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Hypertensive Vascular Disease Hypertensive Heart Disease Introduction • • • Systemic and local blood pressure must be tightly regulated Low pressure • • Inadequate perfusion of organs Dysfunction and death High pressure • • No additional benefit Induces damage Introduction • Elevated blood pressure is called Hypertension • Mechanisms of normal blood pressure • Mechanisms of Hypertension • Pathologic changes in small blood vessels Mechanisms of normal blood pressure • Continuously distributed variable • Hypertension is one end of spectrum • A sustained diastolic pressure of more than 90 mm Hg • A sustained systolic pressure of more than 140 mm Hg • 25% in general population have hypertension Types of Hypertension • Essential or Primary Hypertension • Secondary Hypertension • Renal • Endocrine • Cardiovascular • Neurologic Types of Hypertension • Secondary Hypertension • Renal • • • • • Acute glomerulonephritis Chronic renal disease Polycystic kidney disease Renal artery stenosis Renin Producing tumors Types of Hypertension • Secondary Hypertension • Endocrine • Adrenocortical hyperfunction • Exogenous hormones • Pheochromocytoma • Acromegaly • Hypothyroidism • Hyperthyroidism Types of Hypertension • Secondary Hypertension • Cardiovascular • Coarctation of Aorta • Polyarteritis Nodosa • Increased intravascular volume • Increased cardiac output • Rigidity of Aorta Types of Hypertension • Secondary Hypertension • Neurologic • Psychogenic • Increased intracranial pressure • Sleep apnea • Acute stress including surgery and EXAMS!!! Regulation of normal blood pressure • Blood pressure is proportional to cardiac output and peripheral vascular resistance. • Cardiac output and Peripheral resistance determined by • Genetic factors • Environmental factors • Demographic factors Hypertension • Major factors that determine blood pressure are • Age • Gender • Body mass index • Diet (sodium intake) Normal pressure • Kidney plays an important role • • • • • Renin angiotensin mechanism Kidney produces Prostaglandins and NO counter balance the effect of angiotensin When blood volume decreases, GFR decreases which leads to reabsorption of sodium Natriuretic factors - inhibit sodium reabsorption and cause diuresis When renal excretory function is impaired, increased arterial pressure is a compensatory mechanism Secreted by liver Circulates in blood 11 Renin Juxta Glomerular Apparatus Angiotensinogen Angiotensin 1 11 Medulla Oblangata to increase CO Angiotensin 11 Vasoconstriction ACE Walls of capillaries Adrenal gland Stimulates secretion Aldosterone Of ADH Sodium Mineralocorticoids Constrictors Dilators Angiotensin11 Prostaglandins Catecholamines Kinins Blood Volume Humoral factors = Blood pressure Cardiac factors 0 90 Cardiac factors X Peripheral resistance 0 90 0 90 Cardiac output Heart rate Contractility Constrictors Dilators Alpha adrenergicBeta adrenergic Mechanism in Essential Hypertension • Results from an interaction of genetic and environmental factors that affect cardiac output and peripheral resistance Cardiac output X Peripheral resistance = Blood pressure Genetic disorders • Gene defects in enzymes: Aldosterone synthase, 11b-Hydroxylase • Mutations in proteins: Liddle syndrome Defects in renal sodium balance Defects in vascular Smooth muscle growth and structure Vasoconstriction Inadequate sodium excretion Salt and water retention Increased Plasma and ECF volume Increased cardiac output 360 Increased vascular wall thickness Increased vascular reactivity Increased total peripheral resistance HYPERTENSION Pathology of Hypertension • Accelerates atherogenesis • Causes degenerative changes in the wall of large and medium sized arteries • Also affects small blood vessels • Hyaline aretriolosclerosis • Hyperplastic arteriolosclerosis Hyaline arteriolosclerosis • Consists of homogeneous, pink, hyaline thickening of the walls of arterioles, with loss of underlying structural details and narrowing of lumen • Frequently in elderly, normotensive and hypertensive • Common in diabetes • Major morphologic characteristic of Benign Nephrosclerosis Hyaline arteriolosclerosis • Lesions reflect • leakage of plasma proteins • Excessive ECM production Hyperplastic arteriolosclerosis • Related to more severe