Pharmacology week 3 Autonomic Nervous System - Sympathetic

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• Topic: Autonomic Nervous System (ANS) — Sympathetic Division

• Speaker reference: HEAT, STROMS, DNP, WHNP, RN (contextual cues for exam focus)

• Key idea: Introduction to the SNS within the broader ANS framework, setting the stage for receptors, neurotransmitters, and drug interactions.

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Lecture Objectives

• What are the two divisions of the autonomic nervous system and their activities?

• What is the sympathetic nervous system (SNS)? Key neurotransmitters, their locations, and functions.

• What are the mechanisms of action, therapeutic effects, indications, adverse effects, contraindications, drug interactions, and antidotes for adrenergic agonists and antagonists?

  • Discuss mechanisms of action, therapeutic effects, indications, adverse and toxic effects, cautions, contraindications, drug interactions, and any antidotal management for:

  • alpha antagonists (blockers)

  • beta blockers (selective for β1 and non-selective)

• Describe glaucoma and pharmacological agents that treat or worsen it.

• Describe benign prostatic hyperplasia (BPH) and pharmacological agents that treat or worsen it.

• Describe causes and mechanisms of orthostatic hypotension and reflex tachycardia.

• How does organophosphate poisoning present and what drugs are used for treatment?

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Readings

• Book Chapters:

  • Chapter 18: Adrenergic Drugs

  • Chapter 19: Adrenergic Blocking Drugs

• Scholarly Article: “Treating organophosphates poisoning: management challenges and potential solutions”

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Drugs to Know

• Adrenergic Agonists:

  • Epinephrine

  • Phenylephrine

• Adrenergic Antagonists:

  • Beta Blockers (suffix “-lol”): selective β1 blockers (cardio-selective) e.g., metoprolol; non-selective blockers e.g., carvedilol, labetalol, timolol, propranolol

  • Alpha Blockers (suffix “-sin”): e.g., tamsulosin

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Table Preview: ANS Sympathetic vs Parasympathetic

• Catch Phrases

  • Sympathetic: “Fight or Flight”, “Stressed”

  • Parasympathetic: “Rest and Digest”, “Peace”

• Synonyms (Neurotransmitters / Locks): Adrenergic (SNS) vs Cholinergic (PNS)

• Neurotransmitters (Keys) / Receptors (Locks)

• Target areas (example mappings): Eyes (pupils), Mouth (saliva), Heart (heart rate), Lungs (bronchioles), Arteries (blood pressure), GI tract (motility and secretions), Bladder (sphincter)

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Autonomic Nervous System (ANS) — Two Divisions

• Catch Phrases:

  • Sympathetic = "Fight or Flight", “Stressed”

  • Parasympathetic = "Rest and Digest", “Peace”

• Autonomic Division Control:

  • Generally: Opponent systems (two divisions oppose each other)

  • Rare: Complementary (work in synergy)

  • Rare: Sometimes only one division controls an organ

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Sympathetic “E” — Fight-or-Flight System

• Letter mnemonic: S for Stress; involves E activities – exercise, excitement, emergency, embarrassment

• Purpose: Promote adjustments during exercise; redirect blood flow: reduce flow to some organs, increase to muscles

• Physiologic signs when threatened:

  • Heart rate up; breathing rapid/deep

  • Skin cold and sweaty; pupils dilate

  • Mydriasis: “Wide-eyed with fright”

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Parasympathetic “D” — Rest and Digest System

• Letter mnemonic: D for Digestion, Defecation, Diuresis

• Goal: Keep energy use low; promote maintenance functions

• Activity indicators (relaxed after a meal):

  • Blood pressure, heart rate, and respiratory rate are low

  • GI tract activity high

  • Skin warm; pupils constricted (Miosis)

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Endogenous Neurotransmitters — “KEYS”

• Parasympathetic/Cholinergic Division:

  • Acetylcholine (ACh) → Cholinergic division

• Sympathetic/Adrenergic Division:

  • Adrenaline (epinephrine in the U.S.)

