Topic 4 Lecture Video: Pharmacology Notes: ANS, Adrenergic/Cholinergic Drugs, and CNS/Sleep
Autonomic Nervous System (ANS): Key Concepts and Terminology
Objectives (from the course overview):
Understand mechanism of action, indications for use, and major adverse effects of selected drugs affecting the ANS, CNS, and PNS.
Discuss roles of alternative and complementary therapies (CAM) and interactions with drug classifications.
Identify client-related factors that influence drug effects on ANS/CNS/PNS.
Use pharmacology resources and drug guides to guide nursing interventions.
Apply the nursing process to ensure safe care for clients receiving these drugs.
ANS Overview: two main branches
Sympathetic nervous system (SNS)
Often summarized as "fight or flight" responses.
Adrenergic receptors: $\alpha$ and $\beta$ receptors (further divided as $\alpha1$, $\alpha2$, $\beta1$, $\beta2$).
Parasympathetic nervous system (PSNS)
Often summarized as "rest and digest" responses.
Cholinergic receptors: muscarinic, nicotinic, and dopaminergic (focus on muscarinic here).
Synonyms and what they mean (receptor level and pharmacologic action)
Sympathetic side: sympathomimetic = adrenergic agonist (mimics SNS effects).
Blocking SNS: sympatholytic = adrenergic blocker/antagonist (alpha or beta blockers).
Parasympathetic side: parasympathomimetic = cholinergic agonist; cholinergic blockers = anticholinergic, also called muscarinic blockers.
At receptor level for PSNS: cholinergic agonists (muscarinic, nicotinic receptors) vs anticholinergics (muscarinic blockers).
Be able to map terms across systems:
Sympathomimetic / Adrenergic Agonist = stimulate SNS via adrenergic receptors ($\alpha1$, $\alpha2$, $\beta1$, $\beta2$).
Sympatholytic / Adrenergic Antagonist = block SNS receptors.
Parasympathomimetic / Cholinergic Agonist = stimulate PSNS via cholinergic receptors (muscarinic, nicotinic).
Anticholinergic / Cholinergic Blocker = block PSNS effects; mimics SNS effects.
Graphic organization tip (receptor-level):
SNS receptors: $\alpha$ and $\beta$ families; subtypes $\alpha1$, $\alpha2$, $\beta1$, $\beta2$.
PSNS receptors: cholinergic (muscarinic, nicotinic).
Drugs may be direct agonists, indirect acting, or mixed acting with varying selectivity for receptor subtypes.
Receptors and “rest vs. fight” mapping (key takeaways)
Stimulation of SNS (adrenergic) produces fight/flight: pupil dilation, bronchodilation, increased HR, increased BP, etc.
Stimulation of PSNS (cholinergic) produces rest/digest: pupil constriction, bronchoconstriction, decreased HR, increased GI motility, bladder contraction, salivation.
Adrenergic receptor effects by subtype
$\alpha_1$ receptor: vasoconstriction → ↑ BP; mydriasis (pupil dilation); decreased salivation; bladder/prostate contraction.
$\alpha_2$ receptor: inhibits norepinephrine release → vasodilation; ↓ BP; ↓ GI motility.
$\beta_1$ receptor: ↑ cardiac contractility; ↑ heart rate; ↑ renin release → ↑ BP via renal mechanism.
$\beta_2$ receptor: bronchodilation; ↑ skeletal muscle blood flow; uterine relaxation; ↑ liver glycogenolysis → ↑ blood glucose; ↓ GI motility.
Clinical note: beta-2 agonists can cause hyperglycemia in systemic use due to glycogenolysis; diabetics require closer glucose monitoring.
Adrenergic drugs: categories and examples
Direct acting: bind directly to adrenergic receptors (e.g., epinephrine, phenylephrine, albuterol).
Indirect acting: cause release of NE from nerve endings (e.g., cocaine, amphetamines).
Mixed acting: both receptor stimulation and NE release stimulation.
Catecholamines vs non-catecholamines:
Catecholamines are endogenous or synthetic (epi, NE, dopamine) with shorter duration and require careful dosing.
Non-catecholamines have longer duration; examples include phenylephrine, albuterol (beta-agonists among others).
Note: Do not memorize every drug name yet; focus on mechanism and classifications.
