Autonomic Nervous System

2 Divisions:

Sympathetic ("gross motor control") &

Parasympathetic ("fine tuning" e.g. HR, GI mot.)

Autonomic ("involuntary")

&

Somatic ("voluntary")

Nerve Fiber Classification by Neurotransmitter

a. Cholinergic fibers release:

b. Adrenergic fibers release:

a. Acetylcholine

b. Norepinephrine 

a. Preganglionic fibers inervate:

b. Postganglionic fibers inervate:

a. a ganglion

b. the end organ

Cholinergic or Adrenergic?

a. α1 & α2 receptors

b. Muscarinic receptors

c. Nicotinic receptors

d. β1 & β2 receptors

a. Adrenergic

b. Cholinergic

c. Cholinergic

d. Adrenergic

Mscarinic Receptors

a. M1 stimulates:

b. M2 stimulates:

c. M3 stimulates:

a. ganglia, secretory glands

b. myocardium, smooth muscles

c. smooth muscle, secretory glands

Muscarinic receptors

-inervated by the ____ganglionic parasympathetic fibers except for the ______ which are stimulated by muscarinic receptors in the SNS.

1. Nicotinic receptors are innervated by:

2. In which CNS divisions?

1. PREganglionic fibers (straight from the CNS).

2. Parasympathetic, sympathetic and somatic.

ALL adrenergic receptors are innervated by:

a. postganglionic sympathetic fibers

b. preganglionic sympathetic fibers

c. postganglionic parasympathetic fibers

d. postganglionic sympathetic fibers

a. postganglionic sympathetic fibers

Which of the following are hepatic inducers?

a. Cimetadine

b. St. John's Wort

c. Rifampin

d. Erythromycin

e. Grapefruit juice

f. Phenobarbital

b. St. John's Wort

c. Rifampin

f. Phenobarbital

Hepatic inducers have what effect on serum concentrations of drugs?

a. Increase concentration

b. Decrease concentration

Hepatic inhibitors have what effect on the serum concentratin of drugs:

a. Increase concentration

b. Decrease concentration

a. Increase concentration

Which of the following are hepatic inhibitors?

a. Cimetidine

b. St. John's Wort

c. Erythromycin

d. Grapfruit juice

e. Barbiturates

f. Rifampin

a. Cimetidine

c. Erythromycin

d. Grapefruit juice

Choose the item that does not apply to adrenergic stimulation:

a. Nicotinic receptors

b. Muscarinic receptors

c. Alpha receptors

d. Beta receptors

e. 'Fight or flight'

What are the effects of adrenergic stimulation on

Pupils: dilate or constrict?

Lungs: dilate or constrict?

Heartrate: increase or decrease?

Blood vessels (visceral): dilate or constrict?

Musculoskeletal blood vessels: dilate or constrict? 

GI motility: increase or decrease?

Serum glucose: increase or decrease?

Pupils: dilate

Lungs: dilate

Heartrate: increases

Blood vessels (visceral): constrict

Musculoskeletal blood vessels: dilate

GI motility: decreases

Serum glucose: increases

Targets & effects of α1 stimulation:

a.

b.

c. 

d. 

a. blood vessels: constriction in skin/mucous membranes/viscera --> ↑ peripheral resistance (↑BP)

b. eyes: mydriasis (pupilary dilation)

c. bladder: sphincter contraction

d. prostate: ↑ tension of smooth muscle around prostate gland

Effect of α2 stimulation:

a.

a. CNS: ↓ sympathetic outflow, "off switch"--> peripheral vasodilation

Targets & effects of β1 stimulation:

a.

