
Managing Hypertension: Definition, Classification, and Etiology
Hypertension is a leading global health issue that can increase the risk of cardiovascular diseases, stroke, renal failure, and arterial disease. Learn about its clinical definition, AHA and ESC classifications, measurement techniques, and importance of home blood pressure monitoring.
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Presentation Transcript
HYPERTENSION HYPERTENSION- - DEFINITION,CLASSIFICATION, DEFINITION,CLASSIFICATION, ETIOLOGY ETIOLOGY DR CHAITHRA K JR1 MEDICINE
oHYPERTENSION IS ONE OF THE LEADING CAUSES OF GLOBAL BURDEN OF DISEASE oIT DOUBLES THE RISK OF CARDIOVASCULAR DISEASES, ISCHEMIC AND HEMORRHAGIC STROKE , RENAL FAILURE AND PERIPHERAL ARTERIAL DISEASE oLARGE SEGMENTS OF HYPERTENSIVE POPULATION ARE EITHER UNTREATED OR INADEQUATELY TREATED
oCLINICALLY HYPERTENSION DEFINED AS THAT LEVEL OF BP AT WHICH THE INSTITUTION OF THERAPY REDUCES BP RELATED MORBIDITY AND MORTALITY oIT IS THE PRODUCT OF CARDIAC OUTPUT AND PERIPHERAL RESISTANCE oIT IS BASED ON THE AVERAGE OF TWO OR MORE SEATED BP READINGS DURING EACH OF TWO OR MORE OUT PATIENT VISITS
oSBP IS MORE IMPORTANT THAN DBP IN THE MEASUREMENT OF CARDIOVASCULAR RISK EXCEPT IN YOUNG PATIENTS oPULSE PRESSURE(PP)=SBP-DBP oMEAN ARTERIAL PRESSURE=DBP+1/3PP oISOLATED SYSTOLIC HYPERTENSION oSBP>140 WITH DBP<90 oARTERIOSCLEROSIS/AR/FEVER/THYROTOXICOSIS/AV FISTULA
AHA CLASSIFICATION CATEGORY SYSTOLIC DIASTOLIC NORMAL <120 <80 ELEVATED 120-129 <80 HYPERTENSION STAGE 1 130-139 80-89 STAGE 2 >140 >90
ESC CLASSIFICATION CATEGORY SYSTOLIC DIASTOLIC OPTIMAL <120 <80 NORMAL 120-129 80-84 HIGH NORMAL 130-139 85-89 GRADE 1 140-159 90-99 GRADE 2 160-179 100-109 GRADE 3 >180 >110
SBP DBP OFFICE/CLINIC >_140 90 SELF/HOME BP >_135 85 AMBULATORY(24HR AVG) >_135 85
oHOME BLOOD PRESSURE MEASUREMENT -TO IDENTIFY WHITE COAT HTN -INCREASES ADHERENCE TO MEDICATION -DETECT MASKED HTN oTHE BLADDER LENGTH OF BP CUFF SHOULD BE 80% CIRCUMFERENCE AND IDEAL WIDTH IS 40%
AMBULATORY BP MEASUREMENT OVER A PERIOD OF 24-48 HR DETECT EPISODIC HTN HYPOTENSIVE EPISODES AUTONOMIC DYSFUNCTION EVALUATION OF SLEEP APNEA EVALUATE ANTIHYPERTENSIVES RESISTANT HTN
NORMAL HTN CATEGORY 24 HRS AVG 130/80 135/85 DAY /AWAKE 135/85 140/90 ASLEEP /NIGHTTIME 120/70 125/75
PATHOPHYSIOLOGY PATHOPHYSIOLOGY INCREASED CARDIAC OUTPUT INCREASED PERIPHERAL RESISTANCE ESTABLISHED HTN- INCREASED PERIPHERAL RSISTANCE AND NORMAL CARDIAC OUTPUT
