Cardiac Drugs

Firman Dullah
SMF Ilmu Penyakit Jantung &
Pembuluh Darah
RS Bahteramas Kendari

OVERVIEW
Autonomic nervous system review

Autonomic
Nervous
System
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Autonomic Nervous System

Also known as the

Autonomic Nervous System

Functions
Regulation of cardiac function
Temperature regulation
Fluid & electrolyte balance
Metabolism
Digestion
Excretion

Autonomic Nervous
System
Sympathetic

Norepinephrine
Epinephrine --- released from
adrenal medulla

Acetylcholine
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Actions of autonomic drugs

Increase the amount of
neurotransmitters
Inhibit or augment the breakdown of
neurotransmitters in the synaptic
cleft
Interact with post-synaptic receptors

Receptor Types
Beta-1----- Increased
myocardial contractility &
rate

Vasoconstriction
ureteral contraction

Beta-2-----Vasodilation,
bronchodilation Stimulated
by norepinephrine &
epinephrine 8

Sympathetic Stimuli

Stress
Hypoglycemia
Postural hypotension
Exercise

Receptor Types:
Parasympathetic
Decreased heart rate, increased GI
motility, relaxation of bladder
sphincter
Stimulated by acetylcholine &
baroreceptors

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CARDIAC DRUG`S

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Alpha blockers
Doxazosin (Cardura), Terazosin (Hytrin)

Action: block alpha-1 receptors

smooth muscle relaxation
Uses:
Prostate enlargement
Hypertension

Side effects
Orthostatic hypotension
First dose at bedtime
Change position carefully
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Beta blockers
Bisoprolol(Concor),Propanolol(Inderal), Atenolol(Tenormin), metoprolol
(Fapressor), Carvedilol (VBloc)

Action: Blocks sympathetic nervous system

stimulation
lowers heart rate, BP
reduces myocardial work, lowering oxygen
consumption

Uses:

Blood pressure control

Control of angina
Prolongs survival after MI (prevents arrhythmias)
Prolongs survival in heart failure
Treatment of certain abnormal heart rhythms
Prevention of Migraines
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Beta Blockers
Cautions:
Worsening heart failure in acute CHF
Bradycardia when combined with
calcium channel blockers
(often combined in angina)

Diabetics: masking of hypoglycemia

Exacerbation of wheezing in asthmatics

Adverse effects
Symptomatic bradycardia
Hypotension
Fatigue

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Implications
Check pulse and BP prior to
administration
Goal for pulse in patient with CAD often
50-60, as tolerated

Patient education
Check pulse
Make sure they know why they are
taking it!
Diabetics: hypoglycemia issue
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NITRATE
Isosorbid Mononitrate, Isosorbid
Dinitrate, Isosorbid Trinitrate,
Nitroglycerin(NTG).
Provide an exogenous source of Nitrit
Oxide (NO) ---- cAMP ---- Vasodilator.
Venous dilation predominates.

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Implications
Beware of nitrat tolerance.
Education and Self monitoring
patient`s needed.
Side Effect : Headache, Flushing and
rash, Dizziness, Postural hypotension
and reflex tachycardia.

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ACE Inhibitors
Captopril, Ramipril, Enalapril (Vasotec), Lisinopril (Zestril)

Blocks conversion of Angiotensin I to

Angiotensin II
Blocks vasoconstriction effects of
Angiotensin II
Blocks sodium retention effect of
Aldosterone
Effects: reduced peripheral vascular
resistance, less fluid retention

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ACE inhibitors
Uses
Management of heart failure, prolongs
survival
Decreases preload and afterload

Control of high blood pressure

Diabetics: protective effect on kidneys
Works well with HCTZ

Prolongs survival in MI with LV

dysfunction
Prevents enlargement during remodeling
phase of recovery
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ACE Inhibitors
Adverse effects
Cough ( increase of bradykinin)
Substitute Angiotensin receptor
blocker

