Essential Hypertension - Students
Essential Hypertension - Students
Essential Hypertension - Students
Cindy Chan, MD
Hypertension Outline
I.
Definition of Essential Hypertension II. Epidemiology III. Physiology of Hypertension IV. Diagnosis and Evaluation V. Treatment of Essential Hypertension VI. Complications of uncontrolled HTN
Normal blood pressure: systolic <120 mmHg and diastolic <80 mmHg
Hypertension: Stage 1: systolic 140-159 mmHg or diastolic 90-99 mmHg Stage 2: systolic 160 or diastolic 100 mmHg
If
there is a disparity in category between the systolic and diastolic pressures, the higher value determines the severity of the hypertension.
Isolated systolic hypertension is defined as SBP >140 mm Hg and DBP<90 mm Hg. It occurs predominantly in older persons Occurence in adolescents and young may indicate hyperdynamic circulation and predict future diastolic elevation.
100.00% 90.00% 80.00% 70.00% 60.00% 50.00% 40.00% 30.00% 20.00% 10.00% 0.00%
68.40% 53.60%
27.40%
Treated pharmacologically
Controlled
NHANESIII = Third National Health and Nutrition Examination Survey. 1988 - 1991. Control of hypertension was defined as pharmacologic treatment resulting in systolic BP <140mm Hg and diastolic BP <90 mm Hg. Adapted from Burt VL et al. Hypertension. 1995;25:305-313.
million Americans
Increases with age Greater among Blacks Greater for low-SES groups Greater in Southeastern States
Greater
Prevalence
in men than in women (in young and middle age; thereafter reverse is true)
Source: NHBPEP, Fifth report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure (JNC V),1993.
Sympathetic activity
Filtration fraction
Na reabsorption
Natriuretic hormone
Na-K ATPase
Vascular
Renin angiotensin Intracellular Na*
counters
Hypertension
Vascular resistance
Intracellular Ca**
Primary Membrane defect
Kaplan NM. in: Braunwald E, ed. Heart Disease: A Textbook of Cardiovascular Medicine. 4th ed. Philadelphia, Pa: WB Saunders Co: 1992:829
But really..
????
Unknown etiology
BLOOD PRESSURE
CARDIAC OUTPUT
PERIPHERAL RESISTANCE
Hypertension
Increased CO
and/or
Increased PR
Preload
Fluid Volume Venous Constriction
Contractility
Functional Constriction
Structural hypertrophy
Reninangiotensin excess
Hyperinsulinemia
Genetic alteration
Stress
Genetic alteration
Obesity
Endothelium
derived factors
Adapted from Kaplan NM. Clinical Hypertension. 5th ed. Baltimore, MD: Williams & Wilkins; 1990:57.
Primary or essential hypertension is a multifactorial disease but most hypertensives seem to have at least one of the following mechanisms involved:
An inability to handle sodium and water appropriately in comparison to normotensives Overactivity and overstimulation of the sympathetic/adrenergic nervous system A defect in the handling of intracellular calcium in vascular smooth muscle thereby giving more vasoconstriction in hypertensives versus normotensives A defect in the Renin-Angiotensin-Aldosterone system
Renin-Angiotensin System
ANGIOTENSINOGEN RENIN ANGIOTENSIN I
LOW MACULA DENSA SIGNAL LOW RENAL ARTERY BP HIGH RENAL NERVE ACTIVITY
CONVERTING ENZYME
ANGIOTENSIN II ALDOSTERONE PRODUCTION etc.
Target damage
Eyes
Retinal vein and artery thrombosis
Acute Events
Cerebral
Cerebrovascular accident
Heart
Coronary artery disease Left ventricular hypertrophy Dysrhythmia Congestive heart failure
Heart
Myocardial infarction
Kidney
Renal failure
Vasculature
Atherosclerosis Peripheral vascular disease
Source: Blood Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Pressure. Arch Intem Med. 1993;153:154-183.
Screening
2007
Diagnosis
Posture - initially, check for postural changes by taking readings after five minutes supine, then immediately and two minutes after standing - this is particularly important in patients over age 65, diabetics, or those taking antihypertensive drugs. Sitting pressures are recommended for routine follow-up; the patient should sit quietly with the back supported for five minutes and the arm supported at the level of the heart.
