comp 9

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lingcla
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comp 9
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2013-11-06 19:19:30
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cardiac renal
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cardiac/renal
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  1. inotropic
    force or energy of muscular contractions
  2. positive force
    increase
  3. negative force
    decrease
  4. chronotropic
    rate of the heartbeat
  5. dromotropic
    the conduction of electrical impulses
  6. positive inotropic drugs
    • *drugs that INCREASE the force of myocardial contraction
    • *used to treat heart muscle failure
    •  -cardiac glycosides (DIGOXIN)
    •  -phosphodiesterase inhibitors
    • *poor pump cause heart failure
  7. Heart Failure
    *the heart is unable to pump blood in sufficient amounts from the ventricles to meet the body's metabolic needs
  8. Heart failure symptoms depend on cardiac area affected
    • *Left ventricle failure: pulmonary symptoms
    • *Right ventricle failure: systemic symptoms
  9. Causes of HEART FAILURE
    • *cardiac defect: Myocardiac infarction or valve deficiency
    • *defect outside of heart: coronary artery disease, pulmonary hypertension, and diabetes
    • *supraventricular dysrhythmias: atrial fibrillation, atrial flutter
  10. Cardiac glycosides
    • *originally obtained from Digitallis plant, foxglove
    • *digoxin is the prototype
    • *used in HEART FAILURE and to control ventricular response to atrial fibrillation or flutter (to reduce the frequency of ventricles beating when the atria are going too fast)
  11. cardiac glycosides mechanism of action
    • *INCREASE myocardial contractility
    • *change electrical conduction properties of the heart
    • *result: reduced heart rate and improved cardiac efficiency-> SLOWS AND STRENTHENS THE HEART
    • *narrow therapeutic window on levels
  12. 4 stages of heart failure
    1: high risk for HF w/o symptoms or structural heart disease

    2: some level of cardiac changes, e.g. decrease ejection fraction w/o symptoms of HF

    3: Structural heart disease with symptoms of HF i.e. fatigue, SOB, edema, and decrease in physical activity

    4: severe structural heart disease and marked symptoms of HF at rest
  13. cardiac glycosides: drug effects
    • *positive inotropic effect
    •  -increase in force and velocity of myocardial contractions (w/o an increase in oxygen consumption)
    • *negative chronotropic effect effect
    •  -slows the heart rate
    • *negative dromotropic effect
    •  -slows the rate of the SA node
    •  -conduction through the AV node
    • *increased stroke volume
    • *promotion of diuresis due t improved blood circulation
    • *improving blood flow improves pump
  14. Digoxin AE
    • *cardiovascular: CRITICAL assess->Pulse, if <60 hold and call MD
    •  -dysrhythmias, including BRADYCARDIA or tachycardia
    • *Eye: chg in vision
    •  -colored vision (seeing green, yellow, purple), halo vision, flickering light
    • *GI:
    •  -anorexia, NAUSEA, VOMITING, diarrhea
    •  -if throw up pill never repeat dose
    • *CNS:
    •  -headaches, fatigue, malaise, confusion, convulsion
  15. Digoxin Digitalizing dose
    loading dose  (1 mg)
  16. digoxin maintenance dose
    normal dose 0.125mg or 0.25mg
  17. digoxin toxicity
    • *Digoxin has a VERY NARROW THERAPEUTIC window
    • *drug levels must be monitored
    •  -normal dig level - mg/ml
    • *low potassium levels INCREASE its toxicity
    • *predisposing conditions for digoxin toxicity
    •  -HYPOKALEMIA, hypercalcemia, dysrhythmias, advanced age
    • *treatment of life threatening digoxin toxicity
    •  -digoxin immune fab (digbind)therapy (overdose)
    •  -use for life threatening cardiac effects (severe bradycardia, advanced heart block, dysrhythmias)
    • *Potassium determines effectiveness of heart
  18. cardiac glycosides: nursing implications
    • *CRITICAL ASSESSMENTS: count apical pulse for 1 full minute, check digoxin level
    • *for apical pulse less than 60 or greater than 120 beats/min
    •  -hold dose AND notify prescriber
    • *hold dose and notify prescriber if patient experiences s/sx of toxicity
    • *patients should report immediately a weight gain of 2 or more pounds in one day or 5 or more pounds in one week
    • *infants and children will need BID dosinf (q12hrs)
    • *avoid given with high fiber foods
  19. positive inotropic drugs: nrg implications
    • *monitor for therapeutic effects-
    •  are the symptoms of heart failure resolving?
    •  - ^ urine output
    •  -decreased edema, sob, dyspnea, crackles, fatigue
    •  -resolving of paroxysmal nocturnal dyspnea
    •  -improved peripheral pulses, skin color, temperature
    • *Monitor for adverse effects
    • **DIG TOXICITY**
  20. angina pectors (chest pain)
    • *when supply of oxygen and nutrients in the blood is sufficient to meet the demands of the heart muscle "aches"
    • *the heart requires a lrg supply of o2 to meet the demands placed on it
    • *Ischemia-poor blood supply to an organ
    • *ischemic heart disease-
    •  -poor supply to the heart muscle
    •  -atherosclerosis, coronary artery disease
    • *Myocardial infarction (MI)
    •  -necrosis, or death, of cardiac tissue->disabling or fatal
  21. Antianginals: therapeutic objectives
    • *increase blood flow to ischemic heart muscle and/or
    • *decrease myocardial oxygen demand
    • *minimize the frequency of attacks and decrease the duration and intensity of angina pain
    • *improve the patients functional capacity with as few adverse effects as possible
    • *prevent or delay the worst possible outcome->MI
  22. treatment of angina
    • *Non pharmacologic measures:
    •  -rest, avoid heavy meals, stop smoking, inc exercise, dec stress, extremes in weather
    • *antianginals
    •  -nitrates/nitrites
    •  -B (beta) blockers
    •  -calcium channel blockers
  23. Nitrates/Nitrites
    • *cause vasodilation of coronary vessels due to relaxation of smooth muscles- more blood passes through coronary vessels-> inc o2 to ischemic myocardial tissue
    • *also decrease o2 demand by reducing the volume of blood returning to the heart
    • *used for prevention and treatment of agina
    • *nitrates alleviate coronary artery spasms
  24. Nitrate/Nitrite- Avail forms
    • *SL
    • *Buccal
    • *IV
    • *ointments- (chronic prevent)
    • *transdermal patchs
    • *translingual sprays
    • (all bypass the liver and first pas effect

