N323 QUIZ 2 Study Guide PDF

Title N323 QUIZ 2 Study Guide
Course Pharm Concepts I
Institution Drexel University
Pages 20
File Size 544.9 KB
File Type PDF
Total Downloads 108
Total Views 150

Summary

combined lecture notes for quiz 2 in the class containing notes on heart failure medications (vasodilators, adrenergic agonists, diuretics, beta blockers, dysrhythmic drugs, nitrates, antihyperlipidemic drugs, etc.)...


Description

General: Please know general principles, and how each class of medication works, general precautions etc. HTN (cont)/ Vasodilators and Adrenergic Agonists (2 Qs) nitroprusside (Nipride), hydralazine (Apresoline) Medication Hydralazine (Apresoline)

Class of Medication Direct acting vasodilator - Works DIRECTLY on your blood vessels

Direct acting Nitroprusside vasodilator oo (Nipride) - Only given in an acute care setting; ICU, ER

VASODILATORS How?

Used for To lower BP

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Hypertensive CRISIS DBP >120 Drip med IV use only and MUST be on a pump Relaxes

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decreases the peripheral resistance

Relaxes smooth muscle Vasodilates veins and arteries Causes less workload on heart and lowers BP dramatically – what nursing intervention would we need to do?

ADRENERGIC AGONISTS

S/S and Adverse Effects Adverse Affects: - Lupus like syndrome - Reflex tachycardia - Fluid retention - What can be used to combat reflex tachycardia and fluid retention?

Precautions -

Watch HR Drug interactions – beta blockers

Nursing interventio -

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Protect it from light by wrapping it in foil or using a dark container – light will break it down

Can combine wit a diuretic and/or beta blocker or clonidine Monitor HR

Monitoring BP – CONTINUOUS AND INVASIVE; i an arterial BP line bc of the dramat drop of BP

Medication Epinephrine

Class of Medication Adrenergic agonist - Used for hypotension and shock

Used for -

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Dopamine (Inotropin) - Given IV only in acute care setting

Adrenergic agonist - Catecholamine and a precursor to norepinephrine

Hypotension and shock Very common use for allergies and anaphylactic shock Cardiopulmonary arrest Ventricular fibrillation Asthma Can be given subQ but in an emergency situation, push it IV Treating shock Supports BP

How? -

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Stimulates beta and alpha receptors – its A NONSELECTIVE ADRENERGIC AGONIST What do you alpha and beta receptors do?

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Very powerful vasoconstrictor

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Vasopressor – strong vasoconstrictor Stimulates alpha 1, beta 1, and dopamine receptors

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S/S and Adverse Effects Adverse Effects - CNS - Cardiac effects - Dw about the adverse effects too much

Precautions

Adverse Effects - CV system effects -

WEIGHT BASED DOSING – need accurate weight; the beds do that Dose dependent depends on how much of the dose you give what affects it has on your body

Nursing interventions

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Fix hypovolemia first; it won’t work if pt has low fluid volume Invasive BP monitoring; need an arterial line

Contraindications - Pheochromocytoma - Uncorrected tachyarrhtmias - V-fib Medication Phenylephrine

Class of Medication Adrenergic Agonist

Used for -

Hypotension

How? -

Alpha 1 stimulant –

S/S and Adverse Effects

Precautions -

EXTRAVASATION –

Nursing interventions - WATCH IV

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(NeoSynephrine IV)

A NUMBER 1 VASOCONSTRICTOR; very potent

Shock states Vascular failure

Other (FYI) uses - In Sudafed to clear airway and help w/ inflammation - Eye drops (mydriasis) – dilate pupils to see what’s in your eye Isoproterenol

Adrenergic Agonist

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Drip med Preferred: central IV lines Congestive HF Various types of shock Hypoperfusion

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Inhaled pharmacotherapeutics: - Asthma - Bronchitis - emphysema

Heart Failure (6 Qs) -

HF = heart muscle can’t pump blood around the body properly Not every patient has signs of systemic or pulmonary congestion

Adverse effects Nonselective beta 2 stimulant; so where - r/t cardiac what kind of pts will stimulation these be used for?

