You are on page 1of 89

CARDIOVASCULA

R Agents
Topics to be discussed:
a. Antihypertensives
b. Diuretics
c. Antihyperlipidemics
d. Anticoagulants
e. Antiplatelets
f. Thromnbolytics
g. Cardiac Glycosides
h. Antianginals
i. Antidysrhythmics
Let’s Review… ❖ The cardiovascular system includes the
heart, blood vessels (arteries and veins), and
blood flow.

❖ Blood that is abundant in oxygen (O2),


nutrients, and hormones moves through
vessels called arteries, which narrow to
arterioles and then to capillaries.

❖ Capillaries transport nourished blood to body


cells and absorb waste products, such as
carbon dioxide (CO2), urea, creatinine, and
ammonia.

❖ The deoxygenated blood returns to the


circulation by small venules and larger veins
to be eliminated by the lungs and kidneys
with other waste products.
❖ The heart is composed of four
The Heart chambers including the right and left
atria and the right and left ventricles.

Right Atrium: receives deoxygenated


blood from the circulation
Right Ventricle: pumps blood through the
pulmonary artery to the lungs for gas
exchange (carbon dioxide for oxygen)
Left Atrium: receives oxygenated blood,
Left Ventricle: pumps the blood into the
aorta for systemic circulation
Regulation of Heart Rate and Blood Flow

The heart beats approximately 60 to 80 As blood travels, resistance to The average systemic arterial
times per minute in an adult, pumping blood flow develops, and pressure, known as blood
blood into the systemic circulation. arterial pressure increases. pressure, is 120/80 mm Hg

Arterial blood pressure is determined by Stroke volume, the amount of Three factors—preload,
peripheral resistance and cardiac output, blood ejected from the left contractility, and afterload—
which is the volume of blood expelled ventricle with each heartbeat, is determine the stroke volume .
from the heart in 1 minute, calculated by approximately 70 mL/beat.
multiplying the heart rate by the stroke
volume. The average cardiac output is 4 to
8 L/min.
Factors that determine Stroke Volume
1 2 3

Preload Contractility Afterload


Preload refers to the blood Contractility is the force of Afterload is the resistance to
flow force that stretches the ventricular contraction. ventricular ejection of blood.
ventricle at the end of diastole.
afterload stroke volume
preload stroke volume
afterload stroke volume
preload stroke volume
Specific drugs can increase or decrease preload and afterload, affecting both stroke
volume and cardiac output. Most vasodilators decrease preload and afterload, thus
decreasing arterial pressure and cardiac output.
Circulation
PULMONARY SYSTEMIC CIRCULATION:
CIRCULATION: the heart also called peripheral
pumps deoxygenated blood circulation, the heart pumps
from the right ventricle blood from the left ventricle to
through the pulmonary artery the aorta and into the general
to the lungs. The pulmonary circulation. Arteries and
artery carries blood that has a arterioles carry the blood to
high concentration of carbon capillary beds. Nutrients in the
dioxide. Oxygenated blood capillary blood are transferred
returns to the left atrium by the to cells in exchange for waste
pulmonary vein. products. Blood returns to the
heart through venules and veins.
Blood is composed of plasma,
Blood Plasma, made up of 90% water
red blood cells (erythrocytes), and 10% solutes, constitutes
white blood cells (leukocytes), 55% of the total blood volume.
and The solutes in plasma include
platelets. glucose, protein, lipids, amino
acids, electrolytes, minerals,
lactic and pyruvic acids,
hormones, enzymes, oxygen,
The major function of and carbon dioxide.
blood is to provide
nutrients, including
oxygen, to body cells.
Most of the oxygen is White blood cells (WBCs) are
carried on the hemoglobin the major defense mechanism of
of red blood cells the body and act by engulfing
(RBCs). microorganisms. They also
produce antibodies.
The platelets are large cells
that cause blood to coagulate.
RBCs have a life span of
approximately 120 days,
whereas the life span of a
WBC is only 2 to 24 hours.
Antihypertensives
Hypertension
What is
Hypertension?
Stage Systolic BP Diastolic BP

