• 30% of adults have hypertension. That's 60,000,000 Americans
• 3-4 x risk of coronary artery disease
• White coat syndrome may account for 20% of diagnosed hypertension
• Pathogenesis unknown in most cases (Essential hypertension)
• 50% of patients discontinue their medications in first year

• Hypertension
• Elevated lipids
• Smoking
• Diabetes
• Obesity
• Sedentary lifestyle
• Type A personality
• Family history
• Age

• White males 25-35 1/10,000
• White males 55-64 1/1,000
• Many have abnormal glucose tolerance test

• Monckebergs arteriosclerosis (Calcification of small arteries) (Osler's sign: Artery does not collapse during manometry)
• Arteriosclerosis (Hyalinization of small arteries secondary to hypertension)
• Athrosclerosis (Artheromas=Lipid deposit causes intimal thickening)
• Renal vascular stenosis
• Parenchymal renal disease
• Primary aldosteronism
• Pheochromocytoma
• Cushings syndrome
• Coarctation of the aorta
• Pregnancy
• Drug induced
• Alcohol induced
• Oral birth control meds
• 95% are "essential hypertension" (Cause unknown)

Pressor systems determine blood pressure

• Renin-angiotensin-aldosterone system
• Renin is produced by the kidneys. It acts on angiotensin to produce angiotensin-1 which is then converted to angiotensin-2 by angiotensin-converting enzyme (ACE). Angiotensin-2 stimulates the adrenal glands to release aldosterone, which decreases kidney sodium excretion and causes vasoconstriction acutely and vascular hypertrophy chronically

• Release of epinephrine and norepinephrine causes vasoconstriction and increased cardiac output. Stimulation of renin release and impairment of sodium excretion

• Heredity (2-4 x risk if relatives with hypertension)
• Age
• Sex (Under age 55, more common in males than females. Over age 55, equal distribution among males and females)
• Race (Much more common in Black and Hispanic populations)
• Sensitivity to sodium
• Obesity (2-3 times more common in the obese, especially with upper body obesity)

• First 60 inches height = 106 pounds
• Add 6 pounds for every inch above the 60 inches
• Obesity = 20% or more above ideal weight

• Smoking
• Heavy drinking of alcohol
• 60-80 g ethanol/day
• 10-30 g ethanol/day may decrease BP especially in women
• Moderate drinking is 2 oz of 100 proof liquor, 8 oz wine/day or 24 oz beer/day
• Sedentary lifestyle
• Oral contraceptives
• Stress (Increased cardiac output and peripheral resistance)

Syndrome X carries a very high risk of morbidity

• Increased risk for cardiovascular events
• Hypertension
• Hyperinsulinemia
• Insulin resistance (Like type II diabetics)
• Dyslipidemia
• Elevated triglycerides and reduced HDL

• Borderline systolic hypertension is a pressure between 140-160
• Systolic hypertension is a systolic pressure greater than 160
• High normal diastolic is a diastolic pressure between 85-89
• Mild diastolic hypertension is a diastolic pressure between 90-104
• Moderate diastolic hypertension is a diastolic pressure between 105-114
• Severe diastolic hypertension is a diastolic pressure greater than 114
• Malignant Hypertension is papilledema with altered consciousness due to diastolic greater than 140

• Mild elevation in BP arterioles narrow (Widening of light reflex)
• Arteriol - venous changes (At crossing site they share a common wall and in 70% of crossings the arteriole is over the vein)
• Tapering (Gunns Sign)
• Nicking
• Deflection (Salus's Sign)
• Attenuation (narrowing)
• Straightening
• More acutely angled branching
• Severe or abrupt elevation arterioles spasm in focal constriction. Alternate focal constriction and dilation leads to beading. Sustained elevation causes diffuse dilation and then focal dilation producing tortuosity and eventual exudation.

• Acute, severe hypertension alters choriocapillaris, resulting in choroidal ischemia, producing retinal edema, CME, serous retinal detachments and RPE changes.
• Choroid vascular tone is controlled by sympathetic nervous system. Initially the choroid constricts in response to hypertension. Further hypertension damages the muscle layer and endothelium. Because the choroidal arteries run a short course and supply the choroicapillaris at right angles, systemic pressure is felt stronger than in retinal arterioles. Pressure and flow is higher in macula than periphery. Fluid leakage from the choriocapillaris causes macular edema and serous retinal detachment and the lipid deposits

• Focal infarcts in the choriocapillaris cause yellow spots in the overlying RPE. They are completely obstructed terminal choroidal arterioles and fibrin and necrotic tissue. Overlying retina above the necrotic tissue is detached and leaks on Fluroscein angiopathy. They are also known as Acute Focal RPE Lesions and window defects. With healing the spots become pigmented centrally with a depigmented surround.

• Radially oriented chains of pigmented spots along sclerosed choroidal vessel's. They represent linear foci of RPE disruption and are indicative of malignant hypertension
• Diffuse choroidal ischemia
• Choroidal vasoconstriction in response to hypertension results in reduced blood flow and ischemia of the overlying RPE and sensory retina and subretinal leakage resulting in serous macular detachment and reduced visual acuity. When the blood pressure is reduced visual acuity improves.

• Hard exudates
• Hard exudates are lipid deposits that are often seen in star pattern around the macula
• Cotton wool spots
• These are areas of focal ischemia caused by occlusion of terminal arteries. Some feel a better name might be inner retinal ischemic spot (IRIS).