Drug cards: outline and content to capture for each medication
Name: generic name (lowercase) and brand/trade name (in parentheses after generic).
Classification: e.g., adrenergic agonist (sympathomimetic).
Action: how the drug works on receptors.
Therapeutic effects/uses: what conditions it treats.
Side effects: common, non-serious effects patients should know.
Adverse effects: more serious/less common effects.
Contraindications: when not to use.
Drug–lab–food interactions: other meds, lab test effects, food interactions.
Nursing implications/interventions: assessment, monitoring, patient education.
Evaluation: did the drug achieve its intended effect?
Chapter 2: Sympathetic Nervous System — Adrenergic Agonists and Receptors
Adrenergic agonists and receptor targets
Direct acting agonists stimulate $\alpha$ and/or $\beta$ receptors directly.
Indirect acting agonists promote release of NE from nerve endings.
Mixed acting agonists have both receptor activation and NE release.
Adrenergic receptor subtypes and actions (summary)
$\alpha_1$ stimulation: ↑ BP via vasoconstriction; pupil dilation; reduced salivation; bladder/prostate effects (contraction of bladder sphincter).
$\alpha_2$ stimulation: inhibits NE release → vasodilation; ↓ BP; ↓ GI motility.
$\beta_1$ stimulation: ↑ HR and contractility; ↑ renin release.
$\beta_2$ stimulation: bronchodilation; ↑ skeletal muscle blood flow; uterine relaxation; increased liver glycogenolysis → ↑ blood glucose; ↓ GI motility.
Example drug groups (not exhaustive):
Direct adrenergic agonists: epinephrine, albuterol, phenylephrine.
Indirect adrenergic agonists: cocaine, amphetamines.
Mixed-acting adrenergic agonists: some agents with both mechanisms.
Chapter 3: Epinephrine (Adrenergic Agonist) — In-Depth Case
Classification and action
Classification: sympathomimetic; adrenergic agonist.
Receptor action: nonselective; stimulates $\alpha1$, $\beta1$, and $\beta_2$ receptors.
Indications: anaphylaxis/shock; status asthmaticus; cardiopulmonary resuscitation (CPR).
Routes: IV (emergency); subcutaneous (e.g., EpiPen).
Mechanism and clinical rationale
Nonselective activation yields:
$\alpha_1$: ↑ BP via vasoconstriction.
$\beta_1$: ↑ HR and contractility.
$\beta_2$: bronchodilation (↑ air flow).
In emergencies, all three actions help restore circulation, airway patency, and perfusion.
Contraindications and cautions
High BP and cardiovascular dysrhythmias: may worsen tachyarrhythmias or ischemia.
Hyperthyroidism, diabetes mellitus, pregnancy: require careful consideration due to metabolic and hemodynamic effects.
Caution: use with other agents that may elevate BP or heart rate.
Side effects and adverse effects
Common side effects: tachycardia, palpitations, restlessness, hypertension, hypoglycemia (beta-2 mediated glycogenolysis).
Serious adverse effects: ventricular fibrillation, pulmonary edema.
Drug interactions (illustrative; not exhaustive for exam)
Beta blockers may blunt epi effects (beta receptor blockade can limit therapeutic action).
Digoxin and certain antidepressants can interact and alter cardiac conduction or response.
Nursing assessment and interventions
Assess baseline: vital signs (HR, BP, RR), ECG if available, glucose level, urine output, health history (diabetes, thyroid status).
Monitor: IV site integrity, blood pressure, heart rate, rhythm (EKG), urine output.
Watch for bladder distension ( SNS activation relaxes the bladder; epi may prolong urinary retention).
Nausea prevention and hydration management; monitor glucose in diabetics.
Patient teaching: read labels for OTC decongestants that may contain epi-like components; potential rebound nasal congestion with nasal sprays.
EpiPen use: leg injection for severe anaphylaxis; ensure patients know to report side effects like palpitations, rash, flushing, chest pain, irregular heartbeat, numbness, etc.
Post-use evaluation
Determine if heart rate, BP, and airway status improved; assess perfusion and oxygenation.
Adrenergic Antagonists (Adrenergic Blockers)
Concept
Block adrenergic receptor sites (alpha or beta).
Oppose sympathetic effects; promote rest/digest or reduce sympathetic tone.
