Module 8 Pharma

COLLEGE OF NURSING AND PHARMACY
C-NCM 106 – PHARMACOLOGY

First Semester | AY 2021-2022
Module 8: Drugs Affecting the Cardiovascular System

Time Frame: (3hours)
Schedule of synchronous sessions: 2A Friday 3:00p.m. – 6:00 p.m.
2B Monday 3:00p.m. – 6:00 p.m.
Mapped Learning Outcomes and Course Content for C-NCM 106 Pharmacology, Module 8
Target Learning Outcomes Content and Activities
Hour (At the close of the period allotted, Online Session Offline Session
students should have :)
3hours 1. Recall the anatomy and A. Review of the Anatomy Self – directed Learning
physiology of the and Physiology of the Activities:
cardiovascular system through Cardiovascular System
the illustrations presented. B. Cardiac Glycosides, • Song
2. Describe common disorders of Antianginals and • Medication Monitoring Sheet
the cardiovascular system Antidysrhythmics
(congestive heart failure, C. Diuretics NOTE: Rubrics provided at the
angina pectoris, dysrhythmias D. Antihypertensives end of the module.
and hypertension) E. Antihypotensives
emphasizing on the
pathophysiology.
3. Discuss salient information
related to the different
classifications of the drugs
affecting the cardiovascular
system emphasizing on the
nursing responsibilities and
patient teaching through case
scenario analysis.
4. Create a song about the drugs
that cardiovascular system that
will help recall the concept.
1. Content / Discussion / Learning Resources / Links
A. Review of the Anatomy and Physiology of the Cardiovascular System /

Autonomic Nervous System
Heart
 Composed of 4 chambers – right atrium, right ventricle, left atrium, left ventricle
 Myocardium – heart muscle that surrounds the ventricles and atria
 Pericardium – fibrous covering of the heart that protects it from injury and infection.
 Endocardium – three layered membrane that lines the inner part of the heart chambers.
 Composed of 4 valves (2 atrioventricular – tricuspid and mitral and 2semilunar – pumonic and
aortic)
Faculty: Cherry B. Lazatin, RN,RPh,MAN Page 1 of 34

 Two main coronary arteries- right coronary artery (supply blood to the right atrium and both
ventricles of the heart) left coronary artery (supply blood to the left atrium and both ventricles of the
heart)
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Conduction of Electrical Impulses

 Myocardium – capable of generating and conducting its
own electrical impulses.
 Sinoatrial node – pacemaker; regulates the heart beat by
firing of electrical impulses which is normally 60 to 80
beats /min for adult.
 Atrioventricular node – firing of electrical impulses which
is normally 40 to 60beats/min for adult; takes over as the
pacemaker if the SA node fails; sends impulses to the
ventricles.
 Bundle of His (AV Bundle)
 Drugs that affect the cardiac conduction:
Calcium, digitalis preparations, quinidine and other
preparation
Autonomic nervous system and drugs that stimulate or
inhibit it influence heart contractions.
Sympathetic NS and drugs that stimulate (HR)
Parasympathetic NS and drugs the stimulate ( HR)
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Regulation of Heart and Blood Flow

 Normal heart beat 60 to 80beat/minute pumping blood
to the systemic circulation
 Average systemic arterial pressure (BP) 120/80mmHg.
 Arterial blood pressure is determined by peripheral
resistance and cardiac output
 Cardiac output ( volume of blood expelled from the heart
in 1 minute) = HR X stroke voule
 Average cardiac output = 4 to 8 L/min.
 Stroke volume (amount of blood ejected from the left
ventricle with each heartbeat) = 70ml/beat
 Three factors that determine the stroke volume
a.) Preload – blood flow force that stretches the ventricle
at the end of the diastole;
Direct relationship (preload = stroke volume)
b.) Contractility – force of ventricular contraction
c.) Afterload – resistance to ventricular ejection of blood;
caused by opposing pressures in the aorta and
systemic circulation.
Inverse relationship (afterload = stroke volume)
 Vasodilators decrease preload and afterload, decrease
arterial pressure and cardiac output
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Circulation
 Two types of circulation
a.) Pulmonary circulation – heart pumps
deoxygenated blood from the right ventricle
through the pulmonary artery to the lungs.
Pulmonary artery carries blood that has a high
concentration of carbon dioxide. Oxygenated
blood returns to the left atrium by the
pulmonary vein
b.) Systemic circulation – peripheral circulation –
heart pumps blood from the left ventricle to
the aorta and into the general circulation.
Arteries and arterioles carry the blood to
capillary beds. Nutrients in the capillary blood
are transferred to cells in exchange for waste
products. Blood returns to the heart through
venules and veins.
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Adrenergic and Cholinergic
Autonomic Nervous System – system responsible for autonomic responses like beating of the heart and
other functions involving smooth muscles
Two Specific Branches

1. Adrenergic pathways – sympathetic nervous system
▪ Neurotransmitter (norepinephrine or epinephrine or adrenaline)
▪ Fight or flight response
▪ All other systems increase effect except GI and GU
▪ Receptors – alpha and beta (distributed throughout the body)
2. Cholinergic pathways – parasympathetic nervous system
▪ Neurotransmitter (acetylcholine)
▪ Digest and rest
▪ GI and GU effects increase
▪ Receptors – nicotinic and muscarinic (mostly found in the skeletal muscles)
B. Cardiac Glycosides, Antianginals and Antidysrhythmics

Congestive Health Failure
➢ Heart Failure / Pump Failure / Chronic Heart Failure → heart muscle (myocardium) weakens and
enlarges, it loses its ability to pump blood through the heart and into the systemic circulation.
➢ Acute Heart Failure → when the compensatory mechanisms fail and the peripheral and lung tissues
are congested.
➢ Causes: chronic hypertension, myocardial infarction (MI), coronary artery disease (CAD), valvular
heart disease, congenital heart disease, and arteriosclerosis
➢ Left sided HF – left ventricle does not contract sufficiently to pump the blodd returned from the lungs
and left atrium out through the aorta into the peripheral circulation → excessive amounts of blood to
back up into the lung tissue.
➢ Right sided HF → heart does not sufficiently pump the blood returned into the right atrium from the
systemic circulation → blood and its constituents are backed up into peripheral tissues → peripheral
edema.
1. Cardiac Glycosides
Digoxin and Digitoxin
 Naturally occurring cardiac glycosides are found in a number of plants (digitalis)

 Digitalis – one of the oldest drugs
 It inhibits the sodium potassium pump, which results in an increase in intracellular sodium.
 This increase leads to an influx of calcium, which causes the cardiac muscle fibers to contract
more efficiently.
 Digitalis preparations have three effects on heart muscle:
a.) Positive inotropic action – increases myocardial contraction stroke volume
b.) Negative chronotropic action – decreases heart rate
c.) Negative dromotropic action – decreases conduction of heart cells.
 The increase in myocardial contractility strengthens cardiac, peripheral, and kidney function
by enhancing cardiac output, decreasing preload, improving blood flow to the periphery and
kidneys, decreasing edema, and promoting fluid excretion → fluid retention in the lungs
and extremities
 Cardiac glycosides are also used to correct atrial fibrillation, cardiac dysrhythmia with rapid
uncoordinated contractions of atrial myocardium, and atrial flutter, cardiac dysrhythmia with
rapid contractions of 200 to 300 beats/min.
 Contraindications: Hypersensitivity to digitalis, full digitalization dose should not be given if
client has received digoxin in the previous week
 Drug interaction: Antacids, cholestyramine and colestipol decreases digoxin absorption; IV Ca
+ digoxin = increase risk of cardiac dysrhythmias; erythrocin and nefazadone = increase
digoxin level, diuretics, corticosteroids, amphotericin B, laxatives, Na polystyrene sulfonate
may cause hypokalemia – increase risk of digitalis toxicity
Digoxin
• Absorption in oral tablet is 70% to 80%; liquid 75% to 85%; protein binding power is 20% to 30%;
half life is 30 to 40 hours; need to monitor digitalis toxicity; metabolized int eh liver and excreted in
the kidney.
• Thyroid function can alter the metabolism of cardiac glycosides; decrease dose of digoxin;
hyperthyroidism increase the dose.
• In patients with a failing heart, cardiac glycosides increase myocardial contraction, increases cardiac
output and improves circulation and tissue perfusion.
• Because these drugs decrease conduction through the AV node, the heart rate decreases.
• Drug interactions: Drug interactions can cause digitalis toxicity.
a.) Diuretics promote the loss of potassium from the body (hypokalemia) which increases the effect
of digoxin at its myocardial cell site of action, resulting in digitalis toxicity.
b.) Cortisone preparations promote sodium retention and potassium excretion (hypokalemia) →
consume foods rich in potassium or supplements
• Digoxin therapeutic serum level for dysrhythmias is 0.8 to 2.0 ng/mL.
• Target therapeutic serum level for heart failure is 0.5 to 1.0 ng/mL
Digitalis (Digoxin) Toxicity
• Signs and symptoms: anorexia, diarrhea, nausea and vomiting, bradycardia (pulse rate below 60
beats/min), premature ventricular contractions, cardiac dysrhythmias, headaches, malaise, blurred
vision, visual illusions (white, green, or yellow halos around objects), confusion, and delirium.
• Older adults are more prone to toxicity.
• Cardiotoxicity is a serious adverse reaction to digoxin, and ventricular dysrhythmias result.
• Three cardiac-altered functions can contribute to digoxin-induced ventricular dysrhythmias:
a.) Suppression of AV conduction
b.) Increased automaticity
c.) Decreased refractory period in ventricular muscle
• Phenytoin and lidocaine are effective in treating digoxin induced ventricular dysrhythmias.
• Lidocaine – limited to short-term treatment
Antidote for Cardiac / Digitalis Glycosides
• Digoxin-immune Fab – given to treat severe digitalis toxicity.
• This agent binds with digoxin to form complex molecules that can be excreted in the urine, thus
digoxin is unable to bind at the cellular site of action.