Hypotension < 90 mmHg <60 mmHg

Normal 90 -120mmHg 60 - 80mmHg

Prehypertensio 120 – 139


80 – 89 mmHg
n mmHg
an increase in blood pressure such 140 – 159
that the systolic pressure is greater Stage I 90 – 99 mmHg
mmHg
than 140mmHg and the diastolic
pressure is greater than 90mmHg Stage II ≥ 160 mmHg ≥ 100 mmHg
ABCDs of Antihypertension Drugs

🠶 Angiotensinogen Converting Enzyme Inhibitors

A 🠶 Angiotensinogen Receptors Blockers


🠶 Alpha-adrenergic Blockers

B 🠶 Beta-Blockers

🠶 Centrally-alpha Agonists
C 🠶 Calcium-Channel Blockers

D 🠶 Dilators
🠶 Diuretics
General Consideration in
Antihypertensive Drug Therapy

P R E S
PRESSURE RISE EATING STAY
monitor slowly must be considered on medications

S U R E

SKIPPING UNDESIRABLE REMIND ELIMINATE


is a NO-NO responses (educate) exercise smoking and alchol
Antihypertension Drugs

🠶 Angiotensinogen Converting Enzyme

A (ACE) Inhibitors
🠶 Angiotensinogen Receptors Blockers
🠶 Alpha-adrenergic Blockers
√Captopril √ Enalapril √ Lisinopril
ACE Inhibitors “-prils”
Action: Suppress renin-angiotensin-
aldosterone system, blocks conversion of
Angiotensin I to Angiotensin II, blocks the
release of aldosterone.

ACE inhibitors cause little change in


cardiac output or heart rate, and they lower Side Effects: hypotension, constant, irritated cough,
peripheral resistance. taste alteration, nausea, vomiting, diarrhea, headache,
dizziness, fatigue, insomnia, hyperkalemia, tachycardia,
Indication: Treatment of Hypertension and Angioedema
adjunct therapy for CHF and MI Drug Interaction: Probenecid ↓ elimination of ACE
inhibitors, NSAIDs ↓ hypotensive effects
Contraindication: pregnant because they
reduce placental blood flow, patients with Consideration: monitor Serum Potassium, renal
renal insufficiency sufficiency
ACE Inhibitors

Captopril
Lisinopril

Enalapril
Angiotensin- √Losartan √ Valsartan √ Candesartan
Receptor “-artans”
Indication: Treatment of Hypertension
Blockers Contraindication: pregnancy, patients with renal
insufficiency
Action:
-suppress renin-angiotensin-aldosterone Consideration: monitor Serum Potassium, renal
system, blocks binding of Angiotensin sufficiency
II at the AT1 receptor site
-prevent the release of aldosterone,
cause vasodilation and decrease
peripheral resistance
-may be used as a first-line treatment
for hypertension or with combination
with thiazides to reduce potassium
retention
Angiotensin-Receptor Blockers

Losartan
Candesartan

Valsartan
Alpha- Selective:

adrenergic “-sins” √Doxazosin √ Prazosin√ Terazosin


Nonselective:
blockers √phentolamine √ phenoxybenzamine

Action:
-blocks alpha-1 adrenergic receptors
resulting to relaxation of smooth muscles
-useful in treating hypertension in patients
with lipid abnormalities.
Indication: Primarily used as Treatment of
2 types: selective and nonselective (more Hypertension and maybe used for BPH
potent, newer, for hypertensive crisis due to
Side Effects: orthostatic hypotension, nausea, headache,
pheochromocytomas) drowsiness, nasal congestion, edema, and weight gain.
Drug Interaction: ↑ peripheral edema when taken
together with anti-inflammatory drugs, ↑ syncope when
taken together with nitroglycerin
Alpha-adrenergic blockers
Selective:
Doxazosin
Prazosin

Terazosin
Alpha-adrenergic blockers
Nonselective:
phentolamine

phenoxybenzamine
Antihypertension Drugs

B 🠶Beta-blockers
Beta-blockers “-olols”