IV infiltrates and leak out; can cause damage to veins, underlying tissue and muscle. CAN CAUSE AMPUTATION bc its such a strong vasoconstrictor that the blood isn’t getting to the area

SITES ALMOST CONSTANT MONITORING

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o You can have heart failure with no congestion Different things can happen with HF o Progressive  Once it starts, it progresses o Ventricular dysfunction  L (specifically) is not pumping out blood efficiently to the body (L-ventricle pumps blood out to the body) o Reduced CO  CO tells us how much blood is pumping out with each beat; how strong and efficient your heart is; low CO = HF  Measure CO by ejection fraction (% #); 55-70 is normal o Insufficient tissue perfusion o Signs of fluid retention (heart is not moving to move fluids around) Causes: o Chronic HTN – if BP is high all the time; heart will get tired and start to fail o MI/HA – death of heart muscle due to blockage of coronary artery (oxygen starvation/ decr blood flow) o CAD/coronary artery disease o Valvular disease – valves could not work right o Dysrhythmias – weird rhythm that causes heart to not efficiently work o Fibrillation (heart is shaking) – abnormal rhythm; not being efficient pump; risk for clots; fluid starts to accumulate = dec CO o Aging myocardium o Pregnancy  PPCM – Peripartum/Postpartum cardiomyopathy – get it towards the end of last trimester or w/in 3 mo postpartum  Post cardial myopathy after birth – massive fluid retention  Can be fatal Can result in: o Cardiac Remodeling o Physiologic adaptations to reduced cardiac output  Cardiac dilation in one side or the other  (reduced CO  fibers in the heart stretch  HR increases)  ↑ sympathetic tone  ↑ HR, ↑ contractility/force of contraction, ↑ venous tone, ↑ arteriolar tone  H20 retention and ↑ blood volume  Natriuretic peptides  BNP/brain natriuretic peptide – blood test; measurement of HF  Higher it is, more HF you have bc your heart releases these peptides when it gets stretched and overworked Signs and symptoms o ↓ exercise tolerance o Fatigue

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o SOB o Tachycardia o Cardiomegaly – heart is getting bigger bc its trying to work; can get bigger bc its dilated with fluid o Pulmonary edema o Weight gain – fluid retention o crackles Congestion symptoms include: (you don’t have to have these) o Pulmonary edema ( so full of fluid that you need to be on a ventilator; you have 0 capacity to bring air in bc so full of fluid like breathing through a straw), Peripheral edema hepatomegaly – fluid in liver, JVD – jugular venous distention , Weight gain – fluid retention You have stages in HF (don’t memorize stages) o ACC/AHA Stages of Heart Failure; It gets worse from A to Stage C and D  space your care, struggling to breathe, do not overtax your pt, make sure your pt can tolerate  Washing their face and arms may overtax them, might have to take a 2 hr nap before you can wash the rest of their body Assessment – how do you know HF is improving? o S/S will get better o Measure weight; daily weights!! Treatment overview o Diuretics (Lasix) o ACE Inhibitors/ARB o Beta blockers o Digoxin Medication Loop Diuretics - Furosemide (Lasix) - Profound diuresis - GO-TO HF DRUG - VERY POTENT

Class of Medication Loop Diuretic – K+ depleting

Used for -

HF First line drug with s/s of fluid overload

How? -

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Thiazide Diuretics - Hydrochlorothiazide (HCTZ)

Thiazide Diuretic – K+ depleting

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HF First line drug with

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S/S and Adverse Effects - Ototoxicity - Hypokalemia - Hyperglycemia - Hyperuricemia - gout -

Less fluid for the heart to push against or manage which decreases workload of the heart Dosage for adults is 20-40mg repeated in 1-2 hrs; IV push done slowly over 1-2 min Less fluid for the heart to push against or manage which -

Hypokalemia Hyperglycemia Hyperuricemia -

Precautions K+ DEPLETING Digoxin toxicity Antidote for digoxin toxicity: digibond Don’t need good GFR OR CO/EF

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Nursing interventions Monitor K+ Tinnitus Daily weights I&O Dec Na+ diet Limit fluids

K+ DEPLETING Digoxin toxicity Antidote for

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Monitor K+ Daily weights I&O

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Moderate diuresis

decreases workload of the heart

s/s of fluid overload

- gout -

K+ sparing diuretics - Aldosterone antagonist – Spironolactone (aldactone) - Nonaldosterone antagonist – triamterene (dyrenium) - Mild diuresis

K+ sparing Diuretic

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Aldactone – also affects RAAS and more on HF

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HF First line drug with s/s of fluid overload Aldactone - HTN - “Tyrone the Bouncer” *go to RAAS meds

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Less fluid for the heart to push against or manage which decreases workload of the heart

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Hyperkalemia

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digoxin toxicity: digibond NEED A GOOD GFR Need a good CO/ejection fraction Digoxin will be subtherapeautic

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Dec Na+ diet Limit fluids

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Monitor K+ Daily weights I&O Dec Na+ diet Limit fluids

DIURETICS

Medication ACE Inhibitors “-PRILS” - Angiotensin converting enzyme Inhibitors

Class of Medication ACE Inhibitors

ACE Inhibitors/ARBs (These also fall under RAAS meds) Used for How? S/S and Adverse Effects - Intractable cough - Blocks - HF converting “ACE cough” - Slows down enzyme that cardiac - ANGIOEDEMA – remodeling swelling of lips, makes eyelids, or face angiotensin II which can close which triggers - There are mouth and release of OTHER USES throat aldosterone under RAAS meds - Hypotension esp on first dose - Hyperkalemia