Nursing Implication
1. Check apical PR before administering digoxin. Do not administer if PR is below 60 beats/min.
2. Determine signs of peripheral and pulmonary edema, which indicate HF is present.
3. Monitor serum digoxin level (normal therapeutic drug range is 0.8 to 2 ng/mL).
A serum digoxin level greater than 2 ng/mL is indicative of digitalis toxicity.
4. Monitor serum potassium level (normal range is 3.5 to 5.0 mEq/L), and report if hypokalemia (<3.5
mEq/L) is present.
5. Instruct patients to report side effects: pulse rate less than 60 beats/min, nausea and vomiting,
headache, diarrhea, and visual disturbances, including diplopia.
6. Be cautious in dosing: Digoxin – 0.125 to 0.5mg; Digitoxin – 0.05 to 0.1mg
2. Phosphodiesterase Inhibitors
 Inotropic group of drugs given to treat acute heart failure
 Mechanism of action: inhibits the enzyme phosphodiesterase (PDE) ➔ promotes a positive
inotropic response and vasodilation.
 Increases stroke volume and cardiac output and promotes vasodilation.
 Administered intravenously for no longer than 48 to 72 hours.
 Severe cardiac dysrhythmias might result from the use of PDE inhibitors, so the patient’s
electrocardiogram (ECG) and cardiac status should be closely monitored.
 E.g. Milrinone lactate – high-alert medication that may cause significant harm to a patient
when given inappropriately.
Other Agents Used to Treat Heart Failure

 Vasodilators, ACE inhibitors, angiotensin II–receptor antagonists (blockers), diuretics (thiazides,
furosemide), spironolactone, and some beta blockers
 Vasodilators → decrease venous blood return to the heart and result in a decrease in cardiac filling,
ventricular stretching (preload), and oxygen demand on the heart.
 Arteriolar dilators act in three ways:
a.) Reduce cardiac afterload, which increases cardiac output
b.) Dilate the arterioles of the kidneys, which improves renal perfusion and increases fluid loss
c.) Improve circulation to the skeletal muscles.
 ACE inhibitors → dilate venules and arterioles; improves renal blood flow and decreases blood fluid
volume; moderately decrease the release of aldosterone, which in turn reduces sodium and fluid
retention
 ACE inhibitors can increase potassium levels, so serum potassium levels should be monitored,
 Angiotensin II–receptor blockers (ARBs) e.g.: valsartan and candesartan have been approved for
 HF in patients who cannot tolerate ACE inhibitors.
 Diuretics →first-line drug treatment for reducing fluid volume; frequently prescribed with digoxin
or other agents.
 Spironolactone, a potassium-sparing diuretic, is used in treating moderate to severe HF.
 Aldosterone secretions in HF → promotes body loss of potassium and magnesium needed by the
heart and increases sodium and water retention.
 Spironolactone – blocks the production of aldosterone; improves HR variability and decreases
myocardial fibrosis by its cardioprotective effect of blocking aldosterone in the heart and blood
vessels to promote cardiac remodeling.
 Recommended dose for HF is 12.5 to 25 mg/day.

 Though hyperkalemia is rare unless the patient is receiving 50 mg/day and has renal insufficiency,
serum potassium level should be closely monitored.
 Beta blockers – before it is contraindicated since it reduces cardiac contractility, with dosage
control, beta blockers (carvedilol, metoprolol, and bisoprolol) have been shown to improve cardiac
performance.
 Doses should be low initially and gradually increased.
 It may take 1 to 3 months for a beneficial effect to develop.
 Atrial natriuretic peptide hormone (E.g. Nesiritide) – inhibits antidiuretic hormone (ADH) by
increasing urine sodium loss; promotes vasodilation, natriuresis, and diuresis.
 Useful for treating patients who have acute decompensated HF with dyspnea at rest or who have
dyspnea with little physical exertion.
 BiDil (hydralazine + isosorbide dinitrate) approved by U.S. Food and Drug Administration (FDA) for
the treatment of HF
Angina Pectoris
➢ Condition of acute cardiac pain caused by inadequate blood flow to the myocardium due to either
plaque occlusions within or spasms of the coronary arteries.
➢ Blood flow →  oxygen to the myocardium → pain.
➢ Anginal pain: tightness, pressure in the center of the chest, and pain radiating down the left arm (last
only for few minutes), referred pain felt in the neck and left arm commonly occurs with severe
angina pectoris.
➢ Anginal attacks may lead to MI (heart attack)
➢ Types of angina pectoris
a.) Classic (stable) angina occurs with predictable stress or exertion.
b.) Unstable (preinfarction) angina occurs frequently with progressive severity unrelated to activity
and is unpredictable regarding stress/exertion and intensity; indicates impending MI
(emergency medical attention)
c.) Variant (Prinzmetal, vasospastic) angina occurs during rest.
Antianginal Drugs
 Mechanism of action:  blood flow either by  oxygen supply or by  oxygen demand by the
myocardium
 Three types of antianginals: nitrates, beta blockers, calcium channel blockers.
 Effect of nitrates: Reductions of venous tone →  the workload of the heart and promotes
vasodilation.
 Effects of beta blockers and calcium channel blockers:  the workload of the heart and  oxygen
demand
 Nitrates and calcium channel blockers are effective in treating variant (vasospastic) angina pectoris;
beta blockers are not effective for this type of angina and may aggravate it.
 With stable angina, beta blockers can effectively be used to prevent angina attacks.
 With unstable angina, immediate medical care is necessary.
 Nitrates are usually given sublingually and intravenously as needed.
 If the cardiac pain continues, a beta blocker is given intravenously, and if the patient is unable to
tolerate beta blockers, a calcium channel blocker may be substituted.

1. Nitrates
Isosorbide Dinitrate (Isordil), Isosorbide (Imdur), Nitroglycerin SL (Nitrostat),
Nitroglycerin SR Topical, Transdermal
 First agents used to relieve angina which affects coronary arteries and blood vessels in the
venous circulation → generalized vascular and coronary vasodilation →  blood flow
through the coronary arteries to the myocardial cells.
 Reduces myocardial ischemia but can cause hypotension
 Effects of SL nitroglycerin last for 30 to 60 minutes;
 After a dose of nitroglycerin, the patient may experience dizziness, faintness, or headache as a
result of the peripheral vasodilation.
 Sublingual nitroglycerin is the most commonly used nitrate; not swallowed since it
undergoes first-pass metabolism by the liver; readily absorbed into the circulation through
the SL vessels
 Other dosage forms of nitroglycerin: topical (ointment, transdermal patch), translingual, oral
extended-release capsule and tablet, aerosol spray (inhalation), and IV.
 Pharmacokinetics: Absorbed rapidly and directly into the internal jugular vein and the right
atrium when taken SL; GI absorption inactivated by first pass effect in the liver; slow
absorption if given through ointment and patch; excreted in urine, 60% protein bind; half-life
of 1 to 3 minutes
 Pharmacodynamics: acts directly on the smooth muscle of blood vessels, causing relaxation
and dilation;  cardiac preload (amount of blood in the ventricle at the end of diastole) and
afterload (peripheral vascular resistance) and reduces myocardial O2 demand.
 With dilation of the veins, there is less blood return to the heart, and with dilation of the
arteries, there is less vasoconstriction and resistance
 Onset of action: SL - rapid (1-3 minutes); transdermal method (40-60 minutes).
 Duration of action: transdermal nitroglycerin patch is approximately 18 to 24 hours
 Nitroglycerin ointment is effective for only 4 to 8 hours – need to be reapplied 3 to 4x a day
 Decline use of nitroglycerin ointment since the advent of the transdermal nitroglycerin patch,
which is applied only once a day.
 Side Effects / Adverse Reactions: Headache - most common side effects but become less
frequent with continued use.
 Other side effects: hypotension, dizziness, weakness, and faintness.
 Tapering of the dose over several weeks is important when nitroglycerin ointment or
transdermal patches are discontinued to prevent the rebound effect of severe pain caused by
myocardial ischemia, lack of blood supply to the heart muscle.
 Reflex tachycardia (HR related to overcompensation of the cardiovascular system) may
occur if the nitrate is given too rapidly.
 Contraindications: hypersensitivity to nitrates, hypotension and hypovolemia, severe
bradycardia or severe tachycardia, right vertricular myocardial infarction, use of Viagra
within 24hours
 Drug Interactions: a.) do not mix with any medications in the bottle or IV tubing; b.) use of
sildenafil citrate (Viagra) within 4hours leads to profound hypotension; c.) all other
antihypertensive and vasodilation medications may interact to cause profound hypotension;
d.) IV NTG may antagonize heparin anticoagulant; e.) alcohol consumption should be avoided

Administration Consideration
1. Instruct the client to take no more than 3 nitroglycerin SL tablets (1 tablet every 5 minutes); if pain
persists after a total of 3 tablets, the patient should immediately call for medical assistance.
2. Nitroglycerin SL tablet decompose when exposed to heat and light, so they must be kept in their
original, airtight glass containers.
3. Rotate the location of NTG ointment or patch to reduce skin irritation and enhance absorption;
place on hairless areas for predictable absorption.
4. Patch should be removed nightly to allow for an 8- to 12-hour nitrate-free interval to avoid tolerance
associated with uninterrupted use or continued dosage increases of nitrate preparations.
5. Client may swim or bathe with an NTG in place
6. Hospitalize client – tablet should be at the bedside
2. Beta Blockers
Non-selective beta blockers: propranolol, nadolol, pindolol

Cardioselective beta blokers: atenolol, metoprolol
 Beta-adrenergic blockers block the beta1- and beta2-receptor sites.