Action:
-binds to Beta-receptors to reduce heart Indication: hypertension, angina, MI, migraine headache,
rate, contractility, renin release and tachycardia
relaxation of smooth muscles Contraindication: COPD, asthma, CHF, sinus bradycardia
-used as antihypertensive drugs or in
combination with a diuretic. Side Effects: decreased pulse rate, markedly decreased
blood pressure, and (with noncardioselective beta1 and
-used as antianginals and beta2 blockers) bronchospasm,
antidysrhythmics
Abrupt discontinuation: rebound hypertension, angina,
2 types: selective (beta-1 (heart) and dysrhythmias, and myocardial infarction can result
nonselective beta-1(heart) and 2(lungs)
Noncardioselective beta blockers inhibit the liver’s ability to
convert glycogen to glucose in response to hypoglycemia.
Caution must be done for patients with diabetes mellitus.
Beta-blockers
Selective: Nonselective:
Atenolol

Labetalol

Metropolol
Carvedilol
Antihypertension Drugs

C 🠶 Centrally-alpha Agonists
🠶 Calcium-Channel Blockers
√Clonidine √ Methyldopa
Central Alpha-2
Agonists
Action:
-decrease the release of adrenergic hormones
from the brain which results to reduced
peripheral vascular resistance and increased
vasodilation
-short-acting, maybe used to immediately lower
blood pressure
Indication: hypertension
Contraindication: betablockers
Side effects: Edema (sodium and water retention)
drowsiness, dry mouth, dizziness, and slow heart rate
(bradycardia
Drug Interaction: betablockers ↑ risk for bradycardia
and rebound hypertension
Central Alpha-2 Agonists

clonidine

methyldopa
Calcium-channel
Blockers
Indication: hypertension, angina
pectoris and cardiac dysrhythmia

2 types: Dihydroperidines (selective) Non-Dihydroperidines


and Nondihydroperidines Diltiazem
(Nonselective) Verapamil
Dihydroperidines:
Use cautiously with: Elderly and
Amlodipine
patients with cardiac dysrhythmias
Felodipine
Nifedipine
Drug Interaction: ↑ cardiac depression
Nicardipine
with beta-blockers
Beta-blockers
Dihydroperidines: Non-Dihydroperidines

Amlodipine

Diltiazem

Felodipine
Verapamil
Calcium-channel
✔ Amlodipine
Blockers: ✔ Felodipine
Dihydroperidines ✔ Nifedipine
✔ Nicardipine
Action: Blocks calcium access
to the cells resulting to
vasodilation

Side Effects: Dizziness,


headache, flushing, peripheral
edema and gingival hyperplasia
Calcium-channel ✔ Diltiazem
✔ Verapamil
Blockers:
Non-Dihydroperidines
Action:
-blocks calcium access to the cells
resulting to decrease in contractility,
heart rate, conduction and peripheral
vasodilation but does not affect cardiac
output
-exhibit significant anti-arrhythmic
properties

Side Effects: excessive bradycardia,


cardiac conduction problems,
constipation (with verapamil)
Antihypertension Drugs

D 🠶 Dilators
🠶 Diuretics
3 Major Class:
Diuretics ○ Loop Diuretics
○ Thaizides
○ Potassium-sparring

-drugs that induces diuresis

√Diuresis helps decrease the


volume in the vascular space
decreasing the cardiac output
thereby decreasing blood
pressure
General Consideration in
Diuretic Therapy
Diet, increase
D potassium T Take with or after
meals in AM
R Review heart rate, Bp and
electrolytes
I I and O, monitor
including weight I Increase risk for
orthostatic hypotension
E Elderly, careful

U Undesirable effects
(Elec imbalance) C Cancel Alcohol
Thiazides:
Diuretics ✔ Hydrochlorothiazide (HCTZ)
✔ Chlorothiazide

Action: inhibits sodium, chloride and


water reabsortption in the distal portion
of the ascending loop of Henle
Indication: hypertension and
peripheral edema
Used as combination drug for other
anti-hypertensive meds
Side Effects: Decrease in serum
electrolytes particularly sodium and
potassium but may result to
hypercalcemia, hypeurecemia,
Contraindication: CKD, Oliguria
hyperglycemia
Drug Interaction: Potentiates other anti-HPN meds
and Digoxin
Diuretics: Thiazides

Hydrochlorothiazide
(HCTZ)

