• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/61

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

61 Cards in this Set

  • Front
  • Back
STAGE 1 OF HTN
Stage 1: SB 140-159 & DBP 90-99
*Lifestyle modification needed
Tx w/drugs: f/u q month until goal is reached & then Q 3-6 mths
If compelling indication: antihypertensives plus drug for compelling indication
STAGE 2 OF HTN
SBP >160 & DBP >100 OR w/other compelling situation: need frequent office visits.
LM
Noncompelling: Thiazide & an antihypertensive
Drugs for compeliling indication along with antihypertensives
AHA DEFINES HTN AS
Having SBP 140 mm Hg or highter & DBP 90 mm Hg or greater
taking anti-hypertensive meds
Being told at least 2x by a HCP that an individual has HTN
DIABETES & HTN
BP goal: <130/80 if renal diseae also present, BP goal should be <125/75 mm Hg
Tx goals: Regular self-monitoring blood glucose levels & BP
-Taking medcations as ordered
-Reporting adverse reactions
-Stress reduction strategies
Isolated Systolic HTN
Older adults
SBP >140 coupled w/an average DBP <90 mm Hg
Gender Differences
Men: Before 45, more likely to suffer an MI than a stroke

Women: After 64: more common than in men, menopause,
-ACE-inhibitor induced cough & diuretic induced hyponatremia: more common
-2-3x more common: taking oral contraceptives
Risk factors
Dyslipidemia: elevated serum lipids & triglycerides (elevated)
DM
Family Hx: HTN & CVD
Alcohol Ladies 1 drink men 2 drinks
Normal Regulation of BP
2
-BLOOD PRESSURE-forced exerted by the blood against the walls of the blood vessels.
-determined by the qty of blood flow or CO as well as by resistance in the arterioles
-ARTERIAL BP- Primarily a function of CO and SVR
Normal Regulation of BP
-C/S
CO- amt of blood ejected by each ventricle during a given period (L/min) (50ml)

SV: amt. of blood ejected out by LV/beat 70ml x HR(1 min)
SV=CO/HR (50-70 mL resting HR CO/HR=SV
MECHANISMS THAT MEDIATE AND REG. BP
3
1. ANS- excites/inhibits SNS activity
2. KIDNEYS- Activate RAAS
3. ENDOCRINE- releaes of various hormones to stimulate (SNS) at tissue level (i.e. catecholamine, kinins, serotnin, histamine
SNS
Increase SNS activity INCREASE HR&cardiac contractility produces - vasoc (peripheral arterioles) - release of renin (kidneys)
Net effect SNS activation is to increase BP by increasing CO &SVR
1st Baroreceptors (Pressoreceptors)
1. Arch of aorta & origin of internal carotid arteries -stimulated when arterial walls are stretched by an increae in BP
-impulses from BR inhibit vasomotor center
2nd BR
Peripheral receptors
Sensitive primarily to hypoxemia
stimulated: send ipulses along the vagus nerve to activate a casoc and increase BP
SNS receptors
1/2
1. B-2 receptor: (activated from EN adrenal gland) loc: sm. muscle of blood vessels in heart (e.g. coronary arteries), lungs (e.g bronchi) and skeletal muscle - Response Vasodilation
SNS receptor
2/2
2. Dopamine receptors (located on renal arteries)
-loc: primarily renal blood vessels
-response: vasocilation

Note: Dopamine wks CNS stimulation ot increase BP if low 90/60 causing diuresing
SNS Examples
Interacts w/many areas to maintain normal BP
Ex: Exercise: increase CO & BP to accommodate the increase O2 demand of exercising muscles
-Postural change (lying to stading): transient decrease in BP
Kidneys
Decrease in renal blood flow/pressure decreasees
-kidneys hold Na&H2O
Rise in BP occurse because of:
-fluid retention
-activation of RAAS
RAAS
-vasoc. & Na retention & thus fluid retention
*******RENAL (Kidneys and RAAS)
1. Kidneys: help maintain BP by controlling Na & ECF volume. Na retention = H2O retention = increase in ECF volume

2. RAAS: Plays important role in BP REG.
Renin: enzyme released by the kidneys that converts angiotensinogen to angiotensin I in the liver
*******Renal (ACE, PGE)
3. ACE: COVERS AI to AII; AII: potent vasoconstrictor

4. Prostaglandins (PGE2 & PG12 renal medulla): Vasod. wks on systemic to decrease SVR & BP
****** Renal (Natriuretic peptides)
5. Natriuretic pepties (atrial natriuretic peptide ANP) & bytype natriuretic peptide (BNP) -secreted by cardiac cells antagonize effect of ADH and aldosterone (natriuresis) and diuresis = reduced blood volume and a decreaes in BP.