  • Norepinephrine (NE)

  • Dopamine (DA)

• Note: Classic lock-and-key model in receptor pharmacology

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Autonomic Receptors

• Parasympathetic (Cholinergic):

  • Muscarinic (M)

  • Nicotinic (N)

• Sympathetic (Adrenergic):

  • Alpha receptors: α1, α2

  • Beta receptors: β1, β2

  • Dopamine receptors: D1 (rare in sympathetic context)

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Parasympathetic/Cholinergic Receptor Locations

• Nicotinic Receptors (N):

  • Found at the Neuromuscular Junction (NMJ)

  • Found on effectors all throughout the body; stimulation can either stimulate or inhibit response

• Muscarinic Receptors (M):

  • Found at effectors throughout the body

  • Mediate various cholinergic responses

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Sympathetic/Adrenergic Receptor Locations — Alpha Receptors (α)

• α1 receptors:

  • Eyes (pupillary dilation via radial muscle)

  • Arteries (vascular smooth muscle) – vasoconstriction

  • Nose (mucous membranes) – vasoconstriction

  • Prostate and bladder (bladder base/prostate) – note: complex functional roles

• α2 receptors:

  • Brain (pre-synaptic receptor) – regulatory/feedback roles

  • Eyes (less emphasis in general summaries)

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Sympathetic/Adrenergic Receptor Locations — Beta Receptors (β)

• β1 receptors:

  • Heart

  • Kidney (juxtaglomerular cells)

  • Eye

• β2 receptors:

  • Lungs (bronchioles)

  • Skeletal Muscle

  • Uterine Smooth Muscle

  • Liver

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Additional Receptor Note

• Dopamine receptors (D1):

  • Vascular beds to kidneys (renal vasodilation context)

• Summary: Receptors are located in multiple tissues; focus on the common and exam-tested sites listed above

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Table 14.5 — Effects on Various Organs (Parasympathetic vs Sympathetic)

• Eye (iris):

  • Parasympathetic: constricts pupil (miosis)

  • Sympathetic: dilates pupil (mydriasis)

• Eye (ciliary muscle):

  • Parasympathetic: near vision (bulging lens)

  • Sympathetic: minimal direct effect

• Glands (nasal, lacrimal, gastric, pancreas):

  • Parasympathetic: stimulates secretory activity (watery saliva more typical) and mucous secretions

  • Sympathetic: inhibits secretory activity; vasoconstricts glandular vessels

• Salivary glands:

  • Parasympathetic: stimulates watery saliva

  • Sympathetic: stimulates thick, viscous saliva

• Sweat glands:

  • Sympathetic (cholinergic fibers): stimulates copious sweating

  • Parasympathetic: no significant innervation here

• Adrenal medulla:

  • Sympathetic: stimulates medulla cells to secrete epinephrine and norepinephrine

• Arrector pili muscles (hair):

  • Sympathetic: stimulates contraction (goosebumps)

• Heart muscle:

  • Parasympathetic: decreases rate (cardioinhibitory)

  • Sympathetic: increases rate and force (positive chronotropic and inotropic effects)

• Coronary vessels:

  • Parasympathetic: weak coronary vasodilation

  • Sympathetic: coronary vasodilation in some contexts (epinephrine effects vs baseline tone)

• Digestive tract organs:

  • Parasympathetic: increases motility and secretions; relaxes sphincters

  • Sympathetic: decreases activity; constricts sphincters; diverts blood away from GI tract

• Liver:

  • Parasympathetic: stimulates digestion-related secretion

  • Sympathetic: stimulates glucose release (glycogenolysis and gluconeogenesis via epinephrine)

• Gallbladder:

  • Parasympathetic: contracts to expel bile

  • Sympathetic: relaxes (inhibits contraction)

• Kidneys:

  • Sympathetic: vasoconstriction and renin release (increases BP)

• Reproductive organs:

  • Penis: parasympathetic activity promotes erection; sympathetic activity promotes ejaculation

  • Vagina/clitoris: parasympathetic promotes erection; sympathetic contributes to orgasm (context-dependent phrasing)

