PHARMACOLOGY SEM 01 | CYC 02

LECTURE AUF-CON

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

○ Composed of plasma, erythrocytes, leukocytes

OUTLINE and platelets
I Concept Review ○ Plasma: 90% water, 10% solutes
A Cardiovascular System
B Congestive Heart Failure
II Drugs Acting on the CVS CONCEPTS
A Cardiac Glycosides
B Antianginals ● CONDUCTION OF ELECTRICAL IMPULSES
C Antidysrhythmics ○ SA node “primary pacemaker”: 60-80 bpms
○ AV node “secondary pacemaker”: 40-60 bpms
○ Bundle of His (right and left bundle branches)
CONCEPT REVIEW
○ Purkinje Fibers
CARDIOVASCULAR SYSTEM ● Stimulates the heart to contract

PARTS
📌 REMEMBER: AV node can act as the primary
pacemaker if the SA node is malfunctioning
(bradycardia)
● HEART
○ Composed mainly by myocardium (heart
● CONTROL OF BLOOD PRESSURE
muscles)
○ Arterial blood pressure: determined by
○ Covered externally by the pericardium, lined
peripheral resistance and cardiac output
internally by the endocardium
○ High blood viscosity = high resistance
○ 4 Chambers: LA, LV, RA, RV
○ Longer blood vessel = higher resistance
● Atria: receiving chambers
○ Blood vessel radius increases = lesser
● Ventricles: pumping chambers
resistance produced
○ 4 Valves: Tricuspid and Mitral Valves,
○ Cardiac Output (CO)
Pulmonary and Aortic Semilunar Valves
● Volume of blood pumped by either
○ Perfused through the coronary arteries
ventricles of the heart each minute
● Prevents backflow of blood
○ Stroke Volume (SV)
● Right Coronary Artery, Left Anterior
● Volume of blood pumped per ventricle
Descending Artery, Left Circumflex Artery
each time the heart contracts
● BLOOD FLOW
○ Heart Rate
○ Superior (upper) and Inferior (lower) Vena
● Number of times the heart contracts each
Cava → Right Atrium → Tricuspid valve → Right
minute
Ventricle → Pulmonary semilunar valves →
○ Formula
Pulmonary trunk → Pulmonary artery (lungs,
● CO = HR x Stroke Volume (amount of blood
carrying unoxygenated blood) → Pulmonary
ejected by the ventricle every after
veins → Left Atrium → Bicuspid valve → Left
heartbeat) - 70mL per beat
Ventricle → Aortic semilunar valve → Aorta →
● Normal CO = 4-8 L/m
rest of the body
○ Three Factors affecting Stroke Volume
● BLOOD VESSELS
● Preload: force exerted by blood against
○ Arteries → Arterioles → Capillaries → Venules →
the ventricles at the end of diastole
Veins
○ Blood flow force that stretches the
○ Largest in lumen chena: veins
ventricle
○ Largest lumen in diameter: great veins
○ Higher preload = higher cardiac
○ Thicker wall: arteries
output
○ A lot of medication have their effect on arteries
● Contractility: force of ventricular
specifically of the smooth muscle layer that is
contractions
why the arteries are capable of performing
○ Higher Preload and contractility =
vasoconstriction and vasodilation that is not
higher stroke volume
present in veins
● BLOOD

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 MODULE 12 & 13 – DRUGS ACTING ON THE CARDIOVASCULAR SYSTEM

● Afterload: resistance to ventricular ejection ● Left atrium will return the blood/fluid to the
of blood caused by opposing pressures in lungs
the aorta and systemic circulation ● Nursing Intervention: Do not place patient
○ Afterload increases = flat in bed, dapat orthopneic position
decreased/weaker stroke volume ○ Pulmonary edema
○ Left ventricle has to pump harder due
to the presence of resistance DRUGS ACTING ON THE CVS

