Propedeutics of internal medicine (part 2, 4th ed.) / Kovalyova O. M., Ashcheulova T. V.

Propedeutics of Internal Medicine Part 2

Propede Pr edeuticss off Inte nal Medici Internal M dicine

Part 2

Chapter 2 CARDIOVASCULAR SYSTEM

Syndrome of cardiovascular failure Heart failure is a pathological condition which characterized by decreased contractility of the myocardium, reduction of cardiac output in which the cardiovascular system fails to supply the necessary amount of blood to the organs and tissues for their adequate function.

This condition arises due to the damage of the heart or of the vessels, or it may be combined disorders of the cardiovascular system.

The syndrome of cardiovascular failure is divided into 2 groups: – heart failure: acute (acute left ventricular heart failure, acute left atrial heart failure, acute right ventricular heart failure) and chronic (chronic left ventricular heart failure, chronic left atrial heart failure, chronic right ventricular heart failure and total chronic heart failure); – vascular failure: syncope, collapse and shock. etiology Heart failure may develop in case of overloading or overstrain of the myocardium by “pressure” (hypertension, aortic stenosis, stenosis of the pulmonary orifice), by “volume” (mitral or aortic regurgitation), and also owing to diseases damage primarily the myocardium and its metabolism. Alterations of the myocardium may be due to infectious, inflammatory and toxic damage of the myocardium (myocarditis, cardiomyopathy, intoxication of the myocardium by alcohol, narcotic drugs, other poisons), insufficient blood supply to the myocardium (disordered coronary circulation, anemia), metabolic disorders, endocrine dysfunction.

Common causes of heart failure: – ischemic (coronary) heart disease; – arterial hypertension; – dilated cardiomyopathy; – heart valve diseases; – hypertrophic cardiomyopathy; – restrictive cardiomyopathy; – constrictive pericarditis; – high-output heart failure:

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a) chronic anemia; b) atrioventricular shunts; c) thyrotoxicosis. pathogenesis The clinical syndrome related to organ hypoperfusion and inadequate tissue oxygen delivery due to a low cardiac output and decreased cardiac reserve, as well as pulmonary and systemic venous congestion. Heart failure is associated with complex neurohormonal changes including activation of the renin-angiotensin-aldosterone and the sympathetic nervous systems. At first these changes may help to compensate cardiac function by altering the afterload or preload and by increasing myocardial contractility. Ultimately they become counterproductive and reduce cardiac output by causing an inappropriate and excessive increase in peripheral vascular resistance. A vicious cycle may be established because a fall in cardiac output will cause further neurohormonal activation and increasing peripheral vascular resistance. The onset of peripheral edema is due to salt and water retention caused by impaired renal perfusion and secondary aldosteronism.

Heart failure may develop as a result of impaired myocardial contraction due to decreasing of number functional activity of cardiomyocites – systolic dysfunction, which may observe in patients with inflammation of myocardium, cardiosclerosis, hypertension, non-compensated regurgitation and dilated cardiomyopathy.

Heart failure may arise due to poor ventricular filling caused by disorder of active relaxation and increasing of rigidity of myocardium due to hypertrophy, fibrosis and infiltration – diastolic dysfunction, which may observe in patients with constrictive pericardities, hypertrophic cardiomyopathy.

Systolic and diastolic dysfunctions often coexist, particularly in patients with hypertension, ischemic (coronary) heart disease.

Compensatory mechanisms in heart failure: – tachycardia; – Frank-Starling’s mechanism; – myocardial hypertrophy; – tonogenic dilation; – slow blood flow.

Clinical features Symptoms and signs of heart failure depend on the prevalence of damaged heart chambers. Left ventricular failure corresponds with reduction of the ventricular output and increasing pressure in the left atrium, pulmonary veins and later pulmonary artery. There are clinical picture of congestion in lesser circulation: breathlessness, paroxysmal nocturnal dyspnea, cough, sometimes hemoptysis, orthopnea, cyanosis and crepitation over the lung.

