PHARMACOLOGY SEM 01 | CYC 02

LECTURE AUF-CON

NCM 0106 MODULE 12 & 13 – DRUGS ACTING ON THE CARDIOVASCULAR SYSTEM

OUTLINE
I Concept Review
A Cardiovascular System
B Congestive Heart Failure
II Drugs Acting on the CVS
A Cardiac Glycosides
B Antianginals
C Antidysrhythmics

CONCEPT REVIEW

CARDIOVASCULAR SYSTEM
PARTS
● HEART
○ Shape of a blunt cone and size of clenched fist
○ Composed mainly by myocardium (heart
muscles)
○ Covered externally by the pericardium, lined
internally by the endocardium
○ 4 Chambers: LA, LV, RA, RV
● Atria: receiving chambers; delivers blood to
the right and left ventricles
● Ventricles: pumping chambers
○ 4 Valves
● Tricuspid and Mitral valves
● Pulmonary and Aortic Semilunar valves
● FUNCTION: prevents backflow of blood
○ Perfused through the coronary arteries
● Supplies blood to the myocardium
● Right Coronary Artery, Left Anterior
Descending Artery, Left Circumflex Artery
● BLOOD FLOW
○ Oxygen-rich blood: enters the heart from the
lungs and goes out to the body
○ Oxygen-poor blood: enters the heart from the
body and goes out to the lungs
○ Superior (upper) and Inferior (lower) Vena
Cava → Right Atrium → Tricuspid valve → Right
Ventricle → Pulmonary semilunar valves →
Pulmonary trunk → Pulmonary artery (lungs,
carrying unoxygenated blood) → Pulmonary
veins → Left Atrium → Bicuspid valve → Left
Ventricle → Aortic semilunar valve → Aorta →
rest of the body
● BLOOD VESSELS
○ Arteries → Arterioles → Capillaries → Venules →
Veins
○ Largest in lumen chena: veins
○ Largest lumen in diameter: great veins
○ Thicker wall: arteries
○ A lot of medication have their effect on arteries
specifically of the smooth muscle layer that is
why the arteries are capable of performing
vasoconstriction and vasodilation that is not
present in veins
● BLOOD
○ Composed of plasma, erythrocytes, leukocytes
and platelets
○ Plasma: 90% water, 10% solutes
CONCEPTS
● CONDUCTION OF ELECTRICAL IMPULSES
○ SA (sinoatrial) node
● Primary pacemaker
● 60-80 bpms
● Sets the mood; sets the heart into
contraction
○ AV node (atrioventricular)
● Secondary pacemaker
● 40-60 bpms
○ Bundle of His (right and left bundle branches)
○ Purkinje Fibers
● Stimulates the heart to contract
● 📌 REMEMBER: AV node can act as the primary
pacemaker if the SA node is malfunctioning
○ Assess for bradycardia since AV node delivers
only 40–60 bpms, which is significantly lesser
than the SA node