• With increased BP the pre-capillary arterioles become occluded. With time, the smooth muscle necroses, so the arteriole loses its ability to constrict, which results in increased blood flow and hemorrhaging. Vessel dilation and damage leads to exudation and hemorrhage. Hemorrhages are in the nerve fiber layer so are flame-shaped hemorrhages. Bonnets sign is a small hemorrhage at the site of an arteriol - venous nicking

• Punctate, white opacities that may be round or oval. They can be pinpoint to 1/4 disc diameters in size. They may appear and disappear in crops. They usually are found alongside major artereriols located in deep retinal areas and on disc. They resolve and leave no permanent change. They are independent of other retinopathy signs. Focal dilation of precapillary arterioles leads to increased permeability and plasma deposits They are specific to malignant hypertension.

• Infarction of the nerve head produces ischemia and results in reduced axoplasmic flow. Variable effect n visual acuity based on degree of damage. It is followed by optic atrophy months later

• Disk edema due to malignant hypertension produces increased cerebral spinal fluid. It really is hypertensive encephalopathy. Elevated pressure in the central retinal vein producing stasis in the nerve head capillaries is true cause

• Microaneurysms and macroaneurysms
• Central retinal or branch retinal vein occlusion
• Epiretinal membranes
• Cystoid macular edema
• Extra-ocular muscle palsy (Most often lateral rectus or superior oblique)

• Arteriol - venous changes
• Hollenhorst plaques
• Central retinal or branch retinal vein occlusion
• Transient ischemic attack in the vertrobasilar system or carotid system

• Hemorrhages, cotton wool, retinal edema (Absorb in 3 months)
• Exudates (Can take months to absorb)
• Macular star (Absorption can lead to pigment clumping and reduced visual acuity)

• Early - Focal intraretinal periarteriolar transexudates (FIPT)
• Mid - Macular edema, Acute focal RPE lesions (Acute elschnigs spots), Optic nerve head edema
• Later - Cotton wool, Occasional flame hemorrhage,
• Final - Lipid deposits, CME, Retinal arteriolar changes, Nerve fiber layer loss

• Optic nerve is less able to maintain against IOP. Lower the BP but then IOP problem (AION, CRVO, Acute optic nerve head infarction and sudden and complete blindness)

• Thickening of the arteriole wall as a result of aging or hypertension. As the vessel wall thickens, the light reflex seen widens to be seen as "silver or copper wire" (But not quantifiable)
• Kieth - Wagener grading system
• Grade 1 Mild narrowing of arteriole
• Grade 2 Irregular arteriole narrowing. Moderate Arteriolosclerosis. Ateriol - venous changes
• Grade 3 Edema, hemorrhages, cotton wool
• Grade 4 Papilledema

• History and assessment of risk
• Consider risk factors
• Examination
• Sphygmomanometry (Cuff to large gives low reading, Small cuff reads high)
• Artery to vein ratio
• Arteriol - venous crossing changes
• Hemorrhages
• Exudates
• Choroidopathy
• Optic neuropathy
• Fundus photography

• Lose weight
• Limit alcohol
• Restrict sodium
• Exercise
• Relaxation

Diuretics (Thazides, loop diuretics, potassium sparing)

Andrenergic inhibitors (Centrally acting agents, peripheral acting andrenergic antago

nists which can be alpha-andrenergic blockers, beta-andrenergic blockers or combined

alpha/beta andrenergic blocker)

• Elevate blood cholesterol, triglycerides, glucose, calcium, uric acid
• Lower blood potassium, magnesium, and sodium
• Not favored as much now as before
• Used with impaired kidney function
• More effective in older people and black people
• Contraindicated with:
• Hyperlipidemia
• Gout
• Diabetes (Diet controlled type II would also need an oral hypoglycemic)
• Heart arrhythmia's (Reduced potassium aggravates arrhythmia's)
• Side effects are:
• Fatigue
• Leg cramps
• Impotence

• Better for older patients
• Produce arterial dilation
• Also produce venous relaxation resulting in pooling of blood in viscera and potential hypotension
• Slightly decrease cholesterol and triglycerides and increase in HDL
• Decreases voiding problems with prostatism

• Best for young white people
• Also help other problems (Angina, Arrhythmia's, Migraine, Performance anxiety)
• Not good for some conditions:
• Asthma
• Congestive heart failure
• Diabetes (Decreases awareness of low blood sugar and impairs ability to restore low
• sugar level to normal
• Reduces HDL
• Increases triglycerides
• Side effects are:
• Sedation
• Insomnia
• Fatigue
• Coldness

• Best in young white people
• Slows kidney disease in diabetics
• Helps with congestive heart failure
• Does not effect lipids
• Side effects:
• Cough
• Orthostatic hypotension (Especially if used with a diuretic)
• Angioedema (Face, tongue, lips swell)
• Increased potassium (Problem for diabetics and kidney disease)

• Best for older and black patients
• Side effects are:
• Edema
• Flushing
• Headache
• Rash
• GI upset

• Initially lower BP, but with chronic use they induce fluid retention or stimulate the SNS
• Use with a diuretic or SNS inhibitor (Not monotherapy) 50% Patients can be controlled with montherapy. 90% Patients can be controlled with two drugs.

• Start with one class of drugs and add others later if needed. Better to use two drugs at less than maximum dosage than one drug at maximum dosage "Step down" therapy when the condition is controlled

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Last modified: May 1, 2006