 Decrease the effects of the sympathetic nervous system by blocking the action of the
catecholamines, epinephrine and norepinephrine →  HR and BP.
 Used as antianginal, antidysrhythmic, and antihypertensive drugs.
 Effective as antianginals because by  the HR and myocardial contractility, they reduce the
need for oxygen consumption and consequently reduce anginal pain.
 Most useful for classic (stable) angina
 Tapering of the dose to avoid reflex tachycardia and recurrence of angina pain.
 Patients who have HR and BP, second and third degree AV block cannot take beta blockers.
 Non selective beta blockers – HR and can cause bronchoconstriction
 Cardioselective beta blockers (β1) – HR but avoid vasoconstriction
 Pharmacokinetics: well absorbed orally; half-life of propranolol is 2 to 6 hours, atenolol has a
half-life of 6 to 7hours, metoprolol half-life of 3 to 4 hours.
 Propranolol and metoprolol are metabolized and excreted by the liver.
 Pharmacodynamics: beta blockers  the force of myocardial contraction, oxygen demand by
the myocardium is reduced.
 Effective for classic (stable) angina.
 Onset of action of propranolol 30 minutes, peak action is reached in 2 to 4 hours, and its
duration is 12 to 24 hours. For the cardioselective beta blockers, the onset of action of
atenolol is 60 minutes, its peak action occurs in 2 to 4 hours, and its duration of action is 24
hours. The onset of action of selective metoprolol is reached in 30 to 60 minutes, and the
duration of action is approximately 3 to 6 hours.
 Side Effects / Adverse Reactions: Both nonselective and selective beta blockers: HR and BP
 Nonselective beta blockers, bronchospasm, behavioral or psychotic response, and impotence
(with use of Inderal) are potential adverse reactions.
 Close monitoring of vital signs in early stage of therapy.
 Tapering of dose for 1 or 2 weeks before discontinue to prevent rebound effects (reflex
tachycardia or life-threatening cardiac dysrhythmias)

3. Calcium Channel Blocker / Calcium Blockers
Amlodipine, verapamil, nifedipine, and diltiazem

nicardipine hydrochloride (HCl), felodipine, and nisoldipine
 Used for the treatment of stable and variant angina pectoris, certain dysrhythmias, and
hypertension.
 Calcium activates myocardial contraction, increasing the workload of the heart and the need
for more oxygen.
 Therapeutic effect:
a.) Relax coronary artery spasm (variant angina) and relax peripheral arterioles (stable
angina)
b.) Decreasing cardiac oxygen demand, decrease cardiac contractility (negative inotropic
effect that relaxes smooth muscle), afterload, and peripheral resistance
c.) Reduce the workload of the heart, which decreases the need for oxygen.
 Effectively used for long-term treatment of angina
 Pharmacokinetics: absorbed through the GI mucosa; first-pass metabolism by the liver
decreases the availability of free circulating drug, and only 20% of verapamil, 45% to 65% of
diltiazem, and 35% to 40% of nifedipine are bioavailable: highly protein bound (70% to
98%), and their half-life usually 2 to 12 hours
 Other e.g. of calcium channel blockers highly protein bound (greater than 93%). Nicardipine
has the shortest half-life at 11.5 hours.
 Pharmacodynamics: Bradycardia - common problem with the use of verapamil
 Nifedipine - most potent of the calcium blockers, promotes vasodilation of the coronary and
peripheral vessels, and hypotension can result.
 Onset of action is 10 minutes for verapamil and 30 minutes for nifedipine and diltiazem.
 Verapamil’s duration of action is 6 to 8 hours when given PO and 10 to 20 minutes when
given IV
 Duration of action for nifedipine and diltiazem is 6 to 8 hours.
 Side Effects / Adverse Reactions: headache, hypotension (more common with nifedipine and
less common with diltiazem), dizziness, and flushing of the skin. Reflex tachycardia occurs
with hypotension.
 Peripheral edema may occur with nicardipine, nifedipine, and verapamil; changes in liver and
kidney function, and serum liver enzymes should be checked periodically.
 Frequently given with other antianginal drugs such as nitrates to prevent angina.
 In its immediate-release form (10- and 20-mg capsules), nifedipine is associated with an
increased incidence of sudden cardiac death, especially when prescribed in high doses for
outpatients.
 This is not true of the sustained-release preparations. Immediate release nifedipine is usually
prescribed only as needed in the hospital setting for acute increases in blood pressure.
Cardiac Dysrhythmias / Arrhythmia

➢ Any deviation from the normal rate or pattern of the heartbeat.
➢ Heart rates that are too slow (bradycardia), too fast (tachycardia), or irregular.
➢ Dysrhythmia (disturbed heart rhythm) and arrhythmia (absence of heart rhythm)
➢ ECG identifies the type of dysrhythmia.

➢ P wave of the ECG reflects atrial activation, the QRS complex indicates ventricular depolarization, and
the T wave reflects ventricular repolarization (return of cell membrane potential to resting after
depolarization).
➢ The PR interval indicates AV conduction time, and the QT interval reflects ventricular action
potential duration.
➢ Atrial dysrhythmias prevent proper filling of the ventricles and decrease cardiac output by 33%.
➢ Ventricular dysrhythmias are life threatening because ineffective filling of the ventricle and
ineffective pumping results in decreased or absent cardiac output. With ventricular tachycardia,
ventricular fibrillation is likely to occur, followed by death.
➢ Cardiopulmonary resuscitation (CPR) is necessary to treat these patients.
➢ Cardiac dysrhythmias frequently follow an MI (heart attack) or can result from hypoxia (lack of
oxygen to body tissues), hypercapnia (increased carbon dioxide in the blood), thyroid disease,
coronary artery disease, cardiac surgery, excess catecholamines, or electrolyte imbalance.
Cardiac Action Potentials

➢ Electrolyte transfer occurs through the cardiac muscle cell membrane.
➢ When sodium and calcium enter the cardiac cell, depolarization (myocardial contraction) occurs.
➢ Sodium enters rapidly to start the depolarization, and calcium enters later to maintain it.
➢ Calcium influx leads to an increased release of intracellular calcium from the sarcoplasmic reticulum,
resulting in cardiac contraction.
➢ In the presence of myocardial ischemia, the contraction can be irregular.
➢ Cardiac action potentials are transient depolarizations followed by repolarizations of myocardial
cells.
➢ Five phases:
a.) phase 0 is the rapid depolarization caused by an influx of sodium ions
b.) phase 1 is initial repolarization, which coincides with termination of sodium ion influx
c.) phase 2 is the plateau and is characterized by the influx of calcium ions, which prolong the action
potential and promote atrial and ventricular muscle contraction
d.) phase 3 is rapid repolarization caused by influx of potassium ions
e.) phase 4 is the resting membrane potential between heartbeats and is normally flat in ventricular
muscle, but it begins to rise in the cells of the sinoatrial (SA) node as they slowly depolarize
toward the threshold potential just before depolarization occurs, initiating the next heartbeat.
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Antidysrhythmic Drugs
 Desired action: to restore the cardiac rhythm to normal
1. Class I: Sodium Channel Blockers

 Mechanism of action: decreases sodium influx into cardiac cells.
 Responses to the drug are decreased conduction velocity in cardiac tissues; suppression of
automaticity, which decreases the likelihood of ectopic foci; and increased recovery time
(repolarization or refractory period).
 There are three subgroups of sodium channel blockers:
a.) Class IA slow conduction and prolong repolarization (quinidine, procainamide, disopyramide)
b.) Class IB slow conduction and shorten repolarization (lidocaine, mexiletine HCl, tocainide)
c.) Class IC drugs prolong conduction with little to no effect on repolarization (flecainide,
propafenone)
Lidocaine
• Class IB sodium channel blocker, was used as a local anesthetic and antidysrhythmic properties
• Used to treat acute ventricular dysrhythmias.
• Slows conduction velocity and decreases action potential amplitude.
• Onset of action (IV) is rapid. About one third of lidocaine reaches the general circulation, and a bolus
of lidocaine is short-lived.
2. Class II: Beta Blockers

 Mechanism of action: decrease conduction velocity, automaticity, and recovery time
(refractory period). E.g.: propranolol, acebutolol, esmolol, and sotalol.
 More frequently prescribed for dysrhythmias than are sodium channel blockers.
 Gradually reduced in dose upon discontinuation.
 Acebutolol hydrochloride, which can be prescribed to treat recurrent stable ventricularv
dysrhythmias.
3. Class III: Drugs That Prolong Repolarization

Amiodarone
 Mechanism of action: prolong repolarization and are used in emergency treatment of
ventricular dysrhythmias when other antidysrhythmics are ineffective.
 Amiodarone increases the refractory period (recovery time) and prolongs the action
potential duration (cardiac cell activity)
4. Class IV: Calcium Channel Blockers

 Verapamil and diltiazem.
 Verapamil is a slow (calcium) channel blocker that blocks calcium influx, thereby decreasing
the excitability and (negative inotropic) contractility of the myocardium.
 It increases the refractory period of the AV node, which decreases ventricular response.
 Verapamil is contraindicated for patients with AV block or HF.

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 Side Effects / Adverse Reactions: Quinidine, the first drug used to treat cardiac dysrhythmias:
nausea, vomiting, diarrhea, confusion, and hypotension, heart block and neurologic and psychiatric
symptoms.
 Procainamide causes less cardiac depression than quinidine.
 High doses of lidocaine → cardiovascular depression, bradycardia, hypotension, seizures, blurred
vision, and double vision, less serious side effects may include dizziness, and confusion.
 Use of lidocaine is contraindicated in patients with advanced AV block; used with caution in patients
with hepatic disorders or HF.
 Mexiletine has side effects similar to lidocaine, and both drugs are contraindicated for use in patients
with cardiogenic shock or in those with second- or third-degree heart block.
 Beta blockers are bradycardia and hypotension.
 Bretylium tosylate and amiodarone can cause nausea, vomiting, hypotension, and neurologic
problems.
 Calcium blockers side effects: nausea, vomiting, hypotension, and bradycardia.
 All antidysrhythmic drugs are potentially prodysrhythmic related to both the pharmacologic activity
of the drug on the heart and the inherently unpredictable activity of a diseased heart, with or without
the use of drugs.
 Life-threatening ventricular dysrhythmias can result from appropriate and skillful attempts at drug
therapy to treat patients with heart disease.
 Antidysrhythmic drug therapy is often initiated during continuous cardiac monitoring of the patient’s
heart rhythm in a hospital setting.

