Term
| Principles of HTN treatment |
|
Definition
| majority of pts will require combo therapy of two meds or more to reach goal |
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Term
Major classes of drugs to treat HTN (4) |
|
Definition
- Sypatholytic Agents (inhibit symp. system)
- centrally acting antihypertensives
- alpha blockers (in vasculature)
- beta blockers (I in heart, II in lungs)
- ALL OF THESE AGENTS REDUCE PVR OR CO
- Diuretics (reduce blood vol, which in reduces CO)
- thiazide are the most important agents
- Vasodilators (reduce PVR)
- CCBs (indirect)
- Hydralazine, Minoxidil, Sodium NItroprusside
- ACE Inhibitors & Angio. II receptor antagonists
- reduce PVR/CO, but also reduce blood vol but reducing secretion of aldosterone
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Term
Beta-Adrenergic Blockers all are competitive antagonists; however they can be subdivided according to 3 major properties: |
|
Definition
- selectivity of receptor blockade
- possession of intrinsic sympathomimetrics activity (ISA)
- capacity to block alpha-adrenergic receptors (alpha 1)
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Term
major property of Beta blockers: selectivity of receptor blockade |
|
Definition
some agents are specifically beta I, some II, and some function in combo selectivity is never absolute (always side effects) beta I selective blockers: cardioselective b/c lack unwanted bronchoconstrictors of nonselctive blockers non-selective beta blockers: block both I & II, causing decreased CO/BP (so neg -ino, chrono-, dromo-), peripheral vasoconstriction (b/c alpha I left), decrease glycogen secretion (b/c less need for insulin), increased LDL & decreased HDL (b/c cholesterol prod. may increase) |
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Term
adverse effects of non-selective beta blockers (6) |
|
Definition
Bradycardia (b/c decrease HTN by decreased HR) bronchoconstriction (can result in asthma attack) may hide warning signs of hypoglycemia, i.e. tachycardia fatigue depression sexual dysfunction (vasodilator effect blocked) |
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Term
major property of beta blockers: possession of intrinsic sympathomimetics activity (ISA) |
|
Definition
classified as beta blockers but have some beta-agonistic properties (very mildly stim. both beta I & II receptors; their intrinsic effects are not as strong as those of full-agonists) mimic symp. NS produce bronchoconstriction only at extreme high doses do not induce bradycardia to the degree that full antagonists do (do not decrease resting HR) & cause minimal disruption of lipid & CHO metab. |
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Term
major property of beta blockers: capacity to block alpha-adrenergic receptors (alpha I) |
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Definition
nonselective beta blocking along with alpha I selective blockage, w hich results in peripheral vasodilation rather than the vasoconstriction that occurs w/ the other beta blockers used in tx of HTN or CHF b/c: reduction of symp. activity & improvement of diastolic dysfunction by prolonging diastolic filling time beta-blockers are contraindicated in tx of acute CHF; they are only used when the pt is hemodynamically stable |
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Term
| Pharmacodynamics / Actions of beta blockers |
|
Definition
- interrupt adrenergic stim. to beta I or II receptors by competing w/ NE for available beta receptor sites
- blockage of beta I/II receptors causes decrease in inotropy & chronotropy
- stroke vol. and venous return decreased
- those that inhibit beta II receptors cause vasodilation in skeletal muscles' arterioles
In summary, BBs decrease BP and block adrenergic receptor sites in herat muscle and conduction system, decreasing HR & reducing the force of the heart's contractions, resulting in lower demand for oxygen |
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Term
| Pharmacotherapeutics / Indications of beta blockers |
|
Definition
- management of HTN, used alone or in combo w/ other agents
- management of acute MI and angina
- tx of glaucoma (decrease intraoculara pressure by decreasing prod of aqueous humor by ciliary bodies, b/c beta receptors also found in intraocular fluid)
