cardiology - HTN

what is the leading cause of death and leading reason for PC visits

HTN

people with HTN have a higher risk for developing what?

HF and CVA

what gender and ethnicity are at a higher risk for developing HTN

- lower in women before 50 and after menopause, women risk exceeds men

- African Americans in US and white populations in european countries

Presence of arterial blood pressure elevation that places patients at risk for target end-organ damage

HTN

untreated HTN can lead to what ?

- stroke

- eye damage

- arteriosclerosis

- HF/heart attack

- kidney failure

as one ages, systolic and diastolic blood pressures increase. when does this change?

50s-- diastolic drops and systolic continues to increase

how should pre-hypertensive patients be treated?

- BP followed up to 6 months without medical treatment

** conservative treatment with basic lifestyle changes

what are the recommendations for stage 1 and 2 HTN?

- pharmacologic treatmetn + lifestyle modifications

T/F: people with BP >180/110 require one medication

true

JNC Guidelines for HTN

normal:

what medication should not be used a sole treatment for elderly or stroke patients

beta blockers

the severity of HTN correlates with what?

- absolute level of BP elevation

- rapidity of its development

substantial BP elevations (>180/120) with progressive end organ complications is known as what?

how is treated?

hypertension urgencies

tx: BP reducation w/oral meds within 24-48 hours

T/F: HTN urgencies present with end organ damage

false (just complications)

substantial BP elevations (>180/120) with papilledema and end-organ damage is known as what?

how is it treated?

HTN crisis/emergency

tx: immediate BP reduction w/IV meds by 20-25% + minimize end organ damage

in treating HTN emergencies, resting MAP should not be reduced by how much?

>25%

examples of end organ damage in CNS d/t HTN?

HTN encephalopathy and/or stroke

examples of end organ damage in cardiopulmonary system d/t HTN?

- acute CHF

- acute coronary syndrome

- MI

- pulmonary edema with respiratory failure

- dissecting aortic aneurysm

explain what happens to the eye in papilledema

- absent venous pulsations

- hyperemia of discs and blurring of margins

- flame shaped hemorrhages

what agents are used in HTN emergencies

- clonidine

- diazoxide

- esmolol

- fenoldopam

- nitroprusside

- labetalol

- nicardipine drips

examples of end organ damage associated with HTN?

- •Hypertensive encephalopathy

•Intracranial hemorrhage

•Unstable angina pectoris

•Acute MI (myocardial infarction)

•Acute LV failure with pulmonary edema

•Dissecting aortic aneurysm

•Progressive renal failure

•Eclampsia

where are the majority of intra-parenchymal hemorrhages found

basal ganglia/thalamus

treatment of acute HTN after intracerebral hemorrhage

IV labetalol, nitroprusside or hydralazine

what should be used to immediately slow the progression of aortic dissections

beta blockers or CCBs

T/F: LVH at baseline with HTN and no prior CV history, has a 3 fold increase in CV events

true

how can LVH be treated with anti-hypertensives

use of ACEIs or ARBS and CCBs

normal office BP and elevated home BP. is known as

masked HTN

•elevated office BP and normal home BPs -- increased intermediate risk b/w normotension and sustained HTN

white coat HTN

BP measurements taken in the office and at home are elevated

sustained HTN

what conditions are sustained HTN related to

target organ damage and worse cardiac/renal events

T/F: HTN is usually curable

false

HTN as a symptoms could increase chances for what conditions?

stroke, MI, HF, PVD, aortic dissection, atrial fibrillation, ESRD

what is pulse pressure

difference between systolic and diastolic pressure

systolic HTN after age 50 due to the decreased distensibility of the large conduit arteries:

isolated Sys HTN

secondary causes of HTN include

- renal parenchymal HTN

- renovascular HTN

- coarctation of aorta

- primary hyperaldosteronism

- cushing's syndrome

- pheochromocytoma

- obstructive sleep apnea

- obesity

- autosomal dominant/recessive diseases of adrenal renal gland axis (SALT RETENTION)

why does HTN occur? explain patho.

multisystemi state--> vasoconstriction and renal Na+ retention

OR

cause of failure of vasodilation and renal sodium excretion

how does volume expanded HTN occur

- high Na+ intake and inadeqaute Na+ excretion causes an increased ECF fluid volume which causes (1) Na+-K+ pump inhibitor increases or (2) ANP increases

--> increases BP

when is ANP stimulated

synthesized by atrial myocytes and is released in response to increased atrial distention and hypovolemic states

if there is an abnormal UA, what could be the reason for HTN

renal disease

low serum K+ could be the cause of HTN due to what conditions

1° aldosteronism/Cushing' syndrome

an abnormal HCT could suggest ------ contribution in causing secondary HTN

polycythemia

what is the most common cause of secondary HTN? what is patho behind it?