Other Antiarrhythmic Drug

 Mechanism of action: slow conduction through the SA and AV node; interrupt the re-entry pathways
through the AV node; depress left ventricular function (very temporary); treat supraventricular
dysrhythmias
 Common drug: Adenosine (Adenocard, Adenoscan)
 Administration Consideration: rapid bolus; administer directly into vein as proximal to the insertion
site as possible (half-life 10seconds) follow with rapid normal saline flush → expect sudden slowing
of the HR; store at room temperature to avoid crystallization
 Drug interaction: Dipyridamole can potentiate the effects of adenosine; theophylline can block
electrophysiologic effects of adenosine; carbamazine may increase risk of heart block
 Side effect: flushing of the face
C. Diuretics
 Two main purposes:
a.) To decrease hypertension (lower blood pressure)
b.) To decrease edema, peripheral and pulmonary, in heart failure (HF) and renal or liver disorders
 Can be used alone or in combination in the treatment of hypertension and edema
 Therapeutic effect: increased urine flow, or diuresis, by inhibiting sodium and water reabsorption
from the kidney tubules.
 Most sodium and water reabsorption occurs throughout the renal tubular segments (proximal, loop
of Henle [descending loop and ascending loop], and collecting tubule).
 Diuretics can affect one or more segments of the renal tubules.
 Every 1.5 hours, the total volume of the body’s extracellular fluid (ECF) goes through the kidneys
(glomeruli) for cleansing; first process for urine formation.
 Small particles such as electrolytes, drugs, glucose, and waste products from protein metabolism are
filtered in the glomeruli.
 Larger products such as protein and blood cells are not filtered with normal renal function, and they
remain in the circulation. Sodium and water are the largest filtrate substances.
 Normally, 99% of the filtered sodium that passes through the glomeruli is reabsorbed; 50% to 55%
of sodium reabsorption occurs in the proximal tubules, 35% to 40% occurs in the loop of Henle, 5%
to 10% occurs in the distal tubules, and less than 3% occurs in the collecting tubules.
 Diuretics that act on the tubules closest to the glomeruli have the greatest effect in causing
natriuresis, sodium loss in the urine (E.g. osmotic diuretic mannitol)
 The diuretic effect depends on the drug reaching the kidneys and its concentration in the renal
tubules.
 Antihypertensive effect of diuretics is related to promotion of sodium and water loss by blocking
sodium and chloride reabsorption → fluid volume, which lowers blood pressure.
 Many diuretics cause the loss of other electrolytes, e.g. potassium, magnesium, chloride, and
bicarbonate.
 Potassium wasting – diuretics that promote potassium excretion
 Potassium sparing -- diuretics that promote potassium retention

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1. Thiazides and Thiazide – like Diuretics

 First thiazide, chlorothiazide (1957) and hydrochlorothiazide
 Mechanism of action: act on the distal convoluted renal tubule, beyond the loop of Henle, to
promote sodium, chloride, and water excretion.
 Indication: treatment of hypertension and peripheral edema.
 Not effective for immediate diuresis and should not be used to promote fluid loss in patients
with severe renal dysfunction.
 Used primarily for patients with normal renal function.
  effectiveness of the thiazide if patient has renal disorder and creatinine clearance is <30
mL/min
 Thiazides cause a loss of sodium, potassium, and magnesium, but promote calcium
reabsorption.
 Hypercalcemia (calcium excess) may result, and the condition can be hazardous to the patient
who is digitalized or has cancer that causes hypercalcemia.
 Thiazides affect glucose tolerance → hyperglycemia (caution in patient with diabetes)
 Hydrochlorothiazide + selected angiotensin-converting enzyme (ACE) inhibitors, beta
blockers, alpha blockers, angiotensin II blockers, and centrally acting sympatholytics to
control hypertension (should be taken in the morning to avoid nocturia and sleep
interruption.

 Pharmacokinetics: well absorbed from the gastrontestinal (GI) tract; hydrochlorothiazide -

moderate protein-binding power; half-life of the thiazide drugs is longer than that of the loop
diuretics.
 Pharmacodynamics: act directly on arterioles to cause vasodilation, which can lower blood
pressure; promotion of sodium chloride and water excretion, resulting in a decrease in
vascular fluid volume and a concomitant decrease in cardiac output and blood pressure.
 Onset of action of hydrochlorothiazide occurs within 2 hours; peak concentration times are
long (4 hours).
 Groups of thiazide diuretics according duration of action:
a.) Short acting (duration <12 hours)
b.) Intermediate acting (duration 12–24 hours)
c.) Long acting (duration >24 hours).
 Side Effects and Adverse Reactions: electrolyte imbalances (hypokalemia, hypercalcemia,
hypomagnesemia, and bicarbonate loss), hyperglycemia (elevated blood glucose),
hyperuricemia (elevated serum uric acid level), and hyperlipidemia (elevated blood lipid
level).
 Potassium supplements are frequently needed.
 Thiazides block calcium and uric acid excretion – check serum calcium and uric acid levels
 Thiazides affect the metabolism of carbohydrates (hyperglycemia)
 Thiazides can increase serum cholesterol, low-density lipoprotein, and triglyceride levels.
 A drug may be ordered to lower blood lipids. Other side effects include dizziness, headache,
nausea, vomiting, constipation, urticaria, or hives (rare) and blood dyscrasias (rare).
 Contraindications: renal failure ( urine output,  blood urea nitrogen, serum creatinine)
 Drug Interactions: Thiazides can cause hypokalemia, which enhances the action of digoxin,
and digitalis toxicity
 Thiazides also induce hypercalcemia, which enhances the action of digoxin – digitalis toxicity
 Thiazides enhance the action of lithium, and lithium toxicity can occur.
 Thiazides potentiate the action of other antihypertensive drugs, which may be used to
advantage in combination drug therapy for hypertension.
Nursing Implication
1. Instruct patients to slowly change positions from lying to standing because dizziness may occur as a
result of orthostatic (postural) hypotension.
2. Advise patients to eat foods rich in potassium (fruits, fruit juices, and vegetables). Potassium
supplements may be ordered.
3. Instruct patients to take drugs with food to avoid GI upset (anorexia, nausea, vomiting, diarrhea).
2. Loop (High – Ceiling) Diuretics

 Mechanism of action: act on the thick ascending loop of Henle to inhibit chloride transport of
sodium into the circulation and inhibit passive reabsorption of sodium.
 Sodium and water are lost, together with potassium, calcium, and magnesium.
 Loop diuretics can affect blood glucose and can increase uric acid levels.
 Extremely potent and cause marked depletion of water and electrolytes.
 This high diuretic potential is the reason they are often called high-ceiling diuretics or
potassium-wasting diuretics.
 The effects of loop diuretics are dose related; that is, increasing the dose increases the effect
and response of the drug.

 More potent than thiazides for promoting diuresis, inhibiting reabsorption of sodium two to
three times more effectively, loop diuretics are less effective as antihypertensive agents.
 Loop diuretics should not be prescribed if a thiazide could alleviate body fluid excess.
 Loop diuretics can increase renal blood flow up to 40%.
 Pharmacokinetics: Loop diuretics are rapidly absorbed by the GI tract.
 These drugs are highly protein bound with half life that varies from 1 to 5 hours.
 Loop diuretics compete for protein-binding sites with other highly protein-bound drugs.
 Pharmacodynamics: Loop diuretics have a great saluretic (sodium chloride–losing) or
natriuretic (sodium-losing) effect and can cause rapid diuresis, decreasing vascular fluid
volume and causing a  cardiac output and BP.
 The onset of action of loop diuretics occurs within 30 to 60 minutes.
 The duration of action is shorter than that of the thiazides.
 Side Effects and Adverse Reactions: The most common side effects of loop diuretics are fluid
and electrolyte imbalances such as hypokalemia, hyponatremia, hypocalcemia,
hypomagnesemia, and hypochloremia.
 Hypochloremic metabolic alkalosis may result, which can worsen hypokalemia, and
orthostatic hypotension can occur.
 Thrombocytopenia, skin disturbances, and transient deafness are rarely seen.
 Drug Interactions: digoxin + loop diuretic = digitalis toxicity
 Hypokalemia enhances the action of digoxin and increases the risk for digitalis toxicity.
Furosemide
• If furosemide alone is not effective in removing body fluid, a thiazide may be added.
• Furosemide is usually administered as an oral dose in the morning or intravenously when the
patient’s condition warrants immediate removal of body fluid, for example, in cases of acute heart
failure or pulmonary edema.
• Furosemide is a frequently prescribed diuretic for patients whose creatinine clearance is < 30
mL/min and for those with end-stage renal disease. It causes excretion of calcium
• Derivatives of sulfonamides
• Because furosemide is more potent than thiazide, causes a vasodilatory effect; renal blood flow
increases before diuresis.
• Used when other conservative measures, such as sodium restriction and use of less potent diuretics,
fail.
• The oral dose of furosemide is usually twice that of an intravenous (IV) dose.
• The onset of action for IV furosemide is 5 minutes.
• Take with food to avoid nausea
Ethacynic Acid
• First loop diuretics
• Ethacrynic acid, a phenoxyacetic acid derivative, is a seldom-chosen loop diuretic; reserved for
patients who are allergic to sulfa drugs.
Bumetanide
• Derivatives of sulfonamides

3. Osmotic Diuretics
 Mechanism of action:  osmolality (concentration) and sodium reabsorption in the proximal
tubule and loop of Henle. Sodium, chloride, potassium (to a lesser degree), and water are
excreted.
 Indication: prevent kidney failure,  intracranial pressure (ICP, such as in cerebral edema),
and  intraocular pressure (IOP, such as in glaucoma).
 Mannitol is a potent osmotic, potassium-wasting diuretic frequently used in emergency
situations such as ICP and IOP.
 In addition, mannitol can be used with cisplatin and carboplatin in cancer chemotherapy to
induce a frank diuresis and  side effects of treatment.
 Mannitol is the most frequently prescribed osmotic diuretic, followed by urea.
 Diuresis occurs within 1 to 3 hours after IV administration.
 Side Effects and Adverse Reactions: fluid and electrolyte imbalance, pulmonary edema from
rapid shift of fluids, nausea and vomiting, tachycardia from rapid fluid loss, and acidosis.
 Crystallization of mannitol in the vial may occur when the drug is exposed to a low
temperature; the vial should be warmed to dissolve the crystals.
 The mannitol solution should not be used for IV infusion if crystals are present and have not
been dissolved.
 Contraindication: extreme caution to patients who have heart disease and HF.
 It should be immediately discontinued if the patient develops HF or renal failure.
4. Carbonic Anhydrase Inhibitors

 Mechanism of action: block the action of the enzyme carbonic anhydrase, which is needed to
maintain the body’s acid-base balance (hydrogen and bicarbonate ion balance).
 Inhibition of this enzyme causes increased sodium, potassium, and bicarbonate excretion.
 E.g. acetazolamide and methazolamide
 Prolonged use, metabolic acidosis can occur.
 Indication:  IOP in patients with open-angle (chronic) glaucoma, diuresis, management of
epilepsy, and treatment of high-altitude or acute mountain sickness.
 Not used in narrow-angle or acute glaucoma.
 Such drugs may also be used for patients in metabolic alkalosis who need a diuretic.
 Carbonic anhydrase inhibitors may be alternated with a loop diuretic.
 Side Effects and Adverse Reactions: Acetazolamide can cause fluid and electrolyte imbalance,
metabolic acidosis, nausea, vomiting, anorexia, confusion, orthostatic hypotension, and
crystalluria, hemolytic anemia and renal calculi
 Contraindication: first trimester of pregnancy.
5. Potassium – Sparing Diuretics

 Weaker than thiazides and loop diuretics; used as mild diuretics or in combination with
another diuretic such as hydrochlorothiazide or antihypertensive drug.
 Mechanism of action: act primarily in the collecting duct renal tubules and late distal tubule to
promote sodium and water excretion and potassium retention.
 It interferes with the sodium-potassium pump controlled by the mineralocorticoid hormone
aldosterone (sodium retained and potassium excreted).
 E.g. spironolactone, amiloride, triamterene, and eplerenone
 Amiloride and eplerenone are effective as antihypertensive agents.
 Low doses of spironolactone and eplerenone are effective for chronic HF.