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In patients with right ventricular failure due to the reduction of the ventricular output appear the clinical pictures of congestion in greater circulation: pain in the right hypochondrium, swollen jugular veins, edema on lower extremities, enlarged liver.

Massive accumulation of fluid may cause ascites, pleural and/or pericardial effusion.

Total heart failure: failure of the left and right heart may develop because the disease process affects both ventricles, or because there is primary affection left heart failure with dilation of left atrium, pulmonary hypertension and as a result subsequently development of right heart failure.

The patient’s complaints are fatigue, dyspnea, malaise, edema of legs, the attacks of breathlessness, cough. The general patients condition as usual grave, deranged consciousness, forced posture – orthopnea, cyanosis, anasarca.

Chronic heart failure is sometimes associated with marked weight loss (cardiac cachexia) caused by a combination of anorexia and impaired absorption due to gastrointestinal congestion, poor tissue perfusion due to a low cardiac output and skeletal muscle atrophy due to immobility.

Poor renal perfusion may lead to oliguria and uremia.

Additional methods of examination Clinical blood analysis is required in order to reveal inflammatory process, anemia.

Clinical urine analysis is required for estimation kidney pathology.

Biochemical blood analysis – creatinin, urine acid, total protein levels, potassium, calcium concentration.

ECG is required for detection of main cardiac process.

X-ray examination in order to estimate lung and heart pathology.

Echo-CG is required for estimation of ejection fraction; structural and functional state of heart.

Echo-stress test with dobutamin.

Measurment of pressure in ventricle: – end-diastolic pressure in right ventricle using the catheterization of vena cava superior; – end-diastolic pressure in left ventricle using the Swan-Ganz catheter in pulmonary artery.

Acute heart failure Acute left ventricular failure

Acute left ventricular failure – is state resulted from suddenly sharp decreased contractility of left ventricle and normal one of right ventricle.

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Chapter 2. Cardiovascular system

Causes of acute left ventricular failure: – essential hypertension, espessially hypertensive crisis; – heart valve diseases (aortic regurgitations, aortic stenosis); – ischemic (coronary) heart disease; – myocardial infarction; – myocarditis; – arrhythmias. pathogenesis Acute heart failure may be provoked by infections, intoxications, physical and nervous strain. The lesser circulation becomes overfilled with blood because during a sharply decreased contractility of the left ventricle the right ventricle continues working normal to pump the blood from the greater circulation to the lesser one: arterial blood pressure increases in pulmonary veins and capillaries, its permeability increases, gas exchange is impaired. If congestion in the lesser circulation progresses, hydrostatic pressure in capillaries is equal or higher than oncotic pressure (25–30 mm Hg).

The blood plasma pass from the overfilled pulmonary capillaries to the alveoli and accumulates in the respiratory ducts, pulmonary edema develops. Interstitial edema means the thickening of the alveoli walls due to accumulation of the blood plasma; alveolar edema means the presence of the blood plasma in the alveoli space.

There are two clinical forms of acute left ventricular failure: cardiac asthma and pulmonary edema.

Cardiac asthma

Clinical features The patient complains on severe dyspnea as attack, with more difficulty inspiration, which often arises during night sleep, so called cardiac asthma. May be dry cough or with expectoration of small amount the tenacious sputum. The patient complains on marked weakness, feeling of fear, excitement.

Objective examination. General patient’s condition is from middle grave to extremely grave. Consciousness is clear but if this state lasts a long time, may be cloudiness.

Posture: patient assumes a forced position – sitting with legs hanging down from the bed or he stands up.

The skin becomes pallid and cyanotic, acrocyanosis, cold sweat appears.

Examination of the respiratory system. The accessory muscles take part in the breating, tachypnea – 30–40 per minute. Over the low regions of the both sides of lungs the vocal fremicus is increased. Over the lungs is heard dull-tympanic sound.

Harsh respiration and crepitation in the posterior part of the lungs are heard.

