4. To discover signs inherent to AH.

5. To interpret side effects of antihypertensive drugs. To use diet for AH correction.

Student has to know how to examine patients with cardiovascular disorders.

The main theoretical questions:

1. Definition of arterial hypertension. Essential AH. Secondary AH.

2. Epidemiology and classification of the arterial hypertension.

3. Rick factors for arterial hypertension.

4. Complications in arterial hypertension.

5. Observantional program of the persons with arterial hypertension.

6. Differential diagnosis in AH of different aetiology.

7. General principles of antihypertensive therapy:

a) recommendations on lifestyle modification;

b) the general measures employed;

c) risk factors for an adverse prognosis in hypertension.

8. Recommendations of the European Society of Hypertension for AH treatment.

9. Approach to drug therapy. Antihypertensive “step by step” therapy.

10. Antihypertensive drugs: diuretics, ß-adrenergic blocking agents, angiotensin-convetrting enzyme inhibitors, angiotensin receptor antagonists, calcium channel antagonists, α-adrenergic receptor blockers.

11. Drug combinations.

12. Treatment in AH adjusted to ethnicity, age, pregnancy, concomitant diseases and complications (renal disease, coronary artery disease, diabetes mellitus, obesity).

13. Hypertensive crisis: classification of the hypertensive crises; sequence of clinical events in hypertensive emergencies; treatment of the hypertensive crises.

Assignment for self-assessment

1. What laboratory tests are included to the hypertension management program?

2. At a routine company physical examination, an asymptomatic 46-year-old man is found to have a BP of 150/110 mm Hg, but no other abnormalities are present. What should be done next?

Answers:

1. Urine for protein, blood, and glucose; microscopic urinalysis; serum creatinine and/or blood urea nitrogen; total cholesterol.

2. Obtain repeated BP recording in your office and/or the patient’s home or work site.

REFERENCES

  1. Braunwald E. Harrison’s principles of internal medicine / E. Braunwald, A. S. Fauci, D. L. Kasper, et al. – 15th edition. – New York : McGraw-Hill. Medical Publishing Division, 2000. – 558 p.

  2. Tierney L. M. Jr. Current Medical Diagnosis and Treatment / L. M. Jr. Tierney, S. J. McPhee, M. A. Papadakis, et al. – New York : Lange Medical Books. McGraw-Hill. Health Professions Division, 2000. – 246 p.

  3. Edwards Ch. R. W. Davidson’s principles and practice of medicine / Ch. R. W. Edwards. – 17th edition. – London : Churchill Livingstone. 1996. – 321 p.

  4. Mancia G. Guidelines for the management of arterial hypertension: the task force for the management of arterial hypertension of the European society of hypertension (ESH) and of the European society of cardiology (ESC) / G. Mancia, G. De Backer, A. Dominiczak, еt al. // J. of Hypertens. – 2007. – Vol. 25. – P. 1105–1187.


^ 2. MANAGEMENT OF PATIENS WITH CARDIALGIA. DIFFERENTIATION BETWEEN THE CORONARY AND NONCORONARY CARDIALGIA


Time frame – 6 hours.

Professional motivation. The prevalence of chest pain or chest discomfort varies in different parts of Europe. In a British study of 7735 men, angina pectoris or a history of possible acute myocardial infarction (AMI) was reported in 14% and a further 24% suffered from atypical chest pain. The underlying cause of chest pain varies depending on whether a patient is seen by a general practitioner, calls the dispatch centre, is treated by the ambulance crew or is seen at the emergency department. Not unexpectedly, chest pain of cardiac origin is less commonly seen by the general practitioner (20%), whereas musculoskeletal disorders are common. A summary of prospective studies in general practices in the Netherlands, in England, and in Iceland shown that most of the episodes were caused by musculoskeletal problems and only about 20% were of cardiac origin. Patients with chest pain without a somatic diagnosis often suffer from psychiatric problems such as anxiety, depression or alcohol abuse.

The ischaemic origin of calls about chest pain is much more frequent at dispatch centres. About 25% of all emergency calls to a dispatch centre are initiated because of chest pain. Among such patients, 40% are reported to have confirmed myocardial ischaemia or infarction, and 66% either confirmed or possible myocardial ischaemia or infarction as the cause of their pain. Patients with acute myocardial infarction who call for an ambulance are different from those who do not. They are older, more likely to be female and have a higher prevalence of previous cardiovascular disease and more severe symptoms. They develop more complications and present a higher risk of cardiac arrest and death. The number and proportion of hospital admissions for chest pain vary. Data from the U.S. showed that 20% of all nonsurgical admissions are for chest pain, in patients with chest pain 17% ultimately met the criteria for cardiac ischaemia and 8% had myocardial infarction. Overall, a similar proportion of men and women seek medical care due to non-ischaemic chest pain. In some subsets such as patients with chest pain due to psychiatric causes there might be an over-representation of women. Patients with non-ischaemic chest pain also have a lower prevalence of various risk indicators, such as a history of previous acute myocardial infarction, angina pectoris, hypertension, and diabetes. Smoking is more frequent in this patient population. There are different types of non-ischaemic causes of chest pain: reflux oesophagitis, oesophageal spasm, pulmonary embolism, spontaneous pneumothorax, aortic dissection, pericarditis, pleuritis, early herpes zoster, peptic ulcer, cholecystitis, pancreatitis.