• Blood vessels:

  • Parasympathetic: generally no direct innervation in most vessels

  • Sympathetic: vasoconstriction is common; skeletal muscle vasodilation can occur with epinephrine in exercise contexts

• Cellular metabolism, adipose tissue:

  • Sympathetic: increases metabolic rate; stimulates lipolysis

• Note: “Effects are mediated by epinephrine release from adrenal medulla” in some cases

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Continued Table — Metabolic and Reproductive Effects

• Digestive tract, liver, gallbladder, kidneys, penis, vagina, blood vessels, coagulation, cellular metabolism, adipose tissue (continued)

• Highlights:

  • Sympathetic activation generally reduces GI activity, increases glucose availability, and redirects blood to muscles and brain

  • Parasympathetic activation promotes digestion, storage, and restorative processes

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Cranial and Spinal Cord Pathways (Overview)

• Cranial Sympathetic vs Parasympathetic divisions (schematic references)

• Eye: sympathetic dilates pupil; parasympathetic constricts pupil

• Eye components:

  • Sympathetic: dilator pupillae → mydriasis

  • Parasympathetic: constrictor pupillae → miosis; increased secretions to some eye structures

• Salivation and tears:

  • Parasympathetic promotes watery saliva and lacrimation; sympathetic contributes to minor effects via indirect pathways

• Lungs, Airway tone:

  • Sympathetic: bronchodilation; Parasympathetic: bronchoconstriction

• Heart and Liver:

  • Sympathetic: increases HR and glucose production/release via catecholamines

  • Parasympathetic: slows HR; supports digestion and storage

• Adrenal medulla: sympathetic stimulation leads to epinephrine and norepinephrine release

• Bladder:

  • Sympathetic: relaxes bladder smooth muscle, constricts urethral sphincter → urine retention

  • Parasympathetic: contracts bladder wall, relaxes sphincter → urination

• Reproductive organs:

  • Sympathetic: promotes ejaculation and orgasm pathways; parasympathetic promotes arousal

• Nerves and ganglia layout nuance:

  • Pre- and postganglionic neuron arrangements in various spinal levels (cervical, thoracic, lumbar, sacral)

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Reiteration: Sympathetic “E” Fight-or-Flight (Revisit)

• Re-emphasizes: S for Stress; E activities – exercise, excitement, emergency, embarrassment

• Physiological adjustments during exercise: reduced organ blood flow, increased muscle blood flow

• Threat scenario signs: tachycardia, rapid/deep breathing, cold sweaty skin, mydriasis

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Adrenergic Drugs — Agonists (Overview)

• Synonymous terms: Adrenergic / Sympathomimetic

• Action: Mimic norepinephrine (NE) or epinephrine at target sites

• Pharmacologic class: Generally agonists at α or β receptors

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Pharmacodynamics — Post-Synaptic Receptor Model (Schematic)

• Post-synaptic receptor interactions (NE as endogenous ligand)

• Receptor targets:

  • α1/α2

  • β1/β2

• Presynaptic nerve terminal interactions (autoreceptors): regulatory feedback

• Key terms: ionotropic vs metabotropic signaling

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Vasopressors — Epinephrine (Drug Prototype)

• Uses (routes and indications):

  • Intravenous: Advanced Cardiac Life Support (ACLS); shock, hypotension, bradycardia, or asystole (IV drip in some protocols)

  • Subcutaneous: added to local anesthetics (e.g., lidocaine with epinephrine)

  • Intramuscular: anaphylaxis (epinephrine auto-injector, EpiPen®)

  • Inhaled: asthma (not routine use)

• Context: Epinephrine is a non-selective adrenergic agonist

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Epinephrine — Mechanism and Physiologic Effects

• Mechanism: binds non-selectively to α and β receptors

  • β1 activation → heart: +chronotropic and +inotropic effects (increased HR and contractility)

  • β2 activation → lungs: bronchodilation

  • α1 activation → vascular smooth muscle: vasoconstriction (increased BP)