Effects of β2 stimulation:

a.

b.

c.

d.

e.

f.

g.

h.

a. Lung: dilation of smooth muscle/bronchial tree

b. Blood vessels: dilation of arterioles in skeletal muscles (↓ resistance is overcome by effects of alpha1 stimulation)

c. Liver: glucose release via glycogenolysis & gluconeogenesis

d. Serum potassium: ↓ as it is moves with glucose into cells

e. Bladder: relaxation of detrusor muscle

f. GI: slowed peristalsis

g. Uterus: inhibited contractions

h. Tremor (also seen with drug-induced B2 toxicity)

Parasympathetic stimulation- Muscarinic cholinergic (vagal, cranial nerve X) effects:

Heart:

Eye:

Bladder:

GI:

Lung:

Heart:↓ HR, ↓conduction speed & contractile force (atrium only)

Eye: miosis (pupil constriction), return of accommodation ability, ↓IOP (in pts w glaucoma)

Bladder: contraction of detrusor muscle & relaxation of sphincter

GI: ↑motility,↑gastric acid secretion&pancreatic enz. secretion, ↑bile release, ↑lower esophageal sphincter tone

Lung: ↑smooth muscle tone in bronchial tree

Excessive muscarinic blockade results in...

( eg. 'mad as a hatter')

mad as a hatter: psychosis, seizures

dry as a bone: ↓ secretions (dry mouth/skin)

blind as a bat: loss of accommodation, photophobia

red as a beet: cutaneous vassel dilation

hot as a hare: warm skin

ALSO...

Can't see

Can't pee: urinary retention

Can't spit

Can't ...oh my! GI slowing (constipation, ↓ bowel sounds)

Which of the following are muscarinic agonists and which are muscarinic antagonists?

Bethanechol

Atropine

Pilocarpine

Scopolamine

Ipratropium (Atrovent)

Agonists:

Bethanechol

Pilocarpine

Antagonists:

Atropine

Scopolamine

Ipratropium

Atropine:

in bradycardia, the correct dose must be given! too small--> paradoxical bradycardia with systemic effects

**Atropine will have NO EFFECT on transplanted ♥s!! (disconnected nerves)

flip for clinical uses 

Clinical uses of atropine:

> pre-op to ↓ salivation

> block vagal effects on ♥

> dilate pupil for eye exam (homatropin- not atropine)

> tx of bradycardia (ACLS)

> reverse toxicity of excessive muscarinic stimulation (r/t causative agent)

Bethanechol

Class:

MOA:

Clinical uses:

PRV (patient related variables):

Bethanechol

Class: Muscarinic Agonist

MOA: directly simulates the muscarinic receptor (M1-M3). Relatively selective for the GI tract and bladder.

Clinical uses: GI/bladder atony

PRV: asthma, PUD, cardiac conduction defects

Pilocarpine

Class:

MOA:

Clinical uses:

PRVs:

Pilocarpine

Class: Muscarinic Agonist

MOA: nonspecific direct stimulation of the muscarinic receptor.

Clinical uses: topical application for glaucoma, Sjogren's syndrome

PRVs: (same as for bethanechol) asthma, PUD, ♥ conduction defects

Random words that are fun to say:

Uzbekistan

Pedunculated

Hashimoto

Defenestrate

Don't Panic.

You will master pharmacology.

Atropine

Class:

MOA:

Clinical uses:

PRVs:

Atropine

Class: Muscarinic Antagonist

MOA: competitively blocks muscarinic receptors

Clinical uses: ↓ salivation pre-op, block vagal effects on ♥, dilate pupil for eye exam, tx of bradycardia, tx of toxicity r/t agent causing excessive muscarinic stimulation

PRVs: BPH, high environmental temperature, reflux esophagitis

Scopolamine

Class:

MOA:

Clinical uses:

PRVs:

Scopolamine

Class: Muscarinic Antagonist

MOA: competatively blocks muscarinic receptors

Clinical uses: patch used to prevent motion sickness

PRVs: BPH, high environmental temperatures, reflux esophagitis

** mydriasis can be caused by rubbing eye after applying scopolamine patch!

Ipratropium (Atrovent)

Class:

MOA:

Clinical uses:

PRVs:

Ipratropium (Atrovent)

Class: Muscarinic Antagonist

MOA: nonselectively blocks muscarinic receptors

Clinical uses: asthma/COPD to cause bronchodilation/prevent constriction/spasm

PRVs: ?

