1. Hypertension Dr. Raid Jastania

2. Physics

3. Pressure α Volume of Blood Pressure α Peripheral Resistance

4. Physics Volume of Blood = Heart Rate x Stroke Volume Heart Rate is controlled by SA node, autonomic nervous system Stroke Volume: – Frank–Starling mechanism or law) states that the stoke volume of the heart increases in response to an increase in the volume of blood filling the heart (the end diastolic volume). – Volume of Blood controlled by fluid/salt intake, renal regulation, and aldosterone

5. Physics Peripheral Resistance: – Resistance to flow that must be overcome to push blood through the circulatory system – Results of vascular compliance, vasoconstriction, vasodilatation – Controlled by endocrine and neurogenic system – Who determines the peripheral resistance: Pre capillary arterioles

6. Physics Pressure α Volume of Blood Pressure α Peripheral Resistance What is the effect of: Diuretics, beta-blockers, Ca channel blockers, vasodilators….

7. Hypertension Functional abnormality of the vascular system Not a single disease, it is rather a clinical state of high blood pressure Many causes Types: Primary, Secondary – Primary (no structural abnormality) – Secondary (there is clear structural abnormality)

8. Hypertension Hypertension affects 20% of the population. It is seen in more than half of cases of myocardial infarction, stroke and chronic renal failure. Hypertension is more severe in blacks and results in complications. Hypertension is seen in more than ¾ of cases of dissecting aortic aneurysm, intracerebral hemorrhage, and rupture of myocardial wall. 95% of hypertension is due to unknown cause, “essential” or primary hypertension.

9. Definition Diastolic pressure: – 90 – 104 mild – 105 – 114 moderate – >115 severe Systolic pressure: – >160 Malignant hypertension: – Usually >200/140 – Papilledema Accelerated hypertension: – Rapid increase in blood pressure (our of the norm) in a given person

10. Classification Systemic hypertension with wide pulse pressure: – Arteriosclerosis – Aortic regurgitation – Thyrotoxicosis – Fever – A-V fistula – PDA Systolic and Diastolic hypertension: – Renal: Glomerulonephritis Renal failure Polycystic kidney – Endocrine: Cushing Hyper aldoseronism Pheochormocytoma Oral contraceptives – Neurogenic – Essential Hypertension

11. Etiology/Pathophysiology Hereditary Environmental: – Salt – Obesity – Alcohol – Family size – crowding Renin: – Low-Renin hypertension – Non-modulating – High-Renin hypertension

14. Renin-Angiotensin system In experiment: renal artery occlusion - production of renin - converts Angiotensinogen to AngiotensinI - AngiotensinII which result in: a.Increase sympathetic activity leading to vasoconstriction b.Increase aldosterone production leading to Na and water retention c.Direct vasoconstriction action d.Release ADH e.Stimulate Thirst centers f.Myocardial hypertrophy The end result is increase in cardiac output and increase in the systemic peripheral resistance.

15. Low Renin Hypertension: – Volume overload – ? Unidentified aldosterone – ? Sensitivity of adrenal to Angiotensin II – Corrected by spironolactone High Renin Hypertension: – High Renin – No good response to ACEI – ? Active adrenergic system Non Modulating Hypertension: – No control of Salt intake – Normal Renin level – Salt sensitive – Corrected by ACEI

16. Chloride and Calcium – Cl also cause hypertension – Ca/ Ca channels blockers Cell Membrane defect: – Result in high intracellular Ca – Hyper responsive smooth muscle of vessles Insulin Resistance: – Hyperinsulinemia – Renal Na retention – Vascular smooth muscle hypertrophy – Increase cytosolic Ca Other: – Age: young – Race: Blacks – Sex: male – Obesity, alcohol, cholesterol, glucose intolerance

17. Complications Atherosclerosis Heart: – Increase load – Concentric LV hypertrophy – Dilatation – Ischemic heart disease – Large heart – Aortic Regurgitation – Heart failure Renal: – Arteriosclrosis – Decrease GFR – Tubular dysfunction – Proteinuria – Hematuria – Renal failure

19. Complications Retina: – Vascular spasm, narrowing – Hemorrhage – Excudate – Papilledema – Blurred vision – blindness CNS: – Occipital headaches – Dizziness – Syncope – Infarction – Hemorrhage – Encephalopathy – Increase ICP, Seizures Malignant Hypertension: – Fibrinois necrosis of arterioles and small arteries

20. Secondary Hypertension Renal artery stenosis Chronic renal diseases Conn syndrome Cushing syndrome Pheochromocytoma Hyperthyroidism Coarctation of aorta Renin-secreting tumors Atherosclerosis

21. Pathology Compromised lumen of small muscular arteries and arterioles by: Active contraction of vessels Increase thickness of vessel wall Benign Arterioslerosis and Arteriolosclerosis: – Mild chronic hypertension – Increase thickness of vessel wall with hyaline change due to accumulation of basement membrane material and plasma proteins. – Redublication of internal elastic lamina – Changes seen in kidneys called nephrosclerosis

23. Pathology Malignant (accelerated) hypertension: – Elevated blood pressure >160/110 – Progressive vascular compromise – Affecting brain, heart, kidneys – Retina: segmental constriction and dilatation of arterioles, micro aneurysm, focal hemorrhage, necrosis, edema – Fibrinoid necrosis of muscular small arteries – Smooth muscle proliferation with concentric pattern: “onion-skin” appearance.

25. Hypertensive Heart disease left ventricular hypertrophy in a person with hypertension. – Other causes of left ventricular hypertrophy must be excluded. – This results as an adaptive response to the increase in mechanical stress. – There is change in the genes controlling the expression of myosin and actin and other cellular constituents.

26. Hypertensive Heart disease There is increase in the metabolic requirement, but the hypertrophy makes the left ventricle stiff resulting in increase in the wall tension, and decrease the diastolic filling, and the cardiac output. The changes make the heart at increase risk of ischemic disease, myocardial infarction, arrhythmias and heart failure

27. The heart weight usually exceeds 450g. There is concentric hypertrophy of the left ventricle In long-standing cases dilatation of the left ventricle occurs Cardiac muscles show enlargement of size, and nuclei Coronary artery disease is present in most cases Heart failure may occur