and acute elevations of blood pressure • Characteristic of but not limited to Malignant hypertension (Diastolic pressure > 120 mmHg) • Onion skin, concentric laminated thickening of the walls of arterioles with progressive narrowing of the lumen • If associated deposits of fibrinoid necrosis necrotizing arteriolitis - Hyaline arteriolosclerosis Hyperplastic arteriolosclerosis Necrotizing arteriolitis •Consequences of Hypertension: • Blood Vessels • Atherosclerosis, Arteriolosclerosis. • Heart • Enlarge, Ischemia, Infarction. • Kidney • Ischemia, Infarction, Nephrosclerosis. • Eyes: • Retinopathy – Ischemia, infarction. • Brain: • Ischemia, infarction, Haemorrhages. Malignant Hypertension: •Rapidly progressive end organ damage. •May complicate any type of HTN. •Artery necrosis with thrombosis. •Rapidly developing renal failure. •Hypertensive encephalopathy. •Left ventricular failure. •less time No hypertrophy …! COMPARISON BETWEEN BENIGN AND MALIGNANT HYPERTENSION •characteristic - benign : malignant •aetiology - usually primary : primary or secondary •age - middle age, elderly : young, middle age •incidence - common : uncommon •course - very slow (years) : rapid (months) •blood pressure - diastolic 90-120, very slow rise : diastolic >120, very rapid rise Hypertensive heart disease • Hypertensive heart disease is the response to increased demand induced by systemic hypertension Hypertensive heart disease • Systemic (left sided) hypertensive heart disease • Pulmonary (right sided) hypertensive heart disease (cor pulmonale) Hypertensive heart disease • Systemic (left sided) hypertensive heart disease • Pressure overload can lead to • Myocardial dysfunction • Cardiac dilation • CHF • Sudden death Hypertensive heart disease • Systemic (left sided) hypertensive heart disease • Criteria for diagnosis of Hypertensive heart disease • Left ventricular hypertrophy • History or pathologic evidence of hypertension • Hypertensive heart disease Systemic (left sided) hypertensive heart disease • Morphology • • • • • Overload hypertrophy No dilation of left ventricle Increased ratio of wall thickness to radius Increased weight of the heart disproportionate to the size (wt may exceed 500 gms) Left ventricle over time becomes stiff and impairs ventricular filling leading to left atrial dilation Hypertensive heart disease • Systemic (left sided) hypertensive heart disease • Morphology - Microscopy • Earliest change - increase in the transverse diameter of myocyte (difficult to appreciate on LM) • Later - cellular and nuclear enlargement • Variation in cell size • Interstitial fibrosis Hypertensive heart disease • Systemic (left sided) hypertensive heart disease • Clinical features • • • Compensated HHD may be asymptomatic May present with atrial fibrillation or CHF with cardiac dilation Consequences • • • Normal longevity Progressive ischemic heart disease Progressive renal or cerebral damage Hypertensive heart disease • Pulmonary (right sided) hypertensive heart disease • Cor Pulmonale • Right ventricular hypertrophy • Dilation • Failure secondary to pulmonary hypertension Hypertensive heart disease • Pulmonary (right sided) hypertensive heart disease • May be acute or chronic • Acute - Massive pulmonary embolism • Chronic - implies right ventricular hypertrophy secondary to prolonged pressure overload Hypertensive heart disease • Pulmonary (right sided) hypertensive heart disease • Morphology • Rt ventricular shape is converted to ovoid • Rt ventricular wall thickens • Outflow tract muscle bundle hypertrophy • Secondary compression of left ventricular chamber • Tricuspid regurgitation •Define essential hypertension? •Briefly describe pathogenesis of renal damage in hypertension. •Classify hypertension, briefly describe pathogenesis in each? •Summarize common complications of hptn? •What is nephrosclerosis? Briefly describe its pathogenesis? •What is meant by malignant hypertension? Briefly describe clinical and pathological features? •What are lacunar infarcts? arteriolosclerosis? •How does hptn cause stroke? Damage heart? Lacunar infarcts •Chronic hypertension •Arteriolosclerosis of deep penetrating arterioles of brain stem. Single or multiple cavitary infarcts – lacunes. Lenticular nucleus, thalamus Slit Haemorrhages. • • • • Are there any question?