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Examination of the cardiovascular system. The apex beat displaced to the left and cardiac dullness and configuration of the heart depends on main pathology. The heart sounds are decreased at the apex, accentuated second heart sound over the pulmonary artery, tachycardia, gallop rhythm. Pulse is frequent, arrhythmia, blood pressure may be normal, or decreased.

In case of appropriate treatment may disappear the clinical picture of cardiac asthma. In some case this state transforms in pulmonary edema.

Pulmonary edema

Patients complain on severe breathlessness, cough with expectoration of sputum, heaviness in the heart.

Objective examination. The general patient’s condition is extremely grave, deranged consciousness, disorder of the mental function, forced posture – sitting with trunk slightly bent forward, the skin is pale, cyanosis with grey tint, cold sweet.

Respiration becomes rattling and heard even at the distance. Ample foaming sputum with traces of blood (pink or red) is expectorated.

In percussion over the lungs in the posterior inferior parts of the chest is heard dull sound.

In auscultation harsh respiration, moist rails of various calibers are heard over entire surface of the lungs. The heart sounds are weakened, protodiastolic gallop rhythm, tachycardia.

Pulse – small frequent pulse, alternative, with poor filling.

Blood pressure – decreased.

If patient is not treated urgently, this attack can lead to death.

Additional methods of examination ECG: hypertrophy of the left ventricle, signs of overloading of the left ventricle.

X-ray examination: congestion changes in lungs.

Echo-CG: hypertrophy of the interventricular septum and the back wall of the left ventricle, decreasing myocardial contractility, increasing end-systolic enddiastolic dimensions of the left ventricle.

Acute left atrial heart failure

The syndrome of acute left atrial failure develops in patients with mitral stenosis, myxoma of the left atrium (in mechanical obstruction of the intracardiac blood flow) in markedly weakened contractility of the left atrium and normal function of the right ventricle, which continues pumping blood into the lesser circulation. Clini-

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cally acute left atrial failure manifested by cardiac asthma and pulmonary edema may resemble acute left ventricular heart failure.

Acute right ventricular heart failure

Acute right ventricular heart failure resulted from the sharply suddenly limitation of the lung’s surface from the breathing and consequently development of the congestion in greater circulation. etiology: – thromboembolism of the pulmonary artery trunk or its branches; – spontaneous pneumothorax; – bronchial asthma (status asthmaticus); – lobar pneumonia; – lung atelectasis; – rupture of the aorta aneurism into the pulmonary artery. pathogenesis In thromboembolism of the pulmonary artery or its branches occurs mechanical occlusion of vessel lumen and complete or incomplete blood supply to corresponding part of lung. In case of pulmonary disease develops reduction of blood flow. All these disorders lead to hemodynamic disturbances at first in pulmonary circulation, later intracardial and systemic circulation. As a response to decreasing arterial amount of blood occurs the resistance of pulmonary blood flow. The right ventricular heart failure with dilation of the chamber is developed. Increasing of end diastolic pressure at right ventricle, right atrium and central veins are observed. The features of congestion in greater circulation appear.

Clinical features Clinical features of acute right ventricular heart failure include symptoms and signs due to common process and presence of complication in a form of acute pulmonary heart.

The main complaints according to leading process: severe acute pain in the chest, cough, hemoptysis in patient with thromboembolism of pulmonary artery. The general condition is extremely grave, deranged consciousness, diffuse cyanosis, pallid skin, cold sweat and dyspnea. Acute pulmonary heart is characterized by complaints on the heaviness in the right hypochondrium and edema at the low extremities.

The objective examination of respiratory, cardiovascular systems reveals the clinical features of main pathology: infarction of the lung, pneumonia, pneumothorax, atelectasis.

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The neck veins become swollen, later develops edema of legs. Epigastric pulsation and pulsation left to the sternum are determined as a result of dilation of right ventricle. Right border of the relative heart dullness displaced to the right from the sternum, the heart sounds are diminished, splitting of the second sound over the pulmonary artery, tachycardia, gallop rhythm. The pulse is small and frequent. Blood pressure: hypotension.

In palpation of abdomen the enlarged liver is observed.