Precautions SWELLING/ ANGIOEDEMA

Nursing interventions

ARBs - Angiotensin II Receptor Blockers - SPECIFICALLY: Valsartan (Diovan)

ARBs

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HF Diovan is the only ARB used to treat HF

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ALSO UNDER RAAS meds

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Blocks angiotensin II receptors which blocks the secretion/trigger to release aldosterone

Would choose this over ACE to prevent intractable cough and angioedema

BETA BLOCKERS (also in antidysrhythmia and angina meds) ALDOSTERONE ANTAGONISTS Medication 1. Carvedilol 2. Metoprolol (Lopressor)

Class of Medication Beta Blockers

Used for

How?

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HF

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Metoprolol and Inderal help with angina

Improves LV ejection fraction = improve CO/dec workload of heart Protect heart from excessive sympathetic stimulation

S/S and Adverse Effects Adverse Effects - Fluid retention/edema - Worsening HF - HYPOTENSION - BRADYCARDIA - Heart block

Precautions -

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Nursing interventions Start doses low bc adverse effects might occur MONITOR BP AND HR

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Medication

Spironolactone (Aldactone)

Class of Medication Aldosterone Antagonist

Used for

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How?

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HF

Eplerenone (Inspra) -

Medication Digoxin

Class of Medication Cardiac glycosides

Routes: PO, or SLOW IV PUSH at least over 5 min but always check current IVP rate

Used for -

Protect heart from some dysrhythmias Inc exercise tolerance Slow progression of HF S/S and Adverse Effects

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Nursing interventions

Blocks aldosterone receptors in the heart and on the blood vessels Prevents the HARMFUL effects of aldosterone: Promotes myocardial remodeling Promotes myocardia fibrosis – stiffens heart Activate SNS Promotes vascular fibrosis – veins stiff Promotes baroreceptor dysfunction – doesn’t work properly In response to changes in BP How?

HF antidysrhythmia

Precautions

S/S and Adverse Effects Decreases force Adverse Effects of contraction - Nausea/Vomiting (1st signs) of the heart Inc CO - Yellow halo (1st sign) Dec sympathetic - Mental changes - Visual tone disturbances Dec HR Dec afterload - Abdominal Reduced discomfort, venous pressure blurred vision Inc urine output - Heart rhythm disturbances

Precautions -

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TOXICITY IS LIKELY BC IT IS MOST COMMONLY PAIRED W LASIX K+; seesaw effect Low K+  digoxin toxicity High K+  digoxin subtherapeutic HAS A LOT OF DRUG INTERACTIONS *JUST TAKE PRECAUTION WHEN PT IS ON MULTIPLE MEDS, WATCH FOR SIGNS OF TOXICITY OR

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Nursing interventions NARROW THERAPEUTIC WINDOW: 0.52.0 ng/mL APICAL HR FOR FULL MIN; HOLD IF HR < 60 or CHANGE IN HEART RHYTHM CONTINUOUS CARDIAC MONITORING

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Severe bradycardia

SUBTHERAPEUTIC VALUES  PERIODIC BLOOD TESTS

DIGOXIN (also in antidysrhythmic drugs) NITROGLYCERINE (used in angina meds as well)

Antidysrhythmic drugs (5 Qs) - Dysrhythmia: An abnormality in the rhythm of the heartbeat o 2 Fundamental Causes:  Automaticity: problem w/ impulse formation  Disturbance of impulse conduction - Low ejection fraction = low CO = cannot meet o2 demands - 2 types o **Tachydysrhythmias** = fast one o Bradydysrhythmias – 1 drug = slow one - ANY drug used to treat a dysrhythmia can also CAUSE a dysrhythmia - Supraventricular dysrhythmia = above ventricles = atria - Ventricular dysrhythmia = in the ventricle - Treatment o Dec the conduction/disturbance of impulse conduction or dec of formation of impulse o Termination of the dysrhythmia o Long term suppression with drugs – but heart is still not functioning properly  can lead to complications

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ANTIDOTE: DIGIBIND; standing order

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o Ablation /cardioversion/ defibrillation  Ablation - electrical physiology testing; see the area of the heart is the problem  Can cut off short circuiting of pathway so we can bypass that pathway and get a regular beat Classifications o Class I: Na Channel Blockers (Largest group)  Slows impulse conduction in the atria and ventricles and HIS-Purkinje system o Class II: Beta Blockers o Class III: K+ Channel Blockers o Class IV: Ca+2 Channel Blockers o Class V: Other Antidysrhythmic drugs o *remember all of these drugs can worsen preexisting arrhythmias o these drugs are blocking the movement of ions in order to slow down contraction

