GROUP C

NAMAGANDA ADILAH NGANDA EQ22/MBChB/AUG/0024D

MUKSIN GANYA KAREEM EQ22/BDS/AUG/0001D
THOYA SARAH BUKI EQ22/MBChB/AUG/0011D
WAMBOOZA ISAAC EQ22/MBChB/AUG/0034D
SSEGAWA ROGERS EQ22/MBChB/AUG/0073D
THE ROLE OF ANS DRUGS IN TREATMENT OF CARDIOVASCULAR
DISEASES (hypertension, acute coronary syndrome, heart failure, cardiac
arthymia and shock)
An arrhythmia, or irregular heartbeat, is a problem with the rate or rhythm of
your heartbeat. your heart may beat too quickly, too slowly, or with an irregular
rhythm. its associated with symptoms like fluttering, pounding or racing feeling
in the chest, fast heartbeat ,slow heartbeat, chest pain ,shortness of breath. They
work by modulating the sympathetic and parasympathetic nervous systems.
Beta-Blockers (Sympathetic Nervous System Modulation)
Mechanism: Beta-blockers block α- and β-adrenergic receptors , which are
typically stimulated by the neurotransmitter epinephrine (adrenaline) released by
the sympathetic nervous system. By blocking these receptors, beta-blockers
reduce the effects of sympathetic stimulation on the heart. β-Blockers also
indirectly prevent calcium entry into myocardial cells; therefore slow conduction
velocity, slow automaticity, and prolong the refractory period.
Examples include propranolol ,esmolol,carvedilol etc.
 PROPRANOLOL.
It interacts with β1 and β2 receptors with equal affinity, lacks intrinsic sympathomimetic activity, & does
not block α receptors.

ADME
• Propranolol is highly lipophilic and almost completely absorbed after oral administration
• Much of the drug is metabolized by the liver during its first passage through the portal circulation;
only about 25% reaches the systemic circulation.
• Approximately 90% of the drug in the circulation is bound to plasma proteins
• Despite its short t1/2 in plasma (~4 h), twice-daily administration suffices to produce the
antihypertensive effect in some patients
• Sustained-release formulations of propranolol maintain therapeutic concentrations of propranolol in
plasma throughout a 24-h period
 ADVERSE EFFECTS, PRECAUTIONS & CONTRAINDICATION
• Dizziness, fatigue, diarrhea, constipation, nausea, depression
• Severe: purpura, rash, fever etc.
• Contraindicated in most asthmatics & COPD patients
Dosage propranolol
• 10mg to 40mg, taken 3 or 4 times a day
Drug interactions
• Other hypotensive medications (reserpine, guanethidine, methyldopa)
• Other anti-arrhythmic agents (calcium channel blockers, lidocaine)
• Insulin & oral hypoglycemic drugs (prolongs hypoglycemia & masks signs of
hypoglycemia
Cholinergic Agonists (Parasympathetic Modulation)
Mechanism: Cholinergic agonists, such as acetylcholine or
medications that mimic its effects, stimulate the parasympathetic
nervous system by activating muscarinic receptors(M2).
Anticholinergic Agents (Parasympathetic Modulation):
Mechanism: Anticholinergic agents block the effects of
acetylcholine, reducing parasympathetic activity at the receptor
sites.
 HEART FAILURE
• Heart failure means that the heart is unable to pump blood around the body
properly.
• It is the end stage phenotype of several cardiac diseases such as
hypertension, myocardial infarction, valvular heart disease and
cardiomyopathy
• SIGNS AND SYMPTOMS OF HEART FAILURE
• Difficulty in breathing
• Irregular heart beat
• Swollen legs/edema
• Neck veins stick out
• Pleural effusion
 PARASYMPATHOLYTIC AGENTS
Parasympathetic nervous system activation will conversely act on Sino Atrial node and Atrial
Ventricular nodes to decrease the heart rate which will decrease cardiac output. Examples of
parasympatholytic drugs used in treating cardiac failure are Digoxin, Carvedilol.

Atropine, a parasympathetic agent acts by blocking cholinergic stimulation of the muscarinic receptors
of the heart which usually results in an increase in the sinus rate and shortening of atrioventricular
node conduction time.
Its used to manage bradycardia by increasing heart rate and improving atrioventricular conduction.
Atropine is contra indicated in heart failure in patients with myocardial ischemia as it may result in
increased oxygen demand hence worsening the ischemia.
 Sympathomimetic drugs
Sympathetic nervous system has a wide variety of cardiovascular effects including heart rate acceleration and
increased cardiac contractility. Its stimulation causes Sino atrial node and Atrioventricular node to increase the heart
rate, which increases cardiac output. Examples of sympathomimetic drugs are Dopamine and Dobutamine.
(Are arrythmogenic with small increase in heart rate.)

In initial phases of heart failure the sympathetic nervous system overdrive , plays a compensatory function aimed at
maintaining an adequate cardiac output despite the inotropic dysfunction affecting the myocardium.