 Spironolactone, amiloride, triamterene, and eplerenone should not be taken with ACE
inhibitors and angiotensin II receptor blockers (ARBs) because they can also increase serum
potassium levels.
 Less effective when used alone than when used in combination to reduce body fluid and
sodium
 Usually combined with a potassium-wasting diuretic, primarily hydrochlorothiazide or a loop
diuretic.
 The combination of potassium-sparing and potassium-wasting diuretics intensifies the
diuretic effect and prevents potassium loss.
 The common combination diuretics contain spironolactone and hydrochlorothiazide,
amiloride and hydrochlorothiazide, and triamterene and hydrochlorothiazide.
 Side Effects and Adverse Reactions: hyperkalemia; caution must be used when giving
potassium-sparing diuretics to patients with poor renal function because the kidneys excrete
80% to 90% of potassium. Urine output should be at least 600 mL/day.
 Patients should not use potassium supplements while taking potassium-sparing diuretics,
unless the serum potassium level is low.
 If a potassium-sparing diuretic is given with antihypertensive ACE inhibitors, hyperkalemia
could become severe or life threatening because both drugs retain potassium.
 Monitoring serum potassium levels is essential to safe drug therapy.
 The serum potassium should be periodically monitored when the patient continuously takes a
potassium-sparing diuretic. If the serum potassium level is greater than 5.0 mEq/L, the patient
should discontinue the potassium-sparing diuretic and restrict foods high in potassium.
 Headache, dizziness, weakness, GI disturbances (anorexia, nausea, vomiting, diarrhea)
hyperuricemia, muscle cramps, numbness, and tingling of the hands and feet can occur.
Spironolactone
• Spironolactone, first potassium-sparing diuretic.
• Aldosterone is a mineralocorticoid hormone that promotes sodium retention and potassium
excretion.
• Spironolactone blocks the action of aldosterone and inhibits the sodium-potassium pump (i.e.,
potassium is retained and sodium is excreted).
• Spironolactone has been prescribed by cardiologists for patients with cardiac disorders because of
its potassium-retaining effect.
• As a result of the action of spironolactone, the heart rate is more regular, and the possibility of
myocardial fibrosis is decreased.
• The effects of spironolactone may take 48 hours.
Triamterene
• Useful in the treatment of edema caused by HF or cirrhosis of the liver.

D. Antihypertensive
Hypertension
➢  blood pressure such that the systolic pressure is greater than 140 mm Hg and the diastolic
pressure is greater than 90 mm Hg.
➢ Most common condition leading to myocardial infarction (MI), stroke, renal failure, and death
➢ Essential hypertension – most common type, affecting 90% of persons with high blood pressure,
unknown origin, contributing factors includes: hyperlipidemia, African American race, diabetes,
aging, stress, excessive alcohol ingestion, smoking, obesity, and a family history of hypertension
➢ Secondary hypertension - hypertension cases are related to renal and endocrine disorders (10%)
Guidelines for Hypertension

➢ Purpose of the guidelines: decrease the risk of cardiovascular disease (CVD) in the American
population.
➢ The guideline for normal blood pressure is less than 120/80 mm Hg.
➢ Prehypertension is defined as systolic blood pressure (SBP) of 120 to 139 and diastolic blood
pressure (DBP) of 80 to 89.
➢ Stage 1 hypertension falls between 140/90 and 159/99
➢ Stage 2 hypertension is 160/100 or greater.
➢ Two out of three patients with hypertension have uncontrolled blood pressure or are not optimally
treated.
➢ SBP is more important than DBP as a CVD risk.
➢ According to the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of
High Blood Pressure (JNC 8), a blood pressure of 140/90 is the goal for the population younger than
60 years, with a target of 150/90 for those above 60.
Selected Regulators of Blood Pressure

➢ Kidneys and blood vessels strive to regulate and maintain a “normal” blood pressure
➢ Kidneys regulate BP by control of fluid volume and via the renin-angiotensinaldosterone system
➢ Kidneys control sodium and water elimination and retention, which affect cardiac output and
systemic arterial blood pressure.
➢ Renin from the renal cells stimulates production of angiotensin II, a potent vasoconstrictor that
causes the release of aldosterone, an adrenal hormone that promotes sodium retention and thereby
water retention.
➢ Retention of sodium and water causes fluid volume to increase, elevating BP
➢ The baroreceptors in the aorta and carotid sinus and the vasomotor center in the medulla also assist
in the regulation of blood pressure.
➢ Catecholamines such as norepinephrine, released from the sympathetic nerve terminals, and
epinephrine, released from the adrenal medulla, increase blood pressure through vasoconstrictive
activity.
➢ Other hormones that contribute to blood pressure regulation: antidiuretic hormone (ADH), atrial
natriuretic peptide (ANP) hormone, brain natriuretic peptide (BNP) hormone.
➢ ADH is produced by the hypothalamus and is stored and released by the posterior pituitary gland
(neurohypophysis).
➢ Stimulates the kidneys to conserve and retain water when there is a fluid volume deficit
➢ When there is fluid overload, ADH secretion is inhibited, and the kidneys then excrete more water.

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Pharmacologic Control of Hypertension

➢ Use of individualized approach in the treatment of hypertension
➢ All drugs are considered initial agents when first prescribed for hypertension.
➢ Reduction of other cardiovascular risk factors and the use of fewer drugs (i.e., substituting instead of
adding drugs) at the lowest effective doses are emphasized.
➢ Often more than one antihypertensive is used to control blood pressure, which also may lead to
fewer adverse effects.
1. Diuretics
 Promotes sodium depletion →  extracellular fluid volume (ECFV)
 Diuretics are effective as first-line drugs for treating mild hypertension
 Hydrochlorothiazide is the most frequently prescribed diuretic for controlling mild
hypertension by decreasing excess fluid volume; can be used alone or with other
antihypertensive drugs
 Many antihypertensive drugs can cause fluid retention; therefore diuretics are often
administered together with antihypertensive agents.
 Thiazide diuretics NOT recommended for patients with renal insufficiency (creatinine
clearance <30 mL/min)
 The loop (high-ceiling) diuretics such as furosemide are usually recommended since they do
not depress renal blood flow
 Loop diuretics NOT used if hypertension is the result of RAAS involvement because they tend
to elevate serum renin level immediately.
 Instead of a single thiazide drug, a combination of potassium-wasting and potassium-sparing
diuretics may be useful; less potassium excretion would occur.
 Thiazides can be combined with other antihypertensive drugs to increase their effectiveness.
 Many drug products on the market include combinations of thiazide diuretics and potassium-
sparing diuretics, beta blockers, ACE inhibitors, or ARBs. ACE inhibitors tend to increase
serum potassium (K) levels, so when they are combined with a thiazide diuretic, serum
potassium loss is minimized.
2. Sympatholytics (Sympathetic Depressants)
a.) Beta-Adrenergic Blockers / Beta blockers

 Beta (β+ and β−)-adrenergic blockers reduce cardiac output by diminishing the sympathetic
nervous system response to decrease basal sympathetic tone.
 Beta blockers reduce heart rate, contractility, and renin release.
 The hypotensive response is greater in patients with higher renin levels.
 Continues use of beta blockers, vascular resistance is diminished, and blood pressure is
lowered.
 Types of Beta Blockers:
a.) Nonselective beta blockers (e.g. propranolol and carvedilol) - inhibit β1 (heart) and β2
(bronchial) receptors - HR slows, BP  secondary to the  in HR, and
bronchoconstriction occurs because of unopposed parasympathetic tone.
b.) Cardioselective beta blockers (e.g. acebutolol, atenolol, betaxolol, bisoprolol, and
metoprolol) - blocks β1 receptors; does not confer absolute protection from
bronchoconstriction except atenolol
 If the patient has a pre-existing bronchospasm or other pulmonary disease beta blockers
should be used in caution (alternative contraindication)
 The real value of beta selectivity is in maintaining renal blood flow and minimizing the
hypoglycemic effects of beta blockade.
 The combination of beta blockers with hydrochlorothiazides is packaged together in tablet
form
 Usually the hydrochlorothiazide dose is 12.5 to 25 mg.
 Beta blockers are more effective in lowering BP to patients with elevated serum renin level
 Beta blockers should NOT be used by patients with second- or third-degree atrioventricular
(AV) block or sinus bradycardia.
 A noncardioselective beta blocker (e.g. propranolol) should NOT be given to a patient with
chronic obstructive pulmonary disease (COPD)
 Pharmacokinetics: Metoprolol is well absorbed from the gastrointestinal (GI) tract; short
half-life, low protein binding
 Pharmacodynamics: Cardioselective beta-adrenergic blockers block beta1 receptors -  HR
and BP
 Nonselective beta blockers block beta1 and beta2 receptors, which can result in bronchial
constriction.
 Beta blockers cross the placental barrier; excreted in breast milk
 Onset of action of oral beta blockers is usually 60 minutes or less; duration of action is usually
24 hours with some exceptions.
 Peak for extended release is usually 1 to 7 hours, and the duration is typically 24 hours.
 Beta blockers given IV - onset of action is immediate, peak time is 20 minutes, and duration of
action is approximately 4 to 10 hours.
 Side Effects and Adverse Reactions:  PR; BP; bradycardia,