Dicyclomine (Bentyl)

Class:

MOA:

Clinical use:

PRVs:

Dicyclomine (Bentyl)

Class: Muscarinic ANTagonist

MOA: Blocks M3 receptors (smooth muscle, secretory glands)

Clinical use: IBS, ↓ GI motility/secretion

PRVs:  Tachycardia, confusion, urinary retention, ↑ IOP.

Oxybutynin

Class:

MOA:

Clinical use:

PRVs:

Oxybutynin

Class: Muscarinic ANTagonist

MOA: nonselective blocker of muscarinic receptor

Clinical use: urinary incontinence r/t detrusor spasms

PRVs: tachycardia, confusion, ↑ IOP

Nicotinic ANTagonists

-non-depolarizing (vs depolarizing) neuromuscular blocking agent: pancuronium

MOA:

Clinical use:

Toxicity:

Pancuronium

MOA: competitively blocks the action of ACh at the neuromuscular junction.  Effects reversed by AChase inhibitors (neostigmine).

Clinical use: adjunct to general anesthesia, mechanically ventilated pts.

Toxicity: RESPIRATORY PARALYSIS, hypotension.

Nicotinic ANTagonists

Depolarizing neuromuscular blockers: Succinylcholine

MOA:

Clinical use:

PRVs:

Toxicity:

Succinylcholine

MOA: Produces persistent depolarization resulting in a transient muscular stimulation (fasciculation) followed by neuromuscular blockade (CANNOT be reversed by AChase inhibitors!) RAPID ONSET.

Clinical uses: anesthesia, emergency tracheal intubation

PRVs: deficiency of pseudocholinesterase (=> prolonged effects).  AVOID in: Acute phase following major burn, multiple trauma, Hx sleletal muscle myopathy, Hx malignant hyperthermia! **Associated w FATAL HYPERKALEMIA.

Nicotinic & Muscarinic Agonists-

AChase Inhibitors

MOA:

Clinical uses:

AChase Inhibitors

MOA: reversibly block the action of AChase, allowing more ACh to reach receptors.

**Neostigmine & pyridostigmine do NOT cross the BBB (b/c they are charged).  Physostigmine DOES cross the BBB b/c it is not charged.

Clinical uses: reversal of non-depolarizing neuromuscular blocking agents, tx anticholinergic poisoning (+psychosis, seizures).  Pyrid./neostigmine used in tx Myesthenia gravis.

Excessive Stimulation of ACh-I

Muscarinic & Nicotinic Effects

Muscarinic: N,V,D, ↑ salivation, ↑ bronchial secretions, bronchoconstriction, bradycardia

Nicotinic: Muscle cramps & fasciculations

Organophosphate Insecticides/Nerve Gas

MOA:

Toxicity:

MOA: IRreversibly block the action of AChase, allowing more ACh to reach receptors.

Toxicity: antidote is Pralidoxime & atropine

Isoproterenol

Class:

MOA:

Clinical uses:

PRVs:

Isoproterenol

Class: Adrenergic Agonist

MOA: Binds to adrenergic receptors.

Clinical uses: Rarely used. Primarily for testing (e.g. chem stress test).  Used in place of Atropine for pt's w transplanted ♥ (dobutamine now preferred)? "keeps killing ppl"?

PRVs: B1- ISCHEMIC HEART DISEASE

A1- Hypertension, hypovolemia

Dobutamine

Class:

MOA:

Clinical uses:

PRVs:

Dobutamine

Class: Adrenergic Agonist

MOA: Binds to adrenergic receptors

Clinical uses: Supports cardiac function by increasing rate & force of contraction.

PRVs:B1- ISCHEMIC HEART DISEASE

A1- Hypertension, hypovolemia

Metaproterenol

Class: 

MOA:

Clinical uses:

PRVs:

Metaproterenol

Class: Adrenergic Agonist

MOA: Binds to adrenergic receptors

Clinical uses: BRONCHODILATOR in asthmatics (preferred over Isoproterenol r/t its relative selectivity; stim B2>B1).