IHD is the leading cause of mortality in the United States and the rest of the developed world; it is responsible for more than 20% of deaths. In the United States, approximately 1 million persons suffer from MI, and 500,000 coronary deaths occur each year. IHD is the leading cause of death in the United States for both sexes in both white and black populations. The prevalence of IHD increases with age and is higher in men than in women in every age group. The American Heart Association (AHA) conservatively estimates that more than 6 million persons in the United States experience angina. In addition to posing an increased risk of MI and premature death, chronic stable angina often limits affected persons’ capacity for work and other activities, which, in turn, negatively affects their quality of life. The direct and indirect costs of hospitalization, diagnostic procedures, and revascularization related to angina are substantial. Of patients with angina who undergo a coronary revascularization procedure, 30% or more never return to work.

The major modifiable risk factors for IHD are dyslipidemias – in particular, elevated levels of low-density lipoprotein (LDL) cholesterol and low levels of high-density lipoprotein (HDL) cholesterol – as well as hypertension, diabetes mellitus, and cigarette smoking. Other important, but immutable, risk factors are increasing age, family history of premature coronary disease, and male sex. Obesity, physical inactivity, and atherogenic dietary habits also contribute to cardiovascular risk, although it is difficult to distinguish the risks conferred by these risk factors independently of the risks conferred by the major cardiovascular risk factors because of the potential interaction of these factors. Patients with combinations of risk factors may be at particular risk for developing IHD.

^ Place of carrying out: class-room, wards of the cardiology and rheumatology departments, department of functional diagnostics, X-ray department.

Study objective: to be able to determine extent of examinations to put final diagnosis and assign management.

Basic level:

  1. To be able to collect complaints, case history, carry out objective examination.

  2. To interpret instrumental (ECG, EchoCG, X-ray) and laboratory data in patients with chest pain.

  3. To identify signs from anamnesis and objective data inherent to cardialgia of different origin.

  4. To interpret side effects of antianginal agents. To use physiotherapeutic procedures and diet for correction of chest pain related to diseases of musculoskeletal system, oesophagus, abdominal cavity organs.

Student has to be able to:

  1. Examine patients with cardiovasculal disorders.

  2. Make an algorithm of investigations in patients with cardialgia.

  3. Determine approaches to treatment in different aetiology of cardialgia.

The main theoretical questions:

  1. Aetiology of cardialgia. The main pathogenetic mechanisms in cardialgia development.

  2. Clinical signs of cardialgia depending on aetiology: in coronary diseases, in neurocirculatory dystonia, in pericarditis, myocarditis, valvular disorders, lung and pleural diseases, in oesophageal and abdominal organs pathology, in aortic aneurism.

  3. An algorithm for the diagnosis of acute chest pain.

  4. Management of patients with different aetiology of cardialgia.

  5. The main drugs for treatment of functional disorders of cardiovascular system.

  6. The main drugs for treatment of noncoronary myocardium diseases.

Assignment for self-assessment

  1. A 44-year-old woman is presenting with prolonged stabbing chest pain on the left from sternum, dizziness, paresthesia, general sweating, sleeplessness. She’s sick for a year. The examination reveals emotional lability, a regular heart rate with a systolic murmur above heart apex. Blood pressure is 120/80 mm Hg; pulse is 88 beats/min, regular, respiratory rate is 16 breaths/min. Her lungs are clear. The abdomen is soft without tenderness or distention. The liver spans 10 cm in the midclavicular line with a smooth edge. There is no peripheral oedema, pulse is intact. Her weight is 84 kg, height is 176 cm. She is afebrile. On ECG: sinus rhythm, negative T-waves in V1-V4 leads which disappear (T-waves become positive) after potassium or propranolol test. Suggested diagnosis is:

  1. dishormonal cardiomyopathy;

  2. IHD: stable angina, FCII;

c) infective myocarditis;

d) rheumocarditis.