Chlorothiazide
Loop Diuretic/Potassium-Wasting
Diuretics ✔ Furosemide
✔ Bumetanide

Action: inhibits sodium, chloride and


water reabsortption in the proximal
portion of the ascending loop of
Henle

Indication: Edema, Renal


dysfynction, hypertension

Side Effects: electrolyte imbalance


particlurly sodium and potassium,
hypotension, blurred vision,
dehydration, dizziness, headache,
muscle cramps, constipation,
ototoxicity
Diuretics: Loop Diuretic/Potassium-Wasting

Furosemide

Bumetanide
Potassium-Sparing
✔ Spinorolactone
Diuretics
Action: act primarily in the collecting
duct renal tubules and late distal tubule
to promote sodium and water excretion
and potassium retention. The drugs
interfere with the sodium-potassium
pump controlled by aldosterone

Indication: diuretic-induced
hypokalemia, used with loop or thiazide
diuretic in treating CHF and
hypertension

✔ Mild diuretic, used in combination Side Effects: hyperkalemia, anorexia, nausea,


with other diuretic vomiting, diarrhea, and numbness and tingling of the
hands and feet
Contraindication: CKD, Oliguria
Diuretics: Potassium Sparing

Spironolactone
Antilipidemics
Antilipidemics

-drugs that lower blood lipid

-also known as antihyperlipidemics,


antilipemics, and hypolipidemics

LIPIDS – are any of the diverse group of


organic compounds fats, oils and hormones
and certain components of membranes that Hyperlipidemia- an excess of one more
are grouped together because they do not lipids in the blood
interact appreciably with water.
Lipid Profile- Blood test that measures
lipids- fats and fatty substances used as a
source of energy by your body. Measures
Total Cholesterol, Triglycerides, High and
Low density cholesterol. Risk Screening for
CAD
Hyperlipidemia
Antilipidemics

-drugs that lower blood lipid

-also known as antihyperlipidemics,


antilipemics, and hypolipidemics

Types:

⮚ Bile Acid Sequestrants

⮚ Fibrates (fibric acid)

⮚ Nicotinic Acid

⮚ Cholesterol Absorption Inhibitor

⮚ Hepatic 3-hydroxy-3methylglutaryl
coenzyme A (HMG-CoA)
Antilipidemics: Nursing Considerations
L Liver, renal disease; WARNING

I Intake before sleeping


Increased tendencies for GI upset, constipation

VLDL, LDL , Triglycerides,


V cholesterol monitoring

Encourage low fat, low


E cholesterol diet

R Restrict Alcohol
Antilipidemics: Bile Acid Sequestrants
Drug Prototype: Cholestyramine (Questran)
Colestipol (Colestid)

-one of the first antilipidemic, effective


against hyperlipidemia type II

MOA: bind to bile acids in the intestine and


prevent them from beinf reabsorbed into the
blood. The liver then produces more bile to
replace the bile that has been lost. Because
Side Effects: constipation, flatulence,
the body needs cholesterol to make bile, the
cramping, peptic ulcer
liver uses up cholesterol in the blood, which
reduces the amount of LDL cholesterol
Contraindication: Gallbladder disorder,
circulating in the blood.
pregnancy
Antilipidemics: Fibrates (fibric acid)

Drug Prototype: Gemfibrozil(Lopid) ,


Fenofibrate (Lipway, Lipanthyl)

-primarily to reduce hyperlipidemia type IV,


but it can also be used for type II
hyperlipidemia

MOA: increases activity of Lipase


promoting VLDL, triacylglycocerol
catabolism, promotes transfer of cholesterol
to HDL.