Medication Quinidine

Class of Medication Na Channel Blockers

Used for tachydyshythmias (FYI: supraventricular and ventricular)

Class I: Na Channel Blockers How? S/S and Adverse Effects -

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slows impulse down by blocking Na channels prevents reentry phenomenon  myocardial excitability, contractility, conduction speed

Adverse Effects - Cinchonism – Quinidine toxicity - Arterial embolism – life threatening; clot that cause MI or stroke - Cardiotoxicity - Hypotension with IV use

Precautions -

contraindicated w digoxin

Nursing interventions -

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take oral form with food telemetry monitoring/ heart monitoring VS monitoring Teach pt s/s of embolism

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Ventricular tachydysrhythmias

Slows down Most common contraction of - CV system (dysrhythmias heart and (Suppresses Numbing agent hypOtension) automaticity) - CNS (dizziness, - Numbing contraction lightheadedness, Think that it numbs fatigue, you bc you use it at drowsiness) the dentist Class 1C: Flecainide (Tambocor) and Propafenone (Rhythmol)  Na Channel Blocker Lidocaine (Xylocaine)

Medication Propranolol (Inderal)

Medication

Na Channel Blockers

Class of Medication Nonselective Beta blockers

Used for tachydysrhythmias

Class of Used for How? Medication Amiodarone K+ Channel TachyBlock K+ (Cordarone) Blocker dysrhythmias channels automaticity, contractility,

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Not effective orally NEVER USE IN PREP W/ EPI TO TREAT THIS (BC VASOCONSTRICTION) Only time you use epi with lidocaine is as a local anesthetic

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Class II: BETA BLOCKERS How? S/S and Adverse Effects Block beta 1 and 2 (slows ventric rate)

Adverse Effects: - Severe Hypotension - Bronchospasm (in asthma pts) - Bradycardia

Class III: K+ Channel Blockers S/S and Adverse Effects Adverse effects - CNS – dizziness, tremor, insomnia -

GI – nausea, vomiting

Precautions -

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Nursing interventio

Careful with resp pts bc can cause bronchoconstriction

Precautions -

Short term therapy Monitor ECG a lot

Pregnancy Category D – so don’t give it to pregnant women Long half-life, watch the dosing! MANY DRUG INTERACTIONS

Nursing intervention - Low dos therapy of the pulmona

conduction speed

Changes in skin pigmentation Blurred vision Serious Adverse effects: - Pulmonary toxicity (common) - Exacerbation of the arrhythmia - Photophobia/blurred vision  to blindness - Hyper/hypo thyroidism - SOB and shallow respirations (CONCERN W RESP PTS) -

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Prolongation of the PR & QT intervals; the longer the interval, the WORSE you are Highly lipid soluble Long QT syndrome – heart takes so long to polarize that it goes to asystole; its silent so don’t know that its there – STUDENT ATHLETES SHOULD GET EKG; SUDDEN DEATH CAN OCCUR TOXICITY CAN BE INC BY GRAPEFRUIT Can be subtherapeutic w other meds

y toxicity measure QT every shift

Ami is singing an ode to her banana (K+). Screaming and she’s a really bad singer that it causes bad effects like causing damage to lungs (pulmonary toxicity). Also she’s not attractive and no one’s going to take pictures of her; can’t go outside w/ her bc of the light– photophobic. She’s getting blurry vision from the lights and it looks like she has halos around her. We’re getting nauseated and dizzy listening to her singing. Medication Class of Used for How? S/S and Adverse Effects Precautions Nursing Medication intervention Verapamil (Calan) Ca Channel Tachydysrhythmias Block Ca channel blockers Blockers - slow down HR Diliatazem (Cardizem) Angina Class IV: Ca+2 Channel Blockers (also used for angina) Class V: Other Dysrhythmic Drugs Medication

Class of Medication

Adenosine - must be given IV

Class V antidysrhythmic drug

Used for Tachydysrhythmias

How? -

given a lot of times to reset the heart  conduction through AV node  automaticity in SA node

S/S and Adverse Effects

Precautions -

half-life of 10 seconds heart will be asystole for 6-10 seconds – need code cart, resuscitation equipment, O2

Nursing interventions -

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must be given IV and AS FAST AS YOU CAN then quick saline flush half-life is 10 seconds NEED RESUSCITATION EQUIP IN THE ROOM BC HEART ASYSTOLE; need be ready to code

Digoxin - already talked about dig

Cardiac glycoside Class V antidysrhythmic drug

HF SVT (supraventric tachycardia)

Medication Class of Medication Atropine Anticholinergic drug

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check drug interactions hypokalemia = toxicity hold if apical pulse less than 60

DRUG FOR BRADYDYSRHYTHMIAS Used for How? S/S and Adverse Effects - can’t pee, can’t see, cant Brady- manage dysrhythmias bradycardia...


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