  1. A 28-year-old man is presenting with chest pain, palpitations, and dyspnoea after adenoviral infection. Examination revealed pale skin, acrocyanosis, a regular weakened heart beats, cardiac borders expanded to the left and to the right. Blood pressure is 90/60 mm Hg; pulse is 92 beats/min, respiratory rate is 20 breaths/min. His lungs are clear. The abdomen is soft without tenderness or distention. The liver spans 10 cm in the midclavicular line with a smooth edge. There is no peripheral oedema. On ECG: decreased voltage of R-waves, PQ 0.22 sec. Suggested diagnosis is:

  1. viral myocarditis;

  2. infective endocarditis;

  3. rheumatic myocarditis;

d) exudative pericarditis;

e) dilated cardiomyopathy.

Answers: 1. a. 2 a.

REFERENCES

  1. Braunwald E. Harrison’s principles of internal medicine / E. Braunwald, A. S. Fauci, D. L. Kasper, et al. – 15th edition. – New York : McGraw-Hill. Medical Publishing Division, 2000. – 558 p.

  2. Tierney L. M. Jr. Current Medical Diagnosis and Treatment / L. M. Jr. Tierney, S. J. McPhee, M. A. Papadakis, et al. – New York : Lange Medical Books. McGraw-Hill. Health Professions Division, 2000. – 246 p.

  3. Edwards Ch. R. W. Davidson’s principles and practice of medicine / Ch. R. W. Edwards. – 17th edition. – London : Churchill Livingstone. 1996. – 321 p.


^ 3. MANAGEMENT OF PATIENS WITH ARRHYTHMIAS


Time frame – 6 hours.

Professional motivation. Supraventricular arrhythmias are relatively common, often repetitive, occasionally persistent, and rarely life-threatening. The precipitants of supraventricular arrhythmias vary with age, gender, and associated comorbidity. While supraventricular arrhythmias are a frequent cause of emergency room and primary care physician visits, they are infrequently the primary reason for hospital admission.

The estimated prevalence of paroxysmal supraventricular tachycardia (PSVT) in a 3.5% sample of medical records in the Marshfield (Wisconsin, the USA.). Occurrence rates have been determined for various subtypes of supraventricular arrhythmia after acute myocardial infarction or coronary artery bypass graft surgery and in congestive heart failure (CHF) patients. The incidence rate of supraventricular arrhythmias among patients with CHF is 11.1%; paroxysms are more common in older patients, males, and those with longstanding CHF and radiographic evidence of cardiomegaly.

Age exerts an influence on the occurrence of SVT. The mean age at the time of PSVT onset in the MESA cohort was 57 years (ranging from infancy to more than 90 years old). Among emergency room patients older than 16 years treated with intravenous (IV) adenosine for supraventricular arrhythmias diagnosed by surface electrocardiogram (ECG) criteria, 9% had atrial flutter and 87% had SVT; 70% of these patients (age 51 plus or minus 19 years) reported a history of cardiovascular disease. In the MESA population, compared to those with other cardiovascular disease, “lone” (no cardiac structural disease) PSVT patients without associated structural heart disease were younger (mean age equals 37 vs. 69 years), had faster heart rates (186 vs. 155 beats per minute), and were more likely to present first to an emergency room (69 vs. 30%).

Gender plays a role in the epidemiology of SVT. Female residents in the MESA population had a twofold greater relative risk of PSVT (RR equals 2.0; 95% confidence interval equals 1.0 to 4.2) compared to males. Fifty-eight percent (58%) of symptomatic “lone” PSVT episodes in MESA females without concomitant structural heart disease occurred in the premenopausal age group, as compared to only 9% of episodes in women with cardiovascular disease.

The only reported epidemiologic study of patients with atrial flutter involved a selected sample of individuals treated in the Marshfield Clinic in predominantly white, rural mid-Wisconsin. Over 75% of 58,820 residents and virtually all health events were included in this population database. In approximately 60% of cases, atrial flutter occurred for the first time associated with a specific precipitating event (i.e., major surgery, pneumonia, or acute myocardial infarction). In the remaining patients, atrial flutter was associated with chronic comorbid conditions (i.e., heart failure, hypertension, and chronic lung disease). Only 1.7% of cases had no structural cardiac disease or precipitating cause (lone atrial flutter). The overall incidence of atrial flutter was 0.088%; 58% of these patients also had AF. Atrial flutter alone was seen in 0.037%. The incidence of atrial flutter increased markedly with age, from 5 per 100000 of those more than 50 years old to 587 per 100 000 over age 80. Atrial flutter is 2.5 times more common in men.