Side Effects: GI upset, nausea and vomiting

Contraindication: should not be taken with


anticoagulants
Antilipidemics: Nicotinic Acid

Drug Prototype: Niacin

-for VLDL and LDL: types II, III, IV and V


heperlipidemia

MOA: inhibits free fatty acid release from


adipose tissue by inhibiting the accumulation
of cyclic adenosine monophosphate (cAMP)

Side Effects: itching and flushing, GI upset,


cardiac dysrrhythmia

Contraindication: hepatic disease,


pregnancy, heart failure, MI
Antilipidemics: Cholesterol Absorption Inhibitor

Drug Prototype: Ezetimibe (Zitia)

-reduces total cholesterol LDL, and


triglycerides

MOA: inhibits cholesterol absorption in


small intestine by binding to a critical
mediator of cholesterol absorption, the
Niemann-Pick C1-Like 1 (NPC1L1) protein
on the gastrointestinal tract ephithelial cells
as well as hepatoctyes.
Side Effects: diarrhea, GI upset, URTI

Contraindication: hepatic disease,


pregnancy, lactating mothers
Antilipidemics: Hepatic 3-hydroxy-
3methylglutaryl coenzyme A (HMG-CoA)
Drug Prototype: atorvastatin (Liptor),
Rosuvastatin (Crestor), Simvastatin

-useful in decreasing CAD and reducing


mortality rates

MOA: inhibits HMG-CoA reductase, the


enzyme necessary for hepatic production of
cholesterol, by inhibiting cholesterol
synthesis in the liver, this group of
Side Effects: GI upset, headaches, muscle cramps,
antihyperlipidemics decreases the fatigue, eye cataract, rhabdomyolysis
concentration of cholesterol, decreases LDL,
and slightly increases HDL Cholesterol Contraindication: liver disease, pregnancy

Lifetime maintenance drug, abruptly stopping the


statin drug couls cause a threefold rebound effect that
may cause detah from acute myocardial infarction
Antilipidemics: Nursing Considerations
Administer drug at bedtime

Monitor cholesterol and LDL levels

Monitor results of liver function tests

Ensure patient has initiated a 3-6 month diet and


exercise program

Emphasize the importance of lifestyle


changes

Provide safety and comfort measures


Anti-anginal
Anti-anginals Types of Angina:

⮚ Classic/ Stable – occurs with predicatble


stress or exertion
-drugs that treat Angina Pectoris ⮚ Pre-infarction/ Unstable – occurs
frequently with progressive severity
MOA: drugs increase blow flow either by unrelated to activity; unpredicatble
increasing oxygen supply or decreasing regarding stress/ exertion and intensity
oxygen demand by the myocardium
⮚ Variant/ Prinzmetal / Vasospastic –
ANGINA PECTORIS – condition of acute occurs during rest
cardiac pain caused by inadequate blood
flow to the myocardium due to either plaque
occlusions within or spasms of the coronary
arteries

Types of Angina:
✔ Nitrates
✔ Beta-blockers
✔ Calcium –channel blockers
Anti-anginals: Nitrates
-first agent used to relieve angina

-vasodilator

-caused generalized vascular and coronary


vasodilation, which increases blood flow
through the arteries to the myocardial cells.

-this group of dugs reduces myocardial


ischemia but cause hypotension.

-NITROGLYCERINE

MOA: relaxes the vascular smooth muscle,


decreases myocardial demand for oxygen,
decreasing left ventricular preload by
dilating veins thus decreasing afterload
Anti-anginals: Nursing Considerations
Instruct patient not to swallow sublingual preparations to ensure therapeutic
effects.

Ask for presence of burning sensation to ensure drug potency.

Protect drug from sunlight to protect drug potency.

For sustained-release forms, instruct not to crush and take with water.

Rotate injections sites and provide skin care as appropriate

Avoid abrupt stop of long term therapy, taper doses for 4-6 weeks to
prevent MI
Anticoagulants, Antiplatelet
Thrombolytics
Anticoagulants vs Antiplatelets vs Thrombolytics
-drugs that maintain or restore circulation DIFFERENCE:
Anticoagulants
Anticoagulants Do not dissolve clots that have already formed but
rather act prophylactically to prevent new clots
Prevent the formation of clots that inhibit
from forming , used in patients with venous and
circulation
arterial disorders that put them at high risk for clot

Antiplatelets formation.

I and O, monitor including weight Antiplatelets


Used to prevent thrombosis in arteries by

Thrombolytics suppressing platelet aggregation

Attack and dissolve blood clots that have


Thrombolytics
already formes Promote fibronolytic mechanism (converting
plasminogen to plasmin , which destroys the
fibrin in the blood clot)
Anticoagulants: Heparin
MOA: combines with antithrombin III which
accelerates the anticoagulant cascade of
reactions that prevents thrombosis formation.
By inhibiting the action of thrombin,
coversion of fibrinogen to fibrin does not
occur and the formation of fibrin clot is
prevented.