PRVs: B1- ISCHEMIC HEART DISEASE

A1- Hypertension, hypovolemia

Norepinephrine

Class:

MOA:

Clinical uses:

PRVs:

Norepinephrine

Class: Adrenergic Agonist

MOA: Binds to adrenergic receptors

Clinical uses: Support cardiac function, potent vasoconstrictor

PRVs:B1- ISCHEMIC HEART DISEASE

A1- Hypertension, hypovolemia

Epinephrine

Class: 

MOA:

Clinical uses: 

PRVs: 

Class: Adrenergic Agonist

MOA: Binds to adrenergic receptors

Clinical uses: 1st line drug for cardiac arrest, anaphylaxis, local vasoconstriction to prolong effect of locally administered anesthetics.

PRVs: B1- ISCHEMIC HEART DISEASE

A1- Hypertension, hypovolemia

Phenylephrine

Class:

MOA:

Clinical uses:

PRVs:

Phenylephrine

Class: Adrenergic Agonist

MOA: Binds to α1 adrenergic receptors receptors

Clinical uses: topical decongestant, IV to support blood pressure.

PRVs: B1- ISCHEMIC HEART DISEASE

A1- Hypertension, hypovolemia

Ritodrine & Terbutiline

Class:

MOA:

Clinical uses:

PRVs:

Ritodrine & Terbutiline

Class: Adrenergic Agonist

MOA: Binds selectively to β2 adrenergic receptors

Clinical uses: Inhibit uterine contractions in preterm labor

PRVs:B1- ISCHEMIC HEART DISEASE

A1- Hypertension, hypovolemia

Clonidine

Class:

MOA:

Clinical uses:

PRVs:

Clonidine

Class: Adrenergic Agonist

MOA: Central stimulation of α2 receptors--> ↓ CNS symp. outflow. Stimulates α2 receptors in spinal cord.

Clinical uses: CNS-HTN, narcotic withdrawal. Spinal cord- analgesia.

PRVs:

Toxic Adrenergic Stimulation

a. Beta1:

b. Beta2:

c. Alpha1:

d. Alpha2:

Toxic Adrenergic Stimulation

a. Beta1: tachycardia, cardiac ischemia, arrhythmias

b. Beta2: Hypotension, tremors

c. Alpha1: HTN, ↓ organ perfusion (DO NOT use to tx HoTN)

d. Alpha2: Orthostatic HoTN

Phentolamine (Regitine)

Class:

MOA:

Clinical use:

PRVs:

Phentolamine (Regitine)

Class: Adrenergic Blockers

MOA: Blocks α1 & α2 receptors

Clinical use: Used to reverse the local vasoconstricting effect of extravasated alpha agonist (NE, dopamine). **Blocking Alpha2--> ↑ NE--> tachycardia

PRVs: CHF, asthma

DoxaZOSIN (Cardura)

Class: Adrenergic Blocker

MOA: Blocks Alpha1 receptors

Clinical use: HTN, BPH

PRVs: CHF, asthma

DoxaZOSIN (Cardura)

Class: Adrenergic Blocker

MOA: Blocks Alpha1 receptors

Clinical use: HTN, BPH

PRVs: CHF, asthma

Tamulosin (Flomax)

Class:

MOA:

Clinical use:

PRVs:

Tamulosin (Flomax)

Class: Adrenergic Blocker

MOA:Blocks Alpha1 receptors

Clinical use: BPH

PRVs:CHF, asthma

** SE: ORTHSTATIC HoTN

Propranolol

Class:

MOA:

Clinical use:

PRVs:

Propranolol

Class: BETA Blocker

MOA: Blocks BETA 1&2 receptors

Clinical use: HTN, angina, antiarrhythmic

PRVs: CHF, asthma (choose B1 selective agent)

new onset, at rest, or onset with progressively less exertion.