- management of tachyarrhythmias
- used in tx of anxiety, migraines, and symptoms of hyperthyroidism (where metabolic activities are increased)
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Term
| Contraindications/ Cautions of beta blockers |
|
Definition
- h/o asthma, emphysema, HF, CVA, hypotensioin, sinusbradycardia, AV block (we could worsen conduction condition), dyslipidemia, Raynaud's & peripheral vascular disease
- diabetics on insulin or oral hypoglycemics (may mask symptoms or decrase need for insulin)
- kidney & liver diease (accumulate in serum & cause toxic effects)
- pts w/ depression & impotence
- elderly are at most risk for side effects (so, smaller doses)
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Term
| Drug interactions for beta blockers |
|
Definition
- Digitalis: exacerbation of conduction deficits
- antacids delay absorption of BBs (do not admin. any drugs 2 hrs either way w/ antacids)
- Lidocaine toxicity may occur when lidocaine is taken w/ BBs
- requirements for insulin and PO antidiabetic drugs can be altered by BBs
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Term
| Adverse Effects of beta blockers |
|
Definition
- CV: worsened peripheral vascular disease, intermittent claudication, decreased CO, reduced exercise tolerance, bradyarrhythmias, orthostatic hypotension
- resp: bronchoconstriction
- endo: decreased HDL & increased triglyceride levels, masking symptoms of hypoglycema, exacerbation of hypothyroidism
- other: fatigue, sleep disturbances, impotence, increased serum K+ levels, depression, constipation
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Term
Nursing management / indications for beta blockers |
|
Definition
- beta blockers should NEVER be discontinued abruptly (cause up-regulation of receptors in the heart; discontinuing causes circulating catecholamines and lots of receptors which could cause ventricular fib and death)
- do not take with ETOH, CNS depressants, or OTC decongestants
- admin. at same time everyday
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Term
|
Definition
-olol carvedilol (Coreg) metoprolol (Lopressor, Toprol-XL) |
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Term
| Calcium Channel Blockers (CCBs) |
|
Definition
- Ca ions play important role in excitation and contraction of cardiac and vascular smooth muscle; contraction takes place when extracellular Ca enters cells through channels in membrane
- CCBs act to reduce influx of Ca into cell, which results in relaxation of vascular smooth muscle, dilation of coronary arteries/arterioles, and reduction of myocardial O2 consumption
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Term
| CCBs reduce myocardial oxygen consumption by either: |
|
Definition
slowing HR & decreasing contractility decreasing SVR (afterload) or a combo of both |
|
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Term
| Pharmacodynamics / Action of calcium channel blockers |
|
Definition
- prevent flow of Ca ions into cell
- relax arterial smooth muscle & decrease contraction of heart muscle
- slow AV conduction
- reduce HR
- dilate coronary & peripheral resistance
- increase coronary blood flow (b/c no constriction)
- reduce myocardial O2 demands
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Term
| Pharacotherapeutics / Indications of calcium channel blockers |
|
Definition
- prevent post-MI complications (keep arteries dilated)
- treat HTN
- used for long-term prevention & tx of angina, not short-term relief b/c don't work fast enough
- drug of choice for preventing Prinznetal's angina (vasospasm due to not enough blood supply to this part of the heart --> so vasoconstrict this area)
- Raynaud's syndrome (probs w/ periph. aterial circulation)
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Term
| Contraindications / Cautions of CCBs |
|
Definition
- contraindicated in pts w/ severe HF b/c of myocardial depressant effect
- contraindicated in severe left ventricular dysfunction, heart block, hypotension, bradycardia & hepatic and renal disease
- contraindicated in women who are pregnant or lactating (b/c smooth muscle in uterus)
- should be admin. w/ caution in pts w/ CHF - may worsen HF
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Term
| Drug interactions with CCBs |
|
Definition