  • α2 activation → brain: no significant clinical effect in common practice (often ignored)

• Terminology:

  • Ionotropic: contractility strength

  • Chronotropic: heart rate timing/rate

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Epinephrine — Adverse Effects (Vascular/Cardiac Risks)

• Cardiac system effects lead to:

  • Tachycardia (chronotropic effect)

  • Cardiac dysrhythmias, ischemia/MI risk

• Vasculature effects:

  • Hypertension; potential for MI or stroke; extremities risk due to vasoconstriction

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Epinephrine — Nursing Considerations

• Monitoring focus (any route): vital signs, cardiac rhythm, perfusion, and IV site integrity

• Goals vs unintended outcomes: maximize therapeutic benefits while minimizing adverse effects (e.g., extravasation risk)

• Extravasation risk management: Phentolamine as antidote

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Epinephrine — ACLS Code Scenario (Example)

• Scenario: Cardiac arrest with ACLS protocol; 1 mg IV push epinephrine during CPR

• Question to consider: What is the goal of epinephrine in this context? (Increase coronary/perfusion pressure during CPR)

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Epinephrine — Mnemonics and Real-World Reminders

• Memo: Auto-injector usage steps (Memeplexus style mnemonic in slide)

• Practical steps for Epinephrine auto-injector use in anaphylaxis and emergency settings

• Contacts for emergency care included on slide (organizational detail)

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Drug Class: Vasopressors — Epinephrine (Prototype) and Alternatives

• Other drugs in the category: Norepinephrine (Levophed®), Dopamine, Phenylephrine (Neosynephrine®)

• Therapeutic uses: Subcutaneous for local anesthetic adjuncts; Intramuscular for anaphylaxis; IV for shock/ACLS; Inhaled use limited

• Pharmacology (MOA): as above; adverse effects: tissue extravasation risk; tachycardia; hypertension; potential limb ischemia

• Nursing implications: monitor IV site; continuous vital signs; antidote readiness (Phentolamine)

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Vasopressors — Phenylephrine (Prototype)

• Uses:

  • IV systemic: shock/hypotension

  • Nasal spray: congestion (brief mention; not main focus)

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Phenylephrine — Mechanism

• Mechanism: Selective α1 activation → vascular smooth muscle vasoconstriction

• Result: Increased blood pressure

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Phenylephrine — Adverse Effects

• Systemic vasoconstriction-related hypertension (risk of MI, stroke)

• Nasal spray: rebound congestion with >3 days use (limits on duration)

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Phenylephrine — Nursing Considerations

• Monitoring focus: MAP and SBP/DBP; watch for excessive hypertension

• Infiltration risk and extravasation management: Phentolamine antidote

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Phenylephrine — Clinical Application Example

• ICU scenario: IV infusion at 0.5 mcg/kg/min, titrate by 0.5 mcg/kg/min every 15 min; goal MAP 65–75 mmHg (or SBP 90–140)

• Monitoring: hourly (or per protocol) assessment of MAP/SBP; adjust rate accordingly

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Vasopressors (Phenylephrine) — Summary

• Drug class: Vasopressor

• Prototypical drug: Phenylephrine (Neo-synephrine®)

• Therapeutic uses: IV titration for shock/hypotension; nasal decongestant use

• MOA: Alpha-1 activation → vasoconstriction → increased BP

• Adverse effects: vesicant risk during IV use; tachycardia; hypertension; extremity hypoperfusion

• Nursing considerations: monitor vital signs and IV site; antidote for extravasation: Phentolamine

• Contraindications: none when life-saving but be mindful of tachycardia, hypertension

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Anti-Adrenergic / Adrenergic Blocking Agents — Drugs to Know

• Beta Blockers (the “lols”)

  • Selective Beta1 blockers: metoprolol

  • Non-Selective Beta Blockers: propranolol, carvedilol, labetalol

• Alpha Blockers (the “sins”):

  • Tamsulosin, prazosin

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Selective β1 Antagonists (Beta-1 Blockers) — Metoprolol