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia, occurring in 1–2% of the general population. Over 6 million Europeans suffer from this arrhythmia, and its prevalence is estimated to at least double in the next 50 years as the population ages. AF confers a 5-fold risk of stroke, and one in five of all strokes is attributed to this arrhythmia. Ischaemic strokes in association with AF are often fatal, and those patients who survive are left more disabled by their stroke and more likely to suffer a recurrence than patients with other causes of stroke. In consequence, the risk of death from AF-related stroke is doubled and the cost of care is increased 1.5-fold. AF may long remain undiagnosed (silent AF), and many patients with AF will never present to hospital. Hence, the “true” prevalence of AF is probably closer to 2% of the population. The prevalence of AF increases with age, from < 0.5% at 40–50 years, to 5–15% at 80 years. Men are more often affected than women. The lifetime risk of developing AF is 25% in those who have reached the age of 40. The prevalence and incidence of AF in non-Caucasian populations is less well studied. The incidence of AF appears to be increasing (13% in the past two decades).

AF is associated with increased rates of death, stroke and other thromboembolic events, heart failure and hospitalizations, degraded quality of life, reduced exercise capacity, and left ventricular (LV) dysfunction. Death rates are doubled by AF, independently of other known predictors of mortality. Only antithrombotic therapy has been shown to reduce AF-related deaths. Stroke in AF is often severe and results in long-term disability or death. Approximately every fifth stroke is due to AF; furthermore, undiagnosed “silent AF” is a likely cause of some “cryptogenic” strokes. Paroxysmal AF carries the same stroke risk as permanent or persistent AF.

Hospitalizations due to AF account for one-third of all admissions for cardiac arrhythmias. Acute coronary syndrome (ACS), aggravation of heart failure, thromboembolic complications, and acute arrhythmia management are the main causes. Cognitive dysfunction, including vascular dementia, may be related to AF. Small observational studies suggest that asymptomatic embolic events may contribute to cognitive dysfunction in AF patients in the absence of an overt stroke.

Quality of life and exercise capacity are impaired in patients with AF. Patients with AF have a significantly poorer quality of life compared with healthy controls, the general population, or patients with coronary heart disease in sinus rhythm. Left ventricular (LV) function is often impaired by the irregular, fast ventricular rate and by loss of atrial contractile function and increased end-diastolic LV filling pressure. Both rate control and maintenance of sinus rhythm can improve LV function in AF patients.

Ventricular arrhythmias include premature ventricular contraction, ventricular tachycardia, and ventricular fibrillation. Both of last are life-threatening arrhythmias most commonly associated with heart attacks. The most serious arrhythmia is ventricular fibrillation, which is an uncontrolled, irregular beat. If cardiopulmonary resuscitation (CPR) can be started, or if electrical energy is used to “shock” the heart back to a normal rhythm, then the heart may not be too damaged. About 220,000 deaths from heart attacks each year are thought to be caused by ventricular fibrillation. People who have heart disease or a history of heart attack have the highest risk of ventricular fibrillation.

A less serious type of ventricular arrhythmia is a premature ventricular contraction (PVC). As the name suggests, the condition happens when the ventricles contract too soon, out of sequence with the normal heartbeat. PVCs generally are not a cause for alarm and often do not need treatment. But if patient has heart disease or a history of ventricular tachycardia, PVCs can cause a more serious arrhythmia.

The incidence of ventricular tachycardia (VT) in the United States is not well quantified because of the clinical overlap of VT with ventricular fibrillation (VF). Examination of sudden death data provides a rough estimate of VT incidence. Most sudden cardiac deaths are caused by VT or VF, at an estimated rate of approximately 300,000 deaths per year in the United States, or about half of the estimated cardiac mortality in this country. A prospective surveillance study gave a sudden death incidence of 53 per 100,000, accounting for 5.6% of all mortality. This is only a rough estimate of VT incidence, because many patients have nonfatal VT and because arrhythmic sudden deaths may be associated with VF or bradycardia rather than with VT. Ventricular tachycardia (VT) is observed more frequently in men, because ischaemic heart disease is more prevalent among men. In patients with ischaemic cardiomyopathy and nonsustained VT, sudden death mortality rates approach 30% in 2 years.

^ Place of carrying out: class-room, wards of the cardiology, department of functional diagnostics.

Study objective: to be able to verify supraventricular, ventricular extrasystole and extrasystole from AV-node, to distinguish fibrillation from atrium and ventricles, preexictation syndrome on ECG.