**May be a transition stage b/n stable angina and MI!!

UNSTABLE ANGINA IS A MEDICAL EMERGENCY!! 

Cardiac troponin I

CPK-MB

-Concentration in inspired air

-Lung function

-Hgb

-Blood flow through coronary arteries

-Oxygen extraction

-Diastolic filling time

-Heart rate

-Contractility

-Wall tension

Therapeutic Goal

STEMI

UA/NSTEMI

Chronic Stable Angina

STEMI: achieve rapid, complete reperfusion of the infarct vessel.  Blood thinners and thrombolytic therapy OR PCI[PCTA].  CHEW 300mg or 3 BABY ASA NOW.

UA/NSTEMI: relief from ischemic pain, prevention of recurrent ischemia/MI.  ASA or Plavix, etc.

Chronic Stable Angina: Prevent pain, maintain normal ADLs.  Nitro, BB, ASA/Plavix, ACEI, BP control, CCB, etc.

MI Therapy

MONA

Morphine

Oxygen

Nitroglycerin

Aspirin

-used ONLY in intensive care settings

**MONITOR FOR CYANIDE (Thyocyanate??) POISONING** esp. in compromised renal function

Trembling

Resp. distress

Convulsions

(prevents cells from using O2, accumulation of unused O2 in veins--> decreased A:V ratio)

Antagonizes both the Renin-Angiotensen System and the SNS. Not a first line drug.  Don't use for >72h. 

**Toxicity: HYPOtension.  

Class: Inotropic Agent

MOA: Inhibits Phosphodiesterase III, allowing cyclic-AMP (2nd messenger) to accumulate--> ↑ cardiac contractility. Arterioloar dilation occurs as well, ↓ afterload.

Clinical uses: Severe heart failure  when other therapies have failed.  LONG TERM USE associated with INCREASED MORTALITY.

Class: Inotropic Agents

MOA: Agonist at B1&B2 receptors (Dobutamine), Alpha1 receptor (Dopamine, dose-related effect). 

Clinical uses: Heart Failure

**Dobutamine increases HR & contractility + vasodilation (B receptors) and has MINIMAL effect on MAP. Discouraged in pts on BB (PDE I preferred).  

**Dopamine INCREASES MAP (a1).  Doses>10mcg/Kg/M--> chronotropic/vasoconstrictive effects.

DECREASE MORTALITY RATE.  Every pt with significant heart failure should be on an ACE I unless contraindicated. 

**INCREASE SERUM K! Monitor!

ARBs may not be as effective as ACEI- use ACEI as first choice. 

ACE Inhibitors

SE

1. Low Na Diet

2. Diuretics

3. ACE-I

4. BB or nondihydropyridine CCBs (AVOID IN SYSTOLIC HF)

The RIGHT doses of the CORRECT Beta Blockers helps just enough to decrease the excessive stimulation in HF that damages the heart.

**USE ONLY in STABLE PTs.

NSAIDS (+COX2-I)

Adrenergic stimulators (e.g. decongestants)

TZD (antidiabetic drugs-->H2o reabsorption)

Antiarrhythmics that prolong QT interval

**CCB** Contraindicated in systolic HF

**NEFEDIPINE**

Cardiac Glycosides

(digoxin)

Inhibits the enz. that enables the Na-K pump--> ↑ intracellular Na.  The ↑ in intracellular Na inhibits the influx of Na into the cell from the Na-Ca exchange site.  If Na can't come in, Ca cant leave the cell, and intracellular Ca ↑. Higher levels of intracellular Ca result in more forceful contraction of the muscle fibers.

1. positive inotropic effect-direct effect

2. vagotonic effect (stimulates the vagal nerve-indirect)--> bradycardia

Kidneys: elimination determined by renal function.  Decreased renal function -->longer half life= increased time to SS.

