HTN Flashcards
HTN is more prevalent in:
- Non Hispanic Black Populations
- Older Persons
JNC7 bases BP upon:
-The average of two or more properly measured readings at each of two or more visits after an initial screen
Normal BP
-Systolic: <80
Pre-HTN
- Systolic: 120-139
- Diastolic: 80-89
Hypertension Stage 1
- Systolic 140-159
- Diastolic: 90-99
Hypertension Stage 2
- Systolic > or equal to 160
- Diastolic > or equal to 100
Isolated Systolic HTN
When BP is > or equal to 140/<90mmHg
-Wide pulse pressure present
Isolated Systolic HTN more common in individuals
Over age 60. Have diminished compliance of vasculature
Blood pressure increases with
Age
Non-reversible Risk Factors:
- African-American descent
- Family history of HTN
Reversible Risk Factors
- Pre-HTN
- Obesity
- Sedentary Lifestyle
- High sodium diet
- Excessive alcohol intake
- Metabolic Syndrome
HTN major risk factor for:
- CV disease
- Chronic Kidney Disease
- Dementia
HTN single most important risk factor for?
Stroke
MCC death in persons w/HTN is?
Coronary artery disease
Left Ventricular Hypertrophy
Strong predictor of sudden death and MI in persons with HTN
In HTN, microalbuminuria
Marker for Increased CV risk
Diagnosis: requires SEVERAL BP measurements
1) Use validated sphygmomanometer
2) Correct size cuff on BARE arm
3) Resting quiet for at least 5 minutes
4) Back supported
5) Feet on ground & uncrossed
6) No talking
Masked HTN definition:
Normal in office, but underlying HTN target organ injury
PseudoHTN
See in older persons, falsely increased systolic & diastolic pressure by cuff due to STIFF vascular tree caused by atherosclerosis
Ambulatory reading > office measurements
Classification of bp based on average of 2+ readings obtained more than 1 min. apart on 2 or more visits
Ambulatory BP Monitoring
- Evaluates mean 24 hr B.P.
- Difference b/w mean daytime and mean nighttime bp
- Avg difference used to evaluate for noctural dipping.
- > 10% is dipping (good thing)
Lack of nocturnal dipping causes
More strain on CV system
Non-dipping (bad) often seen in
- African Americans
- Chronic Kidney Disease
- Sleep Disorders
Lack of nocturnal dipping associated with
Increased CV risk
As we grow older our arteries become stiffer and less compliant
- Stiffening, get increased speed of reflected waves
- Faster the pulse wave velocity, the greater the end organ damage.
Measurement of central aortic pressure and pulse wave velocity are better correlated with end-organ damage
> than brachial BP
Most anti-HTNs cannot slow pulse wave velocity
Statins do improve vasculature compliance.
3 questions to ask when evaluating HTN
1) BP: Essential (primary) vs. Secondary
2) CV Risk factors
3) End organ damage
Who is more prone to pseudo HTN?
- Elderly
- Chronically ill
- These groups are also prone to orthostatic hypotension.
Meds that can elevate BP:
- Oral contraceptives
- Corticosteroids
- Monoamine oxidase inhibitors
- NSAIDs
- Sympathomimetic preparations for cold or diet
- Cocaine
- Alcohol
- Serotonin
- Glycyrrhizinic acid (true licorice) in chewing tobacco
Physical Exam:
- Measurement of vital signs
- BMI
- Cardiopulm exam
- Auscultation of major blood vessels to identify bruits
- Fundoscopic examination
- Neuro
- Evaluate extremities for edema and circulatory abnormalities.
Labs:
- CBC
- Lipid and biochem profiles
- Urinalysis
- Electrocardiogram
Wait to measure renin and aldosterone until:
- See pt w/HYPOkalemia or resistant HTN
- Increased plasma aldo:renin ratio: suggests dietary Na+ excess HTN.