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 MODULE 12 – DRUGS ACTING ON THE CARDIOVASCULAR SYSTEM
● CONTROL OF BLOOD PRESSURE
○ Arterial blood pressure: determined by
peripheral resistance and cardiac output
○ High blood viscosity = high resistance
○ Longer blood vessel = higher resistance
○ Blood vessel radius increases = lesser
resistance produced
○ Cardiac Output (CO)
● Volume of blood pumped by either
ventricles of the heart each minute
● FORMULA: CO = HR x Stroke Volume
(amount of blood ejected by the ventricle
every after heartbeat)
● Normal CO = 4-8 L/m
○ Stroke Volume (SV)
● Volume of blood pumped per ventricle
each time the heart contracts
● Three Factors Affecting Stroke Volume
○ Preload: force exerted by blood against
the ventricles at the end of diastole
● Blood flow force that stretches
the ventricle
● Higher preload = higher cardiac
output
○ Contractility: force of ventricular
contractions
● Higher preload and contractility =
higher stroke volume
○ Afterload: resistance to ventricular
ejection of blood caused by opposing
pressures in the aorta and systemic
circulation
● Afterload increases = crackles (due to .. hehe
decreased/weaker stroke volume
● Left ventricle has to pump harder
due to the presence of resistance
○ Heart Rate
● Number of times the heart contracts each
minute
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CONGESTIVE HEART FAILURE
● Heart failure is a condition where the heart can
not pump enough blood to match the body's
needs
WHAT HAPPENS?
● 1. Due to cardiac abnormalities or conditions that
place increase demand on the heart; heart
compensates →
● 2. Heart muscle weakens and enlarges
○ Loses its ability to pump blood to the lungs
and systemic circulation → left or right failure
● 3. Continuous increase, forceful contractions →
● 4. Compensatory mechanism fails → congestive
heart failure → cardiac arrest (heart stops beating
if not treated)
RIGHT-SIDED AND LEFT-SIDED HEART FAILURE
● Right-Sided Heart Failure
○ Right atrium will return blood/fluid to the
systemic circulation
○ Mainly systemic S/Sx
● Abdominal pain (masyadong maraming
blood na nare-receive), fatigue, bloating,
nausea, dependent pitting edema, ankle
edema, ascites, jaundice, hepatomegaly
(enlargement of the liver), decreased urine
output (lesser blood flow going to the
kidneys), increase central venous pressure
(CVP; measures pressure in the right atrium
and nag-i-increase ito since maraming
blood sa RA), hypertension (maraming fluid
sa circulation)
○ Ex. Peripheral edema
● Left-Sided Heart Failure
○ ANO’NG NANGYAYARI?: Naiipon ‘yung blood
(from left atrium) sa left ventricle kasi ayaw na
niyang mag-pump
● Since ayaw i-receive ng left
atrium/ventricle ‘yung blood, nagpu-pool
sila sa blood. Nalulunod ‘yung lungs sa
sobrang daming fluid.
○ Mainly respiratory S/Sx
● Dyspnea, orthopnea, fatigue, restlessness,
:ano raw),
peripheral cyanosis (oxygenated blood
does not reach the periphery), dry
non-productive cough (so much fluid in the
lungs), frothy blood tinged mucus
(nag-iipon ‘yung blood)
 MODULE 12 – DRUGS ACTING ON THE CARDIOVASCULAR SYSTEM

○ Nursing Intervention: Do not place patient flat ● Decrease conduction of heart cells through
in bed, dapat orthopneic position propped with AV node
pillows ○ Increase stroke volume
● They will feel as if they’re drowning if placed ● Due to increased force of contraction
flat on the bed
○ Ex. Pulmonary edema DIGOXIN (LANOXIN)

STAGES OF HEART FAILURE (PUMP FAILURE) ● A secondary drug of choice for heart failure
● Indications: Heart Failure, Atrial Fibrillation (rapid
STAGE CHARACTERISTICS ACCORDING TO STAGE
beating)
High risk to heart failure without symptoms ● Route: PO and IV
A
of structural heart disease ● t ½: 36 hours (long half-life; given only once a day)
Some cardiac changes such as decreased ● Low protein binding power
ejection fraction of heart failure without ● 30% metabolized by the liver
symptoms ● 65% excreted by the kidneys unchanged
B
● Serum level for dysrhythmias: 0.8-2.0 ng/ml
Ejection fraction: how much is expelled from Serum level for heart failure: 0.5–1.0 ng/ml
●
the heart; 50-70% is normal
● Toxic level: >2-3 ng/ml
Structural heart disease with some ● PHARMACOKINETICS
symptoms of heart failure such as fatigue, ○ Contraindications
C
shortness of breath, edema, and decrease in ● Ventricular Fibrillation (fast AV node;
physical activity
hypokalemia)
Severe structural heart disease and marked ○ Side Effects
D
symptoms of heart failure even at rest ● N/V, diarrhea, abdominal pain, confusion,
weakness, blurred vision
DRUGS ACTING ON THE CVS ○ Adverse Reactions
● Bradycardia, cardiac dysrhythmias,
A. CARDIAC GLYCOSIDES Thrombocytopenia
Digitalis Glycosides ● Prior Nursing Intervention: read ECG
● Used since 1200 AD
● Naturally-occurring coming from purple and white DIGITALIS TOXICITY (CARDIOTOXICITY)
foxglove plants, which can be poisonous
● Signaled by emerging side effects
● MECHANISM: inhibits the Na-K pump that leads to
● Serum levels exceed 3 ng/ml
increased intracellular Na
● Elderly are more prone to develop toxicity
○ Leads to calcium influx that causes more
○ Because the elderly have degenerating
efficient cardiac muscle fiber contractions
excretory system, the liver ages, thus having
● INDICATIONS: Heart failure, correcting CHF, atrial
higher chances of not excreting excess level of
fibrillation and atrial flutter
digitalis
○ Atrial fibrillation is a type of cardiac
● S/Sx: Confusion, Irregular pulse, N/V, diarrhea, vision
dysrhythmia characterized by rapid and
changes, appetite loss
uncoordinated contractions of the atria
● Gastrointestinal distress: N/V, anorexia and/or
○ Atrial flutter is characterized by very rapid
diarrhea (earliest signs), salivation and abdominal
contractions (200–300 bpm)
pain
● FOUR EFFECTS OF DIGITALIS ON THE HEART
● Neurological effects: restlessness, irritability,
○ (+) Inotropic
headache, weakness, lethargy, drowsiness, and/or
● Influences the contraction; increases vigor
confusion, visual disturbances (blurred or colored
and force of contraction
vision, halo vision, amblyopia, and diplopia
● Increased CO
● Cardiac effects: cardiac dysrhythmias, bradycardia
○ (-) Chronotropic
and AV block
● Slows down the heart rate
● ANTIDOTES
● Addresses atrial fibrillation and/or flutter
○ Digoxin-Immune Fab (Ovine, Digifab, Digibind)
together with negative dromotropic action
● Bind with digitalis compound = excreted
○ (-) Dromotropic
together = lower digoxin level
● Slower conduction of signals from SA node