    • *chewable tabs
    • *oral capsule/tabs
  25. Nitrate/nitrites
    • *Nitroglycerin (nitrobid, nitrostat)
    •  -prototypical nitrate
    •  -lrg first pass effect with oral forms
    • *isosorbide dinitrate (isordil, sorbitratem dilatrate sr)
    • *isosobide mononitrate (imdur, monoket, ISMO)
    • *used for
    •  -acute relief of angina
    •  -prophylaxis (prevention) in situations that may povoke angina
    • - long term prophylaxis of angina
  26. Nitrates: AE
    • *Headaches (bad, vasodilation of vessels)
    •  -usually diminish in intensity and frequency with continued use
    • *Reflex tachycardia (maintain cardiac output)
    • *postural hypotension (orthostatic)
    • *tolerance may develop
    •  -occurs in patients taking nitrates around the clock or with long acting forms
    •  -prevented by allowing a regular nitrate free period to allow enzyme pathways to replenish
    •   -transdermal forms: remove patch at bedtime for 8 hrs then apply a new patch in the morning
    • *med-med interactions:
    •  -alcohol, anthypertensives, sildenafil
    • **body needs nitrate free period everyday to prevent tolerance
  27. Nitroglycerin Nrg Implications
    • *CRITICAL ASSESSMENT: BP
    • *instruct pts:
    •  -remove topical forms at bedtime and apply new doses in the morning
    •  -never chew or swallow the SL form
    •  -do not stop taking long acting form abruptly
    •  -preserve potency:
    •    -store in an airtight drk glss bottle w/ metal cap & no cotton filter
    •   -obtain new bottle every 3 months
    • *for CP: take lying down to prevent or decrease dizziness and fainting that may occur due to hypotension
  28. nitroglycerin nrg implications cont
    • if anginal pain occurs:
    • -stop activity & sit or lie down
    • -take prn nitrates at the first hint of anginal pain
    • -take a SL tablet and wait 5 min
    • -if no relief in 5 min call 911
    • -can take up to two more doses at min intervals
    • -do not try to drive to hospital
  29. B Blockers
    • *atenolol(Tenormin)
    • *metoprolol (Lopressor)
    • *propranolol (Inderal) -nonspecific b blocker
    • *indications
    •  -angina
    •  -antihypertensive
    •  -cardiac dysrhythmias
    •  -cardioprotective effects, especially after MI
    •  -some used for migraine HA, essential tremors, and stage fright
    • **standard if heart attack
  30. B Blockers
    • *mechanism of action as antianginal
    •  -B1 receptors on the heart are blocked
    •  -dec in HR, resulting in decreases myocardial o2 demand and increased o2 delivery to the heart
    •  -decrease myocardial contractility helping to conserve energy or decrease demand
  31. B Blocker AE:  body system->AE
    • *cardiovascular->bradycardia, hyptension, secon or third heart block, heart failure
    • *Metabolic-> altered glucodse and lipid metabolism
    • *CNS->dizziness, fatigue, mental depression, lethargy, drowsiness, unusual dreams
    • *other-> impotence, WHEEZING, DYSPNEA
  32. b blocker nrsg implications
    • *CRITICAL ASSESS: BP & Apical Pulse
    • *patients taking bblockers should monitor pulse rate daily, and report any rate lower than 60 beats/min
    • *dizziness or fainting should be reported
    • *constipation is a common problems, instruct patients to take in adequate fluids and eat high fiber foods
    • *these medications should never be abruptly discontinued due to risk of rebound hypertensive crisis
    • *inform patients that these medications are for long term prevention of angina, not for immediate relief
  33. calcium channel blockers
    • *Drugs:
    •  -nifedipine (Procardia)
    •  -diltiazem (Cardizem)
    •  -amlodipine (Norvasc)
    •  -verapamil (calan, isoptin)
    • *mechanism of action
    •  -cause smooth muscle relaxation by blocking the binding of calcium to its receptors preventing muscle contraction
    •  -this leads to coronary artery & peripheral arterial vasodilation-> decreasing systemic vascular resistance
    •  -reduce the workload of the heart->decreased myocardial o2 demand
    • **vasodilating means workload decreased
  34. calcium channel blockers INDICATIONS
    *first line drugs for treatment of ANGINA, hypertension, and some dysrhythmias, migraines and Raynaud's disease
  35. Calcium channel blockers AE
    *may cause hypotension, HA, palpitations, reflex tachycardia (due to hypotension) or bradycardia, constipation, change in liver and kidney function
  36. Nrg Implications antianginals
    • *CRITICAL ASSESS BEFORE ADMINISTERING: BP & P
    • *obtain baseline VS, including respiratory patterns and rate
  37. NRG implications antianginals pt instruction
    • *instruct patient in the following: -constipation is a common problem, to prevent drink adequate fluids, and eat high fiber foods -do not take any medications including OTC medications, without checking with the physician -limit caffeine intake
    •  -alcohol consumption and hot baths or spending time in whirlpools, hot tubs, saunas, will result in vasodilation, hypotension, leading to fainting and injury. sit or lie down until symptoms subside
    •  -change positions slowly to avoid postural BP changes
    •  -keep a record of their anginal attacks including precipitating factors, number of pills taken, and therapeutic effects
  38. Antidysrhythmics
    • *Dysrhythmia vs. arrhythmia
    •  -any deviation from the normal rhythm of he heart
    • *antidysrhythmics;
    •  -the desired action of antidysrhythmic drugs to restore the cardiac rhythm to normal
    •  -mechanism of action:
    •   - block adrenergic stimulation of the heart
    •   -depress myocardial excitability and contractility
    •   -decrease conduction velocity in cardiac tissue (slow conduction down)
    •   -increase recovery time (repolarization) of the myocardium
    •   -suppress automatically (spontaneous depolarization to initiate beats)
  39. cardiac cell
    • *inside the resting cardiac cell there exists a net negative charge relative to the outside of the cell.
    • *this difference in the electronegative charge results from an uneven distribution of ions (sodium, potassium, calcium) across the cell membrane
    •  -resting membrane potential (RMP)
    • *sodium potassium pump maintains the uneven distribution of ions
  40. action potential- cardiac cell
    • *a change in the distribution of ions causes cardiac cells to become excited
    • *the movement of ions across the cardiac cell's membrane results in an electrical impulse spreading across the cardiac cells
    • *this electrical impulse leads to contraction of the myocardial muscle
  41. common dysrhythmias
    • *supraventricular dysrhythmia
    •  -atrial fibrillation, atrial flutter
    • *ventricular dysrhythmia
    •  -ventricular tachycardia (Vtach), ventricular fibrillation (Vfib)
    • *Ectropic foci
    •  -premature ventricular contractions (PVC), premature atrial contractions (PAC)
    • *conduction blocks
    •  -first, second or third degree heart blocks
  42. Vaughan Williams Classification
    • *system commonly used to classify antidysrhythmic drugs
    • *based on the electrophysiologic effect of particular drugs on the action potential
    • *class I: sodium channel blockers
    •    class 1a:procainamide (pronestyl, quinidine)
    •    class 1b: lidocaine
    •    class 1c: flecainide
    • *class II: B blockers: atenolol, esmolol, metaprolol,propanolol
    • *class III: prolong repolarization: amiodarone
    • *class IV: calcium channel blockers
    • *other: digoxin, adenosine 
  43. Vaughan Williams class I drugs
    • Class I: procainamide, quinidine, lidocaine
    • *membrane-stabilizing medications- act on the sodium (fast) channel
    • *quinidine: SE: N&V, diarrhea, confusion, low bp
    • *Procainamide: SE: can cause lupus-like syndrome
    • *Lidocaine: SE: bradycardia, Dec BP, CNS symptoms (seizures, confusion), resp depression, blurred or double vision
    •  -given IV, also used as a local anesthetic
    •  -must be careful NOT TO USE LIDOCAINE W/ EPINEPHRINE IV
  44. Vaughan Williams class II drugs
    • Class II: B blockers: atenolol, esmolol, metaprolol, propanolol
    • *reduce or block sympathetic nervous system stimulation, thus reducing transmission of impulses in the hearts conduction system
    • *also used as antianginal & antihypertensive drugs
    • *Cardioselective beta blockers (blocks beta 1)- atenolol, metaprolol, esmolol
    • *nonspecific beta blocker (blocks both beta 1 & beta 2)- propanolol 
  45. Vaughan Williams Class III & IV drugs
    • Class III: adenosine, amiodarone, sotalol
    • *amiodaron:
    •  -SE: hyper or hypothyroidism, visual halos, photophobis, most serious ->pulmonary toxicity
    •  -used for dysrhythmias that difficult to treat

