Unit 4- Andrenergics, Cholinergics, RAAS Flashcards

1
Q

Chronotropic drugs

A

Change the heart rate.
Positive chronotropes - increase heart rate
Negative chronotropes - decrease heart rate

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2
Q

Dromotropic drugs

A

Effect the conduction speed through the AV node and rate of electrical impulses in the heart.
Positive dromotropes - increase conduction speed
Negative dromotropes - decrease conduction speed

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3
Q

Inotropic drugs

A

Affect the strength of muscular contractions (particularly in the heart).
Positive inotropes - increase strength of the heart’s muscular contractions
Negative inotropes - decrease strength of the heart’s muscular contractions

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4
Q

Cardiac output

A

heart rate x stroke volume *(the amount of blood that can be pushed out of the heart in one beat).

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5
Q

Alpha 1 Agonist Drugs (-ine endings, like pseudoephedrine and phenylephrine)

A

MOA: vasoconstriction (which increases blood flow, increases blood pressure, and closes bladder sphincters) and decreases heart rate due to a reflex reaction

Uses: used to treat SVT, but they can also be used as decongestants (vasoconstricting the nose).

Side effects: Hypertension (due to the vasoconstricting)

Considerations: Can’t use longer than 3 days due to a rebound constriction effect and be careful in people who already have high blood pressure.

Memory hint: alpha 1 decrease the heart rate which is no fun!

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6
Q

Alpha 1 Antagonist Drugs (alpha blockers; —Zosin endings, like Prazosin or Tamsulosin.)

A

MOA: Lowers blood pressure and releases bladder sphincters/urinary retention.

Uses: Hypertension and blood circulation problems

Side effects: Orthostatic hypotension and tachycardia (reflex reaction), vertigo, sexual dysfunction, nasal congestion, and the first-dose effect (blood pressure drop/fainting)

Considerations: Slow position changes due to orthostatic hypotension risks. First dose effect can cause fainting so we give the first dose at bedtime.

Memory hint: Alpha blockers block the cock and you take blockers at bedtime

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7
Q

Tamsulosin

A

An alpha 1 antagonist (alpha blocker) that has shown effectiveness in treating BPH (Benign prostatic hyperplasia)

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8
Q

Alpha 2 Agonists (Clonidine)

A

MOA: inhibit norepinephrine, acetylcholine, and insulin release to caaalm the system down (decreased heart rate & blood pressure)

Uses: It can be used to lower anxiety, blood pressure, or even ADHD.

Side effects: drowsiness, hypotension, bradycardia, and rebound hypertension if medication is stopped abruptly.

Considerations: Don’t stop the medication abruptly (rebound hypertension) and monitor blood pressure and vital signs.

Memory hint: Clonidine caaalms the crazy sympathetic system down

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9
Q

Beta 1 Agonists (Dobutamine)

A

MOA: increase heart rate, increase lipolysis (breaks down fats to release fatty acids), increase myocardial contractions, and increase renin (helps the RAAS system to get rid of fluid).

Uses: These effects help the heart beat better in things like heart failure.

Side effects: tachycardia, and cardiac dysrhythmias.

Considerations: Don’t take this with MOIs, general anesthetics, or tricyclic antidepressants. Don’t take it with hyperthyroidism or hypertension (because of the increased heart rate). Don’t give to anyone who already has tachydysrhythmia.

Memory hint: Dobutamine causes fast heart things

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10
Q

Beta 2 Agonists (Albuterol)

A

MOA: vasodilation (decreases peripheral resistance and blood flow), smooth muscle relaxation, and bronchodilation. Also causes glycogenolysis and glucagon release (that part of is SNS Stimulation)

Uses: breathing conditions like asthma and COPD

Side effects: tachycardia (reflex reaction), angina (chest pain), tremors.

Considerations: monitor vital signs especially the blood pressure and respiratory rate, and teach the patient to use their inhalers properly.

Memory hint: Albuterol opens up the asthmatic lungs, blood vessels, and smooth muscle (like our tongues!).

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11
Q

Beta Blockers (1&2 Antagonists; -olol endings)

A

MOAs: decrease heart rate, force of contractions, and the rate of AV conductions.

Uses: hypertension, anxiety, tremors, heart conditions

Side effects: GI upset, bradycardia, hypotension, dehydration, lethargy, depression & drowsiness, and possibly bronchoconstriction.

Long term usage/rarer effects: CHF and AV block.

