1. Cardiovascular Disease

What are the #1 cause of death in men and women in the U.S.?

Cardiovascular disorders

-Hypertension

-Hyperlipidemia (triglycerides and cholesterol)

-Arteriosclerosis

-Atherosclerosis

what is the most modifiable risk factor of stroke

HTN

~50% of all deaths from CVD are from ?

Coronary Artery Disease (CAD)

-atherosclerosis

~33% of deaths are from ?

Cerebral Vascular Accident (CVA)

-15 million people worldwide suffer a CVA annually

-5 million are left permanently disabled

~10% of hypertensive related deaths are due to?

End Stage Renal Disease (ESRD)

What generates blood pressure?

BP = CO x VR

-Cardiac Output (CO): amount of blood pumped by the ventricle per minute

-VR = peripheral resistance

Chronic elevation of BP is Hypertension

Cardiac Output (CO)

CO= SV x HR

-SV= stroke volume

-Amount of blood ejected from ventricles

-HR= heart rate

VR = peripheral resistance

what impacts it

what is HTN

-Vascular resistance is the resistance of blood vessels to blood flow, which is affected by blood volume and blood vessel size (diameter & length)

-smaller diameter is more resistance, longer length is more resistance and higher viscosity is more resistant

-VR increases with obesity & aging

chronic elevation of blood pressure

What is a major contributor to the development of primary HTN and secondary HTN?

which 3 thigns increase renin production

Renin-Angiotensin-Aldosterone System

Angiotensin II has multiple effects

-Obesity increases renin production

-Renin can also be stimulated through sympathetic activation (noradrenaline from adrenal glands)

-Hyper aldosteronism also increases renin production

How common is HTN?

what % are well controlled

Affects 48% of adults in U.S.

-Only ~ 22.5% are adequately controlled

-Geographic, sex, ethnic, and socioeconomic differences

Primary /essential hypertension

-what % of cases

-is it symptomatic

-95% of cases

-Idiopathic

-Asymptomatic "Silent Killer"

Secondary HTN

Increased BP secondary to another cause

-medication, kidney, endocrine disorders, drug use

Hypertensive crisis / malignant hypertension

whcih organs does it impact 4

Acute end-organ damage

-Heart

-Brain

-Retina

-Kidneys

Labile HTN

what is unique about it

-BP that fluctuates repeatedly in response to emotional stress

-HTN medications not effective; usually Rx stress-relieving meds

-Monitor for 24 hours

White Coat Syndrome

amount it increases by

Can increase bp ~20/10mmHg

Gestational/Pregnancy-Induced HTN

when does it return to normal

BP usually returns to normal within 12 weeks of delivery

What is normal BP?

Systolic <120

and

Diastolic <80

What is elevated BP?

Systolic 120-129

and

Diastolic less than 80

Stage 1 HTN

Systolic 130-139

or

Diastolic 80-89

Stage 2 HTN

Systolic 140 or higher

or

Diastolic 90 or higher

Hypertensive crisis

Systolic higher than 180

and/or

Diastolic higher than 120

Consult your doctor immediately

What increases the risk for CV disease 2-fold?

Every 20/10 mmHg increase in BP over 115/75 mmHg

Updated HTN Diagnostic Criteria

in office

24/7

day time

night time

HBPM

ABPM - ambulatory blood pressure monitoring

HBPM - home blood pressure measurement

Whenever possible, the diagnosis should not be made on a single office visit. Usually 2-3 office visits at 1-4-week intervals (depending on the BP level) are required to confirm the diagnosis of hypertension. The diagnosis might be made on a single visit, if BP is ≥180/110 mm Hg and there is evidence of cardiovascular disease (CVD)

What is the difference between HTN urgency & emergency?

Both: Systolic >180 or Diastolic >120

Emergency has end organ damage

HTN Urgency symptoms that DO NOT constitute an emergency 4

-Severe headache

-Shortness of breath

-Nosebleeds

-Severe anxiety

Emergent symptoms

-CVA

-Loss of consciousness

-Memory loss

-MI

-ESRD

-Aortic dissection

-Angina

-Pulmonary edema

-Eclampsia

Hypertension-Risk Factors

-gender

-race

-systemic diseases

-Male gender

-Increased age

-Race: AA

-Family Hx of premature cardiovascular disease

-Sympathetic over-activity

-Sleep apnea

-Concomitant disease

-Lifestyle factors

-BMI: body mass index

What age is a risk for HTN? men vs women

>55 in men; >65 in women

Sympathetic over-activity

what does it cause 4

-stress & pheochromocytoma

-Vasoconstriction, increased heart rate

Concomitant disease

Dyslipidemia, diabetes

Lifestyle factors 5

-Alcohol (moderate to heavy),

-Obesity (BMI>30),

-Sedentary lifestyle

-Cigarette smoking

-Dietary salt intake

BMI: body mass index

= [weight (lb)/height (inches)^2] x 703

= weight (kg)/height (meters)^2

Secondary hypertension manifestations 6

-Edema (pitting)

-Truncal obesity

-Foot ulcers

-Numbness of extremities

-Muscle weakness

-Tachycardia

Blood pressure reading specifications

-Proper size cuff (small cuff = elevated)