**Pt's are dosed BASED ON IDEAL BODY WEIGHT.

**HOLD for APICAL PULSE <60 OR PR Interval>.2sec

Dogoxin Blood Levels

When are blood levels drawn?

Cardiac: Bigeminy/Trigeminy, AV Block, AV arrhythmias, bradycardia

Non-Cardiac: fatigue, visual disturbance (green-yellow perception), muscular weakness, A/N, Hallucinations, confusion, insomnia.

Hypokalemia enhances the effects of Digoxin activity/toxicity without altering the blood levels.

**CAUTION: DIURETIC USE.

Potassium Chloride: Chloride is usually also low- the body won't hold onto K without Cl. So...Potassium Carbonate tastes better, but it doesn't work. 

**Consider using a K-sparing diuretic to minimize K loss (hypokalemia--> ↑ Digoxin effect/toxicity)

**K-sparing diuretics are also Mg-sparing diuretics!!

Vagal Stimulation increases the effect/toxicity of Digoxin.  

Cold stimulates vagal nerves.  

Shower pick massages (drum carotid sinus).

Rectal Exams (any tubes in orifices can stimulate vagal). "Never digitalize someone who's been digitalized."

Drug Interactions

Amiodarone & Verapamil with Digoxin

Drug Interactions

Digoxin + Erythromycin

Drug Interactions

Digoxin + Antacids

+ Rifampin

Decrease Digoxin Levels

*Antacids due to digoxin binding; space by 2 hours.  

1. Decrease the S/S of congestion

2. Maintain a normal life style

3. Prolong life

NSAIDs increase renal retention of Na and water-> increase volume= increased preload (more work for ♥)

Decreased contractility (<40% EF, ↑ LVEDV)

↓ Muscle mass

Dilated cardiomyopathy

Ventricular hypertrophy (pressure overload), volume overload (valve regurgitation)

Reduced ventricular filling (Normal EF & normal/↓ LVEDV):

Ventricular hypertrophy (longterm HTN)

Stiffness of ventricles

Restrictive factors

Vavular stenosis

Pericardial disease

Ischemia

1. ACE-I

2. Diuretics

3. Beta blockers

Ischemic Heart Disease Tx

Clopidogrel (Plavix)

Inactive: must be actived by liver enzyme. **Omeprazole is a PPI that blocks the ENZ that ACTIVATES plavix! 

Use: in STEMI with fibrinolytic therapy

Ischemic Heart Disease Tx

Prasugrel

Nitrates

Nitroglycerin

Nitroglycerin: used to blow up mountains. Dilute and use to venodilation (decrease preload & wall tension-> decreased O2 demand). HIGH FIST PASS EFFECT. Sublingual vasculature by-passes the liver. **Pt must have a NITRATE FREE PERIOD if on patch or ointment.

VIAGRA (Revatio, Cialis)

+

Nitro=

BAD.

Decreased myocardial blood flow and ischemia! Wait 24h for V or R, 48h for Cialis.

DONT GO TOGETHER!

Beta 2 stimulation= vasodilation, prevents constriction. Block it and we're in trouble.  

1. Eliminate excess CV risk & end organ damage, achieve normal pressure

2. Lifestyle changes in preHTN or

3. Simplify drug regimen

4. Satisfy pt and family

Class: Thiazide diuretic

MOA: block Na reabsorption from the proximal part of the renal tubule--> Na loss & water)

Clinical uses: HTN in pts with NORMAL KIDNEY function.

Monitor: Potassium (K)

Class: thiazide diuretic

MOA: blocks renal reabsorption of Na from distal renal tubule--> Na & H2Oloss

Clinical uses: HTN control in pts with normal renal function

Monitor: Potassium

Class: Loop diuretic

MOA: blockes sodium & chloride reabsorption from the ascending loop of Henle.

Clinical uses: HTN control in patients WITH RENAL compromise

a. hypokalemia

b. hyperuricemia

c. hyperglycemia

d. hyperlipidemia

e.hypomagnesemia 

Thiazides +

digoxin

lithium

Class: BB

MOA: nonselectively blocks beta receptors--> decreased CO & a transient increase in peripheral resistance

Clinical uses: HTN in pts with complicated HTN (HF, post MI).