Basic level:

  1. To be able to collect complaints, case history, carry out objective examination.

  2. To be able to register ECG. ECG classification of the rhythm disorders.

  3. Electrophysiology of the heart.

  4. To interpret instrumental and laboratory data in patients with arrhythmias.

  5. To interpret side effects of antiarrhythmic drugs. Preventive measures against arrhythmia development.

Student has to know:

  1. Diseases which are accompanied by arrhythmias.

  2. How to make algorithm of investigations in arrhythmias.

  3. How to differentiate arrhythmias by clinical signs.

The main theoretical questions:

  1. ECG classification of rhythm disorders.

  2. Sinus tachycardia, sinus bradycardia. Clinical signs, ECG signs, management.

  3. Extrasystoles, clinical signs, ECG signs, management.

  4. Supraventricular tachycardias. ECG signs.

  5. Management in paroxysmal tachycardias.

  6. Ventricular paroxysmal tachycardias. ECG signs.

  7. Management in paroxysmal ventricular tachycardias.

  8. Atrial fibrillation and flutter. ECG signs. Management.

  9. ECG signs of the preexcitation syndromes.

  10. Ventricular arrhythmias related to specific pathology (MI, cardiomyopathy, valvular heart diseases). Device therapy.

Assignment for self-assessment

1. 34-year-old patient with sudden onset of fatigue, and palpitation addressed to the doctor’s office. On ECG: presence of frequent and regular P waves and QRS complexes. What rhythm disorder has occured and what drug will you select for treatment?

2. A 52-year-old man arrived to the emergency room with irregular tachycardia, ventricular rate of 250/min, blood pressure of 80/60 mm Hg, and prolonged QRS complexes. It is known he has the Wolff-Parkinson-White syndrome. What medicines should be used for immediate management?

3. Negative P waves were registered on ECG in the II and III standard leads, QRS complexes are not changed and go after P waves. Pacemaker is located in:

a) sinus node;

b) AV node;

c) ventricles;

d) inferior part of the atrium;

e) everything is wrong.

Answers:

1. Paroxysmal superventricular tachycardia; verapamil will terminate over 90% of paroxysmal superventricular tachycardia.

2. Wolff-Parkinson-White syndrome is potentially life-threatening when the anomalous atrioventricular connection has a short refractory period and is capable of rapid atrioventricular con­duction. Very rapid ventricular rates can produce cardiovas­cular collapse or precipitate ventricular fibrillation. Atrial fibrillation should be terminated immediately with cardioversion.

3. d.

REFERENCES

  1. Camm A. J. Guidelines for the management of atrial fibrillation / A. J. Camm, P. Kirchhof, G. Y. H. Lip, et al. // European Heart Journal. – 2010. – Vol. 31. – P. 2369–2429. Access mode: http://www.escardio.org/guidelines-surveys/esc-guidelines/GuidelinesDocuments/guidelines-afib -FT.pdf

  2. Tierney L. M. Jr. Current Medical Diagnosis and Treatment / L. M. Jr. Tierney, S. J. McPhee, M. A. Papadakis, et al. – New York : Lange Medical Books. McGraw-Hill. Health Professions Division, 2000. – 246 p.

  3. Edwards Ch. R. W. Davidson’s principles and practice of medicine / Ch. R. W. Edwards. – 17th edition. – London : Churchill Livingstone. 1996. – 321 p.




  1. ^ MANAGEMENT OF PATIENS WITH BLOCKS


Time frame – 6 hours.

Professional motivation. The exact incidence of sinus node dysfunction (SND) is unknown. The syndrome occurs in approximately one in 600 cardiac patients older than 65 years. Symptoms of SND almost invariably progress over time. The most dramatic symptom in patients with SND is syncope. About 50% of patients with SND develop tachy-brady syndrome over a lifetime; such patients have higher risk of stroke and death. The survival of patients with SND appears to depend primarily on the severity of underlying cardiac disease and is not significantly changed by pacemaker therapy. However, incidence of sudden death owing directly to SND is extremely low.

No racial preponderance exists. Men and women are affected in equal numbers. SND may occur at any age but is primarily a disease of the elderly, with the average age being about 68 years old. SND in young patients is often related to underlying heart diseases.

Sick sinus syndrome describes abnormalities caused by the malfunction of the heart’s natural pacemaker (sinoatrial node) when symptoms such as dizziness or fainting (syncope) are present. Possible complications of sick sinus syndrome include inadequate or inefficient pumping of the heart, heart failure, exercise intolerance, and injuries sustained by fainting spells and falling. Complications may develop from surgery to implant pacemakers, including infection, reaction to medications or anaesthesia, and pacemaker failure. Sick sinus syndrome progresses slowly. No treatment is necessary as long as the individual is not experiencing symptoms. Even with a permanent artificial pacemaker, the long-term prognosis is excellent.

AV blocks occur more frequently in people older than 70 years, especially in those who have structural heart disease. Approximately 5% of patients with heart disease have first-degree AV block, and about 2% have second-degree AV block.

The incidence of AV block increases with age. The incidence of third-degree AV block is highest in people older than 70 years (approximately 5–10% of patients with heart disease). A 60% female preponderance exists in congenital third-degree AV block. For acquired third-degree AV block, a 60% male preponderance exists. No racial proclivity exists in AV blocks.