very safe for noncompliant pts - BBs and other antihypertensive agents - additive effects
- verapamil & diltiazem increase risk of digitalis toxicity (b/c same pharmacodynamics)
- Cimetidine: augments effects of CCB (inhibits P-450, possible toxic effects)
- Ca salts may reduce effectiveness of CCB (clinically insignificant)
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Term
|
Definition
- peripheral edema (dose depend.), bradyarrhythmias, HF
- flushing, sweating (increased blood supply)
- headache (b/c increased cerebral blood flow leads to symptoms of intracranial pressure)
- dizziness, tremor
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Term
| Nursing management / Indications of CCBs |
|
Definition
- efficacious, well tolerated w/ relatively low side effects
- metabolically neutral
- short acting preparations should not be used b/c have been associated w/ greater risk of CV death due to rapid decrease of BP
- admin w/ food/milk to prevent gastric discomfort
- no ETOH b/c acts as a vasodilator and can cause acute drop in BP/extreme dizziness
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Term
|
Definition
- Verapamil (Calan) --> heart; slows HR, reduces contractility, slows AV conduction
- Nifedipine (Adalat) --> peripheral vascular; vasodilation, decreases afterload (usually for those w/ HTN)
- Diltiazem (Cardizem) --> heart & vascular (like partial agonist)
- combined effects of the two, no bad side effects for either but may not work as strongly either
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Term
| Angiotensin-Converting Enzyme (ACE) Inhibitors |
|
Definition
- work by preventing conversion of Angio I to Angio II. As Angio II is reduced, aterioles dilate, reducing peripheral vascular resistance
- by reducing aldosterone secretion, ACE inhibitors promote excretion of Na and water, reducing amt of blood the herat needs to pump and resulting in decreased BP
- unlike other vasodilators, effect of ACE inhibition is not followed by typical reflex actions of the symp. NS (tachycardia, increased output & fluid retention)
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Term
| Pharmacotherapeutics / Indications of ACE inhibitors |
|
Definition
- mild to moderate HTN
- management of HF and left ventricular hypertrophy; improve survival rates
- beneficial in reducing progression of diabetic (& other) nephropathies (renoprotective)
- recommended for a min of 6 mo after acute MI & def. w/ echo evidence of left ventricular systolic dysfunction
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Term
| Contraindications/ Cautions of ACE inhibitors |
|
Definition
- in pts who previously developed angioedema (allergic rxn) after taking ACE inhibitors
- contraindicated in pregnancy; associated w/ fetal abnormalities/death when admin. during 2nd or 3rd trimester (we produce most renin as a fetus)
- pts w/ bilateral renal artery stenosis
- pts on dialysis or who are taking K-sparing diuretics
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Term
| Drug interactions with ACE inhibitors |
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Definition
- all ACE inhibitors enhance hypotensive effects of diuretics and other hyertensives, such as BBs
- can increase serum lithium levels, possibly resulting in lithium toxicity
- Digoxin: increased risk for toxicity
- when used w/ K-sparing diuretics, K supplements, or K-containing salt substitutes, hyperkalemia may occur ("kalemia" = "in serum")
- aspirin & NSAIDS may interfere w/ ACE inhibitor effects
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Term
| Adverse Effects of ACE inhibitors |
|
Definition
- dry cough (1/3 pts) - due to catalyzation of irritating substances by ACE in lungs
- Hyperkalemia (accum. of K+ in serum b/c no pull from Na+) --> in everyone
- renal dysfunction
- angioedema (anaphylactic rxn - swelling in tongue that could occlude airway)
- Rash (rare)
- Hypotension/orthostatic hypotension
- Dysgeusia (altered sense of taste)
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Term
| Nursing Management / implications for ACE inhibitors |
|
Definition
- monitor I & O
- monitor serum electrolytes, in particular K & Mg levels
- assess for angioedema
- monitor blood count for neutropenia
- admin. same time everyday
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|
|
Term
|
Definition