-poorly absorbed in GI thus given SQ or IM

-indicated for anticoagulant effect when a


thrombosis occurs because of a Deep Vein Low Molecular –Weight Heparin:
Thrombosis (DVT), pulmonary embolism enoxaparin sodium (Lovenox) and dalteparin
(PE) or an evolving stroke sodium (Fragmin)

-Heparin prolongs clotting time Selective Factor Xa inhibitor: fondaparinux


(Arixtra)
Lab test: monitor PT, APTT
Antidote: protamine sulfate
Anticoagulants: Heparin

Low Molecular –Weight Heparin:


enoxaparin sodium (Lovenox) and dalteparin
sodium (Fragmin)

Selective Factor Xa inhibitor: fondaparinux


(Arixtra)

Antidote: protamine sulfate


Anticoagulants: Warfarin
MOA: inhibit hepatic synthesis of vitamin
K, thus affecting the clotting factors II, VII,
IX and X

-use mailnly to prevent thromboembolic


conditions such as thromboplebitis,
pulmonary embolism, and embolism caused
by atrial fibrillation, which can lead to stroke
(CVA)

-regular monitoring of PT and APTT

-drug accumulation can occur and lead to


external or internal bleeding, so the nurse
must observe for petechiae, ecchymosis,
tarry stools and hematemesis.

-Antidote: Vitamin K
Anticoagulant : Nursing Considerations
Assess for signs of signifying blood loss (e.g. Petechiae, bruises, dark-colored
stools etc.)
Establish safety precautions (e.g. raising side rails, ensuring
adequate lighting, padding side of bed, etc.) to protect patient
from injury.

Maintain antidotes on bedside to promtply treat drug overdose.

Evaluate effectiveness by monitoring the following: PT and


international normalized ratio (INR) for warfarin; WBCT and APTT
for heparin.

Educate patient on drug therapy including drug name, its indication,


and adverse effects to watch out for, to enhance patient
understanding on drug therapy and thereby promote adherence to
drug regimen.
Antiplatelets
-prevents thrombosis in the arteries by
suppressing platelet aggregation

-prophylactic use in:

✔ Prevention of myocardial infarction (MI)


or stroke for patients with familial
history

✔ Prevention of repeat MI or stroke

✔ Prevention of stroke for patients having


transient ischemic attacks (TIAs)

-commonly used: Aspirin, Clopidrogel and


Cilostazol

Side effects: GI discomfort, increased


bleeding tendencies
Antiplatelets : Nursing Considerations
Administer drug with meals to relieve GI upset.

Provide comfort measures for headache because pain due to


headache may decrease patient compliance to treatment
regimen.

Educate patient on ways to promote safety like using electric razor, soft-
bristled toothbrush, and cautious movement because any injury at this point
can precipitate bleeding.

Educate patient on drug therapy including drug name, its indication,


and adverse effects to watch out for, to enhance patient
understanding on drug therapy and thereby promote adherence to
drug regimen.
Thrombolytics
Streptokinase and urokinase are
-promote the fibrinolytic mechanism enzymes that act systemically to
promote the conversion of plasminogen
MOA: binds with plasminogen causing
to plasmin.
conversion of plasmin to dissolve clots.

-the thrombus, or blood clot, disintegrates Alteplase, also known as tissue


when a thrombolytic drug is administered plasminogen activator (tPA), is a clot-
within 4 hours. Necrosis resulting from specific and binds to the fibrin surface
the blocked artery is prevented or of a clot, promoting the conversion of
minimized, and hospitalization time may plasminogen to plasmin.
be decreased.
Plasmin, an enzyme, digests the fibrin
Common drugs: Streptokinase, urokinase in the clot. Plasmin also degrades
(Abbokinase), altepase tPA (Activase), fibrinogen, prothrombin, and other
reteplase rPA (Retavase), and tenecteplase clotting factors.
TNK-tPA (TNKase)
Thrombolytics : Nursing Considerations
Assess for signs of blood loss (e.g. petechiae, bruises, dark-colored stools, etc.) to
determine therapy effectiveness and promote prompt intervention for bleeding
episodes.