One study examined first-degree AV block in 2123 patients: it was more prevalent in African-American patients in almost all decades of life (third through 10th). In both groups, first-degree AV block became more common at age 50 years and peaked in the 10th decade for black patients versus the ninth decade for white patients. One study examined 24-hour Holter monitors in 625 asymptomatic, heart-disease-free people, aged 15 to 83 years. Transient type I second-degree AV block was seen in 14 (2.2%) patients, more frequently in patients with resting heart rates of < 60 bpm. First-degree AV block has been associated with about a 2-fold increase in the probability of atrial fibrillation, a 3-fold increase in the probability of pacemaker implantation, and an increase in all-cause mortality.

First-degree AV block can be found in healthy adults. At 20 years of age, the PR interval may exceed 0.20 seconds in 0.5–2% of healthy people. At age 60 years, more than 5% of healthy individuals have PR intervals exceeding 0.20 seconds.

Advanced AV block (usually type II second-degree and third-degree) is usually anatomically infranodal and is seen in advanced His-Purkinje disease. One study examined the prevalence of His-Purkinje disease in the Framingham population. Here, QRS intervals of > 0.12 seconds were significantly associated with coronary heart disease, CHF, AV block, hypertension, left ventricular hypertrophy, and ventricular extrasystoles. QRS intervals > 0.12 seconds were rare before 50 to 60 years of age and were found in 11% of older men and 5% of older women. While intraventricular block does not inevitably lead to AV block, it frequently precedes the development of advanced AV block. Thus, this characterisation of a wide-QRS interval population is likely similar to that of the advanced AV block population.

Mobitz II second-degree AV block (Mobitz II) is rare in healthy individuals, whereas Mobitz I (Wenckebach) second-degree AV block is observed in 1–2% of healthy young people, especially during sleep.

Congenital third-degree AV block is rare, at 1 case per 20,000 births. This form of heart block, in the absence of major structural abnormalities, is associated with maternal antibodies to Ro (SS-A) and La (SS-B) and secondary to maternal lupus. It is most commonly diagnosed between 18 and 24 weeks’ gestation and may be first, second, or third degree (complete). Mortality approaches approximately 20%; most surviving children require pacemakers.

Patients treated with permanent pacing to treat AV blocks have an excellent prognosis. Patients with advanced AV blocks who are not treated with permanent pacing remain at high risk of sudden cardiac death.

Although AV block generally is not associated with major morbidity, progressive degrees of AV block carry increasing morbidity and mortality.

The Reykjavik Study, a long-term prospective cardiovascular survey, which included a representative population of 9135 men and 9627 women, 33–79 years old, revealed that Right bundle branch block (RBBB) was found in 126 men and 67 women. The prevalence increased with age, from 0% among men and women 30–39 years of age to 4.1% and 1.6% in men and women, respectively, who were 75–79 years old. In men younger than 60 years RBBB had a significant relationship with hypertension, elevated fasting blood glucose, and increased heart size. In men with RBBB regardless of age, an association was found with cardiomegaly, ischaemic heart disease, arrhythmias, and bradycardia (P<005). A higher mortality from heart disease was found in men with RBBB compared to the control population. RBBB in women younger than 60 years is often associated with hypertension.

^ Place of carrying out: class-room, wards of the cardiology, department of functional diagnostics.

Study objective: to be able to verify different types of blocks, management of patients.

Basic level:

  1. Anatomy and physiology of the conducting system.

  2. To be able to collect complaints, case history, carry out an objective examination.

  3. To be able to register ECG.

  4. To interpret instrumental and laboratory data in patients with blocks.

  5. To interpret side effects of drugs which are used in blocks.

Student has to know:

  1. Diseases which are accompanied by blocks.

  2. How to make algorithm of investigations in blocks.

  3. Indications for pacemaker implantation: single-chamber and dual-chamber pacemaker.

The main theoretical questions:

  1. Sinoatrial blocks. Causes, ECG signs. Treatment.

  2. Intraatrial blocks, ECG signs.

  3. Atrioventricular block. ECG signs. Treatment.

  4. Adams-Stokes attacks. Diagnosis. Emergency.

  5. Bundle branch blocks. Causes. Diagnosis. Classification: right bundle branch block. Block of the left branch of the bundle of His. Anterior/posterior fascicle of the left branch of His bundle.

  6. Sinus node dysfunction. The sick sinus syndrome. Causes, ECG signs, treatment.

  7. External defibrillation and cardioversion. Temporary/permanent pacemakers.

Assignment for self-assessment

  1. A 63-year-old woman was admitted to the coronary care unit with palpitation, weakness and after short period of loss of consciousness. She indicates on impairment of state for about 4 months. Her pulse is 52 per min, arrhythmical, no murmur sounds. On ECG: sinus and irregular rhythm, PQ interval – 0.2 sec, QRS complexes – 0.08, gradual increase R-R interval with subsequent PQRST dropout. What is the reason of such state?

a) sinoatrial block;

b) AV-block, type I;

c) block of 3 fascicles of His bundle;

d) AV-block, type II.