Considerations: slow position changes. Monitor blood pressure and heart rate (hold the medication if they’re below 60 bpm or 100 systolic). Do not stop taking it abruptly. Contraindicated in someone with asthma. Monitor for symptoms of heart failure (edema, cough, chest gurgles) and AV blocks.

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12
Q

Special beta blockers (labetalol and carvedilol)

A

block both beta 1 and 2 receptors, and also block alpha 1 receptors! They’re very effective for hypertensive crises.

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13
Q

Selective beta blockers

A

work primarily on the heart (blocking beta 1), although it can cause these symptoms on the lungs.

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14
Q

Nonselective beta blockers

A

can block both beta 1 and 2 receptors (affecting both heart and lungs)

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15
Q

Timolol

A

a beta blocker that is used to treat glaucomas

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16
Q

Catecholamines (epinephrine, norepi/noradrenaline, and dopamine)

A

drugs that mimic the body’s natural catecholamine neurotransmitters. They’re used to treat hypotension (low blood pressure) and shock

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17
Q

Epinephrine

A

MOA: Stimulates alpha 1, beta 1, and beta 2 receptors = vasoconstriction (increased blood pressure), increased heart rate & cardiac contraction force, increased bronchodilation.

Uses: anaphylaxis or asthma attacks, heart conditions/dysrhythmias

Side effects: hypertension, anxiety, tachycardia and/or palpitations, vomiting

18
Q

Dopamine

A

MOA: Stimulates beta 1 receptors and dopamine receptors. So that = vasoconstriction, increases blood pressure, heart rate, and heart contractility.

Uses: Treats shock related to underperfusion.

Side effects: cardiac dysrhythmias

Considerations: Patients who have been treated with MAOIs will require a VERY reduced dosage.

19
Q

Nicotinic receptor agonists

A

MOA: cause skeletal muscle contraction.

Uses: help withdrawal from nicotine.

Side effects: tremors and muscle spasticity

20
Q

Muscarinic (cholinergic) agonists (bethanechol, tensilon, neostigmine, pilocarpine, pyridostigmine… -gmine endings)

A

MOA: increase GI, genitourinary, and bronchial tone; increase respiratory secretions.

Uses: glaucoma and dry mouth

Side effects: SLUDGE - salivation, lacrimation, urination, diarrhea, GI distress, emesis + bradycardia & dyspnea.

Considerations: Remove contact lenses before administration.

21
Q

Anticholinergics / cholinergic & muscarinic antagonists (atropine, cogentin, dicyclomine, oxybutynin, scopolamine, etc)

A

MOA: Blocks the effect of neurotransmitter acetylcholine; Enhances SNS activity and dries glands out, which will raise the blood pressure

Uses: wide variety of uses, including treating COPD, neurological disorders like Parkinson’s, GI disorders, psychological disorders, and cardiovascular conditions

Side effects: urinary retention, dry mouth, sedation.

Considerations: Watch out for overdose and heatstroke. Be cautious in elderly patients due to the sedation side effect.

22
Q

Symptoms of an overdose of an anticholinergic:

A

“hot as a hare!” - dry/very thirsty, hot, flushed face, confusion & delirium

Antidote: physostigmine or pilocarpine.

23
Q

Antidote for a cholinergic overdose:

A

An anticholinergic like atropine

24
Q

Drugs that will increase blood pressure & heart rate if they’re too low:

A

IDEA -
Isoproterenol, dopamine, epinephrine, atropine.

25
Q

Emergency drugs:

A

LEAN - lidocaine, epinephrine, atropine, narcan

26
Q

RAAS System

A

if there’s not enough salt or water coming into the kidney (and the blood pressure is low), the RAAS system is triggered by the kidney.

  1. kidney produces RENIN.
  2. Renin goes -> liver -> produces angiotensin 1.
  3. Angiotensin 1 -> the heart.
  4. ACE in the heart converts angiotensin 1 -> angiotensin 2.
  5. Angiotensin 2 -> receptors in different places to raise the blood pressure.
  6. Angiotensin 2 triggers ADH release so that the kidneys will reabsorb more fluid.
27
Q

What are all the effects of angiotensin 2?

A
  • it causes vasoconstriction in the cardiac system which raises the blood pressure.
  • It causes salt reabsorption in the adrenals which increases fluid in the kidneys because water follows salt -> raises blood pressure that way.