INCREASED CO INCREASED FLUID VOLUME-EXCESS SODIUM INTAKE INCREASES FLUID VOLUME AND PRELOAD RENAL SODIUM RETENTION RENIN ANGIOTENSIN SYSTEM SYMPATHETIC NERVOUS SYSTEM OVERACTIVITY-
INCREASED PERIPHERAL VASCULAR RESISTANCE INCREASED INTRACELLULAR CALCIUM ANGIOTENSIN 2, IGF,PROSTAGLANDINS,ENDOTHELIN STRUCTURAL VASCULAR REMODELLING AND HYPERTROPHY
PRIMARY HYPERTENSION o80-95% HTN PATIENTS ARE DIAGNOSED AS HAVING PRIMARY OR ESSENTIAL HYPERTENSION INCLUSIVE OF PATIENTS WITH OBESITY AND METABOLIC SYNDROME oFAMILIAL oPREVALENCE INCREASES WITH AGE oOBESITY(BMI>30 kg/m2) HAVE LINEAR CORRELATION WITH BP
oMETABOLIC SYNDROME-INSULIN RESISTANCE ,ABDOMINAL OBESITY,HTN, DYSLIPIDEMIA oHERITABLE AS A POLYGENIC CONDITION oEXPRESSION IS MODIFIED BY ENVIRONMENTAL FACTORS oHYPERINSULINEMIA- MARKER OF INSULIN RESISTANCE-PREDICT THE DEVELOPMENT OF HTN AND CARDIOVASCULAR DISEASE oINSULIN- ANTINATRIURETIC EFFECT
PARENCHYMAL DISEASES, RENAL CYSTS( POLYCYSTIC KIDNEY DISEASE)RENAL TUMOURS(RENIN SECRETING TUMOURS),OBSTRUCTIVE UROPATHY RENOVASCULAR ARTERIOSCLEROTIC, FIBROMUSCULAR DYSPLASIA RENAL ADRENAL PRIMARY ALDESTERONISM, CUSHINGS SYNDROME,PHEOCHROMOCYTOMA,17 ALPHA HYDROXYLASE DEF,11 BETA HYDROXYLASE DEF AORTIC COARCTATION OBSTRUCTIVE SLEEP APNEA PREECLAMPSIA/ ECLAMPSIA NEUROGENIC DIENCEPHALIC SYNDROME,FAMILIAL DYSAUTONOMIA,POLYNEURITIS(A/C PORPHYRIA,LEAD POISONING)RAISED ICT,A/C SPINAL CORD SECTION
ENDOCRINE HYPOTHYROIDISM, HYPERTHYROIDISM,HYPERCALCEMIA,ACROMEGALY MEDICATIONS HIGH DOSE ESTROGENS,ADRENAL STERIODS,DECONGESTANTS,AMPHETAMINES,CYCLOSP ORINE,TCA, ATYPICAL ANTIPSYCHOTICS,MAO- INHIBITORS ,NSAIDS,ALCOHOL,COCAINE MENDELIAN FORMS OF HTN LIDDLES SYNDROME,PCKD,PHEOCHROMOCYTOMA, GORDONS SYNDROME,11BETA HYDROXYLASE DEF 17ALPHA HYDROXYLASE DEF
RENAL PARENCHYMAL DISEASES M/C/C OF SECONDARY HYPERTENSION HTN IS MORE SEVERE IN GLOMERULAR DISEASES THAN IN INTERSTITIAL HTN CAUSES NEPHROSCLEROSIS
RENOVASCULAR HYPERTENSION RENOVASCULAR HYPERTENSION HTN DUE TO AN OCCLUSIVE LESION OF RENAL ARTERY CURABLE PLAQUE OSTRUCTING RENAL ARTERY, FIBROMUSCULAR DYSPLASIA CONSIDERED IN PATIENTS WITH OTHER EVIDENCE OF ATHEROSCLEROTIC VASCULAR DISEASE FT
oSEVERE OR REFRACTORY HTN /RECENT LOSS OF HTN CONTROL/CAROTID OR FEMORAL ARETERY BRUIT/FLASH PULMONARY EDEMA/UNEXPLAINED DETERIORATION OF RFT/DETERIORATION ASSOCIATED WITH ACE INHIBITOR oDOPPLER ULTRASOUND / GADOLINIUM CONTRAST MR ANGIOGRAPHY oFUNCTIONALLY SIGNIFICANT IF STENOSIS IS >70%/ PRESENCE OF COLLATERALS/RENAL VEIN RENIN RATIO>1.5 OF AFFECTED SIDE/CONTRALATERAL SIDE