Additional methods of examination ECG: in II, III standard leads – P-pulmonale, in V1–2 – signs of overloading of the right ventricle.

Chronic heart failure Chronic left ventricular heart failure

Chronic left ventricular heart failure is characterized by congestion in lesser circulation due to the decreasing contractility of the left ventricle. etiology: – essential hypertension; – symptomatic hypertension; – ischemic heart disease; – aortic valve disease; – atherosclerotic cardiosclerosis; – postinfarction cardiosclerosis; – cardiomyopathy. pathogenesis Etiological factor is development relevant to prolonged venous congestion in the lesser circulation which stimulates growth of connective tissue in the lungs and sclerosis of the vessels. in case of increasing pulmonary capillary pressure the elastic ability of lungs is decreased, disorders of ventilation occur. The respiratory centre is stimulated by accumulating under-oxidized metabolites in the blood – lactic acid, bicarbonate alkalis, and carbon dioxide. Relevant to increasing content of the reduced hemoglobin in capillary blood appears acrocyanosis. As a compensatory mechanism may be tachycardia.

Clinical features The patients complain on weakness, decreased work capacity, breathlessness, cough, firstly dry, later with sputum.

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Objective examination. Patient’s condition and consciousness is defined by stage of pathological process. Posture is forced in patients with pronounced heart failure. As usually the orthopnea is observed. The skin is pale and cold, acrocyanosis, trophic disturbances as a rule on the legs.

Objective examination of the respiratory system. The hemoptysis is observed, as a result of rupture of bronchial overfilled arterioles. Tachypnea is determined. At night time may be the attacks of cardiac asthma, transformed in pulmonary edema.

Intermediate sound is observed over the lower lobes of the lung. In auscultation decreased vesicular breathing and moist rales in the posterior-inferior parts on the lung are determined.

Objective examination of the cardiovascular system. Apex beat is displaced to the left. The left border of the relative cardiac dullness displaced to the left. The both heart sounds decreased at the apex. Second sound over the pulmonary artery is accentuated.

Additional methods of examination ECG – hypertrophy of left ventricle, left bundle branch block.

X-ray examination – congestion in lung.

Echocardiography – hypertrophy of left ventricle.

Chronic left atrial heart failure

Chronic left atrial heart failure is due to overloading of left atrium mostly in case of mitral stenosis and mitral regurgitation in late stage. The clinical features resemble the chronic left ventricular heart failure.

Chronic right ventricular heart failure

etiology: – venous congestion in lungs (chronic left ventricular failure); – chronic lung diseases; – congenital heart defects; – tricuspid regurgitation; – stenosis of pulmonary valve orifice; – kyphoscoliotic chest. pathogenesis As a result of pronounced hemodynamic overload appear the decreasing right ventricle pump function, dilation of right ventricle, relative incompetence of tricuspid valve, that lead to the elevation end-diastolic volume and venous pressure at right

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ventricle, right atrium, peripheral veins and capillaries. The central venous pressure is pronouncedly increased. Prolonged venous congestion leads to the enlarged liver, edema, ascites, and transudation of fluid into the pleural cavity and pericardium.

Clinical features The patients complain on the heaviness in right hypochondrium, thirst, loss of appetite, nausea, vomiting, edema at the low extremities.

Objective examination. Patients have a clinical sign of main pathology causing the heart failure. The features of congestion in greater circulation: swallowing of the neck veins, pulsation of the vena jugulars, and edema of the legs. Edema initially arises in the evening on the legs, has ascending character and overspread on the subcutaneous tissue of the whole body – anasarca.

Prolonged edema is accompanied by throphic skin disorders with redness, pigmentation and local ulcers.

The skin color is slightly yellow as a result of liver hypoxia and dysfunction.

Objective examination of the respiratory system may reveal the signs of main process. Due to the hydrothorax dullness and pathologically decreased or even absence of vesicular breathing are determined over one or both lungs.

