Module 2: Hypertension

Question 1

Risks of high bp

Answer 1

MI, heart failure, stroke, renal disease, retinopathy

Question 2

Who has highest prevalence of HTN?

Answer 2

Blacks; highest prevalence, more resistant HTN, develop at a younger age
Black females more so than males
Nocturnal non dipping BP (which means it does not dip more than 10% at night) - increases risk of CVD
More organ damage and highest death rate

Question 3

Hispanics and HTN

Answer 3

Less likely to receive treatment
Lower rate of awareness, treatment, and control

Question 4

Gender differences of HTN

Answer 4

Men - more common before middle age
Women - increased 2-3x with oral contraceptives
More common after menopause, harder to control in older women

Question 5

Factors influencing BP

Answer 5

BP = CO x SVR

CO
Cardiac
-Heart rate, contractility, conductivity

Renal Fluid Volume Control
-Regin-angiotensin-aldosterone system
-Natriuretic peptides

SVR
Sympathetic Nervous System
Alpha 1 + 2 adrenergic receptors (vasoconstriction)
Alpha 2 receptors (vasodilation)

Local Regulation
-Vasodilators (Prostaglandins, nitric oxide)
-Vasoconstrictors (Endothelien)

Nuerohormonal
-Vasoconstrictors (angiotensin, norepinephrine)

Question 6

SVR (systemic vascular resistance)

Answer 6

Force opposing movement of blood within vessels
Principal factor – radius of small arteries and
arterioles
 Small changes in radius of arterioles creates
significant change in SVR
 Increased SVR with constant or increased CO =
increased arterial BP

Question 7

Factors influencing BP

Answer 7

Regulation of BP involves: nervous, CV, endothelial,
renal, endocrine functions
 Sympathetic nervous system (SNS)
 Activation increases HR and cardiac contractility
within seconds
 Vasoconstriction and renin release
 Increases CO and SVR
 PNS stimulation—decreased HR (vagus nerve) and
CO = decreased BP
 SNS
* Baroreceptors—sense decreased BP; send
message to vasomotor center in brainstem leads
to efferent nerves in cardiac and vascular smooth
muscle cells
* Norepinephrine (NE) released from SNS nerve
endings; activate receptors in SA node,
myocardium, and vascular smooth muscle
* Receptors—1, 2, 1, 2, and dopamine

Question 8

SNS Receptors Affecting BP

Answer 8

1—vasoconstriction; increased contractility (+
inotropic)
 2—inhibits release of norepinephrine
 1—increased: contractility (+ inotropic), HR (+
chronotropic), and conduction (+ dromotropic);
renin secretion
 2—vasodilation
 Dopamine—vasodilation

Question 9

Factors Influencing BP: Sympathetic Vasomotor Center

Answer 9

Sympathetic vasomotor center
 Activated during stress, pain, and exercise to
increased CO and BP in response to O2 demands
 Position changes—lying to standing
* Transient decrease in BP leads to SNS stimulation
leads to peripheral vasoconstriction and increased
venous return
* Inadequate response leads to dizziness or syncope

Question 10

Baroreceptors - role in maintaining BP

Answer 10

More on baroreceptors
 Vital role in maintaining BP; sensitive to stretch
* Increased stretch (increased BP)—send inhibitory impulse to vasomotor center to decreased HR,
decreased force of contraction, and vasodilation in
peripheral arterioles
* Decrease stretch (decreased BP)—SNS stimulation leads to peripheral arteriole constriction, increased HR, increased contractility
* Long standing HTN—baroreceptors adjust to increased BP; recognize as new “normal”

Question 11

Vascular Endothelium - Role in maintaining BP

Answer 11

Essential to regulation of substances for:
* Vasodilation—nitric oxide(NO) and prostacyclin
* Vasoconstriction—endothelin (ET)
 Smoking and diabetes—reduce endothelial function leads to increased risk of CVD

Question 12

Renal system - Role in maintaining BP

Answer 12

Control sodium excretion and ECF volume
* Increased Na+ leads to increased H2O leads to increased ECF leads to increased venous return and SV leads to increased CO and BP
 RAAS system—juxtaglomerular apparatus—secretes renin in response to: SNS stimulation, decreased renal blood flow, and decreased serum Na+
* Renin: converts angiotensinogen to angiotensin I
* Angiotensin I converted to angiotensin II (A-II) by ACE
* A-II—potent vasoconstriction and increased SVR; also stimulates adrenal cortex to secrete aldosterone
* A-II remodels vessel walls: contributes to primary HTN and long term effects of HTN
Prostaglandins (PGE2 and PGI2) from renal medulla
leads to systemic vasodilation
* Decreased SVR and BP
 Heart cells: natriuretic peptides: ANP and BNP
* Oppose ADH and aldosterone leads to natriuresis and diuresis leads to decreased blood volume and BP