Note: BNP >500 is indicative of full blown HF.
antagonize effect: block ADH & AL promote Na excreted out of the body.
Mechanism of Action of "Big AL"
↟ AL
↟ Na reabsorption
↟ H2O reabsorption
↟ Blood volume
↟ CO
Endocrine system (3)
1. Epinephrine (adrenal gland) ↟CO by ↟HR & myocardial contractility.
2. AL (adrenal cortex) -stimulates kidneys to retain Na & H2O = ↟ blood volume and CO
3. ADN (posterior pituitary)- released in response to increase blood Na and osmolarity level - ↟ ECF fluid
***** Classification of HTN *******
1. Primary (Essential/idiopathic) HTN: Elevated BP w/o identified cause; Accts for 90-95% of all cases: most prevailent in clinical practice.

2. Secondary...''' with a specific cause that can be identified and corrected. (5-10% in adults: 80% in children)
Secondary HTN (6)
-specific disease & drugs
- renal parenchymal diseaes: most cause SHTN (RENAL ARTERY STENOSIS)
1. Primary aldosteronism
2. Pheochromocytoma - resistant to treatment run 24 hr. urine BP meds that dont wk mean tumor in kidneys
3. Cushings
4. Coarctation of the aorta
5. Brain tumors, emcephalitis, psych disturbances, pregnancy (PIH), sleep apena
****6. Drugs: oral contraceptives: most common cause of secondary HTN in women (e.g. advil, aleve)
Etiology of Hypertension (foods)
Secondary HTN (foods that contain tyramine (e.g. hot dogs, pickels, cold cuts, sour crout fancy cheeses, red wine can cause hyptertensive crisis)
Etiology of Hypertension
-contributing factors
Coarctation of aorta
renal diseaes
endocrine disorders
neurologic disorders
cirrhosis
spleep apnea
Pathophysiology of Primary HTN
-for arterial pressure to rise: increase in either CO/SVR

- Hemodynamic hallmark of HTN: persistently increased SVR
Primary Hypertension
-contributing factors
↥ SNS activity
↥ Na-retaining hormones and vasoc.
DM
>ideal body weight
↥ Na intake
Excessive alcohol intake
Pathophysiology of Primary HTN
hereditary
H2O and Na retention
alterned Renin-Angiotensin Mechanism
Stress & increased SNS activity
Insulin resistance & hyperinsulinemia
Endothelial cell dysfunction
Physical assessment/clinical manifestations
Silent killer
often asymptomatic
visual changes - retinal changes- cotton-wool spots (small infarctions), severe: papilledema: swelling of optic nerve
Note: system it most effects is the heart
Physical assessment/clinical manifestations
- cardiac
sufffers most
arteriolar narrowing
cardiomegaly
LVH increased workload placed on ventricle as it contracts against higher systemic pressure
HF, ACS, atherosclerosis
Abdominal bruit: renal vascular disease
tachycardia , sweating, pallor: phenochromocytoma
COA
Femoral pulses: delayed/absent
Physical assessment/clinical manifestations
-symptoms
dizziness, fainting
nosebleeds (most commonly misconcepted)
headaches
facial flushing
postural (orthostatic changes): orthostatic hypotention - BP (20 mm Hg systolic &/ 10 mm Hg Diastolic when changing position fromlying to standing
Clinical manifestations
Pathologic changes to kidneys: increased BUN/Creat, nocturia, low U.O

Cerebrovascular involvment: stroke/TIA (mini before big stroke) manifested by: Alterations to vision/speech, dizziness, weakness, falls or hemiplegia
Dx Assessment
1. through H&P
2. Eye exam (retinal)
3. Routine labs: U/A: proteiniuria, urine for microalbuminuria; blood chem, lipid profile, BUN/Creat, blood glucose (fasting, CBC, BMP, LFTs (liver function), tsh (thyroid)
4. 12 lead EKG: assess LVH (normal EF 50-70%)
Homocysteine levels 5-15 micromoles
Dx Assessment
Creatine clearance: assess glomerular filtration ability of kidney. Normal: 107-139 mL/min (men), women: 87-107 mL/min. GFR 125 mL/min
Renine level 24 hr urine protein
routine CXR: chow cardiomegaly
risk factor assessment
Complications
target organ diseases
heart hypertensive heart
brain cerebrovascular disease
peripheral vasculature (PVD)
Kidney (ESRD/nephrosclerosis
Eyes (hypertensive retinopathy): retinal damage closed curtains on the eyes)
Hypertensive Heart Disease
CAD, angina, MI
LVH - due to the increased workload placed on ventricles, progressive LVH=HF
HF- pump failure due to the hearts faily compensatory adaptations
Complications
cardio...
peripheral...
Cerebrovascular disease: atherosclerosis: most common cause - stroke

Peripheral vascular disease (PVD): atherosclerosis in peripheral blood vessels, renal failure, blindness, aortic aneurysm and aortic dissection, intermittent claudication
complications
nephro...
Nephrosclerosis (e.g. drunk holiday) ESRD: due to HTN
-gradual narrowing of arteries, arterioles= atrphy of tubules, destruction of glomeruli & death of nephrons
renal dysfuction= direct r esult of schemia intraarenal blood vessels caused by ischemia.
**** Earliest manifestation of renal dysfunction ****
nocturia
Complication
-eyes
-Retinal damage
damage to vessels of the retina

