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Organs/others that regulate ur blood pressure
- Baroreceptor
- chemoreceptor
- Kidneys- regulating fluid
- renin- angiostem I II, aldosterone- vasoconstrict
- Endocrine hypothalmus, adrenal glands (salt, sex, sugar)- mineral corsticords, sex hormones, glucocorticords
- Heart- depends on how well the heart is working- perfusion, oxygen
- blood vessels- narrow, wide, dx
- volume of blood
- electrolytes- K, Na
- ANS
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Blood Pressure
force exerted by the blood against the walls of the blood vessels.
- arterial blood pressure- CO x SVR (systemic Vascular Resistance)
- Arterial blood pressure- blood volume, peripheral resistance, cardiac output
measured in mmHg
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Blood pressure S and D
Systolic blood pressure- the highest pressure during contraction of the heart
diastolic blood pressure- the lowest pressure when the heart relaxes and fills with blood, the vessels propel the blood already in the circulation
- S-tells u what is going on with big vessels
- D- tells u what is going on with small vessels
- coronary vessels- supply the heart
- Brain- stroke
- kidney- renal failure
- eye-
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Blood Pressure- CO
Cardiac output- amount of blood ejected from the LV into the aorta/min
CO= Stroke volume (the volume of blood ejected from the LV with each contraction) * HR
- When CO and SV increases- the BP increases
- cardiac workload- how hard is your heart working (meds are suppose to slow down how hard the heart works)
- ejection friction- how effective is your heart.
Preload, afterload, contractility (HR), some drugs effect these (all or one)
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Factors influencing CO
Heart rate- BPM
Force of the contraction
Blood volume, venous return to the heart
****increase any of these factors- increase CO--- increase BP
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Systems to control BP
- ANS
- - vasomotor center in brain
- - baroreceptor- SNS
Renin Angiostensin Aldosterone system
- Endocrine
- - catecholamines- NE, epinepherine, stimulate beta
- - ADH
- - Aldosterone
p. 331 +332
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Hypertension
a chronic disorder
affects over 70 million people (1 in 3 adults)
very asymptomatic- sometimes pt don't know until they have a stroke, faint, headache
review risk factors for developing HTN- lifestyle, age, diet, obesity, stress, FH, smoking, cholesterol, saturated fats, co morbities ie DM
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HTN risk, SE
- Risk Factors
- - modifable (lifestyle change), non modifable (FH)
- S/S
- often asymptomatic
- often detected at an office visit or the results from complication from HTN
- Consequences of HTN, target organ damage TOD
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HTN
persistent elevation BP > 140/90 more than one occasion
- primary HTN (90%)
- - don't know the cause
- secondary HTN
- -know the reason
- -disease
- - renal failure
- - dm
- - cardiac
- - med treatment
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BP and HTN categories
Normal- < 119/79
preHTN- 120-139, 80-89
Stage 1- 140-159mmHG, 90-99
Stage 2- 160/100
HTN crisis- 210/120mmHg
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HTN categories
if the systolic and diastolic BP readings are in different categories take the higher value
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Stepped approach
Pre HTN- modiable lifestyle change
Drug therapy is recommended for stage 1& 2
Also recommened in pre HTN if risk factors are present (DM, age, heart failure)
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Pre HTN recommendation
lifestyle changes- reducing weight, dietary changes, limiting alcohol, smoking cessation, regular excerise, reduce stress
medication therapy if risk factor is present
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Stage 1 guidlines
lifestyle changes
drug therapy-
- usually a single drug therapy
- - thiazide diuretic
- - combinaion therapy maybe needed ie beta blocker
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Stage 2 and above recommendation
lifestyle changes
- usually combination therapy
- drug of choice will depend on pt's PHM, risk factors
drugs from other catergories
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Stepped care approach
- based on pts response
- always include lifestyle changes
- intially involves a single agent to control bp (stage 1)
- multiple drug therapt for severe or resistant HTN
- start slow and tirate up to control BP
- if therapeutic effect does not occur at moderate does, second drug may be added
- many antihypertensive agents are now in combination form ex lopressorHCT, Hyaar
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Goals
- reduce morbidity and mortality assoc with chronic HTN
- reduce risk of CV disease
beta blocker olol at the end...good to know
