1. CARDIAC INSUFFICIENCY PATHOLOGY OF VASCULAR TONE
Lecturer: PhD Ivanytsa A.
Vinnytsya National Pirogov Memorial Medical University
Pathophysiology Department

2. Insufficiency of blood circulation of is the state when the cardio-vascular system can not provide organs and tissues of an organism with necessary amount of blood .

3. Cardiac insufficiency is the pathological condition characterized by inability of the heart to provide blood supply of organs and tissues in accordance with their necessities.

4. Classification of cardiac insufficiency
1.According to clinical course cardiac insufficiency is divided into:
acute;
chronic.
2.According to clinical manifestations intensity cardiac insufficiency is divided into:
compensated;
decompensated.

5. left ventricle cardiac insufficiency;
3.According to injured parts of the heart cardiac insufficiency is divided into:
left ventricle cardiac insufficiency;
right ventricle cardiac insufficiency;
total cardiac insufficiency.

6. 4.According to pathogenesis cardiac insufficiency is divided into:
cardiac insufficiency due to overload of the heart:
-overload of heart by volume (reasons: heart disease with valvular insufficiency, hypervolemia);
-overload of heart by resistance (reasons: heart disease with valvular stenosis, arterial hypertension);

7. cardiac insufficiency due to damage of myocardium (reasons: arrhythmias, myocarditis, myocardiopathys);
cardiac insufficiency due to violation of the coronary blood circulation (reasons: atherosclerosis, tromboembolism or spasm of coronal vessels);
cardiac insufficiency due to the injury of pericardium (acute and chronic pericarditis, cardiac tamponade);
mixed form.

8. Cardiac insufficiency due overload of the heart
1.overload by blood volume - emerges when the inflow of the blood to a definite part of the heart is increased:
hypervolemia
valvular insufficiency

9. 2. overload by resistance - emerges when the resistance to the heart outflow is increased and develops at:
arterial pressure increase
valvular stenosis (the left ventricle overload develops at aortal stenosis, at mitral stenosis - left atrium, at pulmonary valve artery stenosis - right ventricle, at tricuspid stenosis - right atrium).

10. Cardiac insufficiency due to damage of the myocardium
Etiology:
arrhythmias - related to the damage of the heart conducting system;
myocarditis - related to the damage of myocardium of inflammatory origin (e.g., bacteria, viruses, fungi, allergens, toxic factors);
myocardiopathys - related to the congenital or acquired damage of myocardium noninflammatory origin (e.g., alcohol, anemia, intoxication, hypoxia).

11. Cardiac insufficiency due to violation of the coronary blood circulation
Insufficiency of coronary blood circulation is the pathology which is characterized by inability of coronary vessels to supply blood to the heart in accordance with its requirements.

12. Coronary heart disease (CHD) is illness which develops as a result of absolute insufficiency of coronary circulation and characterized by the myocardium damage.
Etiology:
atherosclerosis of coronary vessels;
thromboembolism of coronary vessels;
primary thrombosis or embolism of coronary vessels
spasm of coronary vessels
inflammation in the coronary vessels ,(e.g., rheumatism); compression of coronary vessels (e.g., scars, tumors, ligature).

13. Main clinical forms of CHD:
1.Stenocardia (angina pectoris) is characterized by attacks of brief (to 20 min) acute myocardium ischemia which are accompanied by a pain syndrome, sense of fear, vegetative reactions, pain is relieved by nitroglycerine
2. the preceding infarction state is the acute focal myocardium dystrophy which develops during myocardial ischemia from 20 to 40 min;

14. 3. the myocardial infarction is the necrosis of myocardium, caused by coronary circulation violation. Emerges at a reversible ischemia continued over min, or at irreversible coronary circulation violation , «-» effect of nitroglycerine
4.cardiosclerosisis the sclerotic changes of cardiac muscle. It can be diffuse (atherosclerotic cardiosclerosis) and focal (postinfarction atherosclerotic cardiosclerosis).

15. Clinical syndromes which characteristic for the myocardial infarction
pain;
acute cardiac insufficiency - develops at the injury of large areas of myocardium and characterized by the cardiac asthma syndrome, pulmonary edema or cardiogenic shock;
arrhythmia - possibly development of all types of arrhythmias at myocardial infarction. Appearance of ventricular fibrillation is the most dangerous;
reperfusion syndrome;
resorption - necrotizing syndrome.