-s/s: blurring of vision, retinal hemorrhage, loss of vision
BP measurement
-Use properly calibrated ad validated instrument
- Pt should be seated quietly for 5 min in a chair (not on an exam table) feet on the floor and arm supported at heart level
Things not to do during a BP measurement
NO SMOKING
EXERCISE
INGESTING CAFFEINE 30 MIN BEFORE
USE APPROP. SIZED CUFF
RECORD FROM BOTH ARMS INITIALLY, then record from arm with highter measurement. Should not vary by more than 5 mm Hg
BP..
Orthostateic hypotenstion
decrease of 20/more in SBP & 10/more in DBP and an increase in HR of >beats/min from supine to standing
common causes: intravascular volume loss, inadequate vasoc. mechanism related to disease or meds
Medical Mgt
To prevent complications and death by achieving and maintaining arterial blood pressure at 140/90 or lower

JNC 7 specifies lower goal of <128/80; Diabetics/Chronomic renal disease <130/80
***What is important in medical mgt?
Lifestyle modification
Collaborative Care: Lifestyle Modifications
Dash diet (besides the obvious)
Drug therapy
2 main actions:
Goal: BP <140/90... DM <130/80

1. decrease the volume of circulating blood
2. decrease SVR.
HTN collaborative care
Drugs used to treat HTN
Diuretics
adrenergic inhibitors
direct vasodilators
Angiotensive-converting enzyme inhibitors (ACE, ARB, sarotene sisters#%$)
AII receptor blockers
Calcium channel blockers
Nursing Hx of Assessment
Hx of risk factos
Assess potential symptoms of target organ damage
-Angina, shortness of breath, altered speech
-cardivascular assessment: apical & peripheal pulses
Interventions
-Patient teaching Life style modification:foundation of HTN control
-support adherence to the drug therapy regimen
-consultation/collaboration
-emphasize f/u care
-emphasize control rather than cure
-a lifelong process
*** Hypertensive Crisis ***
-A hypertensive emergency develops over hours to days. It is a situation in which a patient's BP is severely elevated (often >220/140 mm Hg) with evidence of acute target organ damage
- determined by degress of target organ damage and how quickly BP must be lowered
Hypertensive Crisis
Clinical manifestations
Hypertensive emergency= evidence of acute targe organ damage
-hypertensive encephalopathy, cerebral hemorrhage
-acute renal failure
-myocardial infarction
-HF w/PE
Hypertensive urgency
Pt. BP is severely elevated but there is no clinical evidenceo f targe organ damage
Causes of HTN Crisis
Exacerbation of chronic HTN
renovascular HTN
Preclampsia, eclampsia
Pheochromocytoma
Drugs: Cocaine, amphetamines
MAO: Tyramine containing foods
Rebound HTN: abrupt withdrawl/some hypertensive drugs such as clonidine (catapres) or Beta-adrenergic blockers
necrotizing vasculitis
head injury, acute aortic dissection
Collaborative mgt.
hypertensive...
Hypertensive emergergencies
hospitalization
IV antihypertensive durgs
ICU monitoring
when treating HTN ermgencies
MAP: mean arterial pressure is used instead of systolic and diastolic BP to guide drug therapy
calculated as MAP=(SBP + DPB)/3
UNDER 60 = CHEST PAIN
IV DRUGS
HTN emergencies
Vasodilator: Na nitropruside (Nitropress)
NTG IV (Tridil)
Fenoldopam (Corlopam)
Hydralazine (Apresoline)
Nicardipine (Cardene)
Adrenergic inhibitors : phentolamine (Regitine)
Labetalol (Normodyne)
Esmolol (Breviibloc)
Ace innhibitor enalapril IV (Vasotec IV)
Drugs....
sodium nitropruside (Nitropress) is the most effective IV drug to treat HTN emergencies.

fenoldopam selectively activates dopamine receptors resulting in renal and systemic vasod.

Oral agents may be given w/IV drugs to help make earlier transition to longer term therapy
Labetalol (Normodyne)
-instruct pt. not to discontinue drug abruptly as this may precipitate angina and/or HF.
Managment
IV drugs....
Rapid (within seconds) onset of action
Assess pt closely
use a intraarterial line or an automakted BP noninvasive BP machine to monitor BP as ordered
Titrate drug according to level of MAP/BP
Important to prevent hypotension and its effects
Monitor EKG for dysrhythmias and signs of ischemia
Management
Measure U.O hrly to assess renal perfusion

On IV hypertensive may be restricted to bed
Frequent neuro checks: LOC, pupillary size and reaction, movement of extremities and reaction to stimuli
Detect any lung/renal system changes for decompensation: angina, PE and RF
Management
Hypertensive urgency...
Dont require IV meds but can be managed w/oral agents
May not need hospitalization but requires f/u
oral drugs used
-captopril (capoten)
-Labetalol(Normodyne)
-Clonidine (catapres)
change position slowly to limit orthostatic hypotension
avoid hazardous activities
do not discontinue meds abruptly