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Benefits of mulitple drug therapy
different MOA
administered in lower doses- lowers SE
one agent may offset the s/e of the second agent
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Dosing for HTN
slowly tirate up to control s/s
- slowly withdrawl the medicaiton
- if u withdrawl abruptly- quick drop in bp- stimulate the SNS
after bp controlled for 1 year- attempt to reduce the dosage or the number of meds the pt is on- note pt should not do this themselves
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Overview P. 333
Diuretics: reduce volume overload
lipid lowering agents- lower cholesterol
beta blockers- reduces heart rate, contractility (workload), reduce renin (decrease CO)
ACE inhibitors- dilates blood vessels, reduces blood volume (angiotensin)
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First line Choice
- Thiazide diuretic
- beta blockers
- calcium channel blockers- vasodilates
- ACE inhibitors- angiotensin blockers/renin blockers
- angiotensin II blockers
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Second Line Choices
- Centrally acting Alpha 2 stimulants
- combination alpha 1/beta 1 blockers (olol)
- direct acting vasodilators- work right on the vessels
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another stepped approach
often administered with anti lipid agents
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diuretics
most diurectics share the same basic MOA- block Na and water reabsorption
the site of action that is earlier in the Nephron has the opportunity to block the larger amount of water/Na p300
greater the diuresis the larger amount of Na/water that was blocked
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Thiazide Diuretics
PO
ex- hydrochlorothiazide diurectic (HCTZ) (hydrodiuril)
CI- HTN, edema
- MOA- blocks Na and Cl in the early segment in the distal tubules (far away)
- weak diuretic effect
- dependent on adequate kidney function
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Thiazide Diuretics SE
- electrolyte imbalance
- - loss of Na, K, Cl (K loss can cause muscle weakness- heart)
- -hypercalcemia (holds on to Ca
- dehydration
- hyperglycemia
- muscle weakness/cramps- related to K
- orthostatic hypotension- related to reduce bp
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thiazide diurectics NI
- assess bp, electrolytes, renal function
- drug interaction- digoxin this competes with K whatever is higher wins in the blood.
- effects on are seen in 72 hrs, full effects 2-4 weeks
- contraindicated- severe renal impairment, hypersentivity to thiazide or sulfa
- usually administer in the am
- teaching- safety related to orthostatic hypotension
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Loop diuretics
ex- furosemide (lasix)
CI:reducing peripheral edema associated with CHF, pulmonary edema (fluid in the alveoli), HTN
- MOA: inhibits the reabsorption of Na, Cl, and water in the ascending loop of Henle
- - has a small effect of the distal and proximal tuble
- - high ceiling diuretics
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Loop diuretics SE
- fluid loss loss (fluid volume deficit)
- biggest loss is K
- orthostatic hypotension
- electrolytes imbalance
- - na, k, cl, ca loss
- Ototoxity- esp given IV, give it too fast- ringing in the ear.
- hyperglycemia
- hyperuricemia- concerned bc it can cause gout
- increased LDL, total cholesterol
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Loop diuretics NI
- PO/IV
- assess bp
- k supplements
- IV doses work within 5 minutes last for 2 hours
- PO- works in 1 hr and last 8 hours
- IV dose- (20-40 over 2 mins)
- make to have foley cause it will start to work right away
- drug interaction- digoxin, lithium- levels can go sky high that can get u dehydrated)
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Potassium sparing diuretics
ex- spironolactone (aldactone)
- MOA: blocks the action of aldosterone in the distal tubule
- - aldosterone antagonist
- - increases Na and H2O loss
- - also decreases HCO3, Ca, Cl
- - promotes the retention of K and Mg (be careful of hyperkalemia)
- - interferes with testosterone synthesis (sex, salts, sugar)
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K sparing diuretics CI
- adjunct therapy for HTN, edema associated with CHF, cirrhosis (liver disease, cancer, alcohol abuse)
- DOC ascites
- can be used with thiazide and loop diuretics
- primary hyperaldosteronism
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K sparing diuretics SE
- Hyperkalemia
- electrolyte imbalance
- - loss Na, Cl, HCO3, Ca
- - weak diuretics effect
- - promotes the retention of K, Mg
- weakness, nausea, vomiting
- menstual irregularities, impotence, gynecomastia (men boobs)
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K sparing diuretics NI
- assess K, cardiac arrhythmias
- limit foods high K
- avoid K supplements
- patient teaching
- onset of action 24-48 hours
- drug interaction- drugs that will hold on K Ace inhibitors
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