Toxicity: BRONCHOSPASM, HF, exacerbation of vasospastic disorders, delayed return to euglycemia, masking of S/S of hypoglycemia (tachycardia), Beta Blocker Blues, vivid dreams.

PRVs: Asthma, HF, peripheral vascular insuffiency, DM, Variant angina, drug interaction with Clonidine withdrawal, drug interaction with NSAIDs, Pregnancy (1st trimester).

Class: beta blockers

MOA: selectively blocks B1 receptors

Clinical uses: HTN treatment in noncomplicated pts

Toxicities: bronchospasm, HF, exacerbation of vasospastic disorders, delayed return to euglycemia (post hypo), masked S/S of hypoglycemia (tachycardia), BB Blues, vivid dreams

PRVs: asthma, HF, peripheral vascular insuffiency, DM, variant angina, drug interaction with clonidine withdrawal & NSAIDs, 1st trimester of pregnancy

Class: Beta Blocker

MOA: selectively blocks B1 receptors

Clinical uses: treatment of HTN in noncomplicated pts

Toxicities: BRONCHOSPASM, HF, exacerbation of vasospastic diseases, 1st trimester pregnancy, BB Blues, vivid dreams, delayed return to euglycemia p hypo episode, masked S/S of hypoglycemia (tachycardia)

PRVs: DM, variant angina, asthma, HF, peripheral vascular disease, drug interaction with clonidine & NSAIDs, pregnancy

Class: alpha blocker

MOA: selectively blocks alpha 1 receptors--> decrased peripheral resistance

Clinical use: HTN

Toxicity: dizziness/lightheadedness, reflex tachycardia, orthostatic hypotension (esp in elderly)

Administration: **Take at bedtime to offset the effects of 'First dose syncope'! make sure youre lying flat!

Class: Alpha Agonist

MOA: stimulates alpha 2 receptors centrally (midbrain)-->decreased sympathetic outflow.

Clinical uses: ease opiate withdrawal; analgesic if given epidurally.

Administration: **REBOUND HTN can occur with abrupt D/C. 

Toxicity: rebound HTN, orthostatic hypotension, sedation/confusion in elderly, impotence

Class: ACE-I

MOA: blocks the conversion of Angiotensin I ->Angiontensin II

Clinical uses: HTN

MOA: reduce peripheral resistance by directly dilating arterioles.  Reflex tachycardia is common and aldosterone secretion is stimulated leading to Na & water accumulation.

Clinical uses: HTN EMERGENCIES.  Give at the same time each day with meal?

Toxicity: excessive reflex tachycardia, excessive fluid, SLE-like syndrome (reversible).

**Direct Acting Vasodilators almost always require a BB to tx the reflex tachycardia and a diuretic to tx the fluid accumulation.

Class: direct-acting vasodilator

MOA: directly dilate arterioles

Clinical uses: HTN emergencies.

Toxicity: excessive reflex tachycardia, excessive fluid, hypertrichosis (minoxidil), reversible SLE-like syndrome (hydralazine).

Class: direct-acting vasodilator

MOA: directly dilates the arterioles

Clinical uses: HTN emergencies

Toxicity: excessive reflex tachycardia, excessive fluid accumulation, SLE-like syndrome (hydralazine), hypertrichosis

Class: CCB

**do NOT use with ANGINA! or systolic heart failure

Directly affect the heart:

slowed conduction speed

prolonged refractory period

reduced automaticity

negative inotropic effect

Indirectly affects the heart:

vagoLYTIC effect

MAIN Toxicity: GI, anticholinergic, **quinidine syncope (increases digoxin)

MAIN effect is on ISCHEMIC ventricular muscle fibers, prolong refratory period.

Toxicity: psychosis, seizures, lots others

PRVs: ALLERGY TO LIDOCAINE