CONGESTIVE HEART FAILURE A. CARDIAC GLYCOSIDES

Digitalis
● Due to cardiac abnormalities or conditions that
place increase demand on the heart; heart ● Have been in use as early as 1200 AD
compensates → Heart muscle weakens and ● Naturally occurring come from purple and white
enlarges → Loses its ability to pump blood to the foxglove plants, which can be poisonous
lungs and systemic circulation → Left or right ● Inhibits the Na-K pump that leads to increased
failure → Continuous increase, forceful intracellular Na
contractions → Compensatory mechanism fails → ○ Leads to calcium influx that causes more
Congestive heart failure → Cardiac arrest (if not efficient cardiac muscle fiber contractions
treated) ● Also used to correct CHF, atrial fibrillation (rapid
uncoordinated atrial contraction) and atrial flutter
(200-300 bpm)
STAGES OF HEART FAILURE (PUMP FAILURE)
● FOUR EFFECTS OF DIGITALIS ON THE HEART
STAGE CHARACTERISTICS ACCORDING TO STAGE ○ (+) Inotropic
High risk to heart failure without symptoms ● Influences the contraction; more forceful
A
of structural heart disease contraction
● Increased CO
Some cardiac changes such as decreased
ejection fraction without symptoms of heart ○ (-) Chronotropic
failure ● Slows down the heart rate
B
○ (-) Dromotropic
Ejection fraction: how much is expelled from ● Slower conduction of signals from SA node
the heart; 50-70%: normal
● Decrease conduction of heart cells
Structural heart disease with symptoms of through AV node
heart failure such as fatigue, shortness of ○ Increase stroke volume
C
breath, edema, and decrease in physical
activity DIGOXIN (LANOXIN)
Severe structural heart disease and marked
D ● A secondary drug of choice for heart failure
symptoms of heart failure at rest
● Indications: Heart Failure, Atrial Fibrillation (rapid
Right Sided Heart Failure beating)
●
● Route: PO and IV
○ Mainly systemic s/sx
● t ½: 36 hours (once a day)
● Abdominal pain, fatigue, bloating, nausea,
dependent pitting edema, ankle edema, ● Low protein binding power
ascites, jaundice, hepatomegaly, ● 30% metabolized by the liver
decreased urine output (lesser blood sa ● 65% excreted by the kidneys unchanged
kidneys), increase CVP, HPN ● Serum level for dysrhythmias: 0.8-2.0 ng/ml
● Serum level for heart failure: 0.5 – 1.0 mg/ml
● Right atrium will return blood/fluid to the
systemic circulation ● Toxic level: >2-3 ng/ml
● Contraindications: Ventricular Fibrillation (fast AV
○ Peripheral edema
Left Sided Heart Failure node; hypokalemia)
●
● SIDE EFFECTS
○ Mainly respiratory s/sx
● Dyspnea, orthopnea, fatigue, restlessness, ○ N/V, diarrhea, abdominal pain, confusion,
crackles, peripheral cyanosis, dry weakness, blurred vision
non-productive cough, frothy blood tinged ● ADVERSE REACTIONS
mucus ○ Bradycardia, Cardiac Dysrhythmias,
Thrombocytopenia

