ANTIHYPOTENSIVE

DRUGS
ROGER JOSEPH II RAMOS JECINO, RN, M.D.
• Sympathetic Adrenergic Agonists or Vasopressor
• Sympathomimmetic drugs are the first choice for treating severe hypotension or shock
• E.g Dobutamine, Dopamine, Ephedrine, Epinephrine, Norepinephrine
• MOA: they react with sympathetic adrenergic receptors to cause the effects of a sympathetic
stress response:
• Increase blood pressure
• Increase blood volume
• Increase strength of cardiac muscle contraction
• Adverse Effects:
• Decrease GI activity
• Nausea and constipation
• Increase respiratory rate
• Changes in blood pressure
• Changes in peripheral blood flow with numbness and tingling
• Alpha specific adrenergic agents
• E.g. Midodrine
• Use to treat orthostatic hypotension
• MOA: activate alpha receptors and produce an increase vascular tone, and
increase in the blood pressure
• Metabolized in the liver and excreted in the urine
• Contraindicated in patient with supine hypertension, CAD, or
pheochromocytoma
ANTIARRHYTHMIC
DRUGS
ROGER JOSEPH II RAMOS JECINO
CLASS I ANTIARRHYTHMIC

• MOA: blocks the SODIUM CHANNELS in the cell membrane during an action
potential, depresses phase O of the action potential
• Subclasses
• Class Ia – disopyramide, procainamide, quinidine
• Class Ib – lidocaine, mexiletine
• Class Ic –flecainide, propafenone
• Indications – tachycardia, potentially life threatening Ventricular Tachycardia
• Metabolism – Liver; Excretion – Kidney
• Able to cross placenta and present in milks
• Adverse events: CNS – dizziness, drowsiness, fatigue, twitching, slurred
speech, etc.; GI – changes in taste, nausea and vomiting; Cardiovascular –
proarrhythmic effects (e.g. Heart block), hypotension, vasodilation and
potential cardiac arrest; Respiratory depression
• Drug to Drug interaction
• Never to combine with beta-blockers and digoxin which are known to cause
arrhythmias
• Quinidne competes for renal transport sites with digoxin. Combining the two lead to
digoxin toxicity
• Drug-Food Reaction
• Quinidine requires a slightly acidic urine for excretion. Avoid food that alkalinize the
urine.
• Grapefruit intereferes with the metabolism of quinidine, leading to increased serum
levels.
CLASS II ANTIARRHYTHMIC
• MOA: beta adrenergic blockers that block beta-receptors, causing a depression of phase 4 of the action potential.
• Heart – decrease heart rate, cardiac excitability and cardiac output, slowing of conduction through AV node.
• Kidney – decrease in the release of renin.
• Pharmacokinetics:
• Oral – acebutolol, propranolol; Intravenous – Esmolol, Propranolol
• Exretion – urine; Metabolism - Liver
• Contraindication
• Sinus bradycardia
• AV blocks
• Hypotension
• Heart Failure
• Asthma/COPD
• Caution: diabetes, thyroid dysfunction
• Adverse Effect
• CNS – dizziness, insomnia, dreams and fatigue
• Cardiovascular – hypotension, bradycardia, AV block
• Respiratory – bronchospasm and dyspnea
• Gastrointestinal – nausea, vomiting, anorexia, constipation
• Drug to Drug interaction
• Verapamil – increases the adverse event, use cautiously
• Insulin – may increase possibility of hypoglycemia, patient should be monitored
closely
• Prototype
• Propranolol – indicated for patient with SVT, Vtach induced by digitalis and
catecholamines
CLASS III ANTIARRHYTHMIC