16. Clinical signs which characteristic for the myocardial infarction
Unbearable pain behind the breastbone with irradiation in the left shoulder, arm and others.
The skin is pale, cold.
His face covered with sweat, with a bluish tinge.
Pulse is thready, weak filling, frequent, sometimes arrhythmic.
Pulmonary edema.

17. MI Laboratory Diagnostics: Elevated level of enzymes
MI Laboratory Diagnostics: Elevated level of enzymes !!!!: (damage of cell membranes) ↑ CPK (creatine phosphokinase) ↑ AST, ALT ↑ LDH1,2 2. ↑ troponins 3. neutrophilic leukocytosis, left shift of leukogramm 4. ↑ ESR

18. ECG changes
1. Zone Necrosis - pathological Q wave or QR, QRS, QS 2. Zone damage - domed lifting ST, which is a sign of acute stage and discordant changes of the opposite parts; 3. Zone of ischemia - negative, high, spiky T.

19. Сomplications of myocardial infarction
Reperfusion syndrome emerges as a result of re-establishment blood flow in the area of myocardial ischemia over 40 min ischemia duration.
The pathogenetic basis of the reperfusion syndrome is so-called «oxygen paradox», because of the lipid peroxidation activating and plenty of free radicals
formation which damage the cellular membranes.

20. Cardiogenic shock emerges as a result of the acute falling of the pumping ability of the heart.
Etiology:
myocardial infarction;
congestive heart failure;
cardiomyopathy;
pulmonary edema;
cardiac tamponade;
ineffective pumping due to cardiac dysrhythmias and from acute disruption of valvular function.

21. Pathogenesis of cardiogenic shock:
1. The initial ↓ of arterial pressure 2. Compensatory spasm of arterioles 3. Secondary ↓ of arterial pressure 4. Terminal changes

22. Resorption - necrotizing syndrome at the myocardial infarction is the outcome of the entry of necrotic products of myocardial disintegration into blood
Signs:
fever;
neutrophilic leukocytosis;
increase of ESR;
appearance in the blood of enzymes from damaged cardiomyocytes (creatine kinase, AST, LDH;)

23. Dressler's syndrome - develops as a result of autoantibodies’ production on the changed myocardium proteins and characterized by serous membranes inflammationnism - polyserositis (c.g., pericarditis, pleurisy, peritonitis).

24. Cardiac insufficiency due to pathology of the pericardium
Etiology:
pathology of pericardium, as a result heart’s work is violated during a diastole (e.g., exudate or transudate accumulation in the cavity of pericardium, acute cardiac tamponade).
Clinical signs:
arterial hypotension;
diminishing of ECG wave voltage;
enlargement of the heart.

25. Acute cardiac tamponade
Acute cardiac tamponade is rapid accumulation of liquid in the cavity of pericardium because of hemorrhage at the wound or cardiac rupture, or at quickly developing pericarditis

26. Mechanisms of compensation of the heart's work
urgent mechanisms of compensation:
the heterometric mechanism provides compensation at the cardiac overload by a volume (reasons: heart disease with valvular insufficiency, hypervolemia). Its essence consists in the increase of force of the heartbeats in the case of entrance to the heart of bigger blood volume (а law of Frank-Starling’s) the homeometric mechanism provides compensation at the cardiac overload by resistance (reasons: heart disease with valvular stenosis, arterial hypertension). Its essence consists in the increase of force of the heartbeats in case of the increase of resistance to blood flow.
tachycardia provides constant level of the minute blood volume.

28. Mechanism of long duration adaptation of the heart is the myocardial hypertrophy.
myocardial hypertrophy according to F. Meerson:
myocardial hypertrophy in sportsmen - develops at periodically increasing loadings; it's characterized by the increase of all parts of the heart (myocardiocytes,vessels and nerves)
compensotory myocardial hypertrophy:
1.hypertrophy due to overloads (develops at the cardiac insufficiency, arterial hypertension);
2. hypertrophy due to the damage (e.g., atherosclerosis, myocarditis).