• Therapeutic uses (cardiac):

  • Heart dysrhythmias, prior MI, hypertension, angina, heart failure (compensated)

  • Hyperthyroidism symptoms (thyroid storm/thyrotoxicosis)

• Other uses: migraine prophylaxis; eye drops used for glaucoma

• Mechanism: Block β1 receptors in the heart (and in the kidney to a lesser degree)

• Effects on blood pressure: due to reduced HR (chronotropic) and reduced contractility (inotropic)

• Clinical notes: avoid abrupt stopping; monitor HR and BP; caution in diabetics due to masking of hypoglycemia symptoms; eye drops for glaucoma noted

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Metoprolol — Pharmacology and Safety Notes

• MOA: Antagonist/blocker at β1 receptors (primarily heart; some β1 effects in the eye)

• Adverse effects: bradycardia, hypotension, potential heart failure exacerbation, dizziness

• Important nursing: assess HR and BP before administration; do not give if HR < 60 bpm or BP < 90/60 mmHg

• Special concepts: –chronotropic and –inotropic effects; Boxed FDA warning: abrupt cessation increases MI risk

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Orthostatic/Postural Hypertension (Key Concept)

• Definition: fall in BP with move from supine/seated to standing

• Cause: relaxation of venous smooth muscle

• Signs/symptoms: dizziness, lightheadedness, syncope; high fall risk especially in elderly

• Management: change positions slowly; support during transitions; remain seated if uncertain of tolerance

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Metoprolol — Adverse Effects (Continued)

• Cardiac: bradycardia, hypotension, heart failure exacerbation

• Non-cardiac: sexual dysfunction, mood changes (depression), insomnia, reduced libido

• Diabetes: masking of hypoglycemic symptoms; caution in diabetics; remember epinephrine response

• Additional: do not stop suddenly

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Additional Metoprolol Safety Details

• CNS effects: crossing the blood-brain barrier may affect mood, sleep; sexual side effects

• Important nursing assessment: monitor BP, HR; check for signs of heart failure; assess weight gain as a fluid-retention signal

• Boxed warning: sudden withdrawal risks

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Drug Class: Selective Beta-1 Blockers — Prototypes and Goals

• Prototypes: Metoprolol (and other β1-selective agents with suffix “-olol”) including Atenolol, Bisoprolol, etc.

• Non-cardiac uses: anxiety mitigation, glaucoma (eye drops) for reducing IOP indirectly via β-receptor effects in eye

• Safety and monitoring: baseline BP/HR, avoid abrupt discontinuation, educate about orthostatic risk, diabetic considerations

• Cardiac and non-cardiac indications, with eye-drop usage for glaucoma noted

• MOA recap: selective blockade of β1 receptors; cardiac-specific actions; some systemic effects may occur

• Adverse effects and nursing considerations highlighted above

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Non-Selective Beta Blockers — Carvedilol, Propranolol, Labetalol, Timolol

• Indications:

  • Heart disease: MI history, hypertension, angina, dysrhythmias, heart failure, hyperthyroidism symptoms

  • Anxiety; Timolol (ocular) for glaucoma

• Prototypes and notes:

  • Timolol is used in glaucoma eye drops

  • Carvedilol commonly used in cardiac conditions

  • Propranolol widely used by professionals; Labetalol often used in labor and delivery for hypertension in pregnancy

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Non-Selective Beta Blockers — Mechanism of Action

• MOA: Block β1 receptors in the heart; may also block β2 receptors in lungs, skeletal muscle, liver

• Some agents may block α1 receptors to cause vasodilation (e.g., carvedilol, labetalol)

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Timolol — Glaucoma Context

• Timolol is an eye drop that treats glaucoma by reducing aqueous humor production (IOP)

• Glaucoma types: open-angle and narrow-angle

• Key concept: Glaucoma management is long-term; pupil dilation worsens IOP (mydriasis); pupil constriction lowers IOP (miosis)

• Mnemonic tie-in: SNS activation (fight/flight) leads to mydriasis; PNS reduces IOP in the context of eye meds