Lightheadedness, hypotension
Hyperkalemia
Kidney dysfunction in bilateral renal
artery stenosis
Watch renal function when first started
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Implications
Check BP prior to giving
Note: in heart failure goal systolic BP
may be 85-90,
it may not decrease BP in these patients
Always check with MD before holding dose

Monitor creatinine, potassium

Patient education:
Patient must know why it is being taken
Stopping ACE in CHF can cause
worsening, leading to hospitalization!
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Angiotensin receptor blockers

(ARBs)
Also called Angiotensin II inhibitors
Losartan (Cozaar), Valsartan
(Diovan), Irbesartan, Telmisartan,
Candesartan.
Blocks Angiotensin II effects --/-- the
AT1 receptor`s.
No effects on bradykinin no cough

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Angiotensin receptor
blockers
Uses:
Substitute for ACE, when not
tolerated due to cough
Heart failure management
Hypertension

Adverse effects similar to ACE, no

cough
Generally well-tolerated
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Calcium Channel Blockers

Amlodipine (Norvasc), Diltiazem (Cardizem), Nifedipine
(Procardia), Verapamil (Calan)

Action: Blocks calcium entry into cells,

decreasing the strength of contraction
Relaxation of smooth muscle
Decreased heart work
May slow heart rate

Uses
Blood pressure control
Angina Control
Heart rate control in atrial arrhythmias
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Calcium Channel Blockers

Several types of CCB
Adverse effects
Verapamil: constipation
Dizziness, flushing, peripheral edema

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Diuretics
Prevent sodium reabsorption and
facilitates
excretion
in kidneys.
Prevent
sodium fluid
reabsorption
and facilitates
fluid
excretion in kidneys.

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Loop diuretics
Furosemide (Lasix), Bumetanide (Bumex)
Very potent
Used for fluid overload, especially CHF
Larger doses needed with renal dysfunction
Frequent dose adjustments made
Adverse effects:
potassium and magnesium wasting
Monitor potassium levels with dosage change
Potassium supplements

Dehydration, hypotension,
lightheadedness
Reduce dose, replace fluids

Ototoxicity with rapid IV administration

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Diuretics
Thaizide Diuretics
Hydrochlorothiazide (HCTZ)
Milder than loop diuretics
Used for hypertension, edema
Often combined with other
antihypertensives for synergistic
effect
Adverse effects: potassium and
magnesium loss
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Potassium-sparing Diuretics
Spironolactone, triamterene
Mild diuretics
Used in combination with other
diuretics to prevent potassium
wasting
Side effects:
hyperkalemia

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Implications : diuretics
DAILY WEIGHTS!
Weights are most accurate indicator of fluid
status changes

Monitor electrolyte levels

Check potassium level before giving
potassium supplements

Patient education:
Daily weights
May do sliding scale diuretic doses in CHF
management
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Antithrombotic
Platelet Inhibitors

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Platelet Inhibitors

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Platelet Inhibitors

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Platelet Inhibitors

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Anti-coagulant
CLOTTING

BLEEDING

Anticoagulants tip the balance towards

bleeding
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Anticoagulant
Heparin
Unfractional Heparin(UFH)
Inhibits Factors Xa & the thrombin
also coagulation protease.
Drugs : Inviclot.

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Low Molecular Weight Heparin(LMWH)

One third of the molecular weight of heparin.
Greater bioavailability and a longer plasma
half life than heparin.
Same action with heparin.
Simple and single use but high cost.
Drugs : Fondaparinux(Arixtra),
Enoxaparin(Lovenox), Parnaparin,
Dalteparin.

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Warfarin(Vitamin K Antagonist/VKA)
Oral anticoagulant.
Inhibits/inactivation of Vitamin K in
hepatic microsomes.
Needs monitoring and self-guided
warfarin therapy.
Depends on Index Normalized Ratio
(INR) Level.
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Direct Thrombin Inhibitor

Its acyl gluronides are competitive
and cause thrombin enable the
conversion fibrin to fibrinogen.
Dabigatran etexilate (Pradaxa)
No need Monitoring but high in cost