CKD--> expanded plasma volume and peripheral vasoconstriction d/t activation of vasoconstrictors and inhibition of vasodilators

- UA dipstick: + protein

- serum Cr >1.2 in females and >1.4 in males

- GFR

renal insufficiency

how do you diagnose renal parenchymal disease

renal US or biopsy

main causes of renovascular HTN

- atherosclerosis (older pts)

- fibromuscular dysplasia (women b/w 15-50)

how do you treat renovascular HTN

balloon angioplasty + ACEI

this is caused by underperfusion of juxtaglomerular cells in the kidney which produces renin-dependent HTN in affected kidney, but contralateral kidneys maintain normal blood volume

unilateral renal artery stenosis

if patient presents with flash pulmonary edema, progressive worsening of renal functioning with unilateral small kidney, and flank bruit. when asking of PMH, he states that he was recently hospitalized for emergent HTN. what is condition?

bilateral RAS- renovascular HTN

how do you treat renovascular HTN

- balloon angioplasty

- surgical (for patients undergoing simultaneous aortic reconstruction)

what should be considered in medically refractory HTN, progressive renal failure, and bilateral/unilateral RAS?

revascularization

congenital heart defect involving a narrowing of the aorta

coarctation of aorta

patient presents with higher BP in arms than in legs with weak pulse in groin area and cold legs. She complains of dizziness and nosebleeds. what is condition? how do you diagnose and treat it?

coarctation of aorta

dx: MRI and aortography

tx: surgery

what is found on CXR of someone with coarctation of arota

HTN

chest bruits

rib notching

how is coarctation of aorta diagnosed

MRI and aortography

most common causes of primary hyperaldosteronism

unilateral aldosteorne producing adenoma or bilateral adrenal hyperplasia

patient with HTN and hypokalemia. on testing, increased plasma renin and aldosterone levels were present. what is condition

Primary Hyperaldosteronism (PHA) Mineralocorticoid - Induced HTN

how is PHA mineralocorticoid induced HTN (Conn syndrome) diagnosed

- elevated plasma renin and aldosterone levels

- 24 hour urine K+ and aldosterone; and K+ after salt loading

- adrenal CT

- adrenal vein sampling

how Primary Hyperaldosteronism (PHA) Mineralocorticoid - Induced HTN (Conn Syndrome) treated?

adenoma- surgery

hyperplasia- medical mgmt

the final common pathway for reabsorption of sodium from the distal nephron

epithelial Na+ channel (EnaC)

salt dependent HTN can be caused by what?

- gain of function mutations on ENaC or mineralocorticoid receptor

- increased production of or decreased clearance of mineralocorticoid receptor ligands

15 year old patient with hypokalemia, increased plasma aldosterone and suppressed renin. reports familial HTN. what is condition? how is it diagnosed and treated?

glucocorticoid remedial aldosteronism

dx: southern blot test

tx: dexamethasone

treatment of Glucocorticoid-Remedial Aldosteronism

dexamethasone

effect of aldosterone on kidney tubules

•retain sodium and water. This increases the volume of fluid in the body and drives up blood pressure.

cushing's disease vs cushing's syndrome

DISEASE: hyperstimulation of ACTH from pituitary adenoma and hyperplasia of adrenal gland

SYNDROME: adenoma or carcinoma - excess ACTH

what is iatrogenic cushing's syndrome caused by

exogenous glucocorticoid administration

35 year old female presents with truncal obesity, wide purple blanching striae, and muscle weakness. What is condition?

cushing's syndrome

how do you diagnosis and treat cushing's syndrome

Dx: plasma cortisol, urine free cortisol after dexamethasone suppression, adrenal CT

Tx: surgical (resect lesion), medical + radiation therapy

25 year old patient presents with frequent headaches, palpitations, pallor, and diaphoresis. Family history of early-onset HTN. what is diagnsosi? how do you diagnosis?

pheochromocytoma

dx: plasma metanephrines and normetanephrines, 24 hr catecholamines and adrenal CT

what 2 sympathomimetic agents are confused with pheochromocytomas?

cocaine and methamphetamine

what neurogenic causes are confused with pheochromocytomas?