Clinical marker for LVH:
- S4 gallop
- Apical lift ECG
- ECHO
Clinical marker for angina, prior MI, prior revascularization
History
Clinical marker for heart failure:
-History, lung RALES, S3 gallop, Chest x-ray, Echo
Marker for Stroke, TIA, Leukoariosis (white matter changes on imaging)
History and brain imaging
Marker Chronic Kidney Disease
eGFR, Creatinine, U/A, microalbumin
Marker Peripheral Artery Disease
-Claudication, bruits, diminished pulses
Marker Retinopathy
-Fundoscopic evaluation, general and focal narrowing, AV nicking, Copper wiring, cottom wool spots, microaneurysms, Frame and blot hemorrhages
Essential HTN
90% of patients with htn evaluated in the primary care setting
Classic Features of Essential HTN
- Onset in fourth or fifth decade of life
- A positive family hx for HTN
- Initial BP low categorized as stage 1 HTN
- And easily controlled with 1 or 2 medications
- No target organ damage
- Normal results of routine lab studies
- BP that does not increase from an established level of control over a short period of time
Things that make you think secondary forms of HTN:
- Age of onset, before 30, over 50
- BP >180/110 mmHg at diagnosis, significant target organ damage
- Poor response to an appropriate 3 drug regimen
Lifestyle modifications are appropriate to lower bp in patients with
Pre-HTN
Lifestyle modifications + drug treatment
Stage 1 or greater HTN
Weight Reduction, maintaining normal body weight
5-20 mmHg reduction/10 kg weight loss
Adapting DASH eating plan
8-14 mmHg reduction
Dietary sodium reduction, no more than 1500 mg/day
2-8 mmHg
Physical Activity, 30 minutes/day
4-9 mmHg
Moderation of alcohol consumption
2-4 mmHg
Goal of treatment of HTN:
Reduce CV mortality and morbidity by lowering BP
Goal in general population of anti-HTN treatment
Lower BP below 140/90 mmHg
Linear, progressive increase risk of ischemic heart disease and stroke in patients with bp higher than
115/75 mmHg
Most anti-HTN agents reduce blood pressure by 10-15% and ALL classes of anti-HTN drugs
Reduce CV morbidity and mortality vs. placebo
Treatment of systolic heart failure and proteinuria in kidney disease
ACE Inhibitors and ARBs
Salt sensitive HTN
Diuretics, may be good in:
- Elderly
- Low GFR
Coronary artery disease and migraine headaches
Beta-blockers
Clinical trials have shown that achieving appropriate blood pressure targets is MORE important in reducing morbidity and mortality than
The choice of Anti-HTN therapy
Use these drugs to help lower BP in patients who are likely to be sodium sensitive:
- Older patients
- Black
- Lower pre-txt plasma renin activity
Calcium channel blockers
Diuretics
Use for younger, white, and higher pre-txt plasma renin activity
ACE-Inhibitors or
Beta-blockers
Lifestyle modification and drug treatment are indicated for all patients with
Stage I HTN or greater
Patient with stage II HTN often require treatment with
more than one agent
Resistant HTN
Patients whose BP remains above goal on maximum doses of 3 meds one of which is a diuretic.
10% cases HTN due to secondary htn
Consider in pts who have clinical features inconsistent with essential HTN.
Common secondary causes: drugs, increasing obesity, obstructive sleep apnea
Renal vascular htn
1-3% general HTN population
10% patients with resistant htn
30% pts in htn crisis
Renal artery stenosis does NOT make a diagnosis of
Renal vascular htn
70% or more luminal narrowing
Increases renin production from ischemic kidney
Not all abdominal bruits are from renal artery
Diastolic component to bruit= renal artery lesion
Unilateral disease
-nonischemic kidney increased perfusion, higher Na+ excretion and suppression of renin release
Bilateral disease
-Increases in renin cause ECV expansion and volume dependent htn.
Pulse pressure is a good assessment of
End organ damage
Fibromuscular dysplasia
Most common cause of renovascular htn in younger women, esp childbearing age. Medial subtype most common. “String of beads” on angiography.
- Balloon angioplasty is the treatment of choice
- Stents reserve only if angioplasty fails
Renal revascularization only improves htn in patients with
Anatomic lesion that is hemodynamically significant to activate the renin-angiotensin system.
BOLD MRI
Bilateral renal artery stenosis present, ACE inhibitors and ARBS can make acute renal failure worse.
Gold standard for identifying renal artery stenosis
-Renal angiography
Top causes of secondary HTN
#1: Primary hyperaldosteronism #2: Renal parenchymal disease
HTN is the 2nd most common cause of
End stage renal disease.
3 mechanisms involved in HTN of renal disease
1) volume expansion b/c can’t get rid of salt and water
2) over secretion renin
3) Decreased production renal vasodilators
Primary aldosteronism
- Overproduction of aldosterone by adrenal glands
- HTN, hypokalemia with renal wasting of potassium and metabolic ALKALOSIS.
- Suppressed plasma renin activity
- Increased aldosterone levels
When to suspect primary aldosteronism:
Person with spontaneous hypokalemia, marked hypokalemia precipitated by usual dose of diuretics, resistant HTN, hypertension and adrenal mass, or hypokalemia despite use of ACE inhibitors or ARBs.