"-pril" lisinopril (Zestril) |
|
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Term
| Angiotension II Receptor Antagonists (ARBs) |
|
Definition
| compete w/ Angiotension II for tissue binding sites; block the vasoconstriction & aldosterone secretion produced by Angio, thus lowering BP |
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Term
| Pharmacotherapeutics / Indications of Angio II Receptor Antagonists (ARBs) |
|
Definition
- newest agent against HTN; efficacy comparable to that of ACE inhibitors
- while they appear to be effective for a # of people, long term data does not exist (so, second option after ACE inhibitors)
- more expensive than ACE inhibitors
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Term
| Contraindications / Cautions of ARBs |
|
Definition
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Term
| Drug Interactions of ARBs |
|
Definition
| same as ACE inhibitors (anything that will effect K+) |
|
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Term
|
Definition
- less potential for cough (not completely absent)
- less potential for hyperkalemia
- Dizziness
- Diarrhea
- GI upset
- Kidney impairment
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Term
| Nursing Management / Implications for ARBs |
|
Definition
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Term
|
Definition
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Term
|
Definition
include several different types of drugs, but all reduce BP by inhibiting or blocking symp. NS (like BBs but different action) Classified by their site or mechanism of action and include: - Centrally-acting symp. NS inhibitors
- alpha blockers/ peripherally acting alpha-adrenergic blocking agents: dilate both arteries and veins (alpha in post-syn. neuron)
- direct acting vasodilator (results in decreased PVR & lowered BP; used in severe HTN b/c potent)
- Mixed arterial and venous vasodilators (sodium nitroprusside)
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Term
| Mixed arterial and venous vasodilators (Sodium nitroprusside) |
|
Definition
used in hypertensive crisis: direct acting vasodilator relaxes smooth muscleor arterioles & veins; effects begin in seconds & fade rapidly when admin. ceases (very short half-life) admin by continuous IV infusion; continuous BP monitoring req'd prolonged infusion (longer than 72 hrs) can produce toxic admin. of thiocynate & should be avoided (cyanide toxicity) |
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Term
| Hypoperfusion-Vasopressor Therapy |
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Definition
- when fluid admin. fails to restore adequate BP & organ perfusion, vasopressors are indicated (increased BP & vasoconstriction)
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Term
| Desirable characteristics of a vasopressor: |
|
Definition
- maintain effective circ. blood vol & renal blood flow
- enhance cardiac contractility
- no effect on HR
- not induce or aggravate arrhythmias
- not produce extreme variation in BP
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Term
| Adverse Effects of vasopressors |
|
Definition
- tachycardia
- excessive vasoconstriction (peripheral ischemia & necrosis)
- myocardial ischemia
- arrhythmias
- hypertension
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Term
| Nursing considerations for vasopressors |
|
Definition
- infuse into CL when possible (optimal)
- monitor infusion site frequently (if running peripherally) for signs of infiltration (so it does not go into tissue and kill it)
- treat extravasation w/ Regitine (through infiltrated tissue) --> blocks symp. NS by blocking ganglion
- anticipate a more rapid onset of action when infused w/ a CL rather than peripheral line
- monitor VS at least every 5 min
- monitor ECG for signs of ischmia, arrhythmias
- correct hypovolemia
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Term
| Therapeutic Choices of Vasopressors |
|
Definition
- Dopamine (DA)
- Dobutamine (Dobutrex)
- Norepinephrine (NE), (Levophed)
- Phenylephrine
- Vasopressin
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Term
Vasopressor: Dopamine (DA) |
|
Definition
- catecholamine activating B1 receptors in the heart, dopamine receptors in the kidney & A1 receptors in blood vessels
- action entirely depends on dose admin:
- 1-3mcg/kg/min: stim mainly dop. receptors in renal vasculature causing increased contractility, HR, and CO
- 4-10: stim B1 receptors in heart causing increased contractility, HR, CO & thus BP
- >10: stim A1 receptors in periphery causing vasoconstriction & SVP increase which will increase BP
- 50% of action due to endogenous NE
- many pts respond poorly or fail to respond (so not widely used anymore)
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Term
Vasopressor: Dobutamine (Dobutrex) |
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Definition
| synthetic catecholamine causing selective adtivation of B1 receptors only |
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Term
Vasopressor: Norepinephrine (NE) |
|
Definition
same as NE produced by body stimulate A1 & B1 receptors more potent than DA - most potent vasopressor that we have esp. useful in presence of massive vasodilation (& sepsis) |
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Term
Vasopressor: Phenylephrine |
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Definition
selective A agonist only; no effect on the heart-no risk for dysrrhythmias less potent than NE (so more popular) |
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Term
|
Definition
anti-diuretic hormone (synth. form of what is released by post. pituitary) used in combo w/ NE, or DA, to increase BP |
|
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Term
Extravasation - Phentolamine (Regitine) |
|
Definition
antidote to prevent tissue necrosis potent A blocker - causes vasodilation used for NE, DA, phenylephrine, vasopressin extravasation |
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Term
Coronary Artery Disease (CAD): Angina Pectoris |
|
Definition
- clinical syndrome of crushing chest pain that occurs as a result of cardiac ischemia (when coronary blood flow is inadequate to meet the oxygen demand of the myocardium)
- other sites of pain include left arm, hand, neck, etc.
- it is important to recognize that angina is not a disease but a symptom of an underlying diease-namely ischemic heart disease (due to artherosclerosis, coronary artery disease, etc)
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Term
| Pathophysiology of Angina Pectoris |
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Definition
- simply bad oxygen economics
- there's an imbalance between oxygen supply and demand
- in normal heart, when demand goes up, coronary blood flow increases, so there is an increased supply of oxygen to meet metabolic needs of the myocardium
- in the heart w/ coronary arteries that are obstructed by plaques (or arteries that have vasospasm) when oxygen demands go up, supply isn't always capable of keeping up
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Term
|
Definition
- Stable (classic): pain associated w/ exercise, physical exertion, stress, or eating large meals
- Unstable: occurs in resting heart; greater freq. and duration of attacks, signal impending MI
- Variant (prinzmetal): due to vasospasm in coronary vessel (not blockage) at rest or during exercise (more common in young people)
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Term
| Tx of stable angina has two major purposes: |
|
Definition
prevention of MI & death (increase the quantity of life) --> MI is next step from angina reduction of symptoms and occurrence of ischemia (improve the quality of life) |
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Term
Therapeutics for angina are directed to: (2) and can be accomplished by: (3) |
|
Definition
increased supply (coronary blood flow) & decreased demand (reduced myocard. O2 requirements) decreasing HR and/or contractility decreasing afterload (arterial pressure) decreasing preload (cardiac filling) |
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Term
| Three classes of drugs can be used to treat angina: |
|
Definition
- Organic Nitrates (veins/arteries) - decrease preload
- CCBs (heart/arteries) - reduce HR & contractility,decrease afterload
- BBs (heart) - reduce HR & contractility
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Term
|
Definition
- cornerstone of angina therapy
- provide NO to vascular endothelium & arterial smooth muscles, resulting in vasodilation. All parts of the vascular system relax in response to nitrates.