Alpha-adrenergic antagonists (alpha blockers)
Promote vasodilation → ↓ BP; may cause dizziness and orthostatic hypotension.
Reflex tachycardia as BP falls.
Effects on pupil (miosis) and smooth muscle (e.g., bladder neck and prostate).
Beta-adrenergic antagonists (beta blockers)
Beta-1 blockers: ↓ cardiac contractility and HR;↓ renin release (RAAS impact); useful in hypertension, angina, post-MI prophylaxis.
Beta-2 blockers: cause bronchoconstriction and restrict uterine relaxation; not ideal in asthma/COPD; may precipitate hypoglycemia by inhibiting glycogenolysis in diabetics.
Chapter 4: Specific Drugs in SNS Modulation
Albuterol (beta-2 adrenergic agonist)
Use: asthma, acute bronchospasm, and prevention with regular use.
Mechanism: stimulates beta-2 receptors in lungs → bronchial smooth muscle relaxation → bronchodilation.
Beta blockers (beta-1 selective and nonselective)
Atenolol: beta-1 selective adrenergic blocker; indications include hypertension, angina, MI prevention.
Nonselective beta blockers can block beta-1 and beta-2 receptors; contraindicated in asthma/COPD due to risk of bronchoconstriction.
Common suffix cues
Beta blockers often end in -lol (e.g., atenolol).
Quick practice question (illustrative): Epinephrine in cardiac arrest — primary action is to increase blood flow/pressure and heart rate via SNS receptor stimulation.
Chapter 5: Cholinergic Agents, Anticholinergic Agents, and Atropine Toxidrome
Cholinergic agonists (parasympathomimetics)
Stimulate PSNS via cholinergic receptors (muscarinic, nicotinic).
Direct acting: activate receptors directly.
Indirect acting: inhibit acetylcholinesterase or otherwise enhance acetylcholine availability.
Effects of cholinergic agonists (rest/digest)
Pupils: constriction (miosis).
Lungs: bronchoconstriction; increased secretions.
Heart: bradycardia.
Blood vessels: vasodilation; decreased BP.
GI: increased peristalsis and secretions.
Bladder: contraction; sphincter relaxation → urination.
Salivary glands: increased salivation.
Example: Bethanechol (Urecholine) — a direct-acting cholinergic agonist
Uses: urinary retention; neurogenic bladder.
Mechanism: cholinergic stimulation → bladder contraction; sphincter relaxation.
Contraindications: intestinal/urinary tract obstruction; irritable bowel syndrome; peptic ulcers; severe bradycardia or hypotension; COPD/asthma (bronchoconstriction risk); Parkinson’s; hyperthyroidism; seizures; active asthma.
Side effects: blurred vision, GI effects, urinary frequency/urgency, bronchoconstriction.
Adverse effects: overall weakness; bronchospasm; life-threatening bronchoconstriction.
Assessment: baseline vitals, health history (asthma, obstruction, peptic ulcers), urinary output, GI function.
Nursing interventions: monitor BP/HR, rise slowly (orthostatic hypotension), auscultate breath sounds, record intake/output, monitor for cholinergic crisis.
Anticholinergic agents and toxidrome
Anticholinergic effects mimic sympathetic activation: ↑ HR, bronchodilation, decreased GI motility, urinary retention, pupil dilation, dry mouth.
Anticholinergic toxidrome (MAD AS A HATTER):
Mad as a hatter: altered mental status.
Blind as a bat: mydriasis (pupil dilation).
Red as a beet: flushed skin.
Hot as a hare: dry skin.
Dry as a bone: dry mucous membranes.
Atropine sulfate (an anticholinergic)
Uses: preoperative to reduce salivation; treat bradycardia; pupil dilation for exam.
Contraindications: glaucoma; obstructive GI disorders; tachycardia; BPH; myasthenia gravis; MI; caution in renal/hepatic disease.
Side effects: anticholinergic effects (dry mouth, blurred vision, constipation, urinary retention, photophobia).
Adverse effects: tachycardia, hypertension or hypotension (varies), angina, pulmonary edema, seizures, Stevens-Johnson syndrome (rare but serious).
Assessment and nursing priorities: monitor urinary output due to retention risk; baseline vitals; review drug history; orthostatic precautions.
Test preparation tip: urinary retention is a high-priority nursing assessment in atropine administration.
