Clinical Pathophysiology Of Cardiovascular Diseases

1. Clinical Pathophysiology Of Cardiovascular Diseases Ph. D., M D. Svitlana Dzyha

2. Blood pressure is one of the most variable but best regulated functions of the body. The purpose of the control of blood pressure is to keep blood flow constant to vital organs such as the heart, brain, and kidneys. The continuous elevation of blood pressure that occurs with hypertension is a contributor to premature death and disability due to its effect on the heart, blood vessels, and kidneys.

4. The level of blood pressure in the healthy people is the very stable value. • The stability of blood pressure is supported by regulative systems. • Hayton (1974) divided them into two groups – hemodynamic system and regulative system. Arterial blood pressure normal range: Systolic – 100-125 (equilibration 100-139) mmHg Diastolic – 70-80 (equilibration60-89) mmHg

5. Regulation of arterial pressure (АP)by hemodynamic system Formula: АP = CO · PR CO – cardiac output PR – peripheralvascularresistance (dependedtoarterioles tone) CO leads to PR and АPnormalizes finally PR leads to COand АPnormalizes finally AP normal range: Systolic – 100-125 (equilibration 100-139) mmHg Diastolic – 70-80 (equilibration60-89) mmHg

6. Mechanisms of Blood Pressure Regulation • Short-term regulation • neural mechanisms • hormonal mechanisms • Long-term regulation

7. NEURAL MECHANISMS

8. Location and innervation of the aortic arch andcarotid sinus baroreceptors and the carotid body chemoreceptors.

9. Barroreceptors of the vessels Afferent impulses Medulla oblongata (vessel’s active center) Heart (COincrease atdecreased АP) Arterioles (spasm) Еfferent і impulses Regulative systems 1. Barroreceptors of aorta arch and sinus caroticus

10. Regulative systems

11. Role of the vasopressin in arterial hypertension pathogenesis

12. Classification Arterial hypertension AP above 139/89 mm Hg Arterial hypotension Primary Secondary AP less than 100/60 mm Hg Acute Chronic

13. Arterial hypertension (АH) AP elevation (value above 139/89 mm Hg), which is resulted from rising of peripheral vessels resistance (one of the most common cardiovascular disorders)

14. Classification Primary AH (essential, hypertonic disease) Secondary AH (that is happened in 10 -20 % cases). It’s a symptom of some disease course

15. Etiology (primary AH) Reason is unknown. AH is polyetiological disease. AH arises on the ground of genetically peculiaritiesof metabolism. That is possible to have genetically defect of the systems, which control relaxation of the smooth muscle cells of the arterioles.

16. Contributing factors Risk Factors Family history of hypertension Race Age-related increases in blood pressure Diabetes mellitus

17. Contributing factorsLifestyle Factors Stress High sodium intake Excessive calorie intake and obesity Physical inactivity Excessive alcohol consumption Oral contraceptive drugs

18. Pathogenesis AP = СO х PR Increase of circulative blood volume (CBV) Emotional excitement (SNS activation) Cardiac output (CО) increase Peripheral vessels resistance increase Kidney functions violation

19. Pathogenesis Increase of circulative blood volume (CBV) NaCl (intakemore 5 g/day) Reasons Decrease Naexcretion by kidney (kidneydiseases)

20. Pathogenesis 1. CBV increase Na accumulation in vessels smooth muscle walland increase of its osmotic pressure Naretention in blood Blood osmotic pressure increase Vessels wall edema Vessels smooth musclesensitivity to vasoconstrictive influences increase (noradrenalin, adrenalin, endothelin, angiotensin) Hypervolemia Vessels narrowing Cardiac output increase Vessels spasm Peripheral vessels resistance increase AP elevation Formula: АP = CO · PR

21. Pathogenesis 2. Cardiac output increase (CO) Circulative blood volume increase (CBV) Reasons Emotional stress Physical (overload) stress Hyperthyroidism