 Noncardioselective beta1 and beta2 blockers, bronchospasm. Beta blockers should not be
abruptly discontinued because rebound hypertension, angina, dysrhythmias, and MI can
result.
 Beta blockers can cause dizziness, insomnia, depression, fatigue, nightmares, and sexual
dysfunction.
 Non-cardioselective beta blockers inhibit the liver’s ability to convert glycogen to glucose in
response to hypoglycemia – caution in patients with diabetes
b.) Centrally Acting Alpha2 Agonists

 Mechanism of action:  the sympathetic response from the brainstem to the peripheral
vessels.
 Stimulate the α2 receptors →  sympathetic activity;  vagus activity;  cardiac output; 
serum epinephrine, norepinephrine, and renin release → reduced peripheral vascular
resistance and vasodilation
 With minimal effects on cardiac output and blood flow to the kidneys.
 Not given with beta blockers ➔ accentuation of bradycardia during therapy
 E.g.: methyldopa, clonidine, and guanfacine.
 Side Effects / Adverse Reactions: drowsiness, dry mouth, dizziness, and  heart rate
(bradycardia)
 NOT abruptly discontinued –can result to rebound hypertensive crisis
 If the drug needs to be stopped immediately, another antihypertensive drug is usually
prescribed to avoid rebound hypertensive (symptoms: restlessness, tachycardia, tremors,
headache, and BP)
 The nurse should emphasize the need to take the medication as prescribed.
 Contraindication: pregnant / contemplating pregnancy
Methyldopa
• Methyldopa was one of the first drugs widely used to control hypertension.
• Methyldopa is frequently used to treat chronic or pregnancy-induced hypertension; however, it
crosses the placental barrier, and small amounts may enter the breast milk of a lactating patient.
• Methyldopa NOT used in patients with impaired liver function, and serum liver enzymes
Clonidine
• Can cause sodium and water retention – given together with diuretic
• Clonidine is available in a transdermal preparation that provides a 7-day duration of action. Patches
are replaced every 7 days and may be left on while bathing; skin irritations may occur.
Guanfacine
• Rebound hypertension is less likely to occur
c.) Alpha-Adrenergic Blockers

 Mechanism of action: blocks alpha-adrenergic receptors (alpha blockers)→ vasodilation and
BP
 Helps maintain the renal blood flow rate.
 Useful in treating hypertension in patients with lipid abnormalities ( very-low-density
lipoprotein (VLDL) and the low-density lipoprotein (LDL) responsible for the buildup of fatty
plaques in the arteries (atherosclerosis); high-density lipoprotein (HDL))
 Safe for patients with diabetes because they do not affect glucose metabolism.
 NO affect respiratory function.

 Selective alpha1-adrenergic blocker (e.g. prazosin, terazosin, and doxazosin) used mainly
to reduce blood pressure and can be used to treat benign prostatic hypertrophy (BPH), long
term hypertension.
 Prazosin is a commonly prescribed drug.
 Terazosin and doxazosin have longer half-lives than prazosin, and they are normally given
once at bedtime.
 When prazosin is taken with alcohol or other antihypertensives, the hypotensive state can be
intensified.
 Can cause sodium and water retention with edema (given together with diuretics)
 Pharmacokinetics: Prazosin is absorbed through the GI tract, but a large portion of prazosin
is lost during hepatic first pass metabolism; half-life is short (administered BID)
 Prazosin is highly protein bound, and when it is given with other highly protein-bound drugs,
the patient should be assessed for adverse reactions.
 Pharmacodynamics: Selective alpha-adrenergic blockers dilate the arterioles and venules,
decreasing peripheral resistance and lowering blood pressure.
 With prazosin, the heart rate is only slightly increased, whereas with nonselective alpha
blockers such as phenoxybenzamine, the blood pressure is greatly reduced, and reflex
tachycardia can occur.
 Nonselective alpha blockers – more effective for acute hypertension
 The onset of action of prazosin occurs between 30 minutes and 2 hours.
 The duration of action of prazosin is less than 24 hours.
 Side Effects and Adverse Reactions: prazosin, doxazosin, and terazosin include orthostatic
hypotension (dizziness, faintness, lightheadedness, and  HR, which may occur with first
dose), nausea, headache, drowsiness, nasal congestion caused by vasodilation, edema, and
weight gain.
 Side effects of phentolamine include hypotension, reflex tachycardia caused by the severe
decrease in blood pressure, nasal congestion caused by vasodilation, and GI disturbances.
 Drug Interactions: prazosin + anti-inflammatory = peripheral edema
 Nitroglycerin taken for angina lowers blood pressure.
 Prazosin + nitroglycerin = syncope (faintness) ( blood pressure)
d.) Adrenergic Neuron Blockers (Peripherally Acting Sympatholytics)

 Potent antihypertensive drugs – blocks norepinephrine release from the sympathetic nerve
endings →  in norepinephrine release that result in a lowering of blood pressure.
 Decrease occurs in both cardiac output and peripheral vascular resistance.
 Taken alone or with a diuretic to decrease peripheral edema
 Reserpine, the most potent drug, is used to control severe hypertension.
 Side effect: Orthostatic hypotension (advise client to rise slowly from a reclining or sitting
position, sodium and water retention
 Considered the last choices for treatment of chronic hypertension because these drugs can
cause orthostatic hypotension.
 Reserpine may cause vivid dreams, nightmares, and suicidal ideation.
e.) Alpha1 and Beta1 Adrenergic Blockers

 Mechanism of action: blocks both the alpha1 and beta1 receptor
 Blocking the alpha1 receptor → vasodilation, which  resistance to blood flow
 Alpha receptor is stronger than the effect on the beta receptor → BP and PR is moderately

 Blocking the cardiac beta1 receptor, both HR and AV contractility 

 Large doses of alpha/beta blockers could block beta2-adrenergic receptors →  airway

resistance
 Labetalol is an example of an alpha/beta blocker
 Patients who have severe asthma should not take large doses of labetalol.
 Common side effects: orthostatic hypotension, GI disturbances, nervousness, dry mouth, and
fatigue. Large doses of labetalol may cause AV heart block.
3. Direct Acting Arteriolar Vasodilators

 Potent antihypertensive drugs.
 Mechanism of action: act by relaxing the smooth muscles of the blood vessels, mainly the
arteries, causing vasodilation →  blood flow to the brain and kidneys → BP, sodium and
water are retained (peripheral edema)
 Diuretics can be given with a direct-acting vasodilator to decrease the edema
 Cause little orthostatic hypotension because of minimum dilation of the arterioles.
 Reflex tachycardia and release of renin can occur secondary to vasodilation and  BP
 Beta blocker – given to counteract the effect of reflex tachycardia
Nitroprusside
• Very potent vasodilator that rapidly decreases BP
• Mechanism of action: acts on both arterial and venous vessels
• Given for acute hypertensive emergency, severe (dose-related) hypertension
• Side effect: reflex tachycardia, palpitations, restlessness, agitation, nausea, and confusion.
Minoxidil
• Given for severe (dose-related) hypertension
• Side effects: tachycardia, edema, and excess hair growth, precipitate an anginal attack
Hydralazine
• Side Effects / Adverse Reactions: hydralazine – reflex tachycardia, palpitations, edema, nasal
congestion, headache, dizziness, GI bleeding, lupus-like symptoms, and neurologic symptoms
(tingling, numbness)
4. Angiotensin – Converting Enzyme Inhibitors

 When ACE is inhibited, it in turn inhibits the formation of angiotensin II (vasoconstrictor) and
blocks the release of aldosterone.
 Aldosterone promotes sodium retention and potassium excretion.
 When aldosterone is blocked, sodium is excreted along with water, and potassium is retained.
 ACE inhibitors cause little change in cardiac output or heart rate, and they lower peripheral
resistance.
 Indication: primarily used to treat hypertension, patients who have elevated serum renin
level, heart failure
 E.g. benazepril, captopril, enalapril maleate, fosinopril, lisinopril, moexipril, perindopril,
quinapril, ramipril, and trandolapril,
 First-line antihypertensive therapy with thiazide diuretics
 NOT to be used during pregnancy (it reduce placental blood flow)
 For patients with renal insufficiency, reduction of the drug dose (except for fosinopril) is
necessary
 Administered with meal for maximum effectiveness except moexipril

 Side Effects / Adverse Reactions: constant, irritated cough, nausea, vomiting, diarrhea,
headache, dizziness, fatigue, insomnia, serum potassium excess (hyperkalemia), and
tachycardia.
 Persistent, nonproductive “ACE cough” may be relieved upon discontinuance of the drug.
 Major adverse effects: first-dose hypotension (vasodilating effect) and hyperkalemia.
 First-dose hypotension is more common in patients also taking diuretics.
 Angioedema—swelling of the face, tongue, lips, mucous membranes, and larynx and
extremity edema—may occur due to hypersensitivity and has a higher incidence in African
Americans.
 Occur within hours or 1 week after the first dose; maybe reversed when drug is discontinued
 When laryngeal edema occurs, the patient may require rescue epinephrine.
 Contraindications: pregnancy, not be taken with potassium-sparing diuretics such as
spironolactone or with salt substitutes that contain potassium because of the risk of
hyperkalemia
CTTO: https://www.ncbi.nlm.nih.gov/books/NBK82803/bin/clinacei2f1.jpg
5. Angiotensin II – Receptor Blockers

 Mechanism of action: prevent the release of aldosterone, a sodium-retaining hormone
 Act on the renin-angiotensin-aldosterone system (RAAS)➔ block the vasoconstrictor effects
of angiotensin II at the receptor site.
 ARBs block angiotensin II from the angiotensin I (AT1) receptors found in many tissues
ACE inhibitors inhibit the angiotensin-converting enzyme in the formation of angiotensin II
 ARBs cause vasodilation and decrease peripheral resistance; does not cause the constant,
irritating cough; should not be taken during pregnancy
 E.g.: Losartan, valsartan, irbesartan, candesartan, eprosartan, olmesartan, azilsartan,
telmisartan
 Combination drugs: losartan potassium+ hydrochlorothiazide tablets, valsartan +
hydrochlorothiazide tablets does not cause serum potassium excess or loss
 ARBs may be used as a first-line treatment for hypertension.