    • Class IV: verapamil, dilitiazem
    •  -calcium channel blockers
    •   -inhibit slow channel (calcium dependent) pathways
    •  -reduce AV node conduction
    •  - also used as antianginal & antihypertensive drugs
  46. CLASS III drug: ADENOSINE
    • Adenosine (adenocard)
    • *slows conduction through the AV node
    • *used to convert paroxysmal supraventricular tachycardia to sinus rhythm
    • *very short half life- less than 10 seconds
    • *only administered as fast IV push
    • *may cause ASYSTOLE for a few seconds
    •  *other adverse effects minimal
  47. antidysrhythmics: adverse effects
    • ALL antidysrhythmics can cause dysrhythmias!!
    • *hypersensitivity reactions
    • *N&V
    • *diarrhea
    • *dizziness
    • *blurred vision
    • *HA
  48. Nrsg implications Antidysrhythmics
    • *CRITICAL ASSESS for ADMINISTRATION: heart rate & rhythm, BP
    • *during therapy: monitor cardiac rhythm, general well being, skin color, temperature, heart and lung sounds, serum potassium, and plasma drug levels
    • *instruct patients to take medications as scheduled and NOT TO SKIP DOSES OR DOUBLE UP FOR MISSED DOSES
    • *patients who miss a dose should contact their physician for instructions
    • instruct patients not to crush or chew any oral sustained release preparations 
  49. Ensure that the patient knows to notify health care provider of any worsening of dysrhythmia or toxic effects
    • *SOB
    • *edema
    • *dizziness
    • *syncope
    • *chest pain
    • *GI distress
    • *blurred vision
  50. antidysrhythmic teaching
    patients taking B Blockers, digoxin, and other drugs should be taught how to take their own radial pulse for 1 minute, and to notify MD if pulse is <60 beats /min before taking the next dose of medication
  51. antidysrhythmic monitoring of therapeutic response
    • *decreased BP in hypertensive pts
    • *decrease edema
    • *decrease fatigue
    • *regular pulse rate
    • *pulse rate w/out major irregularities
    • *improved regularity of rhythm
    • *improved cardiac output
  52. Diuretic Drugs
    • *drugs that accelerate the rate of urine formation
    • *result: removal of sodium and water
    • *in the nephron, where sodium goes, water follows
    •  -50-55% of all sodium is reabsorbed into the bloodstream in the proximal tubules
    •  -35-40% in the loop of henle
    •  -5-10% in the distal convoluted tubules 
    •  -3% in collecting ducts
    • *if water is not absorbed it is secreted as urine
  53. Diuretic Drug Classification
    • *potassium- losing diuretics
    •  -thiazide and thiazide like diuretics
    •  -loop diuretics
    •  -carbonic anhydrase inhibitors
    •  -osmotic diuretics
    • *Potassium-sparing diuretics
  54. thiazide & thiazide like diuretics (potassium sparing)
    • *thiazide diuretics
    •  -hydrochlorothiazide (esidrix, hydroDIURIL)
    •  -chlorothiazide (Diuril)
    •  -trichlormethiazide (metahydrin)
    • *thiazide like diuretics
    •  -chlorthalidone (hygroton)
    •  -metolazone (mykrox, zaroxolyn)
    • *mechanism of action:
    •  -inhibit tubular reabsorption of sodium, chloride & potassium ions-> water, sodium, and chloride are excreted, some potassium is also excreted
    •  -dilate the arterioles by direct relaxation
  55. thiazide and thiazide like diuretics AE
    (body system->AE)
    CNS-> dizziness, HA, blurred vision, paresthesia, decrease libido