22. Pathogenesis 2. Cardiac output increase SAS activation Adrenalin excretion Increase of cardiac contractility force Increase of heart beats Increase of cardiac output AP elevation Formula: АP = CO · PR

23. Pathogenesis 3. SAS activation SAS activation Suprarenal glands activation Interaction adrenalin and alpha-adrenoreceptors Venues smooth muscles spasm Arterioles smooth muscles spasm Increase of circulative blood in big blood circle Noradrenalin Аdrenalin adrenoreceptors of heart alpha-adrenoreceptors of vessels Arterioles narrowing Increase of CBV PR increase Arterioles narrowing CO increase CO increase AP increase Formula: АP = CO · PR

24. Pathogenesis 4. Kidney functions violation Long time spasm of kidney arteries • Angiotensin 2 effects • Smooth muscles contraction in the vessels • Stimulation of the vasoactive center in brain • Noradrenalin excretion increase • Adrenalin excretion increase from suprarenal glands • Aldosteron excretion increase from suprarenal glands(Na retention due to kidney) AP decrease in renal capillaries Activation of JGA Renin excretion Angiotensin 2 synthesis AP increase

25. Depressive function of kidney – synthesis of the substances for AP reduce dilates renal arteries, reduces renin synthesis and reduces Na reabsorbing in kidney PG Е 2 ! ! ! Exhaustion of kidney depressive function leads to arterial hypertension stabilization Phospholipid Renin Inhibitor Angiotensinase Phosphatydilcholin alkali ethers

26. Increase of vesseles resistance • It is the defining mechanism. Irrespective of first reason, in the patients with hypertonic disease almost always increases peripheral resistance. • It is considered, that the essence hypertonic disease just is in increase of peripheral vessels tonus. Hyperkinetic phase, which is connected to increase of cardiac output, happens only at early stages of disease and not in all patients.

27. The hereditary predisposition

28. EtiologysecondaryАH • Renal • (resulted from kidney pathology) Glomerulonephritis Acute renal failure Pyelonephritis Acute urinary tract obstruction Kidneydamage at collagenosis Kidneyamiloidosis Kidneytumor Diabetic nephropathy Nephropathy of the pregnant Hereditary defect of renal vessels Renal vessels atherosclerosis, embolism or thrombosis Polycystic kidney disease

29. EtiologysecondaryАH 4. Endocrinopathy (develops in the result of endocrine glands pathology) Acromegaly (Somatotropin over production by the pituitary gland anterior part) Hyperaldosteronism (aldosteronover excretion by suprarenal glands) Cushing's disease (Adrenocorticotropin over productionby the pituitary gland anterior part) Menopause (age-depended decrease of female gonads activity – estrogens excretion decrease) Possible mechanism – deficit of NO synthesis by endotheliocytes Pheochromocytoma

30. EtiologysecondaryАH 5. Neurogene (is accompanying to nerves system pathology) Encephalitis Brain tumor Braintrauma Brainischemia Brainhemorrhage

31. EtiologysecondaryАH 6. Cardiac Heart failure Heart defect 7. Drug-induced Drugs, which cause vessels spasm (influent on kidney), hormonal contraceptives

32. Arterial hypertension after-effects 1stperiod functional violations (heart hypertrophy) • 2dperiod • Pathological changesin arteriesand arterioles (dystrophy): • Arterioles sclerosis • Arteriole’swall infiltration by plasma (leads to dystrophy) • Arterioles necrosis (hypertonic crisis arisesin clinic) • Vein’s wall thickening

33. Arterial hypertension after-effects 3dperiod Secondary changes in organs and systems CNS – brain hypoxia – neurons destruction – apoplexy (because vessels destruction and rupture leads to brain hemorrhagesand brain destruction) Kidney (nephrosclerosisandchronic kidneyinsufficiency) • Organs of vision • retinopathy (retina’svessels injury) • hemorrhages and separation (exfoliation) of retina, that leads to blindness Heart Decompensate heart failure Endocrine system Glands atrophy and sclerosis