 Pharmacokinetics: Valsartan is prescribed primarily to manage hypertension; rapidly
absorbed in the GI tract and undergoes first-pass metabolism in the liver to form active
metabolite; highly protein bound, should not be given during pregnancy (2nd and 3rd
trimester); half-life is approximately 6 hours, excreted in urine and feces
 Pharmacodynamics: Valsartan is a potent vasodilator. It blocks the binding of angiotensin II
to the AT1 receptors found hours) in many tissues; peak time is approximately 6 hours; long
duration of action (24 hours)
 Can cause angioedema.
 Administered with or without food and are suitable for patients with mild hepatic
insufficiency.
6. Direct Renin Inhibitors

 Mechanism of action: binds with renin and causes a reduction of angiotensin I, angiotensin II,
and aldosterone levels
 Indication: mild and moderate hypertension.
 E.g.: Aliskiren which can be used alone or with another antihypertensive agent
 Additive effect in reducing blood pressure when combined with a thiazide diuretic or an ARB.
7. Calcium Channel Blockers / Calcium Antagonist / Calcium Blockers

 Slow calcium channels are found in the myocardium (heart muscle) and vascular smooth
muscle (VSM) cells. Free calcium increases muscle contractility, peripheral resistance, and
blood pressure.
 Mechanism of action: block the calcium channel in the VSM, promoting vasodilation.
 The large central arteries are not as sensitive to calcium blockers as coronary and cerebral
arteries and the peripheral vessels.
 Calcium blockers are highly protein bound but have a short half-life.
 Slow-release preparations decrease the frequency of administration.
 E.g.: verapamil, diltiazem, amlodipine, nifedipine
 Verapamil is used to treat chronic hypertension, angina pectoris, and cardiac dysrhythmias.
 Verapamil and diltiazem act on the arterioles and the heart.
 Nifedipine - BP in older adults and in those with low serum renin values
 Verapamil are potent calcium blockers.
 Can cause reflex tachycardia (prevalent with nifedipine)
 Normally, beta blockers are not prescribed with calcium blockers, because both drugs
decrease myocardium contractility.
 Calcium blockers lower BP better in African Americans than do drugs in other categories.
 Side Effects / Adverse Reactions: flushing, headache, dizziness, ankle edema, bradycardia, AV
block
Nifedipine
• Potent calcium channel blocker
• In its immediate-release form (10- and 20-mg capsules), nifedipine has been associated with an
increased incidence of profound hypotension, MI, and death, especially in older adults; therefore only
extended-release preparations of nifedipine are recommended for chronic hypertension.
• For this reason, immediate-release nifedipine → acute rises in blood pressure only on an as-needed
basis in the hospital setting.

Amlodipine
• Pharmacokinetics: highly protein bound; gradually absorbed via the GI tract; longer half-life (given
OD)
• Pharmacodynamics: may be used alone or with other antihypertensive drugs, long duration of action
• Peripheral edema may occur because of its vasodilator effect, so persons with edema may need to
take another type of antihypertensive drug.
• Amlodipine may be combined with the ACE inhibitor benazepril (Lotrel).
E. Antihypotensive Drugs
norepinephrine, metaraminol, dopamine, dobutamine, isoproterenol
 Mechanism of action: mimic the fight or flight response of the sympathetic nervous system,
selectively stimulating alpha-adrenergic and beta adrenergic receptors
 Stimulation of the alpha adrenergic receptors results in vasoconstriction and increase systemic BP
 Stimulation of beta adrenergic receptors increases the force and rate of myocardial contraction
 Used to treat shock
 Side effects: anxiety, tremor, weakness, dizziness, restlessness, bradycardia, shortness of breath,
nausea, vomiting, flushing, diaphoresis, azotemia, sloughing upon extravasation, bronchospasm,
palpitation
 Administration considerations: drugs must be diluted before administration; client should be
attend constantly during the therapy
 alpha adrenergic blockers
Nursing Consideration
1. Re-evaluate if 3 to 5 treatments in 6 to 12 hours provide minimal to no relief
2. Carefully monitor vital signs, ECG, I&O
3. Monitor for rebound hypertension
4. Constant infusion pump prevents sudden infusion of excessive amounts of drugs
5. Correct blood volume depletion first
6. Antidote for extravasation: 5 to 10mg phentolamine mesylate in 10 to 15ml of normal salide
7. Monitor infusion site frequently
8. Protect solution from light
9. Symphathomimetics are incompatible with sodium bicarbonate

2. Evaluation of Learning
This section will enable you to do self-check of your progress in the discussion. During the self-evaluation,
you are expected to practice the virtue of honesty. A score equivalent to 75% will enable you to proceed to the
assignment section. A separate sheet will be utilized to answer the questions in this section. You may repeat
answering the questions until the required score equivalent is acquired.
Multiple Choices
Select the best answer from the following choices.
1. The patient is receiving digoxin for treatment of heart failure. Which finding would suggest to the nurse that
the heart failure is improving?
A. Pale and cool extremities
B. Absence of peripheral edema
C. Urine output of 60 mL every 4 hours
D. Complaints of increasing dyspnea
2. The patient’s serum digoxin level is 3.0 ng/mL. What does the nurse know about this serum digoxin level?
A. It is in the high (elevated) range.
B. It is in the low (decreased) range.
C. It is within the normal range.
D. It is in the low-average range.
3. The nurse is assessing a patient for possible evidence of digitalis toxicity. Which of these is included in the signs
and symptoms for digitalis toxicity?
A. Apical pulse rate of 100 beats/min
B. Apical pulse of 72 beats/min with an irregular rate
C. Apical pulse of 90 beats/min with an irregular rate
D. Apical pulse of 48 beats/min with an irregular rate
4. A patient is taking a potassium-depleting diuretic and digoxin. The nurse expects that a low potassium level
(hypokalemia) could have what effect on digoxin?
A. Increases serum digoxin sensitivity level
B. Decreases serum digoxin sensitivity level
C. No effect on serum digoxin sensitivity level
D. Causes a low-average serum digoxin sensitivity level
5. A patient takes an initial dose of a nitrate. Which symptom(s) will the nurse expect to occur?
A. Nausea and vomiting
B. Headaches
C. Stomach cramps
D. Irregular pulse rate
6. A patient is prescribed a beta blocker. Beta blockers are as effective as antianginals because they do what?
A. Increase oxygen to the systemic circulation
B. Maintain heart rate and blood pressure
C. Decrease heart rate and decrease myocardial contractility
D. Decrease heart rate and increase myocardial contractility
7. The health care provider is planning to discontinue a patient’s beta blocker. Which instruction will the nurse
give the patient regarding the beta blocker?
A. The beta blocker should be abruptly stopped when another cardiac drug is prescribed.
B. The beta blocker should not be abruptly stopped; the dose should be tapered down.
C. The beta blocker dose should be maintained while taking another antianginal drug.
D. Half the beta blocker dose should be taken for the next several weeks.

8. The beta blocker acebutolol is prescribed for dysrhythmias. What is the primary purpose of the drug?
A. Increase beta1 and beta2 receptors in cardiac tissues
B. Increase the flow of oxygen to cardiac tissues
C. Block beta1-adrenergic receptors in cardiac tissues
D. Block beta2-adrenergic receptors in cardiac tissues
9. A patient who has angina is prescribed nitroglycerin. Which are appropriate nursing interventions for
nitroglycerin? Select all that apply.
A. Have the patient sit or lie down when taking a nitroglycerin sublingual tablet.
B. Teach the patient who has taken a tablet to call 911 in 5 minutes if chest pain persists.
C. Apply the nitroglycerin patch to a hairy area to protect skin from burning.
D. Call the health care provider after taking five tablets if chest pain persists.
E. Warn the patient against ingesting alcohol while taking nitroglycerin.
10. A patient is taking hydrochlorothiazide 50 mg/day and digoxin 0.25 mg/day. The nurse plans to monitor the
patient for which potential electrolyte imbalance?
A. Hypocalcemia
B. Hypokalemia
C. Hyperkalemia
D. Hypermagnesemia
11. The nurse knows that which statement is correct regarding nursing care of a patient receiving
hydrochlorothiazide? Select all that apply.
A. Monitor patients for signs of hypoglycemia.
B. Administer ordered potassium supplements.
C. Monitor serum potassium and uric acid levels.
D. Assess blood pressure before administration.
E. Notify the health care provider if a patient has had oliguria for 24 hours.
F. Assess for decreased cholesterol and triglyceride levels.
12. A patient has heart failure, and a high dose of furosemide is ordered. What suggests a favourable response to
furosemide?
A. A decrease in level of consciousness occurs, and the patient sleeps more.
B. Respiratory rate decreases from 28/min to 20/min, and the depth increases.
C. Increased congestion is heard in breath sounds, and the patient complains of shortness of breath.
D. Urine output is 50 mL/4 h, and intake is 200 mL.
13. What does the nurse know to be correct concerning the use of mannitol in patients?
A. It decreases intracranial pressure
B. It increases intraocular pressure.
C. It causes sodium and potassium retention.
D. It causes diuresis in several days.
14. What should the nurse do when a patient is taking furosemide?
A. Instruct the patient to change positions quickly when getting out of bed.
B. Assess blood pressure before administration.
C. Administer the drug at bedtime for maximum effectiveness.
D. Teach the patient to avoid fruits to prevent hyperkalemia.
15. For the patient taking a diuretic, a combination such as triamterene and hydrochlorothiazide may be
prescribed. The nurse realizes that this combination is ordered for which purpose?
A. To decrease serum potassium level
B. To increase serum potassium level
C. To decrease glucose level
D. To increase glucose level
16. The patient has been receiving spironolactone 50 mg/day for heart failure. The nurse should closely monitor
the patient for which condition?
A. Hypokalemia
B. Hyperkalemia
C. Hypoglycemia
D. Hypermagnesemia