29. stage of complete hypertrophy and relatively proof hyperfunction
Stages of compensatory heart hypertrophy development of according F. Meerson:
emergency stage
stage of complete hypertrophy and relatively proof hyperfunction
stage of gradual exhaustion and progressive cardiosclerosis

30. Dilatation of myocardium
Tonogenic dilatation - this is expansion of heart cavities, that is accompanied by the increase of stroke volume of blood. Develops as a result of activating of heterometric mechanism of provides compensation.
Myogenic dilatation arises up at the dystrophic changes of myocardium. It is accompanied by expansion of cavities of heart and decrease of force of cardiac contractions. Arises up during decompensation of cardiac insufficiency.

31. Indicators hemodynamic:
blood flow velocity;
circulatory blood volume
stroke volume of the heart
cardiac output
heart rate
cardiac index
Arterial pressure
venous pressure
total peripheral resistance
rate of oxygen utilization

32. The indices of hemodynamics change during cardiac decompensation:
cardiac output diminishes;
under the left ventricle cardiac insufficiency:
1)arterial hypotension in the systemic circulation;
2)common peripheral resistance increases;
3)hypertension of the pulmonary circulation, which leads to the lungs edema;
under the right ventricle cardiac insufficiency
1) hypotension of the pulmonary circulation;
2) resistance of the pulmonary circulation vessels increases hereupon;
3)central venous pressure increases which leads to the congestion in the systemic circulation;
the circulatory blood volume increases.

33. Clinical symptoms of cardiac insufficiency:
circulatory hypoxia;
shortness of breath because of acidosis and lungs edema; cyanosis because of venous hyperemia;
edema (under the right ventricle cardiac insufficiency edema develops on the lower extremities, under the left ventricle cardiac insufficiency develops lungs edema);
portal hypertension and cardiac cirrhosis develops under the right ventricle cardiac insufficiency;
ABB violations: metabolic lactate acidosis because of the lactic acid accumulation and gas alkalosis because of shortness of breath; secondary hyperaldosteronism due to activating of the renin-angiotensin- aldosteron system and because of diminishing of aldosteron disintegration in the liver
Cyanosis (↑ concentration of reduced hemoglobin ).

34. Acute cardiac insufficiency develops quickly, at the surplus loading on a heart, when all compensatory mechanisms are not corrected with it , e.g., at the myocardium infarction and its complications (cardiogenic shock, tamponade of heart), at arrhythmias (fibrillation of heart, paroxismal tachycardia, complete atrioventricular blockade), acute pericarditis, myocarditis, embolism of pulmonary artery.

35. Clinical manifestations
1) cardiac asthma, 2) pulmonary edema 3) cardiogenic shock.

36. Acute left ventricular insufficiency

37. Chronic (stagnant) cardiac insufficiency develops gradually, mainly as a result of metabolic violations in myocardium at protracted hyperfunction of heart or different types of myocardium damage (e.g., arterial hypertension, cardiomyopathys, and others).

38. Normal AP: -100 - 120 / 70-80 mm Hg (17 - 20 )
Arterial hypertension is the increase of systolic pressure more than I40mni Hg and diastolic more than 90mm Hg.

39. Classification of arterial hypertension :
primary hypertension (essential or idiopathic hypertension) appears to be a familial disease of unknown etiology
secondary hypertension develops secondary to another disease;
hypertensive crisis is a sudden acute elevation in arterial blood pressure
isolated systolic hypertension refers to an elevation in systolic blood pressure greater than 140 mm Hg without a concurrent elevation in diastolic blood pressure (elderly persons)

40. II. The type of high blood pressure: 1. Systolic. 2. Diastolic. 3
II. The type of high blood pressure: 1. Systolic. 2. Diastolic. 3. Mixed. ІІІ. The value of the cardiac output (cardiac output): Hyperkinetic: ↑cardiac output (↑ circulating blood volume). Hypokinetic: ↑vascular resistance(hypertension) - ↑ diastolic blood pressure. Eukinetic. IV. The level of renin: hyperreninemic. Normoreninemic.Hyporeninemic

41. Etiology:
Primary hypertension results from unknown causes, it accounts for 80% of hypertension cases.
Secondary hypertension 10% of hypertension cases:
renal diseases-may cause accelerated renin release, which, in turn, elevates blood pressure;
Cushing's syndrome, which causes accumulation of extracellular sodium and water;
primary aldosteronism, which causes accumulation of extracellular sodium and water;
hypothyroidism and hyperthyroidism
coarctation of the aorta
excessive alcohol ingestion and prolonged use of oral contraceptives.

