DRUG ACTING ON THE AUNTONOMIC NERVOUS SYSTEM ADRENERGIC AGONIST

- Stimulates the sympathetic nervous system

They are also called adrenergic adrenomimetic, sympathomimetic because
they mimic the effect of sympathetic neurotransmitter such as
Catecholamine- general term for norepinephrine/epinephrine,
adrenaline/noradrenaline
2 sources of catecholamine
1. Endogenous- found naturally in the body (norepinephrine and
epinephrine)
2. Synthetic substances like Dobutemine

Mechanism of Action

If any of the adrenergic drug is given it binds with the alpha or beta receptor and
cause sympathetic response.

The SNS is the counterpart of the parasympathetic NS, together they make up the 1. Direct acting- binds directly to receptor and cause physiologic effect
ANS. They provide a check and balances system for maintaining the normal 2. Indirect acting- stimulates the release catecholamine
homeostasis of the autonomic functions of the human body. 3. Mix- binds directly to receptor cause physiologic effect and stimulates
the release catecholamine
In Parasympathetic, the enzyme responsible is the cholinergic or the acetylcholine.
Indications: (indicated in how it is used in the body)
 Cholinergic receptor- the receptor in Parasympathetic NS
Muscarinic- 1. Respiratory Indications
Cholinergic a. Bronchodilation
 beta adrenergic: albuterol, salbetarol
Acetycholinesterase- degrades the acetylcholine. If acetylcholine is not present in b. Constriction of dilated arterioles and reduction in nasal blood flow
synoptic cleft means we don’t have parasympathetic NS c. Vasoconstriction in arteries of the eyes relieving congestion
2. Alpha Adrenergic Adverse Effect
In sympathetic NS or the adrenergic system has 2 receptor
- Headache, restlessness, excitement, Insomnia and euphoria. Possible
 Alpha receptor (1, 2) If these are stimulated it produces an array of cardiovascular drugs include chest pain, vasoconstriction, hypertension,
 Beta receptor (1, 2) effects in the body tachycardia and palpitation or dysrhythmias.
3. Beta adrenergic adverse effects
SYMPATHETIC EFFECT PARASYMPATHETIC EFFECT a. Stimulates CNS, causing mid tremors, headache, nervousness and
EYES Dilates pupil Constrict pupils dizziness
LUNGS Dilates bronchioles Constrict bronchioles and b. These drugs can also have unwanted effect on the cardiovascular
increase secretion system including increase heart rate and palpitation and fluctuations in
HEART Increase heart rate Decrease heart rate bp
BLOOD VESSEL Constrict blood vessel Dilates blood vessel
ADRENERGIC BLOCKERS
GASTROINTESTINAL Releases smooth muscle Increase peristalsis
in the GI tract - Act as antagonist to adrenergic agonist by blocking the alpha, beta receptor
BLADDER Relaxes Constrict site. Most adrenergic blockers either the alpha receptor or the beta
UTERUS Releases uterine muscle - receptor.
SALIVARY - Increase salivation - Sympatholytic drugs- preventing the action of SNS and producing the
parasympathetic effect
- It is called Adrenergic blockers, adrenolytic
 Blood vessel Dilated Dilated
Heart rate Slowed Increased
1. Alpha Adrenergic Blockers Blood pressure decreased increased
- Interrupt the stimulation of the SNS at the alpha 1 adrenergic receptor EYES Pupil constricted Pupil constricted
- work either by direct competition with receptor or by non-competitive GASTROINTESTINAL
Tone Increased Increased
process
Motility Increased Increased
- example Tamsulosin Sphincter Relaxed none
Competitive blocking- directly the drug goes to the receptor in order for the GENITOURINARY
NE not to bind with the receptor. Tone Increased Increased
Non-competitive blocking- the drug become less responsive with the NE Motility Increased Increased
Sphincter Relaxed Relaxed
Selective blockers- blocks alpha 1 GLANDULAR SECRETIONS Increased intestinal,
lacrimal, salivary and sweat
Non-selective- blocks alpha 1 and 2
gland secretion
- promotes vasodilation, reduces BP. Promotes pupillary constriction and SKELETAL MUSCLE Increased contraction
promotes smooth muscle activity BODY SYSTEM ADVERSE EFFECTS
CARDIOVASCULAR Bradycardia/tachycardia, hypo/hypertension, syncope,
- first effect/dose phenomenon- severe and sudden drop of BP after
conduction abnormalities
administration
CENTRAL NERVOUS Headache, dizziness, convulsions, ataxia
2. Beta Adrenergic Blockers GASTROINTESTINAL Abdominal cramps, increased secretions, n/v, diarrhea
- Drugs that blocks the action of beta adrenergic stimulation RESPIRATORY Increased bronchial secretions, bronchospasm
- Either selective or nonselective cardio blocker Lacrimation, sweating, salivation, miosis
- Some beta blockers are nonselective, blocking both beta 1 and 2 receptor Cholinergic crisis- circulatory collapse
- Example Propanolol (non-selective beta blocker), atenolol (selective beta
blocker) “SLUDGE”- signs and symptoms of toxicity
3. Adrenergic Neuron Blockers
- Drugs that blocks the release of norepinephrine from the sympathetic  Salivation
terminal neurons  Lacrimation
 Urinary incontinence
CHOLINERGIC DRUGS, CHOLINERGIC AGONIST AND PARASYMPATHOMIMETICS
 Diarrhea
Acetylcholine- Is found in the ganglions of the parasympathetic NS  Gastrointestinal cramps
 Emesis
 Muscarinic- found in the heart
 Nicotinic- found mostly in skeletal muscle
CHOLINERGIC BLOCKING DRUGS
Effects of Cholinergic Agonist
- Cholinergic blockers, anticholinergic, parasympatholytics and antimuscarinic
- “rest and digest” system drugs are all terms that refers to the class of drugs that blocks or inhibit the
- Direct acting- promote parasympathetic effect unto specific tissue actions of acetylcholine in the parasympathetic NS.
 Carbachol and pilocarpine - Competitive agonist
- Indirect acting- it block the release of Ache
BODY SYSTEM CHOLINERGIC- BLOCKING EFFECTS
 Aricept- Alzheimer’s CARDIOVASCULAR Small does: decrease heart rate
 Neostigmine- myasthenia gravis Large does: increase heart dose
CENTRAL NERVOUS Small doses: decrease muscle rigidity, tremors
BODY TISSUE/ ORGAN MUSCARINIC NICOTINIC
Large doses: cause drowsiness, disorientation, hallucination
LUNGS Increased secretions, -
EYE Dilate pupils
constriction
GASTROINTESTINAL Relax smooth muscle, decrease intestinal and gastric
CARDIOVASCULAR
 secretions, motility and peristalsis Class II: occurs when ordinary physical activity results in fatigue, dyspnea, or other
GENITOURINARY Relax bladder, increase constriction symptoms
GLANDULAR Decrease bronchial secretions, salivation and sweating
RESPIRATORY Decrease bronchial secretions and dilate bronchial airways Class III: is characterized by a marked limitation in normal physical activity