- dilation of venous system results in venous pooling in the periphery & decresed venous return to the heart, which leads to decreased preload
- arterial dilation decreases systemic vascular pressure, resulting in decreased afterload
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Term
| Together, these effects decrease myocardial oxygen demand: |
|
Definition
- afterload: decreased by CCBs & nitrates
- HR: decreased by BBs
- Preload: decreased by nitrates
- Contractility: decreased by BBs & CCBs
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Term
| Absorption & Distribution of Nitrates |
|
Definition
- well absorbed by oral, buccal, sublingual & transdermal routes
- amyl nitrate is available in an inhaled form, providing for very rapid absorption
- oral nitrats have sig. first-pass effect, so must be given in sufficient high doses to sustain blood levels despite the first-pass effect
- sublingual, transdermal & inhalation routes avoid the first-pass effect route
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Term
|
Definition
Sublingual NTG: every 5 min for up to 3 doses; if the angina is not relieved by the second dose, recommended that you take the third dose, call 911, and go to hospital b/c NG test helps differentiate between angina and MI |
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Term
| Adverse Effects / Contraindications of Nitrates |
|
Definition
- hypotension, especially postural; flushing, pounding headache, blurred vision, dry mouth, peripheral edema, rashes & skin irritations w/ patches
- preg. category C; Amyl nitrate = category X (potent vasodilator)
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Term
| Pt education for Nitrates |
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Definition
- nitrate-free intervals of 10-12 hrs nec. to prevent nitrate intolerance (avoid tachyphylaxis)
- take in sitting or lying pos'n
- use special application paper; wash hands immediately after application and/or use gloves
- to ETOH, even OTC drugs
- take around 5-10 min prior to moderate physical/sexual activity
- notify dentist
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Term
| Drug interactions with nitrates |
|
Definition
- severe hypotension w/ interaction w/ ETOH
- absorption of sublingual nitrates may be dlayed when taken w/ an anticholinergic drug
- marked orthostatic hypotension w/ light-headedness, fainting, & blurred vision may occur when CCB & nitrates are used together
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Term
Coronary Artery Disease (CAD): Heart Failure |
|
Definition
- complex syndrome that occurs when the CO is inadequate to satisfy the O2 demands of the body
- results from any structural or functional cardiac disorder that impairs the ability of ventricle to fill w/ or eject blood
- develops slowly, often years, as the heart grad. loses pumping ability and works less efficiently; some may not become aware until decline
- congestive HF often used to describe all pts w/ HF, actually congestion is just one feature
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Term
Pathophysiology of HF: 3 compensatory mechanisms are activated in HF in an attempt to improve CO; these responses also increase myocardial work load and may perpetuate HF: |
|
Definition
- Sympathetic activation is an early response to reduced CO; syp. NS activation increases HR, contractility, and arterial vasoconstric.
- decreased CO reduces kidney perfusion & leads to vol retention; extra blood vol. increases cardiac preload; higher preload results in more forceful ejection of blood from the heart & improves CO
- cardiac hypertrophy is stim. by elevated myocardial wall tension; hypertrophy adds contractile filaments & improves contractile force
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Term
| Compensatory response in HF: |
|
Definition
- decreased CO
- baroreceptors in circ system cause symp NS stim.
- veins/arteries constrict in increase critital organs (heart & brain) perfusion
- contractile strength & HR increase to promote perfusion
- reduced blood flow to kidneys
- more renin is released from kidneys, starting angio-aldosterone cascade and leading to further vasoconstric. & Na/water retention
- periph. vasoconstricion forces heart to pump harder & renin-angio-aldosterone mech. causes overfilling of the heart
- pulmonary edema,increased syst. circ (liver/spleen become engorged & jug. vein distention/tissue edema become evident)
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Term
Most causes of HF result from dysfunction of the ____ ventricle (systolic & diastolic HF) the ____ ventricle may also be dysfunctional, especially in pulmonary disease (___ ventricular failure) some conditions cause inadequate perfusion despite normal or elevated ___ (high-output failure) |
|
Definition
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Term
|
Definition
Systolic HF: inability of the heart to generate an adequate CO (CO depends of HR & SV); SV is influenced by contractility, preload, afterload) Diastolic HF: occurs when the heart has a problem relaxing; inadequate relaxation to permit normal filling; results from decreased compliance of the left ventricle and abnormal diastolic left HF is characterized by pulmonary congestion which may mainfest w/ dyspnea, orothpnea, crackles, cough, pulmonary edema, and hypoxia (b/c blood backs up into the lungs b/c not being completely ejected from the LV)