42. Risk factors of essential hypertension:
main factors:
psycho-emotional overload (chronic stress situations)
Excessive consumption of salt,
hereditary predisposition,
low body weight at birth
male sex; middle age ; black color of skin; hypodynamia;
insulin resistance;
urban population, bad habits (e.g., cigarette smoking).

43. Pathogenesis of primary (essential) hypertension
Dysregulatory theory - violations of regulatory mechanisms of arterial vessels tone.
There are two phases:
1. Hyperkinetic
1 stage: activation of the sympathetic and adrenal system under the action of stress factors
2 stage: activation of the rennin-angiotensin-aldosteron system
3 stage: activation of aldosteron and vasopressin systems

44. Pathogenesis of primary (essential) hypertension
2. Hypokinetic - is characterized by the irreversible structural changes of compession and resistance vessels, peripheral vascular resistance and arterial vessels tone grows as a result constantly. The main significance has following factors:
constant spasm of arterioles;
hypertrophy of smooth muscles;
atherosclerosis and substitution of smooth muscles by connective tissue.

45. Pathogenesis of primary (essential) hypertension
Membrane theory is the hereditarily conditioned violation of ionic pumps of membranes of smooth muscles fibers:
defect of Ca2+- pump- this leads to the development of permanent contraction and the increase of peripheral vascular resistance.
decrease work of Na -K –pump - the outcome is the thickening of vessel’s wall and diminishing of diameter of vessels increase of sensitization to the action of catecholamine, damage and necrosis of cells, atherosclerosis).

46. Arterial hypotension
is the decrease of systolic pressure less than 100 Hg and diastolic less than 60 mm Hg.
Kinds:
Physiological (it is not accompanied by the symptoms of illnesses).
Pathological:
А) acute (shock and collapse)
B) сhronic (primary and secondary):

47. secondary (symptomatic) arterial hypotension is a result of acute and chronic heart diseases (congenital heart diseases, myocarditis, infarction of myocardium); brain diseases, lungs diseases (croupous pneumonia), liver diseases (hepatitis, mechanical jaundice), blood diseases (anemia), endocrine diseases (Addison’s disease) and intoxications;
primary arterial hypotension develops at patients with neurocirculatory dystonia of hypotension type (essential, primary, idiopathic hypotension).

48. Collapse
Collapse is acute vascular insufficiency which is characterized by the acute dicrease of arterial vessels tone and central- venous pressure and diminished circulatory blood volume.
Types of collapse:
toxic and infectious collapse, - develops at intestinal infections (dysentery, salmonellosis) due to the action of endotoxins (after death of microorganisms).
hemorrhagic collapse - arises up at acute massive bleeding and related to the rapid decrease, of volume of circulatory blood
pancreatic collapse - at the mechanical trauma of pancreas or acute pancreatitis and liberation of tripsin in blood
orthostatic collapse - arises up in acute transition from horizontal position to vertical position
anoxic - arises up at the rapid decrease of partial pressure of oxygen in air, as a result of anoxemia develops, decrease of vessels tone

49. Pathogenesis of collapse
The decrease of volume of circulatory blood and vessels’ tone leads to the decrease of venous return to the heart, decrease of cardiac output decrease of both arterial and venous pressure and disturbance of tissues perfusion and metabolism, which leads to the brain hypoxia.

50. Atherosclerosis
is pathology of vascular wall, which characterize by the sedimentation of lipids, elements of blood, calcium and connecting tissue in its internal membrane (tunica intima).

51. Risk factors of atherosclerosis:
Hypertension;
metabolic disturbances;
hormonal violations;
pathology of vascular wall;
cigarette smoking
elevated serum cholesterol
obesity
diabetes mellitus
Other presumed risk factors include increasing age, physical inactivity, and a family history of arteriosclerosis.
Incidence is higher in men than in women.

52. Pathophysiologic processes and manifestations
It has two theories:
1. primary damage of vessel wall
2.secondary deposit of cholesterol and lipoproteids of low density
Complications of atherosclerosis:
ischemia;
heart attack;
aneurism.