Objective examination of the cardiovascular system. Cardiac beat and epigastric pulsation which increased in deep inspiration are determined. These signs are explained by hypertrophy and dilation of the right ventricle. The right border of the relative cardiac dullness displaced to the right. The heart sounds are decreased at the apex. Second sound over the pulmonary artery is accentuated.

Pulse is frequent. The change of blood pressure depends on main process.

In palpation of abdomen enlarged liver is revealed. In initial stage of chronic right ventricular heart failure liver is soft, with sharp edge, its surface is smooth, and with progression of heart failure liver becomes greater size, with high density.

Prolonged venous congestion in greater circulation leads to development of ascites.

Congestive kidneys are characterized by oliguria.

Additional methods of examination Clinical blood analysis is without specific changes.

Clinical urine analysis: oliguria in edematous phase, proteinuria, cylindruria.

ECG – hypertrophy of right ventricle, right bundle branch block.

X-ray examination reveals the features of main process.

Echocardiography – hypertrophy of right ventricle.

Classification of heart failure 1. Clinical stages according to M. D. Strazhesko and V. H. Vasilenko.

2. Variant of heart failure:

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– with systolic dysfunction of left ventricle (ejection fraction ≤ 40 %); – with normal systolic function of left ventricle (ejection fraction > 40 %).

3. Functional class according to New York Heart Association.

Classification of heart failure according to M. D. Strazhesko and V. H. Vasilenko The three clinical stages of heart failure are distinguished: I stage – initial, latent (Fig. 2.1) there are symptoms during physical exercises: dyspnea, palpitation. These symptoms subside at rest.

II stage is characterized by symptoms and signs of heart failure not only during physical exercises, but at rest. II stage of heart failure subdivided into two stages – II stage A and II stage B. In stage A there are features of congestion or lesser or greater circulation (Fig. 2.2).

The characteristic of II stage B heart failure are the features of congestion in lesser and greater circulation (Fig. 2.3). Patients are fully disabled. At rest pronounced cyanosis, swollen jugular veins, edema and ascites are revealed.

III stage heart failure is defined as final, dystrophic with marked congestion in the lesser and greater circulation, hemodynamic disorders, irreversible morphological changes of all organs, functional and metabolic disorders (Fig. 2.4).

The patient would have extreme asthenia, loss of weight, cardiac cachexia.

Skin is dry, dark, trophic skin ulcers, marked edema, hydrothorax, hydropericardium, ascites, anasarca, fibrosis of liver, lungs and kidney.

II

I

Class

Classification of heart failure according to New York Heart Association New York Heart Association Functional Classification (NYHA)

Canadian Cardiovascular Society Functional Classification

Patients with cardiac disease but without resulting limitations of physical activity; ordinary physical activity does not cause dyspnea (or fatigue, palpitation, or anginal pain) Patients with cardiac disease resulting in slight limitation of physical activity; they are comfortable at rest; ordinary physical activity results in dyspnea (or fatigue, palpitation, or anginal pain)

Ordinary physical activity, such as walking and climbing stairs does not cause angina. Angina with rapid or prolonged exertion at work or recreation Slight limitation of ordinary activity. Walking or climbing stairs rapidly, walking uphill, walking or stair climbing after meals, in cold, in wind, or when under emotional stress, or only during the few hours after awakening. Walking more than two blocks on the level and climbing more than one flight of ordinary stairs and in normal conditions

IV

III

Syndrome of cardiovascular failure

Patients with cardiac disease resulting in marked limitation of physical activity; they are comfortable at rest; less than ordinary physical activity causes dyspnea (or fatigue, palpitation, or anginal pain) Patients with cardiac disease resulting in inability to carry on any physical activity without discomfort; symptoms of dyspnea (or of angina) may be present even at rest; if any physical activity is undertaken, discomfort is increased Venous pressure

Fig. 2.1. Heart failure, stage i

57 Marked limitation of ordinary physical activity. Walking one to two blocks on the level and climbing more than one flight in normal conditions

Inability to carry on any physical activity without discomfort – anginal syndrome may be present at rest

Venous pressure

Fig. 2.2. Heart failure, stage ii a

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Chapter 2. Cardiovascular system Venous pressure

Fig. 2.3. Heart failure, stage ii B

Venous pressure

Fig. 2.4. Heart failure, stage iii

Syndrome of vascular failure

Vascular failure is the pathological condition caused by decreasing of the vascular tone and diminishing of the volume circulating blood.