Class IV: Is defined by symptoms at rest or with any physical activity.

ATROPINE
Drug therapy is individualized on the patient’s class of heart failure
- Atopine ulfate, first derived from the balledonna plant (atropa balledonna)
NON-PHARMACOLOGIC MANAGEMENT
and purified in 1831 is a classic anticholinergic or muscarinic antagonist drug
- Antidote for toxicity 1. The patient should limit salt intake to 2g/day
- Atropine is useful primarily 2. Alcohol intake should be either decreased to 1 drink/day or completely
a. As a preoperative medications to decrease salivary secretions and avoided
b. As an agent to increase heart rate when bradycardia is present 3. Fluid intake may be restricted
4. Smoking should be avoided
DRUG STUDY
5. Mild exercise
Assessment
DRUGS USED IN HEART FAILURE
1. Obtain baseline vital signs for future comparison
1. Inotropic effect- increases the force of myocardial contraction
2. Assess urine output
2. Chronotropic effect- decrease heart rate
3. Check patient’s medical history
3. Dromotropic effect- accelerated the conduction of the heart
4. Obtain patient’s drug history
CARDIAC GLYCOSIDE: DIGOXIN
Nursing diagnosis
- Naturally occurring cardiac glycosides are found in a number of plants,
1. Impaired urinary elimination related to urinary retention
including digitalis
2. Impaired oral mucous membranes related to decreased oral secretions
- This group of drugs inhibits the sodium-potassium pump, resulting in an
3. Risk for injury related to acute confusion
increase in intercellular sodium.
4. Risk for constipation related to decreased peristalsis secondary to atropine
- This increase leads to an influx of calcium, causing the cardiac muscle fibers
side effects
to contract more efficiently
Intervention

1. Monitor v/s
2. Determine fluid intake and output
3. Assess bowel sounds
4. Examine for constipation
5. Used bed alarms for patients
6. Provide mouth care

CARDIOVASCULAR AGENTS DIGOXIN TOXICITY

Heart failure- cause by numerous cardiac abnormalities - Overdose accumulation of digoxin causes digitalis toxicity. Signs and
- Failure of the heart to pump blood to meet the metabolic needs of the body symptoms include anorexia, diarrhea, n/v. bradycardia (below 60 bps),
premature ventricular contractions, cardiac dysrhythmia, headaches,
Class I: describe a patient who is not limited with normal physical activity by malaise, blurred vision, visual illusions, confusions and delirium
symptoms
PHOSPODIESTERASE INHIBITORS
 - This drug group inhibits the enzyme phosphodiesterase, promoting a
positive inotropic response and vasodilation.
- A drug in this group is milrinone lactate

ANTI-ANGINAL DRUGS

- Anti-anginal drug are used to treat angina pectoris

 Classic (stable) occurs with predictable stress or exertion
 Unstable (preinfarction) occurs frequently with progressive severity
unrelated to activity; unpredictable regarding stress/exertion and
intensity
 Variant (prinzmetal, vasopastic) occurs during rest

NONPHARMACOLOGIC MANAGEMENT

- Avoid heavy meals

- Smoking
- Extreme weather changes
- Strenuous exercise
- Emotional upset
- Proper nutrition
- Moderate exercise
- Adequate rest and
- Relaxation technique