Module 2: Hypertension Flashcards
Risks of high bp
MI, heart failure, stroke, renal disease, retinopathy
Who has highest prevalence of HTN?
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
Hispanics and HTN
Less likely to receive treatment
Lower rate of awareness, treatment, and control
Gender differences of HTN
Men - more common before middle age
Women - increased 2-3x with oral contraceptives
More common after menopause, harder to control in older women
Factors influencing BP
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)
SVR (systemic vascular resistance)
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
Factors influencing BP
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
SNS Receptors Affecting BP
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
Factors Influencing BP: Sympathetic Vasomotor Center
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
Baroreceptors - role in maintaining BP
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”
Vascular Endothelium - Role in maintaining BP
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
Renal system - Role in maintaining BP
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
Endocrine system - effect on BP
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
Classification of HTN
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
Primary HTN
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
Normal BP Ranges
Normal: under 120 and 80
Elevated: 120-129, under 80
Stage 1: 130-139, 80-89
Stage 2: Over 140, over 90
Secondary HTN
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
Pathophysiology of primary HTN
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
Risk factors for primary HTN
*Age
Alcohol use
Tobacco use
Diabetes
Elevated serum lipids
Excess dietary sodium
Gender
Family history
Obesity
Ethnicity
Sedentary lifestyle
Socioeconomic status
Stress
Primary HTN Genetic Link
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
Primary HTN Pathophysiology - Na Intake
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
Primary HTN Pathophysiology - Altered Renin-Angiotensin-Aldosterone Mechanism
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?
Primary HTN Pathophysiology - Stress
Stress and Increased SNS activity
Protective response versus pathologic
Prolonged SNS activity
* Causes increased vasoconstriction
* Increased HR
* Increased Renin release
Primary HTN Pathophysiology - Endocrine
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
Primary HTN Pathophysiology - Endothelial Dysfunction
Endothelial dysfunction
Prolonged vasoconstriction response or reduced
vasodilation response
Impaired response to nitric oxide (NO) leads to
vasodilation
Elevated endothelin (ET) leads to vasoconstriction
Most common organ complications in HTN
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
Complications of HTN - common ones
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
HTN Diagnostic Studies
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
ABPM (ambulatory BP monitoring)
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
Goals for Treating HTN
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
HTN Lifestyle Modifications
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
HTN Drugs: Two primary actions of them
- Decrease circulating blood volume
- Reduce SVR (systemic vascular resistance) - resistance to blood flow from systemic vasculature, except for pulmonary vasculature
Caring for Patients with Doxazosin (Cardura)
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
Adrenergic inhibiting agents for HTN
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
Ace Inhibitors for HTN
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.
A-II Receptor Blockers for HTN
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.
Calcium Channel Blockers for HTN
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.
Direct Vasodilators for HTN
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
Diuretics for HTN
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.
Treating Stage I HTN
nonpharmacologic treatment + 1
first line pharmacologic drug
Treating Stage II HTN
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
Resistant HTN Treatment
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
HTN Crisis
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
HTN Crisis - Clinical Manifestations
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
HTN Crisis - Hospital Procedure Treatments
*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)