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Non-Selective Beta Blockers — Adverse Effects (Continued)

• Cardiac: bradycardia, hypotension, potential heart failure escalation; dizziness

• Non-cardiac: sexual dysfunction, mood changes

• Beta-2 effects: bronchoconstriction risk for asthma/COPD; inhibits hepatic glycogenolysis, affecting glucose balance

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Non-Selective Beta Blockers — Contraindications

• Important caution: avoid in asthma/COPD due to β2-mediated bronchospasm risk

• Never stop suddenly (FDA boxed warning) due to MI risk

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Non-Selective Beta Blockers — Summary (Prototypes & Indications)

• Prototypes: carvedilol, propranolol, labetalol, timolol; suffix “-lol”

• Therapeutic uses:

  • Cardiac: dysrhythmias, MI, compensated heart failure, hypertension, hyperthyroidism symptoms

  • Non-cardiac: anxiety; Timolol for glaucoma (eye drops)

• Safety and monitoring: BP, HR; gradual taper; caution in diabetics; weight monitoring in heart failure; education about orthostatic risk; FDA boxed warning

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Alpha-1 Antagonists (Blockers) — Tamsulosin and Prazosin

• Therapeutic uses:

  • Tamsulosin: Benign Prostatic Hyperplasia (BPH); bladder outlet obstruction/kidney stones

  • Prazosin: hypertension

• Extra materials (not test-focused):

  • Prazosin for alcohol withdrawal symptoms, PTSD-related nightmares (informational only)

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Alpha-1 Antagonists — Mechanism of Action

• Mechanism: prevent activation of α1 receptors (antagonist)

• Receptor distribution varies:

  • Peripheral vascular smooth muscle (arteries)

  • Bladder/urethra/prostate

• Some α1 blockers are selective for certain tissues; others are non-selective

• Conceptual effect: reduce sympathetic “fight or flight” tone → lower BP and improved urination (bladder outlet relaxation)

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Hypertension Medication Key Concept #2 — Reflex Tachycardia

• Reflex tachycardia definition: commonly seen with vasodilators that do not act directly on the heart

• Consequences: tachycardia can burden the heart; may negate BP-lowering effects

• Management: pretreatment with a beta blocker (e.g., propranolol) can blunt reflex tachycardia

• BP relationship reminder: BP = (HR × Blood Volume) × Artery Resistance (as a teaching formula)

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Alpha-1 Antagonists — Adverse Effects (First Dose Phenomenon)

• Common: first-dose orthostatic/postural hypotension (often occurs with initial dose)

• Counseling: may lead to falls; consider bedtime dosing to reduce risk

• Rare: reflex tachycardia following sudden BP drop

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Alpha-1 Antagonists — Additional Adverse Effects

• Sexual dysfunction (common with antihypertensives)

• Rebound hypertension if stopped abruptly

• Compare to beta-blocker caution (avoid abrupt withdrawal)

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Administration Considerations for Alpha-1 Blockers

• Often given at bedtime to reduce orthostatic risk

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Nursing Process for Alpha-1 Blockers

• Assessment: measure BP before dosing; hold if < 90/60

• Planning/Implementation: start low, titrate slowly; educate on First Dose Phenomenon; avoid abrupt cessation

• Evaluation: monitor BP for 2–6 hours post-initiation; monitor urine output and urinary retention symptoms; assess orthostatic changes

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Alpha-1 Blockers — Drug Prototype Summary

• Drug class: Alpha-1 blockers

• Prototypes: tamsulosin, prazosin, terazosin, silodosin, doxazosin

• Therapeutic uses:

  • BPH, urinary retention, bladder obstruction; hypertension (less common)

• Safety and pharmacology:

  • MOA: prevent α1 receptor activation in vascular smooth muscle and bladder/ prostate tissue

  • Adverse effects: First-dose hypotension, reflex tachycardia, sexual dysfunction

• Nursing considerations:

  • Check BP prior to dosing; counsel on orthostatic risk; bedtime dosing recommended; avoid abrupt cessation