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 MODULE 12 – DRUGS ACTING ON THE CARDIOVASCULAR SYSTEM

○ Phenytoin and Lidocaine are effective in ● Predictable

treating digoxin-toxicity-induced ventricular ● Occurs following physical exertion or stress
dysrhythmias ● Can be relieved by rest
● Controls only the symptoms brought about ○ Unstable Angina (Preinfarction)
by the toxicity but not correct the toxicity ● Unpredictable, may occur even at rest
● Occurs frequently over the course of a day
DIGOXIN DRUG INTERACTIONS with progressive severity
○ Variant (Prinzmetal, Vasospastic)
● (+) potent diuretics – digitalis toxicity ● Occurs during rest, worsens overtime
○ Potassium-wasting diuretics: Furosemide ● Typical pain is described as originating in the
(Lasix), Hydrochlorothiazide (Hydrodiuril) center of the chest, radiating to the left arm and
○ Furosemide and thiazides promote K loss neck
(hypokalemia) ● Decreased blood flow, decreased oxygen
● Normal potassium level: 3.5-5 mmol/L myocardium leading to pain lasting for a few
● Hypokalemia may intensify the minutes
concentration of digitalis ● S/sx: tightness, pressure in the center of the chest
○ Results in higher risk for patients to and pain radiating down the left arm, neck (severe
have digitalis toxicity because the AP)
digitalis bind at the same receptor site ○ Usually starts with epigastric pain
of potassium
○ Digoxin have stronger effect – it sapaws
the potassium
● (+) Cortisone preparations – digitalis toxicity
○ Promotes Na retention and K loss when taken
systematically
● (+) Antacids, bulk forming laxatives – decreased
digitalis absorption

NURSING RESPONSIBILITIES

● Obtain drug history

● Record baseline PR at the apical pulse for one full
minute; withhold drug if pulse is >60 bpm
○ Baka bumagal lalo since may negative
chronotropic/dromotropic action
bradycardia
● Recommend potassium rich food sources as
permitted in diet
○ We are preventing hypokalemia
● Monitor serum digoxin levels (NORMAL: 0.8–2
ng/ml); monitor I&O
● Space the time of medications
● Instruct to report signs and symptoms of toxicity
B. ANTIANGINALS
● Drugs used to treat Angina Pectoris
○ A condition of acute cardiac/chest pain caused
by inadequate myocardial perfusion due to
either plaque formation or coronary artery
spasms
● Could lead to Myocardial Infarction or a
heart attack
● THREE TYPES OF ANGINA PECTORIS
○ Stable Angina (Classic)
THREE TYPES OF ANTIANGINALS
● MECHANISM: increase blood flow either by
= increasing oxygen supply or by decreasing oxygen
demand by the myocardium
NITRATES
● Developed in 1840s
● First agent used to relieve angina
● Act on smooth muscle and the blood vessels
causing relaxation and dilation
○ Promotes generalized and coronary
vasodilation
● When nitrate is ingested and flows through
the bloodstream, they enter the cells and
smooth muscles located at the arteries and
are converted to nitric oxide
● They increase Cyclic Guanosine
Monophosphate that causes the relaxation
of the of smooth muscle layer of blood
vessels causing vasodilation