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Term
|
Definition
- can result from left HF which eventually increases the burden on the R heart and may cause it to fail as well
- causes must hterefore include all of the left HF (less blood ejected to pul. circ, so back up into systemic circ)
- pure right HF is rare (usually due to R ventricular infraction or pulmonary disease)
- pulmon. disorders that relsut in PVR impose a high afterload against which the RV must pump; the resultant RV hypertrophy (called cor pulmonale) may progress to right ventricular failure as the lung disease worsens
- RHF is characterized by systemic venous congestion, which may maifest w/ jugular vein distention, hepatomegaly, spenomegaly & peripheral edema
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Term
|
Definition
- rare form that takes place when the demads of the body are so great that even increased CO is insufficient
- heart increases output but body's metabolic needs are still not met
- causes include hyperthyroidism, anemia, septicemia
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Term
| Causes/Risk factors of HF |
|
Definition
- age, cardiac arrhythmias, idiopathic dilated cardiomyopathy, HTN, diabetes, obesity, smoking, dyslipidemia
- single risk factor may be sufficient, but a combo of factors dramatically increase the risk
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Term
|
Definition
- fatigue, SOB, reduced exercise tolerance, tachycardia, dilation of heart, venous distention, cough (pulmonary edema), weight gain, hepatomegaly, distention of jugular vein
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Term
|
Definition
overall tx aimed at altering & controlling compensatory mechanisms - diuretics: reduce blood vol: first line = loop diuretics, second line = spironolactone
- cardiotonic-inotropic agents: (digitalis) strengthen the failing heart; increase contractility
- vasodilators: decrease PVR (ACE inhib, CCBs)
- ACEI/ARBs: dilate veins/arterioles, decrease preload/afterload, reduce detrimental effects of aldosterone, decrease workload of heart
- beta blockers: reduce excessive adrenergic stim. of heart (decrease work); new approach, whether due to ischemic heart diesase or cardiomyopathy, is to use low doses of BBs
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Term
| Digitalis Glycosides (Cardiac Glycosides) |
|
Definition
- group of drugs derived from digitalis, substance that occurs naturally in foxglove plant species
- most prequently used is dixogin
- another, digotoxin, is no longer avail. in US
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Term
| Pharmacodynamics/Action of Digitalis Glycosides |
|
Definition
- increase the force of myocardial contraction (pos. inotropic effect)
- by inhibiting ATPase which normally decrases move't of Na out of cell after contraction
- slow HR due to both direct & indirect actions on the SA node (neg. chrono. effect)
- cause decreased conductivity through AV node, whichcan lead to varying degree of heart block (neg dromo. effect)
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Term
| Pharmacokinetics of Digitalis Glycosides |
|
Definition
- route of admin. (PO, IV, IM)
- intestinal absorption of digoxin varies greatly; capsules are absorbed most efficiently follwed by elixer, then tablets
- digoxin is distributed widely throughout body, bound extensively to skeletal muscles & does not penetrate body fat easily
- most of drug is excreted by kidneys as unchanged drug
- half-life = 36-48 hrs
- preg. category C
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Term
| Pharmacotherapeutics / Indications of Digitalis Glycosides |
|
Definition
- CHF
- atrial fib/flutter, supraventricular tachycardia, paroxysmal atrial tachycardia
- Digitalization:
- b/c digoxin has long half-life, loading does must be given to a pt who requires immediate drug effects to achieve the steady state
- if no loading dose, may take up to two weeks (4-5 half-lives) before steady state plasma concs are achieved
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Term
| Contraindications/ Cautions of Digitalis |
|
Definition
- Contraindicated for pts w/ heart blocks or bradycardia
- caution in:
- elderly (possible toxicity due to renal insufficiency)
- pts who are taking any drugs that can interact
- IV digitalis should be admin slowly; too rapid infusion can precipitate toxicity
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Term
| Drug interactions w/ Digitalis |
|
Definition
- adrenergic agent: increased risk for toxicity; BBs may cause bradycardia & arrhythmias when taken w/ digoxin
- Ibuprofen, anticholinergic agents, etc increase digitalis absorption, serum level, and risk of toxicity
- antacids, laxatives, etc decrease digitalis absorption, reducing therapeutic effect
- Ca preparations increase risk of dysrrhythmias; IV Ca contraindicated when digoxin is admin.