• Amiodarone, dofetelide, ibutilide and sotalol

• MOA: blocks potassium channels and slow the outward movement of
potassium during phase 3 of the action potential, prolonging it.
• Amiodarone – drug of choice for treating Ventricular fibrillation or pulses
Vtach in cardiac arrest situation
• Pharmacokinetics
• Amiodarone – available on oral and IV forms
• Metabolized in the liver and excreted by the kidney
• Contraindications
• No contraindication when used to life-threatening arrhythmias
• Caution: hypotension, respiratory depression, prolonged QT interval
• Adverse effect
• Liver toxicity – amiodarione
• Ocular abnormality
• Drug to Drug interaction
• Cause serious toxic effects if they are combined with digoxin or quinidine
• Increase risk of proarrhythmia if combined with antihistamines,
phenothiazines, tricyclic antidepressants
CLASS IV ANTIARRHYTHMIC
• MOA: Calcium Channel blockers that blocks the movement of calcium ions across the membrane,
depressing the generation of action potential and delaying phases 1 and 2
• E.g. Diltiazem and Verapamil
• Pharmacokinetics:
• Diltiazem is administered intravenously
• Verapamil is used intravenously when used as an antiarrhythmic
• Metabolized in the liver and excreted in the kidney
• Contraindication:
• Allergy to any calcium channel blocker
• Sick sinus syndrome or heart block
• Pregnancy and lactation
• Heart failure and hypotension
• Adverse events
• Adverse event related to their vasodilation of blood vessels
throughout the body
• CNS: dizziness, weakness, fatigue, depression with beta blockers
• GI upset, nausea and vomiting
• Drug to Drug interaction
• Beta blockers – increases risk of cardiac depression
• Digoxin – additive AV slowing
• Digoxin, carbamazepine, prazosin, and quinidine – increases levels of
toxicity
OTHER ANTIARRHYTHMIC
• Adenosine
• DOC for Supraventircular Tachycardia (SVT)
• It slow the conduction at the AV node, prolongs the refractory period
• Decreases automacity in the AV node.
• Digoxin
• Use to treat atrial arrhythmia
• Slows calcium from leaving the cell prolonging the action potential, slowing
conduction and heart rate
• Positive inotropic effect
NURSING CONSIDERATION
• Assessment
• Assess for contraindications or cautions
• Perform physical assessment
• Assess neurological status
• Assess cardiac status
• Monitor respiratory rate and depth
• Inspect abdomen
• Evaluate skin color, lesions and temperature
• Obtain a baseline ECG
• Nursing Diagnoses
• Decreased cardiac output related to cardiac effects
• Disturbed sensory perception
• Risk for injury related to adverse effect
• Deficient knowledge regarding the drug therapy
• Implementation
• Titrate the dose to the smallest amount needed to achieve control
of arrhythmia
• Monitor cardiac rhythm when initiating or changing the dose
• Ensure emergency life support equipment is readily available
• Administer parenteral forms as ordered
• Consult with the prescriber to reduce the dose in patients with
renal or hepatic dysfunction
• Establish safety precaution
• Arrange for periodic monitoring of cardiac rhythm
• Provide comfort measures
CARDIOTONIC AGENTS
ROGER JOSEPH II RAMOS JECINO
• Cardiotonic Agents – drugs used to increase the contractility of heart muscle
for patient experiencing heart failure
• Heart Failure – heart condition in which the heart fails to pump blood
around the body effectively
• Causes of heart failure
• Coronary Artery Disease – leading cause of heart failure, insufficient supply of blood
to meet the oxygen demands of the myocardium
• Cardiomyopathy – disease of the heart muscle that leads to an enlarge heart and
eventually to complete muscle failure and death
• Hypertensive Heart Disease – eventually leads to an enlarged cardiac muscle
because the heart must work harder than normal to pump against the high pressure
in the arteries
• Valvular Heart Disease – overload of ventricles because the valves do not close
tightly
CARDIOTONIC AGENTS
• Cardiac Glycoside (Digoxin)
• MOA: Increases intracellular calcium and allows more calcium to enter myocardial cells
during depolarization causing the following effects:
• Increased force of myocardial contraction (positive inotropic effect)
• Increased cardiac output and renal perfusion
• Slowed heart rate, owing to slowing of the rate of cellular repolarization (negative
chronotropic effect)
• Decrease conduction velocity through the AV node
• Overall effect is a decrease in the myocardial workload and relief of HF
• Other indications: Atrial flutter, atril fibrillation, paroxysmal atrial tachycardia
• Digoxin has a very narrow margin of safety
• Pharmacokinetics
• Available in oral and IV form
• Excreted in the urine
• Contraindications
• Ventricular tachycardia or fibrillation
• Heart block or sick sinus syndrome
• Idiopathic hypertrophic subaortic stenosis
• Acute MI
• Renal insufficiency
• Electrolyte abnormalities – increased calcium, decreased potassium, decreased
magnesium
• Adverse events
• Headache, weakness, drowsiness and vision changes (yellow halo)
• GI upset and anorexia
• Digitalis toxicity – anorexia, nausea, vomiting, malaise, depression, irregular HR
• Digoxin Immune Fab – antidote for digitalis toxicity
NURSING CONSIDERATION
• Implementation
• Consult with the prescriber about the need for a loading dose when
beginning a therapy
• Monitor apical pulse for 1 full minute before administering the drug, hold
if HR is less than 60 then repeat HR after 1 hr if still low withhold the drug
and inform the prescriber
• Monitor the pulse for any change in quality of rhythm
• Check the dose and preparation carefully
• Administer IV doses slowly for 5 minutes
• Maintain emergency drugs/equipment on standby
• Obtain digoxin level as ordered
• Phosphodiesterase Inhibitors
• E.g. Inamrinone and milrinone
• MOA: blocks the phosphodiesterase enzyme which increases cAMP which increases cellular
calcium levels in the cell
• Indications: short term treat of HF that has not responded to digoxin of diuretic alone
• Pharmacokinetics: available only on IV form, metabolized in the liver and excreted in the urine
• Adverse events: ventricular arrhythmias, hypotension and chest pain
• Drug to drug interaction:
• Furosemide – causes precipitation of inamrinone
• Contraindications
• Severe aortic and pulmonary valvular disease
• Acute MI
• Fluid volume deficit
• Ventricular arrhythmias
• Caution: elderly