2. The ECG examination of the 32-year-old male shows the PR interval of conducted beats is normal but some P waves are not conducted. What type of block is it? What is the management of this disorder?

  1. A type of AV block characterised by progressive lengthening of the PR interval until the P wave fails to conduct is:

a) second degree AV-block: Mobiz type II;

b) second degree AV block: Mobiz type I;

c) first degree  AV block;

d) third degree block.

4. Rhythms required permanent pacing in patients with cardiac disorders include:

a) supraventricular tachycardia;

b) second-degree AV block: Mobiz type I;

c) complete heart block;

d) Wolf-Parkinson-White syndrome.

Answers:

1. a.

2. Mobitz type II second degree AV block. A permanent pacemaker is indicated.

3. b. 4. c.

REFERENCES

  1. Adan V. Diagnosis and treatment of sick sinus syndrome / V. Adan, L. Crown // American family physician. – 2003. – Vol. 67, №8. – P. 1725–1732.

  2. Tierney L. M. Jr. Current Medical Diagnosis and Treatment / L. M. Jr. Tierney, S. J. McPhee, M. A. Papadakis, et al. – New York : Lange Medical Books. McGraw-Hill. Health Professions Division, 2000. – 246 p.

  3. Edwards Ch. R. W. Davidson’s principles and practice of medicine / Ch. R. W. Edwards. – 17th edition. – London : Churchill Livingstone. 1996. – 321 p.


^ 5. MANAGEMENT OF PATIENS WITH STABLE ANGINA, CRITERIA FOR DIAGNOSIS


Time frame – 6 hours.

Professional motivation. Stable angina is the initial manifestation of ischaemic heart disease in approximately 50% of these patients. The prevalence of angina in community studies increases sharply with age in both sexes from 0.1–1% in women aged 45–54 to 10–15% in women aged 65–74 and from 2–5% in men aged 45–54 to 10–20% in men aged 65–74. Therefore, it can be estimated that in most European countries, 20,000–40,000 individuals of the population per million suffer from angina.

Statistics released by the American Heart Association in 2010 indicate that approximately 10.2 million people in the United States suffer from angina pectoris. In 2007 the overall death rate from coronary artery disease was 251.2 per 100,000 people, and coronary artery disease accounted for 33.6% of total deaths from all causes. Though the death rate from coronary artery disease decreased by 27.8% from 1997 to 2007, the over all burden of the disease remains high secondary to high prevalence of risk factors such as smoking, hypertension, diabetes, obesity. People in the Mediterranean region and Eskimos have a lower incidence of coronary artery disease due to higher consumption of canola oil and fish oil, respectively.

In the past, the incidence and prevalence of coronary artery disease were low in developing countries in comparison to developed countries. But with the westernization of developing regions in Middle East, India, and Central and South America, the incidence of CAD is increasing. The prevalence of coronary artery disease among adults in India has risen 4-fold over the last 40 years. By the year 2005, it was the leading cause of death accounting for 29% of the total deaths from all causes. The prevalence of coronary artery disease has been increasing in China with increase in risk factors such as smoking and mean cholesterol levels which have increased from 166 mg/dL to 206 mg/dL over the past 15 years.

According to the Framingham Heart Study, the lifetime risk of developing coronary artery disease at the age of 40 is 49% in men and 32% in women while the risk at 75 years of age is 35% in men and 24% in women. During 26 years of follow-up in the Framingham Heart Study, 80% of women under 75 years of age presented with angina pectoris rather than myocardial infraction. In contrast, only 20% of men presented with angina pectoris as their first manifestation.

Patients with stable angina are at risk of ACS developing: unstable angina, non-ST-elevation MI or ST-elevation MI. Data from the Framingham Heart Study showed that for men and women with an initial clinical presentation of stable angina, the 2-year incidence rates of nonfatal MI and CHD death were 14.3 and 5.5% in men and 6.2 and 3.8% in women, respectively. More contemporary data regarding prognosis can be gleaned from clinical trials of antianginal therapy and/or revascularization, although these data are biased by the selected nature of the populations studied. From these, estimates for annual mortality rates range from 0.9–1.4% per annum, with an annual incidence of nonfatal MI between 0.5% (INVEST) and 2.6% (TIBET).