- sympathomimetic agents

- baroreflex failure

- OSA (snoring/hypersomnolence and CPAP)

repeated arterial desaturation causes what?

sensitizes carotid body chemoreceptors and sustained sympathetic overactivity

how does obesity contribute to HTN?

expands plasma volume and overactivity of sympathetic nervous system (to burn fat-- increase in vasoconstriction and renal salt/water retention)

HTN, male pattern obesity, insulin resistance/glucose intolerance, dyslipidemic pattern (increase trigs and decrease HDLs)

metabolic syndrome

what is metabolic syndrome caused by?

increased calories and salt

patient presents with T2 DM, high blood pressure, and central obesity. After labs, it showed, decreased HDLs and elevated triglycerides. what is condition?

metabolic syndrome

is HTN genetic?

- greater with families, between monozygotic twins, and between biologic siblings

how is HTN diagnosed?

often an incidental finding seen in BP elevation

T/F: HTN can be diagnosed based on a single reading

false (multiple readings at separate visits)

SBP vs DBP can be heard at what time when measuring BP

systolic-- onset of korotkoff sounds

diastolic-- disappearance of korotkoff sounds

what is auscultatory gap

Korotkoff sounds disappear then reappear

if readings in 2 arms are grossly different, which number should be recorded

higher

how is orthostatic hypotension evaluated?

checking BPs in seated, supine and upright postures

when is ambulatory BP monitoring indicated

- suspected white coat HTN

- suspected white coat aggravation in patient with medically refractory HTN

- suspected masked HTN/nocturnal HTN

- HTN of pregnancy

- suspected orthostatic hypotension or autonomic failure

- as people get older, walls of arteries get thicker and calcium is deposited which makes them difficult to compress

-BP reading is very high over time, but the patient has no signs of organ damage or other complications OR when treating high BP causes symptoms of low BP symptoms--> actually normal

pseudohypertension

•Detecting a palpable artery that persists even after the cuff is inflated is known as what?

osler sign

what are the goals for the initial evaluation for HTN

1.Correctly Stage the BP according to the JNC-8

2.Assess overall CV risk for the patient

3.Detect clues for secondary forms of HTN

** thorough and complete H&P + labs

HTN guidelines

Normal:

when should antiHTN meds be initiated:

1.BP > 140/90 in pts less than 60yo

2. BP > 150/90 in pts older than 60yo

3.BP > 140/90 in high-risk pts (DM,CKD,...)!!!

first line treatment for HTN In general nonblack population

thiazides, CCB, ACEI or ARBs

first line for HTN in black population

thiazides or CCB

first treatment for someone with HTN and CKD

ACEi or ARB

when should HTN medication be up-titrated or added to?

after 1 month if BP still not achieved

what meds cause an increase in BP

decongestants, OCPs, appetite suppressants, NSAIDs, exogenous thyroid hormones, alcohol, ilicit drug use, steroids

when should secondary HTN be considered?

- age of onset

- difficult to control after Rx started

- stable HTN that suddenly becomes difficult to control

- clinical occurrence of HTN-ive crisis

- s/s of secondary cause

why does copper wiring occur in HTN?

Retinal arteriolar narrowing due to thickening and opacification of arteriolar walls (copper wiring) caused by hypertensive arteriosclerosis.

- intra-retinal hemorrhages

- yellow hard exudates

- cotton wool spots

hypertensive retinopathy

when is first and second heart sound heard?

first: "lub" - when AV valves close

second: "dub"- when SL valves close

labs ordered in HTN patient

•UA

•Hematocrit

•Plasma Glucose

•Serum Potassium

•Serum Creatinine

•Serum Calcium

•Uric Acid

•CXR

•ECG - (check for LVH)

•Fasting Cholesterol and Triglycerides

what lifestyle modifications can be made for HTN patient

- Na+ restriction

- DASH diet

- smoking cessation

- weight loss

- minimal caffeine and alcohol

- exercise

- control stress

examples of diuretics used for HTN

THIAZIDES: HCTZ, cholthalidone LOOP: furosemide, bumetanide

K-SPARING: spironolactone