Clinical Manifestion of Essential Hypertension Flashcards Preview

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Flashcards in Clinical Manifestion of Essential Hypertension Deck (16)
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Proper BP Testing Criteria

Patient seated quietly for five minutes, feet on the floor, and arm supported at heart level

Avoid Caffeine, exercise and smoking 30 minutes prior to measurement

Cuff bladder should encircle at least 80% of the arm

Inflate the cuff 20-30 mmHg past the loss of the radial pulse


JNC and Guidelines

The Joint National Committee on the Prevention, Detection and Treatment of High Blood Pressure

Recommended attaining measurements outside the clinic – “white coat syndrome” in order to make a proper dx
Patient can get home BP monitor or ambulatory BP monitoring which takes the BP throughout the day


Stages of Hypertension

Normal: 120/80
As you increase systolic by 20, you go up a stage
120-139 = pre-hypertension
140-159 = stage 1
160 + = stage 2

Diastolic increase by 10 to go up a stage
80-89 = pre-hypertension
90-99 = stage 1
100 + = stage 2

Systolic vs. diastolic – go by which one is highest for staging level


Ambulatory BP Monitoring

Indicated for:
Suspected “white coat hypertension”
Symptomatic hypotension with antihypertensive medications
Episodic hypertension

BP values are lower than clinical readings:
Upper normal is 135/85 while awake
Average 120/75 while asleep
BP should “dip” by 10-20% at night. “Non-dippers” are at increased risk for cardiovascular events


JNC 8 Tx Goals

60 or older: 150/90 is the upper limit of normal; no significant difference between 140 and 150 for elderly people in studies, but controversial

Younger than 60, CKD, and diabetes patients: 140/90 is the upper limit of normal


Systolic Blood Pressure Intervention Trial (SPRINT)

Patients were all over 50
Two groups: under 120 and under 140
Had to be 50 or older, systolic BP of 130-180, and at least one CV risk factor

At least one of the following:
Additional cardiovascular disease (CVD) risk
Clinical or subclinical CVD (excluding stroke)
Chronic kidney disease (CKD), defined as eGFR 20 –


CV Risk Factors

Look at CV risk factors of patients and limit them as much as possible
Think about secondary causes of HTN, but not necessarily test for them unless strongly think this is the case

CV Risk Factors: HTN, smoking, obesity, physical inactivity, dyslipidemia, diabetes, GFR greater than 60, age (55+ for men, 65+ for women), family hx


Causes of HTN

Identifiable Causes of HTN: sleep apnea, drug induced, CKD, primary aldosteronism, renovascular disease, chronic steroid therapy, Cushing’s, pheochromocytoma, coarctation of the aorta, thyroid/parathyroid disease


Lifestyle Modifications

DASH diet has effects similar to single drug therapy
Lifestyle modifications: can be just as effective as medications, but are harder to implement

Weight reduction: 5-20mmHg
DASH diet: 8-14mmHg
Sodium Reduction: 2-8mmHg
Physical Activity: 4-9mmHg
Moderation of Alcohol: 2-4mmHg


Recommended Lab Tests for HTN

Blood Glucose
Serum potassium, creatinine, calcium
Lipid profile

More extensive testing for secondary causes is not indicated unless BP control is not achieved or there are signs and symptoms strongly suggestive of other underlying causes


Recommended Drug Classes

Black patients- have increased vascular contractility and increased salt sensitivity. My be related to low levels of NO and high levels of CK

For non AA: ACEIs, Angiotensin Receptor Blockers, Thiazide Type Diuretics, and Ca2+ Channel Blockers

For AA: Thiazide Type Diuretics and Ca2+ Channel Blockers


Tx for CKD and Diabetes Patients

Patients with diabetes and CKD: efferent arteriole narrows and get high BP within nephron itself and relieve this with ARB and ACE inhibitors, but should not be used together since increases chance of side effects

These two meds protect the kidney


Pregnant Women HTN Tx

Cannot give ARB and ACE inhibitors because can cause high BP in fetus; fetuses need the pressure gradient created by constriction of glomerulus, so if give these drugs then vasodilates and causes renal failure


ACE Inhibitors

ACE inhibitors may cause hyperkalemia. Suppression of angiotensin II leads to a decrease in aldosterone levels. Since aldosterone is responsible for increasing the excretion of potassium, ACE inhibitors can cause retention of potassium. Some people, however, can continue to lose potassium while on an ACE inhibitor

The bradykinin buildup causes the cough: effect doesn’t come on when you first begin the drug, but then comes on 2-3 months later; must be careful and monitor patient = captopril is the ACE inhibitor that causes cough


Antihypertensive Tx Strategies

A. Start one drug, titrate to max dose, then add second drug
B. Start one drug and then add second before achieving max dose of initial drug; lower doses of two drugs for lower side effects
C. Begin with 2 drugs at same time (separate pills or combination)

Say BP goes below the goal BP with treatments: as long as patient is tolerating and asymptomatic, can leave the medication and dosage alone; if asymptomatic must change/back off dosing


Individual Drug Class Indications

CHF: anything but hydralazine and minoxidil. Aldos include Eplerenone (Inspra) and Spironolactone (Aldactone)

Heart Failure: thiazides, BB, ACEI, ARB, aldosterone antagonist

Post-MI: BB, ACEI, aldosterone antagonist