Establish safety precautions (e.g. raising side rails, ensuring adequate room
lighting, padding sides of bed, etc.)

Evaluate effectiveness by monitoring coagulation studies to adjust drug dose


appropriately.

Educate patient on drug therapy including drug name, its indication,


and adverse effects to watch out for, to enhance patient
understanding on drug therapy and thereby promote adherence to
drug regimen.
Anti-arrythmic Drugs
Anti-arrythmics
-drugs that restore cardiac rhythm to
normal

-also known as ANTIDYSRRYTHMIC

CARDIAC DYSRRYTHMIA – any


deviation from the normal rate or pattern
of the heartbeat, can be too slow
(bradycardia), too fast (tachycardia) or
irregular. It can be atrial, ventricular or
both.

ELECTROCARDIOGRAM (ECG) –
test that measures electrical impulses in
heart to identify the cardiac rhythm.
Mechanisms of HEART BEAT
The heart’s conduction system consists of special electrical cells that
generate and coordinate electrical impulses to the myocardial cells.

Properties of the myocardial cells:

✔ RHYTHMICITY-regularity of impulse transmission

✔ AUTOMACITY-ability to initiate electrical impulses

✔ CONDUCTIVITY-ability to transmit electrical impulses from


one cell to another

✔ CONTRACTILITY- ability to contract in response to the flow


of electric impulse

✔ EXCITABILITY-ability to respond to electrical stimuli


Example of Arrythmia
Anti-arrhythmics
-drugs that restore the cardiac rhythm to
normal

-also known as antidysrrhythmic

Four Types:

1. Sodium Channel Blockers (Fast)

2. Beta Blockers

3. Drugs that prolong repolarization

4. Calcium Channel Blockers (Slow)


Anti-arrhythmics: Sodium Channel Blocker Class IA

-slows conduction and prolong ✔ QUINIDINE


repolarization ✔ PROCAINAMIDE
-for atrial and ventricular dysarrhytmias, ✔ DISOPYRAMIDE
proxysmal atrial tachcardia (PAT),
supraventricular arrhythmias

MOA: stabilize cell membrane by


depressing action potential by binding to
sodium channels and change the duration
of action potentials of the cells.
Anti-arrhythmics: Sodium Channel Blocker Class IB
✔ LIDOCAINE
-slows conduction and shortens
repolarization ✔ MEXILITINE HCl

-for acute ventricular arrhythmias


MOA: stabilize cell membrane by
depressing action potential by
binding to sodium channels and
change the duration of action
potentials of the cells.
Anti-arrhythmics: Sodium Channel Blocker Class IC
✔ FLECAINIDE (TAMBOCOR)
-prolongs conduction with little to
no effect on repolarization ✔ PROPAFENONE HCl
(RYTHYMOL)
-for life threatening ventricular
arrhythmias
MOA: stabilize cell membrane by
depressing action potential by
binding to sodium channels and
change the duration of action
potentials of the cells.
Anti-arrhythmics: Class II Beta-blockers
-decrease conduction velocity, automaticity
and recovery time

-atrial flutter and fibrillation,


tachydysrhythmias, ventricular and
supraventricular dysrhythmias

- “-OLOLS”

MOA: binds to beta-receptos to reduce HR,


contractility and relaxation of smooth muscles
through inhibiting stimulation of beta-
receptors

ESMOLOL-very short acting beta blocker


Anti-arrhythmics: Class III drugs that prolong repolarization
-prolong repolarization during ventricular
disarrhythmias, prolongaction potential
duartion

-life-threatening atrial and ventricular


dysrhythmias resistant to other drugs

- AMIODARONE, ADENOSINE

MOA: prolongs and slows down the outward


movement of potassium during action
potential

-these drugs act directly on the heart muscles


to prolong repolarization and refractory
period.
Anti-arrhythmics: Class IV Calcium Channel Blockers
-block calcium influx, slow conduction
velocity, decrease myocardial
contractility and increase refraction in
AV node

-supraventricular tachydysrhythmias;
prevention of PSVT

- DILTIAZEM, VERAPAMIL

MOA: blocks the movement of calcium


towards the cell membrane slowing
down both conduction and automaticity
Anti-arryhythmics: Nursing Considerations
Titrate the dose to the smallest amount enough to manage arrhythmia to decrease
the risk of drug toxicity.