Question 13

Endocrine system - effect on BP

Answer 13

Epinephrine and norepinephrine from adrenal medulla
* Epinephrine—Increased HR and contractility leads to increased CO; vasodilation of peripheral arterioles in skeletal muscle (2 receptors); vasoconstriction in skin and kidneys (1 receptors)
 Aldosterone from adrenal cortex
* Retain Na+ and H2O—increased blood volume and CO
 ADH from posterior pituitary
* increased ECF—reabsorption of H2O in kidneys leads to increased blood volume leads to increased CO and BP

Question 14

Classification of HTN

Answer 14

The higher measurement when either SBP or DBP
are outside a range determines the classification
 SBP increases with age
 DBP rises until about age 55, then declines
 BP classification is based on
- 2 or more readings
- Accurately performed on both arms
- On 2 separate occasions

Question 15

Primary HTN

Answer 15

Also called essential or idiopathic HTN
 Elevated BP of unknown cause
 90% to 95% of all cases
 Many contributing factors
* Altered endothelial function, increased SNS activity, increased Na+ intake, overproduction of Na+ retaining hormones, overweight, diabetes, tobacco, excess alcohol

Question 15

Normal BP Ranges

Answer 15

Normal: under 120 and 80
Elevated: 120-129, under 80
Stage 1: 130-139, 80-89
Stage 2: Over 140, over 90

Question 16

Secondary HTN

Answer 16

Elevated BP with a specific cause; sudden
development
 5% to 10% of adult cases
 Clinical findings relate to underlying cause
* Cirrhosis; aortic problems; drug-related; endocrine, neurologic, or renal problems; pregnancy-induced, or sleep apnea
 Treatment aimed at removing or treating cause

Question 17

Pathophysiology of primary HTN

Answer 17

Increased CO or SVR = increased BP
 Persistently increased SVR
 Risk factors for primary hypertension
 Contribute to progression or consequences
 Abnormalities in any mechanisms involved in
maintenance of normal BP can result in HTN

Question 18

Risk factors for primary HTN

Answer 18

*Age
 Alcohol use
 Tobacco use
 Diabetes
 Elevated serum lipids
 Excess dietary sodium
 Gender
 Family history
 Obesity
 Ethnicity
 Sedentary lifestyle
 Socioeconomic status
 Stress

Question 19

Primary HTN Genetic Link

Answer 19

Different sets of genes regulate BP at different times
 Research—endothelial dysfunction
 Children and siblings of persons with hypertension should be screened and strongly advised to adopt healthy lifestyles to reduce their risk of hypertension

Question 20

Primary HTN Pathophysiology - Na Intake

Answer 20

Water and sodium retention
 Only 1 in 3 people who consume high sodium diet
develop hypertension
 The effect of sodium on BP has a strong genetic
component
* Salt sensitive (increased BP) versus salt resistant (little change)
* Blacks; middle-aged and older adults
 Increased risk for renal dysfunction, endothelial
dysfunction and HF

Question 21

Primary HTN Pathophysiology - Altered Renin-Angiotensin-Aldosterone Mechanism

Answer 21

Altered Renin-Angiotensin-Aldosterone Mechanism
 High plasma renin activity (PRA)
* Increases angiotensinogen to angiotensin I
* increased BP inhibits release of renin
* Expect low PRA with primary HTN but not the findings
* Possibly ischemic nephrons release renin?

Question 22

Primary HTN Pathophysiology - Stress

Answer 22

Stress and Increased SNS activity
 Protective response versus pathologic
 Prolonged SNS activity
* Causes increased vasoconstriction
* Increased HR
* Increased Renin release

Question 23

Primary HTN Pathophysiology - Endocrine

Answer 23

Insulin resistance and hyperinsulinemia
 Defects in glucose, insulin, and lipoprotein
metabolism are common
 High insulin levels:
* Stimulate SNS activity and impair nitric oxide–mediated vasodilation
* Vascular hypertrophy
* Increased renal sodium absorption

Question 24

Primary HTN Pathophysiology - Endothelial Dysfunction

Answer 24

Endothelial dysfunction
 Prolonged vasoconstriction response or reduced
vasodilation response
 Impaired response to nitric oxide (NO) leads to
vasodilation
 Elevated endothelin (ET) leads to vasoconstriction

Question 25

Most common organ complications in HTN

Answer 25

Target organ diseases occur most frequently in
 Heart
* Coronary artery disease; atherosclerosis
* Left ventricular hypertrophy
* Heart failure
 Brain—cerebrovascular disease
* TIA/Stroke; atherosclerosis
* Hypertensive encephalopathy; changes in
autoregulation

