Meds for HTN

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  1. 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
  2. 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
  3. 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-
  4. 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)
  5. 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
  6. 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
  7. 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
  8. 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
  9. 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
  10. 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
  11. HTN categories
    if the systolic and diastolic BP readings are in different categories take the higher value
  12. 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)
  13. Pre HTN recommendation
    lifestyle changes- reducing weight, dietary changes, limiting alcohol, smoking cessation, regular excerise, reduce stress

    medication therapy if risk factor is present
  14. Stage 1 guidlines
    lifestyle changes

    drug therapy-

    • usually a single drug therapy
    • - thiazide diuretic
    • - combinaion therapy maybe needed ie beta blocker
  15. 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
  16. 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
  17. Goals
    • reduce morbidity and mortality assoc with chronic HTN
    • reduce risk of CV disease

    beta blocker olol at the end...good to know
  18. Benefits of mulitple drug therapy
    different MOA

    administered in lower doses- lowers SE

    one agent may offset the s/e of the second agent
  19. 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
  20. 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)
  21. First line Choice
    • Thiazide diuretic
    • beta blockers
    • calcium channel blockers- vasodilates
    • ACE inhibitors- angiotensin blockers/renin blockers
    • angiotensin II blockers
  22. Second Line Choices
    • Centrally acting Alpha 2 stimulants 
    • combination alpha 1/beta 1 blockers (olol)
    • direct acting vasodilators- work right on the vessels
  23. another stepped approach
    often administered with anti lipid agents
  24. 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
  25. Thiazide Diuretics

    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
  26. 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
  27. 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
  28. 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
  29. 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
  30. 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)
  31. 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)
  32. 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
  33. 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)
  34. 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
Card Set:
Meds for HTN
2014-06-20 03:49:22

FUN summer
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