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 MODULE 12 – DRUGS ACTING ON THE CARDIOVASCULAR SYSTEM

● Decreases preload and afterload = ○ Do not touch the medication portion

decreases workload of heart = reduces ● You might absorb the medication
myocardial oxygen demand systemically
● NITROGLYCERIN (NTG) ● Rotate sites: thighs and arms can be used
○ Most used nitrate ○ Do not repeatedly use one site only
○ Preparations: Sublingual (SL) tablets ● Avoid hairy areas (may shave to increase
(commonly used), ointment, transdermal patch absorption)
(kept for patient up to 8-12 hrs OD, usually in ● Do not apply on the chest in the vicinity of
anterior chest), extended release capsules, defibrillator-cardioverter paddle
aerosol sprays ● Avoid alcohol ingestion
● NTG SL → internal jugular vein → right ● Store bottle away from light
atrium ○ Might lose potency
○ Given in 3 doses, 5 minutes interval ● Burning and stinging sensation means the drug is
● PO is avoided because nitrates undergo potent
hepatic first pass (medications that ● Instruct client not to discontinue these drugs
undergoes hepatic first pass effect are without healthcare provider’s approval =
greatly metabolized before going to withdrawal symptoms may be severe
bloodstream); sa liver pa lang ubos na ● NON-PHARMACOLOGICAL WAYS
yung gamot ○ Avoid heavy meals, smoking, extremes weather
○ Side Effects: H/A (can be given changes, strenuous exercise, emotional upset
acetaminophen), postural hypotension, ● These might put extra workload in the heart
dizziness, weakness and faintness, myocardial and decrease oxygen
ischemia (rebound effect; lalala ‘yung ○ Moderate exercise, rest, relaxation techniques
condition), reflex tachycardia (compensatory ● Perform pain assessment
mechanism), and syncope because of ● Monitor blood pressure, report hypotension
vasodilating effect ● If NTG patch is about to be discontinued, taper
○ Drug Interactions down dose prior to discontinuation of drug
● (+) other vasodilators = risk for hypotension ○ If abruptly discontinued, nitrates can cause
greatly increases spasms
● (+) heparin = antagonized heparin effect ● Wear gloves when applying transdermal
when given NTG is given as an IV dose preparations
● Advise patient to refrain from doing activities
NURSING RESPONSIBILITIES requiring alertness as it can cause fainting
● Educate patient about orthostatic hypotension
● Monitor vital signs especially blood pressure
○ Monitor orthostatic hypotension BETA BLOCKERS
● Have client sit and lie down during
administration ● Blocks Beta receptors → decrease effects of
● Tolerance to nitrates may develop due to continued sympathetic NS → block release of catecholamines
increase in dosage and prolonged use (NE/Epi) → decrease HR and BP
● SUBLINGUAL ROUTE OF ADMINISTRATION ● Blocks Beta 1 and Beta 2 receptors
○ Offer sips of water before giving sublingual ● For classic angina (anti-angina) decrease HR,
nitroglycerin decrease myocardial contractility → decrease
● Dryness of the oral mucosa might affect the oxygen consumption → decrease pain of angina
absorption of the medication ● Decreases sympathetic nervous stimulation of
● DO NOT give after administration cardiac muscles
○ If chest pain persists after 3 doses of NTG SL, ● Decreased HR leads to decreased cardiac muscle
instruct client to do to nearest hospital oxygen demand which can reduce angina
● May be a sign of impending myocardial
infarction NON-SELECTIVE BETA BLOCKERS
● OINTMENT ROUTE OF ADMINISTRATION
○ Do not use finger, instead use gloves or tongue ● Blocks Beta 1 and 2 (decrease HR and
depressor bronchoconstriction)
● TRANSDERMAL PATCH ROUTE OF ADMINISTRATION

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 MODULE 12 – DRUGS ACTING ON THE CARDIOVASCULAR SYSTEM

● Ex: Propranolol (Inderal), Nadolol (Cogard), Pindolol ○ Dysrhythmia (distured heart rhythm)
(Visken) ○ Arrhythmia (absence of rhythm)
● Contraindications: Asthma because of the
bronchoconstriction effect ELECTROCARDIOGRAM (ECG)
● S/E: bronchospasm, psychotic response,
impotence, bradycardia, hypotension

SELECTIVE BETA BLOCKERS (CARDIOSELECTIVE)

● Blocks Beta 1 (decreases HR)