    • CV-> hypotension
    •  
    • GI -> anorexia, N&V, diarrhea, constipation

    Integumentary -> uticaria, photosensitivity

    Metabolic-> HYPOKALEMIA, hypomagnesiumia, hypecalciumia, HYPERGLYCEMIA, hypochloremia, HYPEURICEMIA
  56. LOOP DIURETICS
    • *furosemide (Lasix)
    • *bumetanide (bumex)
    • *ethacrynic acid (edecrin)
    • *mechanism of action:
    •  -act directly on the ascending limb of the loop of henle to inhibit chloride and sodium absorption
    • *potent diuresis and subsequent loss of fluid
    • *decreased fluid volume causes reduced BP
    • *increased loss of potassium and sodium
  57. LOOP diuretics: AE
    (body system->AE)
    CNS->dizziness, HA, tinnitus, blurred vision

    CV-> hypotension

    GI->N&V, diarrhea

    Hematologic-> agranulocytosis, neutropenia, decease platelets

    Metobolic-> HYPOKALEMIA, hyponatremia, dec calcium, magnesium, hyperglycemia, hyperuricemia, inc BUN & CREAT
  58. Carbonic anhydrase inhibitors (CAIs)
    potassium losing diuretic
    • *acetazolamide (Diamox)
    • *methazolamide
    • *dichlorphenamide
    • *mechanismof action
    •  -the enzyme catrbonic anhydrase helps to make H+ ions available for exchange with sodium and water in the proximal tubules
    •  -CAIs blocks the action of carbonic anhydrase prevents the exchange of H+ ions w/ sodium and water -> decreased resorption of water
    • -RESULT -> THERE IS INCREASED EXCRETION OF BIOCARBONATE, SODIUM, WATER, AND POASSIUM, URINE VOLUME IN INCREASED
  59. carbonic anhydrase inhibitors:AE
    • *metabolic acidosis
    • *anorexia
    • *hematuria
    • *photosensitivity
    • *melena
    • *hypokalemia
    • *drowsiness
    • *paresthesias
    • *urtucaria
  60. osmotic diuretics (potassium losing diuretic)
    • *mannitol (osmitrol)
    • *mechanism of action
    •  -pulls water into the renal tubules from the surrounding tissues
    •  -inhibits tubular resorption of water and solutes, producing a rapid diuresis
    • *drug effects
    •  -increase glomerular filtration and renal plasma flow-helps to prevent kidney damage, during acute renal failure
    •  -reduces excessive intraocular pressure
  61. osmotic diuretics
    • *used in the treatment of patients, with acute renal failure, TO REDUCE INTRACRANIAL PRESSURE, and treat cerebral edema
    • *NOT used for peripheral edema
    • *AE: convulsions, thrombophlebitis, pulmonary congestion
    • * given by IV infusion only
  62. potassium sparing diuretics
    • *amiloride (midamor)
    • *spironolactone (aldactone)
    • *triamterene (dyrenium)

    • *mechanism of action:
    •  -interfers with the sodium-potassium exchange-> blocks the absorption of sodium and water

    • *indications: 
    •  -hypertension, hyperaldosteronism, heart failure
    • -reversing the potassium loss caused by potassium losing drugs
  63. potassium sparing diuretics AE
    CNS->dizziness, HA