-And lastly it triggers ADH so that the kidneys reabsorb more fluid -> raises blood pressure

28
Q

ACE inhibitors (-pril ending drugs like enalapril)

A

MOA: prevent ACE From converting angiotensin 1 to angiotensin 2, so it will decreases peripheral vascular resistance without changing the cardiac output, rate, or contractility.

Uses: lower blood pressure.

Side effects: Dizziness, orthostatic hypotension, GI upset, headache, nonproductive cough.

Considerations: slow position changes.

Memory hint: ACE inhibitors ACE the blood pressure changes w/o affecting the heart. They also make the stomach ACE /ACHE

29
Q

Angiotensin 2 receptor blockers (ARBs; -sartan endings like losartan)

A

MOA: Blocks angiotensin 2 so we won’t get the vasoconstriction.

Uses: lower blood pressure.

Side effects: hyperkalemia. Kidney insufficiency, possible angioedema, dry cough.

Considerations: Monitor potassium levels and kidney functions. Slow position changes. Should not be used in pregnancy.

Memory hint: Pregnant women can’t have too many cARBs

30
Q

Direct renin inhibitors (Aliskiren)

A

MOA: Blocks renin (the very first step of the RAAS), so we won’t get vasoconstriction and all the fluid increasing RAAS effects

Uses: lowers blood pressure and retains potassium.

Side effects: dyspepsia (heartburn), headache/dizziness, rash, hypotension, hyperkalemia.

Considerations: Monitor potassium levels and blood pressure.

Memory hint: Renin RETAINS potassium (hyperkal), and really rashes

31
Q

Aldosterone antagonists (Spironolactone and eplerenone)

A

MOA: potassium sparing diuretics. These decrease the effects of aldosterone which promotes potassium retention and make you pee more.

Uses: hypertension, heart failure, and fluid retention

Side effects: hyperkalemia, orthostatic hypotension, hyponatremia. Spironolactone causes GI upset and libido changes as well.

Considerations:
Epleronone has fewer sexual and GI side effects than spironolactone.
Monitor sodium & potassium levels.
Slow position changes.
Monitor I’s & O’s and daily weights.

Memory hint: spironolactone makes my sodium go low

32
Q

Vasodilators (hydralazine, nitroprusside, sildenafil aka viagra)

A

MOA: vasodilation.

Uses: Hypertension, peripheral vascular insufficiency

Side effects: orthostatic hypotension.

Considerations: some of them have strict storage requirements like keeping the vials very clean and out of sunlight. Encourage slow position changes.

33
Q

What effects are seen in stimulation of the sympathetic vs parasympathetic nervous systems?

A

Sympathetic - Dilated pupils, increased heart rate (tachycardia), respiratory rate and blood pressure, hyperglycemia, urinary/bowel retention and decreased digestion

Parasympathetic - Constricted pupils, decreased heart rate, respiratory rate, and blood pressure, relaxed muscles, increased digestion, urinary output (bladder contraction) & bowel movements, and bronchoconstriction strangely enough

34
Q

What are some side effects of adrenergic antagonist (sympatholytic) medications?

A

Bronchoconstriction and bradycardia

35
Q

Which of the following medications is considered a sympathomimetic (drug that stimulates the SNS)?

A

Epinephrine, dopamine, and albuterol

36
Q

Beta 1 receptors are located where?

A

The heart and kidney’s

37
Q

Beta 2 receptors are where?

A

The heart, lungs, smooth muscle (including GI tract), and skeletal muscle

38
Q

A client is admitted with a cardiac condition and the physician prescribes propranolol. Which of the following client statements would require the nurse to hold the ordered dose and notify the physician?

A

I use an inhaler at home for asthma.

Why?: You can’t take a beta blocker (selective or not) if you have asthma due to the risk of bronchospasms

39
Q

The nurse is caring for a client who is scheduled to take a dose of atenolol. Which of the following findings would require the nurse to hold the scheduled dose and notify the physician?

A

Dyspnea in lung fields, crackles (or any abnormal sound in lung fields), and swelling in lower extremities.

Why?: Atenolol is a selective (beta 1) beta blocker. If someone takes it and suddenly has lung issues (swelling in lower extremities could mean Pulmonary embolism!), it is contraindicated for them,

40
Q

The nurse will monitor the client taking albuterol for which of the following conditions?

A

Bronchospasms.

Why?: Albuterol is supposed to treat respiratory conditions (and bronchospasms), so if they are still having them while on albuterol, you would want to notify the physician to adjust the dose / change to a more effective med.