Atropine-related nursing questions (sample NCLEX-style prompts)
Priority assessment after atropine: urinary retention risk is high; monitor for tachycardia, blood pressure, and respiratory status.
Anticholinergic drug interactions and substitutes: CAMs like kava kava, valerian, chamomile can increase sedation with benzodiazepines; use caution with polypharmacy.
Chapter 6: Central Nervous System (CNS) Pharmacology — Stimulants and Sedatives
CNS stimulants overview
Indications: ADHD, narcolepsy, reversal of respiratory distress.
Categories: amphetamines, caffeine; analeptics; anorexiants.
Abuse potential: high risk of psychological dependence and tolerance; short-term use preferred (often up to ~12 weeks).
Withdrawal: may cause depressive symptoms.
ADHD and narcolepsy (brief overview)
ADHD: dysregulation of serotonin, norepinephrine, and dopamine; typically presents before age 7; more common in boys; features include inattention, hyperactivity, impulsivity; often associated with learning disabilities and sometimes abnormal EEG findings.
Narcolepsy: recurrent daytime drowsiness; sleep paralysis; episodes can occur during tasks or awakening; may involve muscle paralysis during sleep-wake transitions.
Sleep and insomnia management
Stages of sleep: REM and non-REM; insomnia is difficulty sleeping.
Nonpharmacologic strategies first: maintain regular sleep schedules, avoid caffeine/alcohol/nicotine near bedtime, limit daytime naps, avoid heavy meals and fluids late, minimize screen time before bed, create a quiet, dark environment, warm drink or light activity to promote sleep.
Pharmacologic options (sedative-hypnotics):
Benzodiazepines (ending in -azepam/-zolam, etc.).
Non-benzodiazepine hypnotics (e.g., zolpidem).
General side effects of sedative-hypnotics: residual daytime drowsiness, vivid dreams/nightmares, dependence/tolerance, potential depression, respiratory depression, hypersensitivity.
Benzodiazepines (e.g., Alprazolam)
Indications: anxiety, panic disorders; insomnia (short-term).
Mechanism: GABA-A receptor modulation increases CNS inhibition.
Side effects: drowsiness, dizziness, amnesia, GI effects; potential depressive mood; risk of Stevens-Johnson syndrome (rare).
Contraindications/cautions: respiratory depression; active alcohol intoxication; psychotic disorders; pregnancy; elderly/debilitated patients; history of alcohol or sedative misuse.
Antidote for overdose: Flumazenil.
CAM interactions: avoid kava kava, valerian, chamomile due to additive sedation.
Nursing implications: assess sleep history, monitor vitals and mental status; be cautious with elderly; screen for suicidality; avoid driving until effects are known; drug reconciliation to avoid additive CNS depression.
Zolpidem (non-benzodiazepine hypnotic, Ambien)
Use: short-term insomnia (< 10 days recommended).
Onset/duration: onset ~30 minutes; duration ~6–8 hours.
Side effects: residual sedation, memory impairment, nightmares; sleep-related behaviors including sleep-driving and binge eating due to amnesia.
Adverse effects: tolerance, dependence, withdrawal; angioedema; suicidal ideation; pulmonary edema and renal issues in rare cases.
Special populations: caution in elderly, renal/hepatic impairment, pregnancy, depression, suicidal ideation, children; avoid in nursing mothers.
Counseling points: take right before bed; avoid alcohol and other CNS depressants; discourage daytime activities that require alertness; monitor for complex sleep behaviors.
Special considerations for older adults (insomnia/sedatives)
Prefer short-to-intermediate acting agents.
Avoid long-acting agents to reduce daytime sedation and falls risk.
Use nonpharmacologic methods first; limit use to four days/week or less when possible.
Chapter 7: Anesthetics — General and Local
General vs Local anesthesia
General: depresses CNS broadly; provides analgesia, amnesia, and loss of consciousness.
Local: blocks pain at the site of administration; consciousness is preserved; routes include topical, local infiltration, nerve blocks, regional blocks, spinal/epidural, inhalation, or IV.
Practical considerations during anesthesia
Obtain accurate drug history and reconciliation to identify cardiopulmonary interactions.
Monitor post-procedure sensorium (alertness and orientation).
Monitor urinary output (hourly or per eight hours).
Monitor vital signs for hypotension and respiratory depression.