    GI-> cramps, N&V, diarrhea

    other-> urinary frequency, weakness

    **HYPERKALEMIA**
  64. nrsg implications diuretics
    • *CRITICAL ASSESSMENT BEFORE ADMINSTERING: BP & POTSSIUM LEVELS'
    • *assess baseline fluid volume status, I&O, serum electrolyte values, wt, and VS especially postural BP
    • *Foods high in potassium include bananas, oranges, dates, raisins, plums, fresh veg, potatoes, meat, and fish, apricots, whole grain cereals, legumes
    • *s/sx of hypokalemia include muscle weakness, constipation, irregular pulse rate, and over all feeling of lethargy
  65. diuretics- INSTRUCT PATIENTS
    • *take in the morning as much as possible tgo avoid interference with sleep patterns
    • *change position slowly, and rise slowly after sitting or lying to prevent dizziness & fainting
    • *keep log of their daily wt and return for f/u visits and lab work
    • *eat more potassium rich foods when taking any but potassium sparing drugs
    • *notify the md immediately if they experience rapid heart rates or syncope (reflects hypotension or fluid loss) or a wt gain of 2 or more lb/day or 5 or more pounds a week
  66. Hypertension=High blood pressure
    *blood pressure=CO x SVR

    • CO=cardiac output
    • SVR=systemic vascular resistance

    *antihypertensives = medications used to treat hypertension
  67. Hypertension
    • Selected regulators of blood pressure
    •  -kidneys via reninangiotension system
    •  -autonomic nervous system
    •  -hormones such as antidiuretic hormone (ADH)
  68. JNC-7
    four stages, based on BP measurements
    • *normal <120/80
    • *prehypertension 120-138/80-89
    • *stage 1 hypertension 140-159/90-99
    • *stage 2 hypertension 160 or higher/100 or higher
  69. JNC-7: significant changes
    • *studies have shown that elevated BP is strongly associated with heart failure, stroke, and renal failure
    • *risk factors for hypertension:
    •  -excess fat and carbohydrate intake
    •  -alcohol
    •  -obesity
    • *nonpharmacologic control of hypertension
    • *prehypertensive BP are no longer considered high normal and require lifestyle modifications to prevent CVD
  70. Classification of BP
    • *hypertension can be defined by its cause
    •  -unknown cause:
    •   *known as essential, idiopathic or primary hypertension
    •   *90% of the cases
  71. HTN cultural considerations
    • *African americans higher risk of HTN
    •  -meds less effective: beta blockers, ACE inibitors
    •  -effective anti HTN: alpha, blockers, and calcium channel blockers
    • *Asian americans are 2x as sensitive to beta blockers
  72. Antihypertensive Drugs: categories
    • *Diuretics
    • *Sympathoulytics
    •  -beta adrenergic blockers
    •  -centrally acting alpha 2 agonists
    •  -alpha adrenergic blockers
    •  -adrenergic neuron blockers (peripherally acting sympatholytics)
    • *direct acting arteriolar vasodilation
    • *angiotensin converting enzyme (ace) inhibitors
    • *angiotensin II receptor blocker (ARBs)
    • *calcium channel blockers (CCBs)
  73. Diuretics
    • *decrease the plasma and extracellular fluid volumes
    • *results: decreased preload, cardiac output and total peripheral resistance
    • *overall effect: decreased workload of the heart and decrease bp
    • *thiazide diuretics are the most commonly used diuretics for hypertension
  74. Sympathetics (sympathetic depressants)
    • *beta adrenergic blockers
    • *centrally acting alpha 2 agonists
    • *alpha adrenergic blockers
    • *adrenergic neuron blockers (peripherally acting sympatholytics)
    • *alpha1 & beta1 agrenergic blockers
    • *ALL CAN CAUSE 1ST DOSE SYNCOPE
  75. Sympathetics beta adrenergic blockers (beta blockers)
    • *reduce cardiac output by reducing heart rate, contractablity and renin release -> thus Low bp
    •  -nonspecific beta blocker (block both beta1 & beta2)
    •    *propanolol (Inderal)
    •    *can cause bronchoconstriction
    •  -selective beta1 blockers are preferred
    •    *atenolol (Tenormin)
    •    *metoprolol (Lopressor)
    •    *less likely to have bronchoconstriction or hypoglycemia
    • *adverse effects include insomnia, depression and impotence
  76. sympathetic centrally acting alpha2 agonists
    • *stimulate the alpha2 receptors which decreases the sympathetic response from brainstem to the peripheral vessels-> dec peripheral vascular resisitance and inc vasodilation
    •  -clonidine (catapres) - 7 day patch
    •   -useful in the management of withdrawl symptoms in opiod or nicotine dependent persons
    •  -guanfacine (tenex)
    •  -methyldopa (aldomet)
    •   -drug of choice for hypertension in pregnancy
    • *contraindications: impaired liver function
    • *SE: sodium and water retention, dry mouth, bradycardia
    •  -also may be used for treatment of sever dysmenorrhea, menopause flushing, glaucoma
  77. sympathetic alpha adrenergic blockers
    • *blocks the alpha adrenergic receptors-> vasodilation and decrease BP
    •  -selective alpha 1- treat HTN and BPH
    •   -doxazosin (Cardura)
    •   -terazosin (hytrin)
    •   -prazosin (minipress)
    •  - Non selective alpha blockers- HTN crisis 
    •    -phentolamine (regitine)
    •    -tolazoline HCL (prescoline HCl)
    • *do not affect glucose metabolism
    • *can cause sodium and water retention
  78. sympathetic adrenergic neuron blockers -peripherally acting sympathetics
    • *block norepinephrine release that results in lowering of Bp
    • *dec in cardiac output and peripheral vascular resistance
    •  -reserpine
    •    -seldom used because of frequent AE
    • *last choice for treating hypertension due to orthostatic hypotension
  79. sympatholytic alpha1 and beta1 receptor blockers
    • *dual action: alpha1 & beta1 receptor blockers
    • *labetalol (normodyne)
    • *carteolol (catrol)
    • *carvedilol (coreg)
    •  -block the a1 adrenergic receptors
    •  -reduction of the heart rate (b1 receptor blockade)
    •  -vasodilation (a1 receptor blockade)
    • *large doses can cause AV heart block
  80. Sympatholytics AE
    *most common: dry mouth, sedation, drowsiness, constipation

