Meds for HTN

• 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

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

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-

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)

Heart rate- BPM

Force of the contraction

Blood volume, venous return to the heart

****increase any of these factors- increase CO--- increase BP

• ANS
• - vasomotor center in brain
• - baroreceptor- SNS

Renin Angiostensin Aldosterone system

• Endocrine
• - catecholamines- NE, epinepherine, stimulate beta
• - ADH
• - Aldosterone

p. 331 +332

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

• 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

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

Normal- < 119/79

preHTN- 120-139, 80-89

Stage 1- 140-159mmHG, 90-99

Stage 2- 160/100

HTN crisis- 210/120mmHg

if the systolic and diastolic BP readings are in different categories take the higher value

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)

lifestyle changes- reducing weight, dietary changes, limiting alcohol, smoking cessation, regular excerise, reduce stress

medication therapy if risk factor is present

lifestyle changes

drug therapy-

• usually a single drug therapy
• - thiazide diuretic
• - combinaion therapy maybe needed ie beta blocker

lifestyle changes

• usually combination therapy
• drug of choice will depend on pt's PHM, risk factors

drugs from other catergories

• 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

• reduce morbidity and mortality assoc with chronic HTN
• reduce risk of CV disease

beta blocker olol at the end...good to know

different MOA

administered in lower doses- lowers SE

one agent may offset the s/e of the second agent

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

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)

• Thiazide diuretic
• beta blockers
• calcium channel blockers- vasodilates
• ACE inhibitors- angiotensin blockers/renin blockers
• angiotensin II blockers

• Centrally acting Alpha 2 stimulants 
• combination alpha 1/beta 1 blockers (olol)
• direct acting vasodilators- work right on the vessels

often administered with anti lipid agents

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

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

• 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

• 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

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

• 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

• 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)

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)

• 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

• 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)

• 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