Monitor cardiac rhythm closely to detect potentially serious adverse effects and
to evaluate drug effectiveness.

Provide comfort and safety measures. Ensure maintenance of emergency


drugs at bedside.

Educate patient on drug therapy including drug name, its indication,


and adverse effects to watch out for, to enhance patient
understanding on drug therapy and thereby promote adherence to
drug regimen.
Cardiotonic Drugs
Cardiotonic Drugs
Types:
-drugs that have a strengthening effect on the heart
or that can increase cardiac output ✔ Cardiac Glycosides
-used as teatment for cognitive heart failure ✔ Phosphodiesterase Inhibitors
Effects:

INOTROPIC: modifying the force or speed of


contraction of muscles

CHRONOTROPIC: modifying the heart rate and


rhythm by affecting the elctrical conduction
system particularly at SA node

DROMOTROPIC: modifying the heart rate and


rhythm by affecting the electrical conduction
system particularly at AV Node
Cardiac Glycoside: Digoxin
Therapeutic Serum Level: 0.8-2.0 ng/ML
-derived from the plant, Digitalis
Half-life: 30-40 hours (high risk for toxicity)
Brand Name: Lanoxin, Digoxin, Digox
Digoxin Toxicity S/Sx: anorexia, diarrhea, nausea
MOA: inhibit the sodium-potassium pump, and vomiting, bradycardia, premature ventricular
resulting in increase in intracellular sodium. This contractions, cardiac dysrhythmias, headaches,
increase leads to an influx of calcium, causing the malaise, blurred vision, visual illusions (white,
cardiac musclefibers to contract more efficiently green, yellow halos around objects), confusion and
delirium
Indication: Cardiac arrhythmia, atrial fibrillation,
atrial flutter, paroxysmal supraventricular
tachycardia

Effects:
✔ Positive inotropic action
✔ Negative chronotropic action Antidote: Digoxin Immune Fab
✔ Negative dromotropic action (ovine, Digibind)
Digoxin: Nursing Considerations
Check drug dose and preparation carefully to avoid medication errors because
drug has narrow safety margin.

Do not administer drug with food and antacids to prevent decreased in drug
absorption.

IMPORTANT: count apical pulse or one whole minute before administering


drug to monitor adverse effects.

Drug is withheld if pulse is less than 60 beats per minute in adults


and 90 beats per minute in infants.
Digoxin: Nursing Considerations
Monitor serum digoxin level to evaluate dosing and devleopment of adverse
effects.

Promote rest periods and relaxation techniques to balance supply and demand of
oxygen.

Ensure maintenance of emergency drugs and equipment at bedside to promote


prompt treatment in cases of severe toxicty.

Educate patient on drug therapy including drug name, its indication,


and adverse effects to watch out for, to enhance patient
understanding on drug therapy and thereby promote adherence to
drug regimen.
Phoshodiesterase Inhibitors
MOA: inhibits the enzyme phosphodiesterase,
promoting a positive inotropic response and
vasodilation.

-it increases stroke volume and cardiac output and


promotes vasodilation

-it is administered IV for no longer than 48 to 72


hours

Indication: short-term treatment of patients not


responding to cardiac glycosides, vasodilators and
diuretics.

-drug use is only limited to severe situations


because it is associated with fatal ventricular
arrhythmias.

AMIRINONE, MILRINONE
Phoshodiesterase Inhibitors: Nursing Considerations

Protect drug from light to prevent drug from degradation.

Ensure patency of IV access to promote safe administration of drug.

Assess skin condition, noting presence of petechiae and other manifestations


of bruising and bleeding to assess presence of thrombocytopenia.

Educate patient on drug therapy including drug name, its indication,


and adverse effects to watch out for, to enhance patient
understanding on drug therapy and thereby promote adherence to
drug regimen.
CREDITS: This presentation template was created by Slidesgo, including
icons by Flaticon, and infographics & images by Freepik

You might also like