Pathogenesis and clinical features of Hypertension Prof KR Sethuraman. MD Thanks to: Dr. Suresh, for the PPT set

Learning objectives Definition and classification of hypertension Pathogenesis of hypertension Regulation of blood pressure & recording of BP Pathogenesis of essential hypertension and secondary hypertension and their causes Pathophysiology of complications due to hypertension Clinical features and diagnosis of hypertension

Hypertension - Introduction Silent Killer – painless & complication is first hint Complications bring to diagnosis but late… Chronic, vascular & end organ damage. It is the leading risk factor – Myocardial Infarction, Heart failure and Stroke Responsible for the majority of hospital visits, 20 to 25% of population is affected, 70 to 80% of them are aware and out of them only 20% have BP under control ..! (“rule of halves”)

Definition of Hypertension Classification of blood pressure (in mm Hg) for adults aged 18 years or older in the 7th Report of the Joint National Committee of Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VII), the is as follows: Normal† Systolic <120, diastolic <80 Pre hypertension Systolic 120-139, diastolic 80-99 Stage 1 Systolic 140-159, diastolic 90-99 Stage 2 Systolic >= 160, diastolic >= 100

Pathogenesis of Hypertension It is multifactorial Humoral mediators Vascular reactivity – especially the arterioles Blood volume Vascular caliber Blood viscosity Cardiac output (= Heart rate x Stroke volume) Blood vessel elasticity Neural stimulation

Regulation of BP: BP = Cardiac Output x Peripheral Resistance (Cardiac output= heart rate x stroke volume) Endocrine Factors Renin, Angiotensin, ANP, ADH, Aldosterone. Neural Factors Sympathetic & Parasympathetic Blood Volume Sodium, Mineralocorticoids, ANP Cardiac Factors Heart rate & Contractility.

Control of Blood Pressure: Humoral Factors Vasoconstrictors Angiotensin II Catecholamines Vasodilators Pg & Kinins Blood Volume Na+, Aldosterone BP Cardiac Output Peripheral Resistance Cardiac Factors Rate & Contract.. Local Factors pH, Hypoxia Neural Factors Adrenergic – Cons ß Adrenergic - Dil

Etiologic Classification: Primary or Essential Hypertension(95%) rule out “white coat hypertension” Artifact: BP cuff too small Secondary Hypertension (5-10%) Renal – Chronic kidney disease, Acute and chronic glomerulonephritis, Polycystic kidney disease, Rennin secreting tumors Endocrine – Cushing’s syndrome, Thyroid disorders, Pheochromocytoma, Acromegaly.

Secondary Hypertension: causes Renovascular hypertension Vascular: coarctation of aorta, polyarteritis nodosa, Neurogenic: raised intracranial pressure, psychogenic, etc. Drugs and toxins: oral contraceptives, alcohol, NSAIDs, cocaine, cyclosporin, etc. Pregnancy induced hypertension Hypercalcemia and hyperparathyroidism Obstructive sleep apnoea

Pathogenesis of Hypertension: Pathogenesis in Essential hypertension - Multifactorial Increased blood volume - Sodium retention ADH, Aldosterone. Increased sympathetic tone - Adrenal tumours, sympathetic stimulation. Increased vasoactive hormones - Cushings, Pheochromocytoma,

Pathogenesis of Essential HT It is also multifactorial Genetic predisposition Excess dietary salt intake Increased adrenergic tone Stress Obesity Endothelium derived factors

Pathogenesis of Renovascular HTN: GFR Renin by JGA Aldosterone Angiotensin II Sodium Retention Blood Volume Vasoconstriction  P. Resistance Hypertension

Pathophysiology of target organ damage due to hypertension Cardiovascular system: Left ventricular hypertrophy Aortic root dilatation Congestive cardiac failure Ischemic heart disease

Left ventricular hypertrophy Myocardium undergoes structural changes in response to increased afterload Cardiac myocytes respond by hypertrophy, allowing the heart to pump more strongly against the elevated pressure However the contractile function of LV remains normal until late stages Eventually LVH lessens the chamber lumen, limiting diastolic filling and stroke volume LV diastolic function is markedly compromised in long standing hypertension

Left Ventricular Hypertrophy:

Hypertension and CNS Long-standing hypertension may manifest as hemorrhagic and athero embolic stroke or encephalopathy. High systolic pressure (> 160 mm Hg) and a diastolic pressure (>100 mm Hg) have led to a significant incidence of strokes. Others - dementia.

Cerebral Infarction (Stroke) : Haemorrhagic Necrosis

Subarachnoid Haemorrhage: Cerebral Blood vessels Special features: Thin walled* End arteries* Cong. Aneurisms May present as “Thunder clap Headache”

Lacunar Infarcts: Single or multiple cavitary infarcts – lacunes. Arteriolosclerosis of deep penetrating arterioles of brain stem. Lenticular nucleus, thalamus Slit Haemorrhages.