Vascular failure includes: syncope, collapse, shock.

Syndrome of a syncope

Syncope – is a sudden transient loss of consciousness with rapid recovery not requiring electrical or chemical cardioversion.

Classification Classification of syncope due to the etiology: – neurally mediated syncopal syndromes vasovagal (carotid sinus, situational);

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– cardiac arrhythmias as primary cause (bradycardia, tachycardia); – structural cardiac or cardiopulmonary disease (acute myocardial infarction/ ischemia, aortic dissection, pulmonary embolus).

The underlying mechanism of pathogenesis is a relatively abrupt cerebral hypoperfusion.

Clinical features Presyncope is characterised by weakness, nausea, darkening in the eyes, noise in the ears. Syncope is characterized by loss of consciousness.

Objective examination. The person has a pallid skin, cold sweat, cold limbs, pupils are narrow, its reaction to light is present, pulse is thread, arterial pressure is decreased.

Initial evaluation may lead to a certain diagnosis based on symptoms, signs or ECG finding. This applies to the following cases: – vasovagal syncope is diagnosed if precipitating events such as fear, severe pain, emotional distress, instrumentation or prolonged standing are associated with typical prodromal symptoms; – situational syncope is diagnosed if syncope occurs during or immediately after urination, defecation, cough or swallowing; – orthostatic syncope is diagnosed when there is a documentation of orthostatic hypotension (decrease of SBP ≥ 20 mm Hg or to < 90 mm Hg) associated with syncope or pre-syncope; – syncope due to cardiac ischemia is diagnosed when symptoms are present with ECG evidence of acute ischemia with or without myocardial infarction; – syncope due to cardiac arrhythmia is diagnosed by ECG when there is: • sinus bradycardia < 40 beats/min or sinoatrial blocks or sinus pauses > 3 sec; • atrioventricular block (2nd degree Mobitz II or 3rd degree atrioventricular block); • alternating left and right bundle branch block; • rapid paroxysmal supraventricular tachycardia or ventricular tachycardia; • pacemaker malfunction with cardiac pauses.

Syndrome of collapse

The collapse is acute vascular failure due to the affection of the vascular tone primary or secondary origin. etiology: – toxicosis, acute infections; – profuse blood loss; – dehydratation; – myocardial infarction;

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– embolism of the pulmonary artery; – disordered vasomotor innervation of central origin; – after taking some drugs; – metabolic disorders. pathogenesis Collapse develops due to upset central nervous regulation of the vascular tone.

Diminished vascular tone disturbs normal distribution of blood in the body: the amount of deposited blood increases, especially in the vessels of the abdominal organs, whereas the volume of circulating blood decreases. The stroke volume of blood is decreased and arterial and venous pressure is diminished as well.

Clinical features A collapse characterizes by giddiness, darkening in the eyes, noise in the ears, weakness, then often by loss of consciousness.

Objective examination. Pallid skin with a marble tint, cold sweat, cold limbs, decreasing of body temperature, accelerating and superficial respiration. The heart sounds are decreased, tachycardia, small, accelerated and thread pulse, decreasing arterial and venous blood pressure.

Syndrome of shock

Shock is the clinical syndrome that develops when there is critical impairment of tissue perfusion to some organs.

Classification according to pathophisiological picture Hypovolemic shock secondary to any condition provoking a major reduction in blood volume: – internal/external hemorrhage; – severe burns; – acute pancreatitis; – dehydration.

Normovolemic shock secondary to capillary damage, arteriovenous shunting and inappropriate vasodilatation: – septic shock; – anaphylactic shock.

Cardiogenic shock, caused by any form of severe heart failure: – myocardial infarction; – acute massive pulmonary embolism; – heart tamponade due to pericardial enfusion.