INTERVENTIONS-PTRA, PLACEMENT OF STENT,SURGICAL RENAL REVASCULARIZATION BP ADEQUATELY CONTROLLED +RFT STABLE- NO INTERVENTION NEEDED FIBROMUSCULAR D/S -YOUNG AGE ,FAVOURABLE OUTCOME
PRIMARY ALDOSTERONISM PRIMARY ALDOSTERONISM INDEPENDENT OF RENIN ANGIOTENSIN SYSTEM SODIUM RETENTION, HTN, HYPOKALEMIA, LOW PRA,KIDNEY DAMAGE AND CVS DISEASES DIAGNOSED AT 3RDOR 4THDECADE ASYPTOMATIC POLYURIA,POLYDYPSIA,PARESTHESIA ,MUSCLE WEAKNESS DUE TO HYPOKALEMIC ALKALOSIS
REFRACTORY HTN/ HTN WITH UNPROVOKED HYPOKALEMIA PATIENTS ON DIURETICS- S POTASSIUM<3.1 SCREENING TEST PA/PRA >30:1 PA>550 pmol(20ng/dl) ARB & ACEI AFFECT THIS RATIO- SHOULD BE STOPPED 4-6 WKS BEFORE TESTING ALDOSTERONE BIOSYNTHESIS IS K+ DEPENDENT- HYPOKALEMIA CORRECTED WITH ORAL SUPPLEMENTS
PATIENTS WITH ELEVATED PA/PRA RATIO DIAGNOSIS CONFIRMED WITH FAILURE TO SUPRESS PA BY ORAL SODIUM LOADING/SALINE INFUSION FLUDROCORTISONE/CAPTOPRIL
SPORADIC / FAMILIAL SPORADIC- ADENOMA/ BILATERAL ADRENAL HYPERPLASIA/ADRENAL CARCINOMA/ECTOPIC MALIGNANCY IMAGING- HIGH RESOLUTION CT/ADRENAL SCINTIGRAPHY B/L ADRENAL VENOUS SAMPLING- HIGH SENSITIVITY AND SPECIFICITY TO DIFFERENTIATES U/L & B/L
ADENOMA- SURGICAL MX-U/L ADRENELECTOMY HYPERPLASIA MEDICAL MX- ALDOSTERONE BLOCKERS SPIRONOLACTONE, EPLERENONE
GLUCOCORTICOID REMEDIABLE HYPERALDOSTERONISM- AD/ MOD TO SEVERE HTN AT YOUNG AGE OVER PRODUCTION OF BOTH ALDOSTERONE AND STEROID Rx- SUPRESSION OF ACTH BY LOWDOSE GLUCOCORTICOIDS
CUSHINGS SYNDROME CUSHING S SYNDROME M/C/C- IATROGENIC STEROIDS ACTH DEPENDENT-PITUTARY ADENOMA/ ECTOPIC ACTH ACTH INDEPENDENT- ADRENAL TUMOURS OVERNIGHT DEXAMETHASONE SUPRESSION TEST OR 24 HOUR URINARY CORTISOL OR LATE NIGHT SALIVARY CORTISOL Rx SURGICAL AND MEDICAL
PHEOCHROMOCYTOMA PHEOCHROMOCYTOMA oCATECHOLAMINE SECRETING TUMOURS IN ADRENALS oIN EXTRA ADRENAL PARAGANGLION TISSUE PARAGANGLIOMA oHEADACHE/PALPITAION/SWEATING/EPISODIC HTN/ORTHOSTSIC HYPOTENSION oINV-24HR FRACTIONATED METANEPHRINS/PLSMA FREE METANEPHRINS oCT/MRI oRx-ALPHA BLOCKERS- BETA BLOCKERS-SURGERY
OBSTRUCTIVE SLEEP APNEA OBSTRUCTIVE SLEEP APNEA oHTN DUE TO SYMPATHETIC ACTIVATION CAUSED BY INTERMITTENT HYPOXIA AND FRAGMENTED SLEEP oBP REMAIN ELEVATED DURING NIGHT TIME- REVERS DIPPERS oCPAP VENTILATION IS THE TREATMENT oIT ABOLISHES APNEA,PREVENTS INTERMITTENT BP SURGES,RETORES NORMAL DIPPING PATTERN