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Term
| Adverse Effects of Digitalis |
|
Definition
- potential for toxicity is the major side effect; cardiac arrhythmias are most life threatening & major contributing factor is serum levels of K+ (too high or low)
- cardiac glycosides have a low therapeutic index
- serum levels greater than 2 indicate toxicity
- doses should be individualized based on pt's serum digitalis conc.
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|
Term
| Signs/Symptoms of digitalis toxicity include: |
|
Definition
- CNS: drowsiness, HA, confusion (more in elderly)
- CV: cardiac arrhythmias, ventricular bigeminy/trigeminy - initial sign of toxicity in adults
- GI:
- anorexia (initial sign in adults)
- upset stomach (intial sign in kids)
- Visual disturbances: blurred vision, halo-appearance, single color vision
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Term
| Nursing Management / Implications |
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Definition
- withhold drug if apical pulse rate is below 60 in adults, 70 in kids, 90 in infants or if there is a dysrrhythmia (pulse >120 = toxicity)
- admin. orally at same time of day
- toxicity occurs in 10-25% of pts
- admin. of antiarrhythmic agents if indicated
- toxicity may be treated w/ digoxin ammune Fab (antibody fractions specific for digoxin) -->these bind to the glycosides and the combo is excreted in the urine
- monitor serum levels of K, Ca, Mg, kidney & liver function status
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Term
| contributing factors leading to development of digitalis toxicity: |
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Definition
- larger than nec. maintentance dose
- rapid loading dose
- impaired liver/renal function prolonging metabolism and excretion of drug
- old/young pts
- electrolyte imbalance (esp K+)
- hypoxia (increases myocardial sensitivity to digitalis)
- hypothyroidism (slows metabolism)
- concurrent tx w/ other cardiac drugs
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Term
| Other cardiac inotropic drugs -- Phosphodiestarase Inhibitors |
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Definition
used for short-term therapy for HF when digitalis & diuretic therapy do not control symptoms differ from digitalis b/c also act as vasodilators |
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Term
| Pharmacodynamics / Actions of Phosphodiestarase Inhibitors |
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Definition
- inhibit phosphodiestarase which leads to increased levels of cAMP and intracellular Ca; this results in increased contractility
- vasodilator effect relaxes vascular smooth muscles, decreasing peripheral resistance, increasing SV, ejection fraction & HR
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Term
| Pharmacokinetics of Phosphdiestarase inhibitors |
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Definition
- IV admin. is the only route, so absorption is immediate
- renal elimination
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Term
| Contraindications / Cautions of Phosphodiestarase inhibitors |
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Definition
- hypersensitivity reactions
- used w/ caution in arrhythmias, past MI, thrombocytopenia
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Term
| drug interactions w/ phosphodiestarase inhibitors |
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Definition
- digitalis: digoxin toxicity
- diuretics: increased diuretic effect
- should not be infused w/ furosemide due to formation of precipitations; when giving both drugs IV, use separate lines
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Term
| adverse effects of phophodiestarase inhibitors |
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Definition
- dysrrhythmias
- thrombocytopenia (platelet count should be monitored)
- hypotension
- anorexia
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Term
| Common phosphodiestarase inhibitors |
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Definition
"-none" inamrinone (Incor) milrinone (Primacor) - analog or inamrinone but 20x more potent |
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