LV function is the strongest predictor of survival in patients with chronic stable coronary disease; the next most important factor is the distribution and severity of coronary stenosis. Left main (LM) disease, three-vessel disease, and the proximal involvement of the left anterior descending are common characteristics predicting a poor outcome and increase the risk of ischaemic events. Myocardial revascularization can reduce the risk of death in selected anatomical subgroups, reduce the number of ischaemic episodes (ACIP), and in some instances may improve the LV function in high-risk patients. However, disease progression and the occurrence of acute events may not necessarily be related to the severity of stenosis at coronary arteriography. In all patients, smaller lipid filled plaques are present in addition to those that cause severe stenoses.

The risk of acute events is related to the overall plaque burden and to plaque vulnerability. Although an area of great research interest, our capabilities to identify vulnerable plaque remain limited.

^ Place of carrying out: class-room, wards of the cardiology and rheumatology departments, department of functional diagnostics.

Study objective: to be able to determine extent of examinations to put final diagnosis and assign management.

Basic level:

1. To know classification and rick factors of the ischaemic heart disease.

2. To be able to collect complaints, case history, carry out objective examination.

3. To interpret instrumental (ECG, 24 hour ECG monitoring (ECG Holter monitor), EchoCG) and laboratory data in patients with chest pain.

4. To identify signs from anamnesis and objective data inherent to stable angina.

5. To interpret side effects of antianginal agents.

Student has to be able to:

  1. Examine patients with cardiovascular disorders.

  2. Make an algorithm of stable angina management.

The main theoretical questions:

  1. Classification of the angina pectoris (functional classes). Diagnostic criteria.

  2. Stress and pharmacology testing, evidence for performing and interpretation.

  3. Treatment and preventive measurements in stable angina.

  4. Importance of ECG, 24 hour ECG monitoring and coronarography in painless form of ischaemia.

Assignment for self-assessment

  1. A 53-year-old man complains of pressing chest pain on 100 m walking that lasts about 15 min. The examination reveals a regular heart rate with a reduced intensity S1 and normal S2. Blood pressure is 140/90 mm Hg; pulse is 90 beats/min, regular, respiratory rate is 20 breaths/min. His lungs are clear. The abdomen is soft without tenderness or distention. On ECG: sinus rhythm, high and sharp T waves in V2–V4 leads. During the last week pain appears at night and at rest, not stopped after taking 1 tab. of nitroglycerin. What disease can you think of?

a) progressive angina;

b) stable angina, FC4;

c) myocardial infarction;

d) vasospastic angina;

e) stable angina, FC3.

2. A 38-year-old man complains of angina attacks and dyspnoea on excersises. The patient suffers from obstructive form of hypertrophic cardiomyopathy. The examination reveals a regular heart rate. Blood pressure is 145/85 mm Hg; pulse is 80 beats/min. What medicine is contraindicated in this situation?

a) bisoprolol;

b) verapamil;

c) aspirin;

d) nitroglycerin.

3. What ECG sign is typical for myocardial ischaemia?

a) ST elevation less than 1 mm;

b) ST depression less than 1 mm;

c) ST depression more than 1 mm;

d) ST elevation more than 5 mm.

4. What test should be made in inefficiency of 24 hour ECG monitoring for revealing of painless form of ischaemia?

a) pharmacological test with propranolol;

b) pacemaker setting;

c) excersise test.

5. A 58-year-old man complains of dyspnoea on excersises and mild oedema on the legs. He has never complained of chest pain, never used nitrates and other medicines. There are no pathological changes of ST segment and T wave on ECG at rest; in excersise test there is ST segment depression more than 2 mm. What should be suspected?

a) painless form of myocardial ischaemia;

b) vasospastic angina;

c) lung pathology;

d) state of absolute health.

Answers: 1. a. 2. d. 3. c. 4. c. 5. a.

REFERENCES

  1. Fox K. Guidelines on the management of stable angina pectoris / K. Fox, M. A. Alonso Garcia, D. Ardissino, et al. // European Heart Journal. – 2006. – Vol. 27. – P. 1341–1381. Access mode: http://www.escardio.org/guidelines-surveys/esc-guidelines/GuidelinesDocuments/guidelines-ang ina-FT.pdf

  2. Tierney L. M. Jr. Current Medical Diagnosis and Treatment / L. M. Jr. Tierney, S. J. McPhee, M. A. Papadakis, et al. – New York : Lange Medical Books. McGraw-Hill. Health Professions Division, 2000. – 246 p.

  3. Edwards Ch. R. W. Davidson’s principles and practice of medicine / Ch. R. W. Edwards. – 17th edition. – London : Churchill Livingstone. 1996. – 321 p.




  1. ^ ISCHAEMIC HEART DISEASE. MANAGEMENT OF PATIENTS WITH UNSTABLE ANGINA, CRITERIA FOR DIAGNOSIS


Time frame – 6 hours.
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