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 MODULE 12 & 13 – DRUGS ACTING ON THE CARDIOVASCULAR SYSTEM

● Prior Nursing Intervention: read ECG
DIGITALIS TOXICITY (CARDIOTOXICITY)
● Signaled by emerging side effects
● Serum levels exceeds 3 ng/ml
● Elderly are more prone to develop toxicity
○ Because the elderly have degenerating
excretory system, the liver ages, thus having
higher chances of not excreting excess level of
digitalis
○ S/Sx: Confusion, Irregular pulse, N/V, Diarrhea,
Vision Changes, Appetite Loss
○ Gastrointestinal distress: Anorexia and/or
diarrhea (earliest signs), salivation and
abdominal pain
○ Neurological effects: restlessness, irritability,
headache, weakness, lethargy, drowsiness, and
/or confusion, visual disturbances (blurred or
colored vision, halo vision, amblyopia, and
diplopia
○ Cardiac effects: cardiac dysrhythmias, - -
● Phenytoin and Lidocaine are effective in treating
digoxin toxicity induced ventricular dysrhythmias
○ Controls only the symptoms brought about by
the toxicity but not correct the toxicity
● Antidote: Digoxin-Immune Fab (Digifab, Digibind)
○ These antidotes bind with digitalis compound =
excreted together = lower digoxin level
DIGOXIN DRUG INTERACTIONS
● (+) potent diuretics – digitalis toxicity
○ Diuretics: Furosemide (Lasix),
Hydrochlorothiazide (Hydrodiuril)
○ Furosemide and thiazides promote K loss
(hypokalemia)
● (+) 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
● Recommend potassium rich food sources as
permitted in diet
● Monitor serum digoxin levels (0.8 – 2 ng/ml)
● 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 (Classis): Predictable, occurs
following physical exertion or stress
○ Unstable Angina (Preinfarction)
● Unpredictable, may occur even at rest.
● Occurs frequently over the course of a day
with progressive severity
○ Variant (Prinzmetal, Vasospastic): occurs
during rest
● Typical pain is described as originating in the
center of the chest, radiating to the left arm and
neck
● Decreased blood flow, decreased oxygen
myocardium leading to pain lasting for a few
minutes
● S/sx: tightness, pressure in the center of the chest
and pain radiating down the left arm, neck (severe
AP)
THREE TYPES OF ANTIANGINALS
● Increase blood flow either by increasing oxygen
supply od by decreasing oxygen demand by
myocardium
NITRATES
● Developed in 1840s
● First agents used to relieve angina
● Act on smooth muscle and the blood vessels
causing relaxation and dilation
○ Promotes generalized and coronary
vasodilation
● Decreases preload and afterload and reduces
myocardial oxygen demand
● NITROGLYCERIN (NTG)
○ Most used nitrate
○ Preparations: Sublingual (SL) tablets, ointment,
transdermal patch, extended release capsules,
aerosol sprays
○ NTG SL → internal jugular vein → right atrium
○ Side Effects: HA, postural hypotension, dizziness,
weakness and faintness, myocardial ischemia
(rebound effect), reflex tachycardia, and
syncope
○ Drug Interactions
● (+) other vasodilators = risk for
hypotension greatly increases