Question 26

Complications of HTN - common ones

Answer 26

Peripheral vascular disease
* Atherosclerosis leads to PVD, aortic aneurysm, aortic dissection
* Intermittent claudication
 Kidney
* Nephrosclerosis leads to chronic kidney disease (CKD)
 Eyes—retinal damage
* Blurry or loss of vision; retinal hemorrhage
 Damaged retinal vessels indicate concurrent
damage to vessels in heart, brain, and kidneys

Question 27

HTN Diagnostic Studies

Answer 27

Measurement of BP
Labs to:
1) identify or rule out secondary HTN
2) evaluate target organ disease
3) determine CV risk
4) establish baselines before starting therapy
Renal function, U/A, BMP, CBC, serum lipid profile, uric acid, ECG, ophthalmic exam
Other: Echo, LFTs, TSH

Question 28

ABPM (ambulatory BP monitoring)

Answer 28

Noninvasive, fully automated system that measures BP at preset intervals over 12 to 24-hour period. Teach patient to hold arm still while device reads BP and keep diary of activities
 Other applications for use:
* Antihypertensive drug resistance
* Hypotensive symptoms with antihypertensive therapy
* SNS dysfunction
* Episodic HTN
* Diurnal variability; nondippers; reverse dippers

Question 29

Goals for Treating HTN

Answer 29

Achieve and maintain goal BP
 Reduce CV risk factors and target organ disease
 Lifestyle modifications
* AHA Life’s Simple 7
(1) Manage BP
(2) Control cholesterol
(3) Reduce blood sugar
(4) Get active
(5) Eat better
(6) Lose weight
(7) Stop smoking

Question 30

HTN Lifestyle Modifications

Answer 30

Weight reduction
 Weight loss of 1 kg will decrease SBP by 1 mm Hg
 Calorie restriction and physical activity
 DASH eating plan
 Fruits, vegetables, fat-free or low-fat milk/milk
products, whole grains, fish, poultry, beans, seeds,
and nuts

Dietary sodium reduction
 Less than 2300 mg/day for healthy adults
 Less than 1500 mg/day for
* Blacks, middle-aged and older, those with
hypertension, diabetes, or chronic kidney disease
* Salty Six (AHA): bread/rolls, lunch and cured meats, sandwiches, pizza, soup, poultry
 Read labels food, OTC meds, and health products
(e.g., toothpaste with baking soda)

Moderation of Alcohol Intake
 Men: 2 drinks/day; women: 1 drink/day
 Physical activity
 150 minutes moderate or 75 minutes vigorous exercise/wk
 Combine moderate and vigorous activities
 Age-associated guidelines
 Muscle-strengthening activities at least 2 times/wk
 Flexibility and balance exercises 2 times/wk; especially older adults (decreased falls)

Avoid tobacco products
 Nicotine causes vasoconstriction and elevated BP
 Smoking cessation reduces risk factors within 1 year

Question 31

HTN Drugs: Two primary actions of them

Answer 31

1. Decrease circulating blood volume
2. Reduce SVR (systemic vascular resistance) - resistance to blood flow from systemic vasculature, except for pulmonary vasculature

Question 32

Caring for Patients with Doxazosin (Cardura)

Answer 32

Give 1st dose at bedtime to reduce first dose BP drop
 Watch for syncope
* 30-90 minutes after 1st does
* Too-rapid increase in dose
* Given with other antihypertensive agent(s)
 Severe hypotension can occur with
phosphodiesterase inhibitors

Question 33

Adrenergic inhibiting agents for HTN

Answer 33

Meds that inhibit actions of the adrenergic (sympathetic) nervous system
Examples: alpha blockers, beta blockers, Alpha 2 agonists, combined alpha and beta blockers

Decrease SNS stimulation; work centrally on vasomotor center and peripherally to inhibit NE release or block adrenergic receptors on blood vessel

Question 34

Ace Inhibitors for HTN

Answer 34

Prevent conversion of angiotensin I to angiotensin II; reduce vasoconstriction and sodium and water retention

(stands for angiotensin conversion enzyme inhibitors)

They work by relaxing blood vessels and making it easier for heart to pump blood. ACE inhibitors are often chosen because they not only reduce blood pressure but also have protective effects on the heart and kidneys, especially beneficial in patients with diabetes or mild-to-moderate kidney diseases.

Question 35

A-II Receptor Blockers for HTN

Answer 35

Prevent angiotensin II (a chemical in your body that narrows blood vessels) from binding to receptors in blood vessel walls. This leads to relaxation of blood vessels and a decrease in blood pressure.