• Warnings/contraindications:

  • Priapism risk; floppy iris syndrome during cataract surgery

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Quick Reference — “ANS Answers” Cheat Sheet ( summarized )

• Sympathetic vs Parasympathetic Catch Phrases:

  • Sympathetic: Fight or Flight

  • Parasympathetic: Rest and Digest

• Synonyms:

  • Adrenergic (SNS)

  • Cholinergic (PNS) and Neuromuscular (NMJ) for certain sites

• Neurotransmitters (Keys):

  • Epinephrine (Epi), Dopamine (DA), Norepinephrine (NE)

  • Acetylcholine (ACh)

• Receptors (Locks):

  • A1, A2, B1, B2, DA

  • Muscarinic (M), Nicotinic (N)

• Eye/pupil: Mydriasis (SNS) vs Miosis (PNS)

  • Mydriasis note: increases intraocular pressure (IOP) – relevant to glaucoma

• Mouth: Dry mouth (SNS) vs saliva secretion (PNS: SLUDGE strengths)

• Heart: Tachycardia (SNS) vs bradycardia (PNS)

• Lungs: Dilation (SNS) vs constriction (PNS)

• GI tract: Minimal activity (SNS) vs increased motility and secretions (PNS)

• Bladder: Detru­sor muscle relaxation and sphincter contraction (SNS) vs detrusor contraction and sphincter relaxation (PNS)

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Practice on the Bladder

• Question prompts:

  • What receptors are found in the bladder and/or prostate?

  • Which drugs allow a patient to void?

  • Which drugs can stop an overactive bladder?

Page 58

Practice on the Eye

• Question prompts:

  • What drugs cause mydriasis?

  • What drugs cause miosis?

  • What drugs treat glaucoma?

  • What drugs can worsen glaucoma?

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Practice on the Heart

• Question prompts:

  • What receptors are found on the heart?

  • What drugs can increase heart rate and cardiac output?

  • What drugs can decrease heart rate and cardiac output?

Summary Notes for Exam Preparation

• The ANS comprises two divisions with generally opposing roles: the SNS (fight/flight) and PNS (rest/digest). While most organs are innervated by one or both, the overall effect is context-dependent and mediated by receptor subtype distribution and signaling pathways.

• Key receptor families to know:

  • Adrenergic (SNS): α1, α2, β1, β2, DA (D1)

  • Cholinergic (PNS): Muscarinic (M), Nicotinic (N)

• Primary neurotransmitters:

  • SNS: norepinephrine (NE) and epinephrine (Epi) – with DA in certain CNS/peripheral roles

  • PNS: acetylcholine (ACh)

• Core pharmacology concepts:

  • Agonists mimic NE/Epi at adrenergic receptors; antagonists block receptor activation

  • Beta-blockers reduce heart rate and contractility; alpha-blockers reduce vascular tone; alpha-1 blockers can affect urinary function and BP; glaucoma therapies often involve beta-blocker eye drops (timolol) to reduce IOP; beta-2 blockade can worsen asthma/COPD; reflex tachycardia can arise with some vasodilators, mitigated by beta-blockers

• Clinical and safety themes:

  • Orthostatic/postural hypotension is a common risk with alpha-1 blockers and other antihypertensives; educate on slow position changes and first-dose effects

  • Never abruptly discontinue beta-blockers or other antihypertensives without clinician guidance (FDA boxed warnings for sudden withdrawal)

  • Extravasation of vasopressors (e.g., epinephrine) requires prompt management with phentolamine

  • Glaucoma management often implicates β-blockers (eye drops) and the role of pupil size in IOP control

Formulas (as seen in slides):

• Standard physiology: $BP = CO imes SVR$ where $CO = HR imes SV$

• Alternate expression from slides: $BP = (HR imes Blood\,Volume) imes Arterial\;Resistance$ (illustrative teaching form)

• Blood pressure relation reminder: $BP = (HR imes BV) imes AR$ (contexted in lecture materials)

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