    *other: HA, sleep disturbances, nausea, rash, cardiac disturances (palpitations), others

    **HIGH INCIDENCES OF ORTHOSTATIC HYPOTENSION**
  81. Direct acting arteriloar vasodilators
    • *diazoxide (hyperstat)
    • *hydralazine HCl (apresoline)
    • *minoxidil (loniten)
    • *sodium nitropusside (nipride, nitropress)
    • *mechanism of action
    •  -directly relax arterior and/or venous smooth muscle
    • *result: decreased systemic vascular response, decrease afterload and peripheral vasodilation
  82. Vasodilators: AE
    • *hydralazine
    •  -dizziness, HA, anxiety, tachycardia, N&V, diarrhea, anemia, dypsnea, edema, nasal congestion, others
    • *sodium nitroprusside
    •  -bradycardia, hypotension, possible cyanide toxicity (rare)
    • * Diazide
    •  -dizziness, HA, anxiety, orthostatic hypotension, dysrhythmias, sodium and water retention, N&V, hyperglycemia in diabetic patients, others
  83. Angiotension converting enzyme inhibitors (ACE inhibitors)
    • *captopril (capoten)
    •  -very short half life
    • *enapril (vasotec)
    •  -avail in oral and parenteral forms
    • *lisinopril (prinivil & zestril) and quinapril (accupril), others
    •  -newer drugs long half lifes, once a day dosing.
    • *indications: HTN and types of heart failure
  84. ACE inhibitors Mechanism of action
    • renin angiotensin-aldosterone system
    • *ace inhibitors block the angiotensin converting enzyme (ACE) thus preventing the conversion of angiotensin II from angiotensin I
    • *blocks release of aldosterone
    • *result: decrease systemic vascular resistance (afterload), vasodilation-> decrease blood pressure
  85. ACE inhibitors AE
    • fatigue, HA, inpaired taste, dizziness, mood changes, possible hyperkalema, DRY NONPRODUCTIVE COUGH, which reverses when therapy is stopped,
    • angioedema: rare but potentioally fatal
    • NOTE: first dose hypotension effect may occur!!!!
  86. angiotensin II receptor blockers (A II blockers, or ARBs)
    • *losartan (cozaar, Hyzaar)
    • *valsartan (diovan)
    • *eprosartan
    • *irbesartan
    • *newer class, well tolerated
    • *do not cause a dry cough
    • *allow angiotensin I to be converted to angiotensin II, but block receptors that recieve angiotensinII
  87. angiotensin II receptor blockers: AE
    • *URI
    • *HA
    • *may cause occasional dizziness inability to sleepm diarrhea, dypsnea, heart burn, nasal congestion, back pain fatigue
    • *hyperkalemia much less likely to occur
  88. calcium channel blockers
    • *bezothiazepines
    •  -diltiazem (cardizem, dilacor)
    • *phenylalkamins
    •  -verapamil (calan, isoptin)
    • *dihydropyridines
    •  -amlodipine (norvasc), bepridil (vascor), nicardipine (cardene)
    •  -nifedipine (procardia), nimodipine (nimotop)
    • *decreased pripheral smooth muscle tone and decreases systemic vascular resistance-> lowers BP
  89. NRSG Implications ANTI HYPERTENSIVES
    • *critical assessment before administering: BP & P
    • *instruct clietns in the following:
    •  -do not miss a dose, take meds exactly as prescribed and NEVER DOUBLE UP ON DOSES
    •  -if a dose is missed check w/ physician for instruction on what to do
    •  -DO NOT STOP THESE MEDS ABRUPTLY-> may caus a rebound hypertensive crisis, and perhaps lead to stroke
    •  -CHANGE POSITION SLOWLY to avoid syncope from postural hypotension
  90. NRSG implications antihypertensives
    • *Impotence is an expected effect- counsel male clietns to talk to their md
    • *if they are experiencing serious AE or believe that the dose or medication needs to be changes, they should contact their physician immediately
    • * use sugar free hard candy or frequent fluidsto manage AE of dry mouth
    • *consider lifestyle changes; low sodium, low fat diet, manage stress level weight and alcohol intake
    • *avoid smoking and eating high sodium
    • *excercise w/ supervision
    • *hot tubs, showers, baths hot weather, prolonged sitting or standing ophysical excercise and alcohol igestiong may aggravate low bp leading to fainting and injury sit or lie down until symptoms subside
    • *don take any other medications including OTC drugs w./out first gettting the approval of the md
    • *keep journal of regula BP
  91. Antihypertensives AE
    dizziness, orthostatic hypotension, fatigue and toxic effects
  92. antihypertensives Therapeutic effects
    • *blood pressure should be maintaiined at less than 130/90
    • *if a pt with htn also has diabetes or renal disease the bp goal is less than 130/90
  93. coagulation modifier drugs
    • *anticoagulants
    •  -inhibit the action or formation of clotting factors
    •  -prevent clot formation
    • *antiplatelet
    •  -inhibit platelet aggregation
    •  -prevetn platelet plugs
    • *thrombolytic drugs
    •  -lyse (break down) existing clots
  94. hemostasis system
    • *the process that halts bleeding after injury to a blood vessel
    • *complex relationship between subsances that promote clot formatin and either inhibit coagulation or dissolve a formed clot
  95. coagulation system
    • *'cascade'
    • *each activated factor serves as a catalyst that amplifies the next reaction
    • *result is fibrin, a clot forming substance
    • *intrinsic pathway and exrtinsic pathway
  96. anticoagulants
    • * have no direct effect on a blood clot that is already formed- DO NOT LYSE existing clots
    • *used to prophylactically to prevent
    •  -clot formation (thrombus)
    •  -an embolus (dislodged clot)
    • *work on different points of the clottign cascade
    • *all ultimately PREVENT clot formation
    • *heparin and low molecular weight heparing
    •  -turn off coagulation pathway and prevent clot formation
    • *warfarin (coumadin)
    •  -works by inhibiting vit K synthesis by bacteria in intestinal tract-.inhibits clotting factors
    •  
  97. Prevention of clot formation also prevents
    • *stroke
    • *MI
    • *DVT
    • *PE
    • *use to prevent clot formation in certain settings where clot formation is likely:
    •  _MI, unstable angina, afib, indwelling devices, such as heart valves, major orthopedic surgery
    • **AE: BLEEDING 
  98. Heparin
    • *monitored by activated partial thromboplastin times (aPTTs)
    • *toxicity: effects reversed by protamine sulfate
    • *parenteral (IV or SQ)
    • *short half life (1-2 hrs)
  99. low molecular weight heparins
    • *enoxaparin(lovenox) and dalteparin (fragmin)
    • *more predictable anticoagulatant response
    • *do not require frequent laboratory monitoring of aPTT, however MUST MONITOR PLATELET COUNT
    • *give SQ
  100. Heparin nrsg implications
    • *CRITICAL ASSESS FOR ADMIN: aPTT, platelets
    • *IV doses are usually double checked  w/ another nurse
    • *ensure the SC doses are given SC not IM
    • *SC doses should be given in areas of deep SC fat, and sites rotated
    • *LMWH must be given in th eabd SC
    • *do not give SC doses w/in 2 inches of:
    •  -the umbilicusm abd incisions, or open wounds, scars, drainage tubes, stomas
    • *donot aspirate SC injections or massase injection site
    •  -may cause hematoma formation
  101. Warfarin (coumadin)
    • *given orally only