ARBs are particularly beneficial for patients who experience side effects with ACE inhibitors, as they provide similar benefits but are often better tolerated. They are also an important treatment option for protecting the kidneys in patients with diabetes.

Question 36

Calcium Channel Blockers for HTN

Answer 36

increase Na+ excretion and cause arteriolar vasodilation by preventing the movement of extracellular Ca into cells

They work by preventing calcium from entering cells of the heart and blood vessel walls, leading to relaxation of the blood vessels and a decrease in heart rate. This helps lower blood pressure and can improve blood flow.

Question 37

Direct Vasodilators for HTN

Answer 37

relax vascular smooth muscle and reduce SVR

Directly relax the muscles in the walls of blood vessels, leading to their dilation (widening). This dilation reduces blood pressure by decreasing the resistance against which the heart has to pump

Question 38

Diuretics for HTN

Answer 38

reduce plasma volume by increased sodium and water excretion and reduce vascular response to catecholamines

often called “water pills,” are a class of medications that promote the elimination of salt (sodium) and water from the body through the urine. They are widely used to treat high blood pressure (hypertension), heart failure, kidney disorders, and sometimes edema (swelling) caused by various conditions. Diuretics work by acting on the kidneys to increase urine production.

Question 39

Treating Stage I HTN

Answer 39

nonpharmacologic treatment + 1
first line pharmacologic drug

Question 40

Treating Stage II HTN

Answer 40

nonpharmacologic therapy + 2 antihypertensives from two different classifications
 If a drug is not tolerated, then another classification will be used
 Monthly follow-up visits until at goal BP; then 3 to 6 months
 Stage 2 HTN or comorbidities—more frequent

Question 41

Resistant HTN Treatment

Answer 41

Failure to reach goal BP with appropriate therapy
and drug regimen: increased risk of stroke or MI
 Causes
* Improper BP measurement
* Volume overload
* Drug-induced or other causes
* Associated conditions
* Secondary HTN
 Treatment: determine cause
* Overactive renal nerve - renal nerve ablation

Question 42

HTN Crisis

Answer 42

SBP >180 mmHg and/or DBP >120 mmHg
 Hypertensive emergency
* Target organ damage
* Requires hospitalization
* Very severe problems can result if prompt recognition and treatment is not obtained
 Encephalopathy, intracranial or subarachnoid
hemorrhage, HF, MI, Renal failure dissecting aortic
aneurysm or retinopathy
* Untreated = 79% mortality in one year

Hypertensive urgency—more common
 No evidence of target organ disease
 Hospitalization usually not required
 Associated with chronic stable disorders
* Stable angina, chronic HF, prior MI or CVA
 Hypertensive crisis
* History of HTN; not adherent or undermedicated
* Cocaine, amphetamines, PCP, LSD leads to seizures, stroke, MI, or encephalopathy

Question 43

HTN Crisis - Clinical Manifestations

Answer 43

Hypertensive encephalopathy - syndrome
 Severe headache, nausea/vomiting, seizures, confusion, coma; retinal changes
 Renal insufficiency
 Cardiac decompensation
- MI, HF, pulmonary edema, chest pain, dyspnea
 Aortic dissection
- Sudden severe chest and back pain, reduced/absent peripheral pulses

Question 44

HTN Crisis - Hospital Procedure Treatments

Answer 44

*Treatment related to BP and evidence of target organ disease (When high blood pressure has caused damage to organs like the heart, brain, kidneys, or eyes (known as target organ damage), treatment becomes more urgent and intensive. The goal is to lower the blood pressure to prevent further damage)

*IV Drugs, Slow titration; MAP (mean arterial pressure, average pressure in person’s arteries during one heartbeat cycle) 110-115 mm HG
-MAP = (SBP + 2 DBP) / 3
*this number is for sufficient blood flow to organs without causing further damage

Drugs: vasodilators (sodium nitroprusside, help widen vessels), adrenergic inhibitors (reduce affects of adrenaline and similar hormones to lower BP and HR), Ca channel blockers (prevent Ca from entering cells of heart and blood vessel walls, which lowers BP)
-have rapid onset, monitor HR and BP q 2-3 min

Special considerations:

aortic dissection (This is a serious condition where the inner layer of the aorta, the large blood vessel branching off the heart, tears. Blood pressure must be carefully and quickly controlled to prevent further tearing)

acute ischemic stroke (In the case of a stroke caused by a blood clot, blood pressure management is complex. While high blood pressure needs to be lowered, it’s also crucial to maintain enough blood flow to the brain)

post stroke patients (After a stroke, blood pressure management is essential to prevent another stroke and to minimize further brain damage. However, overly aggressive lowering of blood pressure can potentially reduce blood flow to the brain, which is already vulnerable)