It can negatively impact cardiovascular system in heart failure by

• Down regulating beta one receptors
• Exerting direct toxic effects on myocardium
• Contributing to myocardial remodeling
• Life threatening arrhythmias
 HYPERTENSION
• Hypertension or high blood pressure is when the pressure in the blood vessels is too high.
• Normal blood pressure is 120/80mmHg
• Clinically its divided into 2 ; 1. primary or essential hypertension: this is where the cause for the
rise in blood pressure is not known.
2. Secondary hypertension: this is where the cause for the rise in blood pressure is known
CLASSIFICATIONS OF HYPERTENSIVES
a. Sympatholytic drugs: Drugs acting on adrenergic receptors
i. Alpha adrenergic blocking agents; e.g prazosin, indoramin, phenoxybenzamine.
These drugs block the action of norepinephrine at alpha receptors. They dilate blood vessels by
relaxing the smooth muscles in the walls of arteries and veins.
By blocking the effect of norepinephrine on alpha receptors ,these blockers reduce the
constriction of blood vessels leading to vasodilation, this leads to decreased Peripheral resistance
and improve blood flow helping to lower blood pressure.
CONT’D
i. Beta adrenergic blocking agents: e.g propranolol, atenolol, metoprolol
These drugs block the effects of adrenaline on beta receptors ,this results in reduction of heart rate and contractility leading
to decreased cardiac output and lower blood pressure .
These drugs can also dilate blood vessels
ii. Both alpha and beta adrenergic blocking agents: e.g labetalol
Central sympatholytic
Alpha 2 adrenergic receptor stimulants.e.g chlonidine, alpha methyldopa
They act centrally in the brain .
These drugs stimulants these receptors leading to decreased norepinephrine release and subsequent decrease in PVR and
heart rate.
Adrenergic neuron blockers e.g reserpine, guanethidine.
They inhibit the release of norepinephrine from sympathetic nerve terminals there by reducing the stimulation of
adrenergic receptors on blood vessels and the heart.
Ganglion blocking agents e.g hexamethonium, trimethaphan.
They act by blocking ganglionic transmission which disrupts the communication between sympathetic and parasympathetic
nervous system ,this lead to vasodilation and decreased heart rate hence lowering blood pressure.
CONT’D
• Calcium channel blockers e.g nifedipine, amlodipine, verapamil, diltiazem.
They relax blood vessels by inhibiting the influx of calcium ions into vascular smooth muscle
cells. This results in vasodilation and decreased PVR hence lowering blood pressure
Oral diuretics e.g thiazides, chlorthalidone.
They promote the excretion of sodium ions and water through the urine .by reducing blood
volume diuretics help decrease blood pressure with in the blood vessels.
Drugs acting directly on the vascular smooth muscles e.g hydralazine, diazoxide, minoxidil
Potassium channel activators e.g diazoxide, minoxidil, pinacidil, nicorandil
Metyrosine
This drug inhibits the production of catecholamines by reducing the levels of these
hormones , this drug helps control blood pressure in individuals with pheochromocytoma or
paraganglioma.
 Acute coronary syndrome.
• Define: any condition brought on by a sudden reduction or blockage of blood flow to the heart
1. Acute coronary syndrome is most often caused by clot formation in the hearts arteries.
2. Symptoms may include : heart attack-like chest pressure or sudden heart stoppage.
3. Chest pain radiating towards left arm and jaw
on ECG it shows ST elevation.
• TREATMENT;
• Give beta blockers these include carvedilol, this helps to slow down heart rate and decrease
blood pressure.
• They reduce chances of arrhythmias because they are leading causes of death
• If the patient develops bradycardia and is unstable , give IV atropine , this blocks the
parasympathetic system and sympathetic system and sympathetic system takes over makes
the heart pump more and corrects Brady cardia.
 SHOCK
Shock is a critical condition brought on by the sudden drop in blood
flow through the body in response to the body's demand.
Shock is a critical medical condition where there is insufficient blood
flow to meet the body's demands, leading to impaired organ function.
. Various drugs are used to manage shock by influencing vascular tone
and cardiac output:
• Vasopressors: These drugs constrict blood vessels, increasing blood
pressure. Common examples include norepinephrine and dopamine
they are used to improve perfusion to vital organs during shock
CONT’D
• Inotropes: These medications enhance the force of the heart's contractions, thereby increasing
cardiac output. They are used to improve the heart's pumping ability. Examples include
dobutamine and milrinone.
• Fluid Resuscitation: While not directly affecting the ANS, intravenous fluids are a crucial part of
managing shock. They help increase blood volume, improving cardiac output and tissue
perfusion.
• Vasodilators: In certain types of shock, such as distributive shock, vasodilators like nitroglycerin
may be used to relax blood vessels and improve blood flow example.prostaglandin
• Corticosteroids: In some cases of shock, particularly septic shock, corticosteroids may be
administered to modulate the inflammatory response and support blood pressure. Example
Fludrocortisone

The choice of drugs depends on the type and cause of shock

References;
• Pharmacology and pharmacotherapeutics by R.S. Satoskar Nirmala
N Rege Raakhi K. Tripathi S.D. Bhandarkar.
• Goodman and Gilman’s. The Pharmacological Basis of Therapeutics