Hypertension and kidney disease Nephrosclerosis is one of the possible complications of long-standing hypertension. The renin-angiotensin system activity influences the progression of renal disease. Angiotensin II acts more on the efferent arteriole, which leads to an increase of the intraglomerular pressure. Volume expansion is the main cause of hypertension in patients with glomerular disease (nephrotic and nephritic syndrome).

Benign Nephrosclerosis: Leathery Granularity due to minute scarring

Hypertension and kidney disease Hypertension in patients with vascular disease is the result of the activation of the renin-angiotensin system, which is often secondary to ischemia. The combination of volume expansion and the activation of the renin-angiotensin system is believed to be the main factor behind hypertension in patients with chronic renal failure

Consequences of Hypertension: Blood Vessels Atherosclerosis and its complications like aortic aneurysm, aortic dissection, Rupture, necrosis. Heart Left Ventricular Hypertrophy, Cardiac failure, IHD, MI. Kidney Benign/Malignant nephrosclerosis. Infarction Eyes: Hypertensive retinopathy Brain: Haemorrhage, infarction, dementia, etc.

Hyperplastic Arteriolosclerosis: Narrow Lumen Onion Skin Thickening Of arterioles.

Normal Retina - Fundoscopy

Hypertensive Retinopathy: Grade I – Thickening of arterioles. Grade II – Focal Arteriolar spasms. Vein constriction. Grade III – Hemorrhages (Flame shape), dot-blot and Cotton wool and hard waxy exudates. Grade IV - Papilloedema

Malignant Hypertension: Defined as High BP >220mmHg over 110mmHg associated with evidence of target organ damage. May lead to Intravascular thrombosis. Renal failure Hypertensive encephalopathy. Left ventricular failure.

Clinical features of Hypertension Part 2 Clinical features of Hypertension

Common Presentation of HT Usually asymptomatic Occipital headaches characteristic but uncommon Blurring of vision (retinal involvement) Breathlessness and chest pain (cardiopulmonary involvement) Irritability, confusion and somnolence are signs of encephalopathy

Diagnostic clues of Hypertension Following the presentation of patients with suspected symptoms, Hypertension which is confirmed after properly measuring BP on atleast 3 separate occasions (based on the average of 2 or more readings taken at each of 2 or more visits after initial screening) A history of cardiovascular risk factors includes hypercholesterolemia, diabetes mellitus, and tobacco use (including chewing tobacco).

Diagnostic clues of Hypertension History of over-the-counter medication use, ethanol intake. The historical and physical findings that suggest the possibility of secondary hypertension are a history of known renal disease, abdominal masses, anemia, A history of sweating, labile hypertension, and palpitations suggests the diagnosis of pheochromocytoma.

Diagnostic clues of Hypertension A history of cold or heat tolerance, sweating, lack of energy, and bradycardia or tachycardia may indicate hypothyroidism or hyperthyroidism. A history of weakness suggests hyperaldosteronism. Abdominal bruit suggests the possibility of renal artery stenosis. Absence of femoral pulses suggests coarctation of aorta. Kidney stones raise the possibility of hyperparathyroidism.

Methodology of recording BP An accurate measurement of blood pressure is the key to diagnosis. Several determinations should be made over a period of several weeks. At any given visit, an average of 3 blood pressure readings taken 2 minutes apart using a mercury manometer is preferable. Blood pressure should be measured in both the supine and sitting positions, auscultating with the bell of the stethoscope..

Methodology of recording BP As the improper cuff size may influence blood pressure measurement, a wider cuff is preferable, particularly if the patient's arm circumference exceeds 30 cm. The patient should rest quietly for at least 5 minutes before the measurement. Although somewhat controversial, the common practice is to document phase V (a disappearance of all sounds) of Korotkoff sounds as the diastolic pressure.

Physical signs of Hypertension A fundoscopic evaluation of the eyes should be performed to detect any evidence of hypertensive retinopathy. These are flame-shaped hemorrhages and cotton wool exudates. Palpation of all peripheral pulses should be performed.

Physical signs of Hypertension Look for renal artery bruit over the upper abdomen; the presence of a unilateral bruit suggests renal artery stenosis. A careful cardiac examination is performed to evaluate signs of LVH. These include displacement of apex, a sustained and enlarged apical impulse, and the presence of an S4.

Conclusion: Persistent increased blood pressure (140/90) 95% Essential, 5% secondary - Renovascular Benign and Malignant types (>120Diastolic) Vessel damage & Arteriolosclerosis Complicates - Atherosclerosis, Diabetes, IHD Ischemia or Infarction in end organs. Kidney, Brain, Heart & Eyes. Nephrosclerosis, renal damage, IHD, MI, Stroke & Retinopathy.

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Thank you Any questions??