Cardiac Conditions

PNS Anatomy

Neurons in midbrain, brainstem and sacral region of SC

CN X

Chronotropic effects

Only one organ or tissue target

SNS Anatomy

Neurons in t and l/s

Chronotropic and inotropic effects

Diffuse

Cholinergic receptor types

Nicotinic and muscarinic

Nicotinic cholinergic receptors, location, function

Type 1 in ANS

Type 2 in NMJ

ACh binds to them

Muscarinic Receptor types and their location

M1,4,5 in CNS

M2 in heart

M3 in pancreas, bladder

Adrenergic receptor types

Alpha 1 (SM in peripheral vasculature, intestinal wall, urethra, urinary sphincter, spleen capsule)

Alpha 2 (spinal interneurons, CNS nonadrenergic neurons, pancreas, GI, vasculature)

Beta 1 (heart and kidneys)

Beta 2 (SM of vasculature, bronchioles, gallbladder, uterus)

Beta 3 (adipose, heart, bladder)

Cholinergic stimulants

Increases synaptic activity either directly (to cholinergic receptors) or indirectly (inhibit AChE)

Adverse effects of cholinergic stimulants

GI distress

Salivation

Bronchoconstriction

Bradycardia

What diseases are treated with cholinergic stimulants

Alzheimer (atrophy of cholinergic neurons)

Glaucoma (increases PNS to remove humor in eye)

Myasthenia Gravis (downregulation of postsynaptic receptor)

Anticholinergic Drugs

Antimuscarinic (atropine) is tissue specific

Antinicotinic (trimethaphan and mecamylamine)

Use for Anticholinergic Drugs

IBS

Parkinson’s (overactivity of CNS cholinergic)

Motion sickness (scopolamine)

Urinary tract hypertonicity

Respiratory tract relaxation

Adverse effects of Anticholinergic Drugs

Dry mouth

Blurred vision

Urinary retention

Constipation

Tachycardia

Confusion/dizziness

What do A1 selevtive agonists bind to?

Directly and activate the receptor on vascular SM

Action of A1 selective agonists

SM contraction

Vasocontriction (increases BP by increased PVR (increase BP and decrease HR) (improves nasal congestion)

Pseudoephedrine (sudafed), phenylephrine

Adverse effects of A1 selective agonists

Increase BP, headache, abdnormally slow HR, chest pain, dyspnea

Alpha 2 selective agonist action

Treats HTN (stims receptors in brain and BS (inhibitory effect on SNS))

Spasticity (interneuron inhibition in SC → decreases MN excitability)

Clonidine, tizanidine

Adverse effects of A2 selective agonists

Dizziness, dry mouth, dyspnea, bradycardia, fainting

B1 selective agonists

Stimulation → increased HR and CO (myocaridum) in emergency

Dopamine and dobutamine

Adverse effects of B1 selective agonists

Chest pain, SOB, arrhythmias

B2 selective agonists

Relaxation of bronchioles in bronchospasm/construction

Uterine muscle relaxation

“ol” albuterol, metaproterenol

Adverse effects of B2 selective agonists

Nervousness, restlessness, trembling

Mixed alpha-beta

Amphetamines (increase NE and decrease reuptake)

Ephedrine (increase NE release; acute hypotension)

Epi (local vasoconstriction, prolongs anesthetic, anaphylactic shock, reestablished rhythm during MI)

NE (hypotension)

Metaraminol (hypotension)

Alpha antagonists

Reduce peripheral vascular tone → vasodilation (decreases BP by decreasing resistance)

HTN, vascular insufficiency, raynaud’s, hyperplasia

Alfuzosin, phenoxybenzamine, phentoalamine, flomax

Adverse effects of alpha antagonists

Tachycardia, Orthostatic hypotension, increase in plasma volume → increase risk of CHF

Beta blockers

Reduce rate and force of myocardial contractions

HTN, angina pectoris, CHF, prevent infarction

Metoprolol, propanolol, acebutolol, atenolol

Adverse effects of beta blockers

Nonspecific can target bronchiole SM and depression of cardiac function

Sympatholytics

Interfere with SNS discharge: B-adrenergic blockers, a-adrenergic blockers, presynmaptic adrenergic NT depeletors (reserpine), central acting agents (clonidine; A2), ganglionic blockers

Diuretics

Increase renal excretion of water and Na → decrease fluid in vascular system

What are the classes of diueretics

Thiazide (inhibit Na reabsorption; for HTN)

Loop (inhibit reabsorption of Na and Cl; furosemide/lasix)

Potassium sparing (sprionolactone/aldactone)

Vasodilators

Reduce PVR by directly acting on vascular SM using second messengers

Hydralazine, minoxidil, fenoldopam, NO

Venous dilation, decreases preload

Calcium channel blockers

Dihydropyridine (inhib Ca entry → vasodilation and decreased vascular resistance; amlodipine, nifedipine)

Nondihydropyridine (decrease HR and contractile force; diltiazem, verapamil)

“Pines”

Anticoagulants

Platelet inhibitors (inhibit syn of PGEs which are responsible for activating platelets)

Clopidogrel (plavix) or prasugrel are stronger

Heparin inhibits thrombin

Renin

enzyme in kidneys released when BP falls

Angiotensinogen

peptide produced by liver that circulates continuously

Angiotensin 2/3

increase aldosterone secretion from adrenal cortex which increases Na reabsorption from kidneys

Thickens vessel walls when in excess

Sodium channel blockers

Bind to membrane Na channels to normalize rate of firing

Class 1A (disopyramide, procainamide, quinidine)

Class 1B (lidocaine, mexiletine)

Class 1C (flecainide, propafenone)

Potassium channel blockers

Delay depolarization of cardiac cells prolongs the effective refractory period → slowing HR

Prevents K from leaving

Amiodarone, dofetilide, dronedarone, ibulitide

Digitalis

Inhibits Na/K pump → increased sodium = increased calcium in cell → more Ca in SR → greater cardiac contraction

Toxicity