17. A patient’s blood pressure is 130/84. The health care provider plans to suggest non-pharmacologic methods to
lower blood pressure. Which should the nurse include in teaching? Select all that apply.
A. Stress-reduction techniques
B. An exercise program
C. Salt restriction
D. Smoking cessation
E. A diet with increased protein
18. A patient has developed mild hypertension. The nurse acknowledges that the first-line drug for treating this
patient’s blood pressure might be which drug?
A. Diuretic
B. Alpha blocker
C. Angiotensin-converting enzyme inhibitor
D. Alpha/beta blocker
19. An African American patient has developed hypertension. The nurse is aware that which groups of
antihypertensive drugs are less effective in African American patients?
A. Diuretics
B. Calcium channel blockers and vasodilators
C. Beta blockers and angiotensin-converting enzyme inhibitors
D. Alpha blockers
20. The patient, 62 years old, is taking amlodipine and complains of swelling in her ankles. What is the nurse’s best
response to her concern?
A. “Swelling is common when taking Norvasc. You should cut the tablet in half to reduce your dosage.”
B. “Swelling may occur with Norvasc. I will contact your health care provider to determine if the drug should
be changed or if another drug should be added.”
C. “You should not be taking that drug because of your age. I will see what other antihypertensive drug you can
take.”
D. “You should stop taking the drug for several days and check that the swelling has decreased.”
21. What classification of drug is bisoprolol?
A. ACE inhibitor
B. Beta blocker
C. Calcium blocker
D. Diuretic
22. What classification of drug is pindolol?
A. ACE inhibitor
B. Beta blocker
C. Calcium blocker
D. Diuretic
23. What is/are the advantage(s) of using cardioselective beta-adrenergic blockers as an antihypertensive? Select all
that apply.
A. They can be abruptly discontinued without causing rebound symptoms.
B. They increase serum electrolyte levels.
C. They maintain renal blood flow.
D. They minimize hypoglycemic effect.
24. ARBs have gained popularity for treating hypertension. Which is/are example(s) of ARB agents? Select all that
apply.
A. Losartan potassium
B. Valsartan
C. Lisinopril
D. Metoprolol
25. Which statement best describes the direct renin inhibitor aliskiren?
A. It is effective for treating severe hypertension.
B. It can be combined with another antihypertensive drug such as an ARB.
C. It can cause hypokalemia when taken as a monotherapy drug.
D. It is more effective than calcium channel blockers in treating hypertension in African-American patient

3. Evaluation of Learning
For the evaluation of learning for Module 8, a scheduled quiz will be assigned in the Google Classroom and
will be taken before the start of the next Module during the Synchronous Class.
Activities for Self-Directed Learning
1. Creation of a Song
A. Learning Outcomes
▪ Apply appropriate nursing concepts and actions holistically and comprehensively
B. Description of the Activity

▪ Create a song that will summarize the drugs affecting the cardiovascular system. You will be divided
according to your RLE group. The song should be composed of 4 stanzas with a chorus. You can choose
from the song of the group assign to the group. You may also opt to have a medley
Group 1 ➔ any song of 1970’s
Group 3 ➔ any songs of 1990’s
▪ After the creation of the song, you need to create a video that will show your group singing the song
with the lyrics in it.
▪ Include in your output the tasks that is done by the member of the group.
C. Rubrics for Grading

RUBRIC - SONG COMPOSITION AND PRESENTATION
CRITERIA OUTSTANDING GOOD FAIR POOR Remarks

(9-10points) (7-8points) (5-6points) (1-4point)
Lyrics Lyrics are extremely Lyrics are catchy and Lyrics somewhat Lyrics are not catchy
(x3) catchy and contains all contains the most catchy and contains a and lacks concepts of 30
significant concepts of concepts of the few concepts of the the subject matter
the subject matter subject matter subject matter
Melody Sings entire song with Sings entire song Sings entire song with Sings entire song out
(x2) appropriate melody with only 1 – 2 lapses 3 – 4 lapses in melody of tune 20
in melody
Rhythm Sings entire song with Sings entire song Sings entire song with Sings entire song
appropriate rhythm with only 1 – 2 lapses 3 – 4 lapses in rhythm entirely out of rhythm 10
patterns in melody patterns patters
Vocal Tone Sings entire song with Sings entire song Sings entire song with Sings entire song with
exceptional voice with good voice with ordinary voice quality poor voice quality 10
quality good quality
Performance Sings with enthusiasm Sings with some Sings with little Sings with no
Delivery and energy during the enthusiasm and enthusiasm and enthusiasm and 30
(x3) entire song energy during the energy during eh energy
entire song entire song
Timely Timely submission
Submission Timely submission = 5
Submitted 1 day after the deadline = 3;
Submitted 2 days after the deadline = 2
Failure to submit 2 days after the deadline = Output will not be accepted but it should still be done as part of the
portfolio for this module

2. Creation of a Medication Monitoring Sheet
A. Learning Outcomes
1. Apply appropriate nursing concepts and actions holistically and comprehensively
2. Implement safe and quality interventions with the client to address the health needs, problems and
issues
3. Customize nursing interventions based on Philippine Culture and values
B. Description of the Activity

• Create your own medication monitoring sheet for one member of a family who is taking a lot
medication starting November 15 until November 26. Ensure that the rights to medication are
followed. You may use the format which you think will help you in monitoring the documentation of
the correct intake of your client. You may do your research but be sure to include the reference in your
output.
• The medication monitoring sheet should include the following:
(minimum elements) – order of the physician, monitoring for frequency of giving the medication,
standard abbreviation/acronym – if the drug is not taken or other circumstances, date, time
• In case you do not have a family member who is taking the medication, you may look for a relative and
monitor the intake of medications virtually.
• The medication monitoring sheet maybe hand made or computerized. Its application should be clearly
done.
• After November 30, prepare a video that explains the medication monitoring sheet that you have
created. Maximum time of the video is 2minutes.
C. Rubrics for Grading the Output
CRITERIA OUTSTANDING GOOD FAIR POOR Remarks

(9-10points) (7-8points) (5-6points) (1-4point)
Content Complete elements 1-2 missing elements 3-4 missing elements 5 or more elements
(x2) in the medication of the medication of the medication not included in the 20
monitoring sheet monitoring sheet sheet medication sheet
Useability and Easy to use and Somewhat easy to Somewhat difficult to Difficult to use, creates
Application applied to the client use and applied to use, creates some confusion in its 30
(x3) the client confusion in its application
application.
Creativity – Presentation was Presentation was Limited creativity No creativity in the 20

video very creative using a creative using using a limited presentation.
(x2) variety of resources. several resources resource
Quality of the The explanation Some elements of the Few elements are Very few elements are
explanation of covers all of the monitoring sheet are covered in the covered in the 30
the medication elements of the not covered in the explanation. explanation. Difficult
monitoring monitoring sheet. explanation. Somewhat difficult to to use and quiet
sheet – video Clear and easy to Somewhat clear and use and some parts are confusing.
(x3) follow easy to follow confusing.
Timely Timely submission
Submission Timely submission = 5
Submitted 1 day after the deadline = 3;
Submitted 2 days after the deadline = 2
Failure to submit 2 days after the deadline = Output will not be accepted but it should still be done as part of
the portfolio for this module
References
Burchum, Jacqueline Rosenjack, Rosenthal Laura D. Lehne’s Pharmacology for Nursing. 10th Edition.
(2018). Elsevier Inc. St. Louis, Missouri USA.
Kee, Joyce LeFever, Hayes, Evelyn R., McCuistion, Linda E. Pharmacology: A Patient-Centered Nursing
Process Approach. 8th Edition. (2015). Elsevier Pte. Ltd. Singapore.
McCuistion, Linda, Vuljoin-DiMaggio, Kathleen, Winton, Mary, Yeager, Jennifer. Pharmacology: A

Patient-Centered Nursing Process Approach. 9th Edition. (2018). Elsevier Inc. St. Louis,
Missouri USA.
Pacitti, Diane, Smith, Blaine T. (editor). Pharmacology for Nurses. 2nd Edition. (2020). Jones &
Bartlett Learning. Burlington, MA.
Zerwekh, JoAnn, Miller, C.J., Harvey, Pamela, Ye, Robin. Mosby’s Pharmacology Memory NoteCards:
Visual, Mnemonic, & Memory Aids for Nurses. 5th Edition. (2019). Elsevier Inc., Missouri, USA
Congratulations for having completed this C-NCM 106 Module 8! See you in the next Module

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COLLEGE OF NURSING AND PHARMACY

C-NCM 106 – PHARMACOLOGY

Module 8: Drugs Affecting the Cardiovascular System

1. Content / Discussion / Learning Resources / Links

A. Review of the Anatomy and Physiology of the Cardiovascular System /

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Conduction of Electrical Impulses

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Regulation of Heart and Blood Flow

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Adrenergic and Cholinergic

Two Specific Branches

B. Cardiac Glycosides, Antianginals and Antidysrhythmics

 Naturally occurring cardiac glycosides are found in a number of plants (digitalis)

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Other Agents Used to Treat Heart Failure

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Non-selective beta blockers: propranolol, nadolol, pindolol

 Beta-adrenergic blockers block the beta1- and beta2-receptor sites.

Faculty: Cherry B. Lazatin, RN,RPh,MAN Page 9 of 34

3. Calcium Channel Blocker / Calcium Blockers

Amlodipine, verapamil, nifedipine, and diltiazem

Cardiac Dysrhythmias / Arrhythmia

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Cardiac Action Potentials

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1. Class I: Sodium Channel Blockers

2. Class II: Beta Blockers

3. Class III: Drugs That Prolong Repolarization

4. Class IV: Calcium Channel Blockers

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Other Antiarrhythmic Drug

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1. Thiazides and Thiazide – like Diuretics

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 Pharmacokinetics: well absorbed from the gastrontestinal (GI) tract; hydrochlorothiazide -

2. Loop (High – Ceiling) Diuretics

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4. Carbonic Anhydrase Inhibitors

5. Potassium – Sparing Diuretics

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Guidelines for Hypertension

Selected Regulators of Blood Pressure

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Pharmacologic Control of Hypertension

2. Sympatholytics (Sympathetic Depressants)

a.) Beta-Adrenergic Blockers / Beta blockers

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b.) Centrally Acting Alpha2 Agonists

c.) Alpha-Adrenergic Blockers

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d.) Adrenergic Neuron Blockers (Peripherally Acting Sympatholytics)

e.) Alpha1 and Beta1 Adrenergic Blockers

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