● Ex: Atenolol (Tenormin), Metoprolol (Neobloc,
Lopressor)
● S/E: decrease HR (bradycardia), decrease BP
(hypotension)

CALCIUM CHANNEL BLOCKERS

● Also known as CCBs

● First introduced in 1982 for the treatment of stable
and variant angina, hypertension and certain
dysrhythmias
● Calcium
○ Increases myocardial contractions
○ Increases workload of the heart
○ Increases oxygen need/consumption
● Calcium Channel Blockers (blocks Ca)
○ Exert dilating effect on coronary arteries and
peripheral blood vessels by inhibiting calcium
→ coronary vasodilation and increase blood
flow and lower BP
○ Negative inotropics and decreases afterload
which help decrease cardiac oxygen demands
Examples
●
○ “-dipine” (Amlodipine, Nifedipine, Nicardipine,
Felodipine)
○ Verapamil HCl, Diltiazem HCl
● Routes: PO, IV
● Common side effects: Hypotension (vasodilation),
Bradycardia, Dizziness, Headache
● P wave: atrial depolarization (contraction)
● QRS wave: ventricular depolarization (contraction)
● T wave: ventricular repolarization (relaxation)
● PQ interval: atrial repolarization (relaxation)
5 PHASES OF A HEARTBEAT
Travel of the cardiac action potential across the heart
PHASE EVENT
0 Rapid depolarization caused by Na influx
Initial repolarization which coincides with
1
the termination of Na ions influx
2 Plateau associated with the influx of Ca ions
Rapid repolarization caused by the influx of
3
K ions
4 Resting membrane potential
TYPES OF ANTIDYSRHYTHMIC DRUGS

C. ANTIARRHYTHMICS CLASS 1 - NA CHANNEL BLOCKERS – FAST

Antidysrhythmia
● Decreases Na ion influx which decreases
● Cardiac Dysrhythmia (Arrhythmia) conduction velocity and suppresses automaticity
○ Any deviation from the normal rate and pattern ● 1A
(normal sinus rhythm) of the heartbeat; ○ Slows conduction and prolong repolarization
bradycardia, tachycardia, irregular heart ○ Longer relaxation phase
rhythm ○ Ex: Quinidine, Procainamide
○ Often follow a myocardial infarction or as a ● 1B
result of hypoxia or hypercapnia ○ Slows conduction and shortens repolarization
○ Atrial dysrhythmia: prevent proper filling of ○ Faster relaxation phase
ventricles and decrease the CO by ⅓ ○ Ex: Lidocaine HCl
○ Ventricular dysrhythmia: – ● 1C
● NOTE: DYS- VS ARRHYTHMIA

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 MODULE 12 – DRUGS ACTING ON THE CARDIOVASCULAR SYSTEM

○ Prolongs conduction with little effect on

repolarization
○ Given for fast arrhythmias
○ Ex: Propafenone

CLASS 2 - BETA BLOCKERS

● Block sympathetic activity

○ Leads to decreased contractility, BP, AV node
conduction, and enhance repolarization
○ Shortens cardiac action potential across the
heart
● Decreases conduction velocity, automaticity and
refractory time
● Ex: Propranolol (Inderal)

CLASS 3 - POTASSIUM CHANNEL BLOCKERS

● Drugs that prolong repolarization

● Prolong action potential and delay repolarization
and refractory period
● Increases the refractory period, and prolongs the
action potential duration
● Longer relaxation phase = lower HR
● Ex: Amiodarone HCl (Cordarone)

CLASS 4 - CA CHANNEL BLOCKERS

● Inhibit movement of calcium ions decreasing

excitability and contractility of the myocardium
● Most effective at the SA and AV nodes to reduce
rate of contraction
● Dilate coronary arteries and increase blood flow to
the myocardium
● A negative inotropic agent
● Ex: Verapamil (Calan), Diltiazem (Cardizem)
● SIDE EFFECTS
○ Cardiovascular depression, hypotension,
bradycardia, confusion, nausea and vomiting,
headache, dizziness
● NURSING RESPONSIBILITIES
○ Obtain baseline VS and ECG
● Hypotension and bradycardia
○ Perform objective pain assessment
● They may manifest chest pain
○ Monitor cardiac enzymes/markers
● Might indicate Myocardial infarction
○ Promote rest

REFERENCES
Synchronous Lecture: 15 Nov 2022 (CI: Ma’am Jennie
Junio)
Module: NCM 0106 - Module 12

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