-Patient relaxed

-Remove constricted clothing

-No caffeine or tobacco use prior

-At rest for 5 or more minutes

-Feet on floor, legs uncrossed

-Void bladder before

Diagnostic Tests or Procedures Prior to Treatment

-EKG, ECG

-Urinalysis

-Blood glucose

-Hematocrit

-Electrolytes: Na, K, Ca, Chloride, Bicarbonate

-BUN (kidney function)

-Creatinine (or glomerular filtration rate)

-CRP

-Homocysteine

-Lipid profile (total, HDL, LDL, triglycerides)

-Liver profile (Albumin)

C-Reactive Protein

what is it

Inflammation-promoting globulin in blood that is produced when blood vessel walls become damaged

C-Reactive Protein values

normal

moderate

high

-Normal - <0.11 mg/dL

-Moderate - 0.12 to 0.19 mg/dL

-High - 0.20 to 1.50 mg/dL

Factors that increase CRP

-HTN

-Body mass index

-Smoking

-Metabolic syndrome

-Hyperglycemia

-Low HDL/ High triglycerides

-Estrogen/progesterone use

-Chronic infection

-Rheumatoid arthritis

-Genetic mutation

-Vasculitis

Homocysteine

what does it cause 3

Amino acid in blood that converts cholesterol to LDL

-Further damages arterial walls

-Causes blood to clot

-Increases risk of vessel blockage / ischemic stroke

Homocysteine values

normal

increased risk cardiovascular disease

-<12 µmol/L - desirable

-12 to 15 µmol/L - increases risk for cardiovascular disease

Homocysteine treatment

B vitamins (folic acid/B9; cobalamin/B12; pyridoxine/B6)

Hypertension Treatment

Reduce BP gradually (consult with internist)

-First Line Agents

-Second Line Agents

-Lifestyle modifications

First Line Agents 4

which is the preferred treatment for diabetics

-Diuretics: furosemide, hydrochlorothiazide

-ACE inhibitors (preferred treatment for diabetics): captopril

-Angiotensin-receptor blockers (ARB): valsartan

-Ca 2+ channel blockers: diltiazem, nifedipine, verapamil

Second Line Agents

-b-blockers: e.g. metoprolol

-Alpha agonist/antagonist: clonidine, terazosin

-Methyldopa

-Vasodilators: hydralazine

Lifestyle modifications 5

what is a normal BMI

-Weight reduction (normal BMI=18.5-24.9)

-Adopt Mediterranean Diet

-Dietary sodium decrease

-Increase physical activity

-Moderation of alcohol consumption

HTN Effects on Heart Muscle 2

what do they cause

Increased workload

Stronger contractions

-Left ventricular hypertrophy (can lead to left sided heart failure, and then right sided will follow)

-Congestive heart failure (CHF)

stiffening & narrowing of BVs puts stress on heart

Hypertensive Retinopathy

-what is it second to in prevalence

-Second only to diabetic retinopathy in prevalence

-Clinical presentation depends upon severity, duration, and degree of control

Keith-Wagener-Barker grade 1

Arterial narrowing

-Chronic, asymptomatic hypertension, adequate cardiac and kidney function

-Mild retinopathy does not correlate with mortality and morbidity

Grade 2: appearance

is it reversible

where

-Irreversible

-Damage and thickening of arterial wall

-Caliber of arterioles is reduced

-Best observed about 1DD out

-Attenuation of arterioles (Normal A/V=2/3)

-Thickening of arterial light reflex (normal ALR=1/3)

Keith-Wagener-Barker grade 2

-Focal arteriolar narrowing (ALR thickening d/t steepening)

-AV crossing changes

AV Nicking & Banking - Grade 2 appearance

-Occurs at AV crossings

-Most common in superior temporal arcade

-Compression of the retinal vein at their common sheath causes venous nicking/banking, dilation, and tortuosity

Keith-Wagener-Barker grade 3

Exudates, hemes, CWS, vessel occlusions, microaneurysms, macroaneurysms

Microaneurysms- Grade 3 appearance

where are they usually located

how are they best visualized

Small out-pouch of an capillary wall

May be the direct result of an increase in pressure from a sclerosed arteriole

-Usually near AV crossing change

Often associated with CWS

Difficult to visualize

-Best seen with IVFA

Exudation- Grade 3 appearance

what does it result from

Results from prolonged hypertension or abrupt acute episode

Tight junctions damaged

Blood leaks into retina

-Flame & intraretinal (dot/blot) hemes

Hard exudates

Retinal NFL ischemia (CWS)

what are the two different type of macroaneurysms and how do they appear

what is the most common location for it

fusiform: spindle shaped and associated with exudation. ruptured ones cause hemorrhage and exudation at any level of the retina

saccular RAM: small sac. more likely to reslut in hemorrhaging

superior temporal arcade

Vascular Occlusion- Grade 3 appearance

-what is this a complication of

-what is it the most common cause of

Complications of retinal arteriosclerosis

-BRVO, CRVO (ischemic vs. non-ischemic): Most common etiology of BRVO

-Retinal, optic nerve, and/or anterior segment neovascularization

-BRAO, CRAO

-Retinal macroaneurysm

Keith-Wagener-Barker grade 4

what is this called

what is it most commonly associated with

where do exudates form (which layer)

hypertensive encephalopathy/malignant HTN: most commonly associated with acute, severe HTN

Optic nerve head edema, macular edema, venous engorgement and arteriolar constriction

rapid rise in BP damages the small vessel endothelium. Lipid exudates in the outer plexiform layer form a radiating pattern called a macular star