    • *monitored by PT & INR
    • *clients not on warfarin should have INR of 1.0
    • *client on warfarin-therapeutic range of 2-3.5 depending on indication
    • *toxicity: antidote is Vitamin K
    • *long duration of action 2-5 days
    • *long half life of 1/2 -3 days
  102. warfarin nrg implications
    • * may be started while the pt is still on heparin until PTINR levels indicate adequate anticoagulation
    • *full therapeutic effect takes several days
    • *monitor PTINR regularly- keep f/u appts
    • *antidote is Vit K
    • *many herbal products have potential interactions- increas bleeding may occur
    •  -capsicum, garlic, ginger, gingko, ginseng, feverfew
  103. warfarin & ADE
    • *one of the primary causes of admissin for adverse drug reactions
    • *study published in 2011 in NEJM
    • *approx 100,000 emergency hospitalizations for ADEs per year
    • *warfarin was te cause for 33% of emergency adverse drug events hospitalizations
    • *two thirds of all ADE due to 4 drugs/classes; warfarin, oral antiplatelet meds, insulins, and oral hypoglycemic agents
  104. Direct thrombin inhibitors: parental anticoagulantsII
    • *four anticoagulants inhibit thrombin directly, not directly
    • *adminitered IV
    •  -argatroban (acova)
    •  -bivalirubin (angiomax)
    •  -lepirudin (refludan)
    • *administered SC
    •  -desrudin (Ipravask)
  105. anticoagulants PT Education
    • *importance of regular lab testing
    • *signs of abnormal bleeding
    • *measures to prevent bruising, bleeding, or tissue injury
    • * wearing a medical alert bracelet
    • *avoiding foods high in Vit K (tomatoes, drk leafy green vegetables)
    • *consultin md before taking other meds or OTC productsm, including herbals
  106. antiplatelet drugs
    • *prevent platelet adhesion
    •  -aspirin
    •  -dipridamole (persantine)
    •  -clopidogrel (plavix and ticlopidine (Ticlid)
    •    -ADP inhibitors
    •  -tirofiban (aggrastat), eptifibatide (integrilin)
    •   -new class, GP IIb/IIa inhibitors
    • *ised to reduce risk of fatal and nonfatal strokes
    • *AE: bleeding, heartburn, decrease platelets
  107. antiplatelet drugs Nrsg implications
    • *concerns and teaching tips same as for ancoagulants
    •  -dipyridamole should be taken on an empty stomach
    • -drug-drug interactions
    • -adverse reactions to report
    • -monitoring for abnormal bleeding
  108. Thrombolytic drugs
    • *streptokinase (streptase);anistreplase (eminase); alteplase (t-PA, activase); reteplase (retavase); tenecteplase (TNKase); droctrecogin alfa (Xigris)
    • *mechanism of action:
    •  -activate the fibrinolytic system to break down the clot in the blood vessel quickly
    •  activate plasminogen and convert it to plasmin which can digest fibrin
    • *reestablish blood flow to the heart muscle via coronary arteries, preventing tissue destruction
    • *contraindications: stroke, contusion
  109. thrombolytic drugs Indications
    -acute MI, artrial thrombolysis, DVT, occlusion of shunts or catheters, pulmonary embolus, acute ischemic stroke
  110. thrombolytic drug AE
    • -BLEEDING: internal, intracranial, superficial
    • -other effects: N&V, hypotension, anaphylactiod reactions, cardiac dysrhythmias
  111. nrsg implications/pt teaching thrombolytic drugs
    • *follow strict manufactureres guidelines for preparation and administraton
    • *monitor for bleeding from IV sies, gums, mucous membranes, nose, injection sites
    • *observe for signs of internal bleeding (decr BP, restlessness, inc pulse)
  112. coagulation modifier drugs nrsg implications
    • * monitor for therapeutc effects
    • *monitor for signs of excessive bleeding
    •  -bleeding of gums while brushing teeth, unexplained nosebleeds, heavier menstrual bleeding, bloody or tarry stools, bloody urine or sputum, abdominal pain, vomiting blood
    • *monitor for AE
    •  -inc BP, HA, hematoma formation, hemorrhage, SOB, chills, fever
  113. antilipemics
    • *drugs used to lower lipid levels
    • *triglycerides & cholesterol
    •  -two primary forms of lipids in the blood
    •  -water soluble fats that must be bound to apolipoproteins, specialized lipid carrying proteins
    •  -lipoprotein is the combination of triglyceride or cholesterol w/ apoliprotein
    • *the risk of CHD in patients w/ cholesterol levels of 300mg/dl is three to four times greater than that in patients w/ levels less than 200mg/dl
  114. lipoproteins
    • *very low density lipoprotein (VLDL)
    •  -produces by the liver
    •  -transports endogenous lipids to the cells
    • *low density lipoprotein (LDL)
    • *high density lipoprotein (HDL)
    •  -responsible for "recycling" of cholesterol
    •  -also known as "good cholesterol"
  115. antilipemics
    *non pharmacologic methods for cholersterol reduction
  116. types of antilipidemics
    • *resin antilipidemics (bile acid sequestrants)
    • *folic acid derivatives (fibrates)
    • *nicotinic acid
    • *cholesterol absorption inhibitor
    • *statins/vastatins
    • *combination anticholesterol drugs
  117. Bile acid sequestrants
    • *cholestyramine (questran)
    • *colestipol hydrochloride (colestid)
    • *colesevelam (tablet form)
    • *may be used along with stains
    • *mechanism of action: prevent resorption of bile acids from small intestine
    • *AE: constipation, heartburn, nausea, belching, bloating-- these AE tend to disappear over time
  118. fibric acid derivatives (fibrates)
    • *gemfibrozil (lopid)
    • *fenofibrate (tricor)
    • *drug effects
    •  -dec the triglyceride levels
    •  -inc HDL by as much as 25%
    • *AE:
    •  -abd discomfort, diarrhea, nausea, blurred vision, HA, inc risk of gallstones, prolonged prothrombin time, liver studies may show increase function
  119. niacin (nicotinic acid)
    • *Vit B3
    • *lipid lowering properties require much higher doses than when used as a vitamin
    • *effective, inexpensive, often used in combination w/ other lipid lowering drugs
    • *indications:
    •  -effective in lowering triglyceride, total serum cholersterol,and LDL levels, inc HDL levels
    • *AE:
    •  -flushing (due to histamine release)
    •  -pruritus
    •  -GI distress
  120. Cholesterol absorption inhibitor
    • *ezetimibe (zetia)
    •  -inhibits absorption of cholesterol and related sterols from the small intestine
    •  -results in reduced total cholesterol, LDL, triglyceride levels
    •  -also inc HDL levels
    •  -works well when taken with a statin drug
  121. antilidemics: HMG-CoA reductase inhibitors (HMGs, or statins)
    • most potent LDL reducers
    •   -lovastatin (mevacor)
    •   -pravastatin (pravachol)
    •   -simvastatin (Zocor)
    •   -atorvastatin (Lipitor)
    •   -fluvastatin (lescol)
    •  
    • *mechanism of action
    •  -inhibit HMG CoA reductase, which is used by the liver to produce cholesterol
    •  -lower the rate of cholesterol production
  122. HMG-CoA reductase Inhibitors
    • *indications
    •  -first line drug therapy for hypercholesterolemia
    •  -tx of types IIa & IIb hyperlipidemias
    •   -reduce LDL levels by 30-40%
    •   -inc HDL levels by 2-15%
    •   -reduce triglycerides by 10-30%