Administer analgesics with caution to avoid excessive CNS depression until fully recovered from anesthesia.
CAMs and Interactions Across Classifications
Each section (SNS, PSNS, CNS stimulants, sedative-hypnotics) includes CAM interactions to avoid.
Examples mentioned: kava kava, valerian, chamomile (increased sedation when combined with benzodiazepines).
Patient education: always check labels for decongestants with adrenergic activity; consider sleep hygiene strategies before resorting to sedatives.
Practice Questions (Sample NCLEX-style prompts)
Prompt 1: After giving a sedative-hypnotic, which sign indicates more patient teaching is needed?
Answer: Taking a caffeinated beverage or other stimulant (e.g., option D in the scenario) would indicate missing education about sedation interactions.
Prompt 2: An older adult with insomnia asks for advice. The most appropriate initial recommendation?
Answer: Nonpharmacologic strategies (e.g., warm milk or chamomile tea) before resorting to sedatives; avoid daily dosing of sedatives in older adults.
Quick Reference: Key Drug Group Highlights
Epinephrine (nonselective adrenergic agonist)
Receptors: $\alpha1$, $\beta1$, $\beta_2$; indications include anaphylaxis, status asthmaticus, CPR.
Contraindications: certain arrhythmias, hyperthyroidism, diabetes, pregnancy; caution in HTN.
Monitoring: vitals, glucose (diabetes), ECG; IV site; urine output.
Bethanechol (Cholinergic agonist)
Indication: urinary retention; neurogenic bladder.
Mechanism: stimulates PSNS → bladder contraction; sphincter relaxation.
Cautions: GI/urinary obstruction; peptic ulcers; bradycardia; asthma/COPD; pregnancy.
Atropine (Anticholinergic)
Indication: preop to reduce secretions; bradycardia; mydriasis.
Anticholinergic toxidrome awareness (MAD AS A HATTER).
Albuterol (beta-2 agonist)
Indication: asthma; acute bronchospasm; prevention.
Atenolol (beta-1 selective blocker)
Indication: hypertension, angina, post-MI protection.
Caution: avoid in asthma/COPD due to possible bronchospasm from beta-2 blockade if nonselective.
Alprazolam (benzodiazepine)
Indication: anxiety, panic; insomnia (short term).
Antidote: Flumazenil.
CAMs: avoid kava kava, valerian, chamomile due to sedation interactions.
Zolpidem (non-benzodiazepine hypnotic)
Indication: short-term management of insomnia; onset ~30 min; duration ~6–8 h.
Risks: sleep-related behaviors (sleep driving, binge eating), dependency, withdrawal; monitor for respiratory depression.
Sleep and Behavioral Health: Quick Takeaways
Insomnia management prioritizes nonpharmacologic approaches first.
When meds are used, prefer short acting agents in older adults to reduce fall risk and cognitive impairment.
Assess mental health history (depression, suicidality) before prescribing CNS depressants.
Ensure safe driving and activity plans during sedative use; assess for interactions with alcohol and other CNS depressants.
Closing: Connections to Foundational Principles
Mechanisms of action (receptor targeting) explain why specific adverse effects occur and guide safety monitoring (e.g., beta-2 effects on glucose, bronchoconstriction with beta-blockers in asthma).
The nursing process (assessment, diagnosis, planning, implementation, evaluation) remains central to safe pharmacotherapy across all ANS-related drugs.
CAM interactions highlight the need for holistic patient education and comprehensive medication reconciliation to avoid additive sedation, cardiovascular effects, or CNS depression.
Ethical and practical implications:
In emergencies (e.g., epinephrine for anaphylaxis/CPR), rapid action justifies broad receptor stimulation despite potential adverse effects.
In chronic conditions (HTN, asthma, insomnia), selectivity and duration of action minimize systemic adverse effects and improve adherence.
Foundational math/quantitative notes
Receptor subtypes and their physiological responses can be summarized as mappings, not equations. When using mathematical notation, apply $\alpha1$, $\alpha2$, $\beta1$, $\beta2$ to differentiate subtypes and keep pharmacology terminology precise within a mathematical-like framework where appropriate. For example, the effect of stimulating $\beta2$ on bronchodilation can be denoted as: Bronchodilation \text{via } \beta2 \text{ receptor activation}.