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 MODULE 12 & 13 – DRUGS ACTING ON THE CARDIOVASCULAR SYSTEM

● (+) heparin = antagonized heparin effect

when given NTG is given as an IV dose ● Blocks Beta receptors → decrease effects of
○ NURSING RESPONSIBILITIES sympathetic NS → block release of catecholamines
● Monitor vital signs (NE/Epi) → decrease HR and BP
● Have client sit and lie down during ● Blocks Beta 1 and Beta 2 receptors
administration ● For classic angina (anti-angina) decrease HR,
● Offer sips of water before giving sublingual decrease myocardial contractility → decrease
nitroglycerin oxygen consumption → decrease pain of angina
○ Dryness of the oral mucosa might
● Decreases sympathetic nervous stimulation of
affect the absorption of the
cardiac muscles
medication
● Decreased HR leads to decreased cardiac muscle
● If chest pain persists after 3 doses of NTG
oxygen demand which can reduce angina
SL, instruct client to do to nearest hospital
● Non-selective beta blockers
● Tolerance to nitrates may develop die to
○ Blocks Beta 1 & 2
continued increase in dosage and
○ Decrease HR, bronchoconstriction
prolonged use
○ Ex: Propranolol (Inderal), Nadolol (Cogard),
● Ointment: do not use finger, instead use
Pindolol (Visken)
gloves of tongue depressor
○ Contraindications: Asthma because of the
● Transderm patch: do not touch the
broconstricting effect
medication portion
○ S/E: bronchospasm, psychotic response,
○ Rotate sites: thighs and arms can be
impotence, bradycardia, hypotension
used
● Selective beta blockers (Cardioselective)
○ Avoid hairy areas (may shave to
○ Blocks Beta 1
increase absorption)
○ Decrease HR
● Do not apply on the chest in the vicinity of
○ Ex: Atenolol (Tenormin), Metoprolol (Neobloc,
defibrillator-cardioverter paddle
Lopressor)
● Avoid alcohol ingestion
○ S/E: decrease HR (bradycardia), decrease BP
● Store bottle away from light
(hypotension)
○ Might lose potency
● Burning and stinging sensation means the
CALCIUM CHANNEL BLOCKERS
drug is potent
● Instruct client not to discontinue these ● Also known as CCBs
drugs without healthcare provider’s ● First introduced in 1982 for the treatment of stable
approval = withdrawal symptoms may be and variant angina, hypertension and certain
severe dysrhythmias
● NON-PHARMACOLOGICAL WAYS ● Calcium
○ Avoid heavy meals, smoking, ○ Increases myocardial contractions
extremes weather changes, ○ Increased workload of the heart
strenuous exercise, emotional upset ○ Increases oxygen need/consumption
○ Moderate exercise, rest, relaxation ● Calcium-channel blockers - blocks Ca
techniques ○ Exert dilating effect on coronary arteries and
● Perform pain assessment peripheral blood vessels by inhibiting calcium
● Monitor blood pressure, report hypotension → coronary vasodilation and increase blood
● If NTG patch is about to be discontinued, flow and lower BP
taper down dose prior to discontinuation ○ Negative inotropics and decreases afterload
of drug which help decrease cardiac oxygen demands
● Wear gloves when applying transdermal ● CCBs relax coronary artery spasms and peripheral
preparations arterioles
● Advise patient to refrain from doing ● CCBs are negative inotropes and decreases
activities requiring alertness afterload which help decrease cardiac oxygen
● Educate patient about orthostatic demand
hypotension ● Examples
○ “-dipine”
BETA BLOCKERS ○ Amlodipine, Nifedipine, Nicardipine, Felodipine

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 MODULE 12 & 13 – DRUGS ACTING ON THE CARDIOVASCULAR SYSTEM
○ **Verapamil HCl, Diltiazem HCl
● Routes: PO, IV
● Common side effects: Hypotension, Bradycardia,
Dizziness, Headache
C. ANTIDYSRHYTHMICS
● Cardiac Dysrhythmia (Arrhythmia)
○ Any deviation from the normal rate and pattern
(normal sinus rhythm) of the heartbeat;
bradycardia, tachycardia, irregular heart
rhythm
○ Often follow a myocardial infarction or as a
result of hypoxia or hypercapnia
○ Dysrhythmia (distured heart rhythm)
○ Arrhythmia (absence of rhythm)
○ Atrial dysrhythmia - prevent proper filling of
ventricles and decrease the CO by ⅓
ELECTROCARDIOGRAM (ECG)
● 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 ○ Cardiovascular
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
CLASS 1 - NA CHANNEL BLOCKERS – FAST
● Decreases Na ion influx which decreases
conduction velocity and suppresses automaticity
● 1A
○ Slows conduction and prolong repolarization
○ Ex: Quinidine, Procainamide
● 1B
○ Slows conduction and shortens repolarization
○ Ex: Lidocaine HCl
● 1C
○ Prolongs conduction with little effect on
repolarization
○ Ex: Propafenone
CLASS 2 - BETA BLOCKERS
● Block sympathetic activity → decrease
contractility, BP, AV node conduction, and enhance
repolarization
● 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
● 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
● Decreasing excitability and is a negative inotropic
agent
● Ex: Verapamil (Calan), Diltiazem (Cardizem)
● SIDE EFFECTS
depression, hypotension,
bradycardia, confusion, nausea and vomiting
● NURSING RESPONSIBILITIES
○ Obtain baseline VS and ECG
● Hypotension and bradycardia
○ Perform objective pain assessment
○ Monitor cardiac enzymes/markers
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