Almost half of patients with primary aldosteronism have
Normal potassium levels
Plasma aldosterone: renin ratio
Screening test for primary aldosteronism
urine aldosterone excretion 12 mcg/24 hours (33.2nmol/day) or higher after correction of hypokalemia and adherence to HIGH sodium diet for 3 days.
Adrenal imaging
- Aldosterone producing adenoma (Conn syndrome)
- Primary unilateral adrenal hyperplasia
Can use spironolactone for treatment of
Primary aldosteronism
Sometimes obese pts or with resistant htn can see dramatic decrease in bp when started on
Aldosterone antagonist
Pheochromocytoma
Tumors of chromaffin cells, derived from neural crest.
- Cause paroxysmal or sustained htn
- excess production of catecholamines
- Diaphoresis, headache, and anxiety frequently associated symtpoms
Complications of pheochromocytoma
- MI, stroke, cardiovascular collapse
- Can have germ-line mutations
Familial pheochromocytoma occurs in
- multiple endocrine neoplasia type II
- von Hippel-Lindau disease
- Neurofibromatosis
- Familial paraganglioma
Diagnosis pheo
- Confirm excess catecholamine production supported by imaging studies
- Fractionated catecholamines and metanephrines can be measured in the serum or via a 24-hour urine collection
- MRI
- CT scanning can localize
Treatment of choice for pheochromocytoma
Surgical resection
-10-14 days before surgery give alpha blocker phenoxybenzamine , then beta-blockers started
**Do NOT use Beta blockers without alpha blockage b/c
-Can lead to unopposed alpha stimulation and an increase in BP
Catecholamines can induce vasoconstriction and pressure naturesis can cause decrease in plasma volume
-We can institute high sodium diet and avoid diuretics.
HTN patient with impaired fasting glucose
Cushing syndrome
Hypothyroidism
- associated with diastolic htn
- state of decreased cardiac output and contractility
- Tissue perfusion maintained by increase in peripheral vasc. resistance mediated by increased activity of the sympathetic nervous system
Hyperthyroidism
- Associated with systolic HTN
- Wide pulse pressure due to increased CO and decreased peripheral vasc. resistance
Hyperparathyroidism
-Hypercalcemia may increase BP directly by increasing peripheral vascular resistance and indirectly by increasing vascular sensitivity to catecholamines
Acromegaly
-Can develop HTN due to Na+ retaining effects of GH.
Coarctation of aorta
- Constriction of vessel, detected in childhood
- More common males
- Assoc. with bicuspid aortic valve
- Classic feature: increased BP in upper extremities and low BP in lower extremitie
Symptoms of coarctation of aorta
Headache, cold feet, and claudication (pain by too little blood flow during exercise)
-Clinical signs: elevated bp in arms, murmurs in front and back of chest and delay in femoral pulse when radial and femoral pulses palpated.
**NOTCHED ribs
Coarctation! Do surgical repair or balloon angioplasty
Obstructive Sleep apnea
- Upper body obesity
- Overweight pts that snore loudly
- Complains: morning headaches, daytime sleepiness
- Sleep study**
- Increased sympathetic nervous system
- Treatment: continuous POSITIVE pressure, lower BP 3-5 mmHg.
- Encourage to lose weight
HTN emergency:
- Need to hospitalize
- Parenteral therapy!!!
- HTN encephalopathy, aortic dissection, unstable angina, MI, eclampsia, pulmonary edema, and acute renal failure
- Fibrinoid necrosis vascular lesion of malignant HTN
HTN urgency
- Severe HTN without evidence acute organ injury but occurring in setting in which it is important to decrease bp.
- Oral therapy
Common causes HTN urgency
- Neglected essential HTN
- Discontinuation of anti-htn therapy
- Renovascular disease
- Scleroderma
- Stroke
Sodium nitroprusside
- DOC htn emergency
- Don’t use in pts with kidney disease
- Raises intracranial pressure in animals
- Nitroprusside: worry about cyanide and thiocynate toxicity
Labetalol
A combo of alpha and beta blocker
can use orally & IV
Nicardipine and clevidipine
Ca2+ channel blockers
Fenoldapam
IV dopamine agonist
Preserves renal perfusion and is good for patients with Increased creatinines
Nitroglycerin
Good for pts w/acute congestive heart failure or coronary ischemia
Esmolol
DOC for Aortic dissection!