Circumstances - no caffeine during the hour preceding the reading and no smoking during the preceding 30 minutes. No exogenous adrenergic stimulants, such as phenylephrine in decongestants or eye drops for pupillary dilatation. A quite, warm setting. Home readings should be taken upon varying circumstances. Equipment - cuff size: length of the bladder should be 80 percent and the width of the bladder should be at least 40 percent of the circumference of the upper arm
Manometer - aneroid gauges should be calibrated every six months against a mercury manometer
Diagnosis
Technique - number of readings. Take at least two readings on each visit, separated by as much time as possible; if readings vary by more than 5 mmHg, take additional reading until two consecutive readings are close. For the diagnosis of hypertension, take three readings at least one week apart. Initially, take blood pressure in both arms; if pressures differ, use the higher arm. If the arm pressure is elevated, take the pressure in one leg, particularly in patients under age 30 Performance - inflate the bladder quickly to 20 mmHg above the systolic pressure as estimated from loss of radial pulse. Deflate the bladder 3 mmHg per second. Record the Korotkoff phase V (disappearance) as the diastolic pressure except in children in whom use of phase IV (muffling) may be preferable. If the Korotkoff sounds are weak, have the patient raise the arm, open and close the hand five to ten times, and then inflate the bladder quickly. Recordings - note the pressure, patient position, arm, and cuff size: eg, 140/90, seated, right arm, large adult cuff.
20 to 25 percent of patients with mild office hypertension (diastolic pressure 90 to 104 mmHg) blood pressure is repeatedly normal when measured at home, at work, or by ambulatory blood pressure monitoring
ABPM typically involves automated inflation of the BP cuff and recording of the blood pressure at preset intervals (usually every 15 to 20 minutes during the day and every 30 to 60 minutes during sleep) White Coat HTN Suspected episodic hypertension (eg, pheochromocytoma) Hypertension resistant to increasing medication Hypotensive symptoms while taking antihypertensive medications Autonomic dysfunction
Evaluation
Hx meds, lifestyle, diet, family hx, sleep, symptoms of end-organ damage PE papilledema, cotton-wool spots, palpation and auscultation of carotids, cardiac & pulm exam, renal bruits pulses, edema, visual disturbance, confusion Labs - Hematocrit, urinalysis, routine blood chemistries (glucose, creatinine, electrolytes), estimated glomerular filtration rate, fasting lipid profile Electrocardiogram
Fundus Changes
I Minimal changes II Arteriovenous Nicking III Exudate, flame-shaped hemorrhages IV Papilledema and changes I through III
Grade I
Grade IV
(check fundi, consult ophthalmology) Cardiac/EKG (assess for any prior CAD) CNS (assess for any prior Stroke) Renal (assess urinalysis - U/A, BUN, creatinine) Cholesterol/Glucose
reduce morbidity and mortality by the least intrusive means possible Achieving and maintaining the following levels; lower if tolerated
<140/90 mmHg <130/80 mmHg All patients Diabetes mellitus Renal disease
Complications
Premature CHF LVH
CVD
CVA
Intracerebral
Definitions
Malignant hypertension/Hypertensive emergency Hypertension with end-organ damage (retinal hemorrhages, exudates, or papilledema), usually associated with a diastolic pressure above 120 mmHg. Hypertensive encephalopathy Altered mental status (AMS) secondary to HTN, can be seen at diastolic pressures as low as 100 mmHg (in previously normotensive patients with acute hypertension due to preeclampsia or acute glomerulonephritis).
Hypertensive urgency Severe hypertension (as defined by a diastolic blood pressure above 120 mmHg) in asymptomatic patients. (No proven benefit from rapid reduction in BP in asymptomatic patients who have no evidence of acute endorgan damage and are at little short-term risk)
Hypertensive Emergency
Accelerated-malignant hypertension with papilloedema Cerebrovascular Hypertensive encephalopathy Atherothrombotic brain infarction with severe hypertension Intracerebral hemorrhage Subarachnoid hemorrhage Cardiac Acute aortic dissection Acute left ventricular failure Acute or impending myocardial infarction After coronary bypass surgery Renal Acute glomerulonephritis Renal crises from collagen vascular diseases Severe hypertension after kidney transplantation Excessive circulating catecholamines Pheochromocytoma crisis Food or drug interactions with monoamineoxidase inhibitors Sympathomimetic drug use (cocaine) Rebound hypertension after sudden cessation of antihypertensive drugs Eclampsia Surgical Severe hypertension in patients requiring immediate surgery Postoperative hypertension Postoperative bleeding from vascular suture lines Severe body burns Severe epistaxis
A bit of pharm.
First
Break Time!!