    • *AE;
    •  -mild transient GI disturbances
    •  -rash
    •  -HA
    •  -myopathy (muscle pain) possibly leading to the serious condition rhabdomyolysis
    •  -elevations in liver enzymes or liver disease
  123. antilipidemics nrg implications
    • *assess dietary patterns, exercise level, weight, height, VS, tobacco, and alcohol use in family history
    • *contraindications include biliary obstruction, liver dysfunction, active liver disease
    • *obtain baseline liver function studies
    • *patients on long tern therapy may need supplement fat soluble vitamins (A,D,K)
  124. antilipidemics- pts should be instructed
    • *take with meals to dec GI upset
    • *powder forms must be taken with at least 4-6 oz ofliquid, mixed thoroughly but not stirred, and NEVER taken dry
    • *eat a low fat diet
    • *enc high intake of raw vegetables and fruits and at least 2000 ml fluid to prevent constipation
    • *other medications should be taken 1hour before or 4-6 hrs after meals to avoid interference w/ absorption
    • *NIACIN:
    •  -to minimize AE, start on low initial dose and gradually inc it and take with meals
    •  -small doses of aspirin or NSAIDs may be taken 30 min before niacin to minimize cutaneous flushing
  125. Nrg implications antilipidemics
    • *instruct pts to report persistant GI upset, constipation, abnormal or unusual bleeding, and yellow  discoloration of the skin
    • *monitor for AE including inc liver enzyme studies
    • *monitor for therapeutic effects
    •  0reduces cholesterol and triglyceride levels

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