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Anti X-a Agents

Directly inhibits of factor X
Rivaroxaban (Xarelto), Apixaban
No Need Monitoring

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Fibrinolytic
Thrombolytic/Reperfusion therapy
The generation of plasmin
---plasminogen that binds to the clot
surface to lyse the clot
Needs special preparation and
checklist
Be careful of allergic paients --- rare
case
Drugs : Streptokinase, Urokinase
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Fibrinolytic
Tissue Plasminogen Activator (tPA)
Is a naturally occuring enzyme that
binds to fibrin with a greater afinity
than streptokinase/urokinase.
Needs special preparation and
checklist
Drugs : Alteplase, Reteplase,
Tenecteplase
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AntiArrhytmia
Divided by Vaughan Wiiliams Class.
Class I --- IA, IB & IC
Class II
Class III
Class IV

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Anti-arrhythmic Agents

Classification of anti-arrhythmic agents

with the Vaughan-Williams system
(Classes I, II, III and IV)
Based on their effects on certain ion
channels and/or receptors
Class I agents further divided into
subclasses IA, IB and IC based one
electrophysiological effects
Class I agents
Mechanism of Action: block Na+ channels,
slow conduction velocity, prolong
refractoriness, decrease automaticity of
sodium-dependent tissues
Subclasses due to differences in effect on
repolarization (recovery)
Subclass IA block K+ channels (prolonged
recovery phase) resulting in QRS widening and
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QT prolongation

 Subclass indications:
Class IA Atrial and
ventricular arrhythmias
Class IB Ventricular
arrhythmias
Class IC - Atrial and
ventricular arrhythmias
Class II agents
Mechanism of Action: Betaadrenergic antagonist with
decreased heart rate

Indications:
Slow ventricular rate in Atrial
Flutter/Fibrillation and
Paroxysmal SupraVentricular
Tachycardia (PSVT) 48

Anti-arrhythmic Agents

Classification of anti-arrhythmic
agents with the VaughanWilliams system (Classes I, II, III
and IV) continued:
Class III agents
Mechanism of Action: block K+
channels leading to prolonged
repolarization and QT prolongation
Indications:
Amiodarone Atrial and ventricular
arrhythmias
Bretylium Ventricular arrhythmias
Sotalol Ventricular arrhythmias 49

 Class IV agents
Mechanism of action: Ca+2
channel blockers decreasing the
heart rate
Indications: slow ventricular
rate in atrial flutter/fibrillation
and PSVT

Misc. Agents
Digoxin - slow ventricular rate in
atrial flutter/fibrillation and
PSVT
Adenosine endogenous
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Anti Arrhytmia Drug Classes

Class

Channel Effect

Repolarization Time

Drugs

IA

Sodium Block Effect

++

Prolongs

Quinidine
Disopiramide
Procainamide

IB

Sodium Block Effect

+

Shortens

Lidocaine
Phenitoin
Mexiletine
Tocainide

IC

Sodium Block Effect

+++

Unchanged

Flecainide
Propafenone

II

A pacemaker and
Unchaged
Depolarizing current;
indirect Ca Channel
Block

Beta Blocker

III

Repolarizing K
currents

Markedly Prolongs

Amiodarone
Sotalol
Ibutilide
Dofetilide

IV

Av Nodal Ca Block

Unchaged

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Verapamil

Cardiac glycosides
Definitions--preload, afterload,
inotrope, chronotrope, cardiac output
Clinical effects--increase myocardial
contractile force, the positive
inotropic action increases CO, RBF
and diuresis; decreases preload
Uses--CHF, arrhythmias (afib and
aflutter)
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Cardiac glycosides--Digoxin
Mechanism of action-inhibition of the Na-K
pump and increasing intracellular sodium
to activate the Na-Ca carrier to increase
calcium concentration inside the cell
Results in an increase in the force of
contraction of myocardial muscle fibers
and increase in SV and CO
Blood volume decreases, venous pressures
and EDV decreases and distended heart
returns to normal
Decrease in sympathetic stimulation-renal
elimination of sodium and water53improves
secondary to improved renal perfusion,

Digoxin
Adverse effects--digitalis intoxication,
electrolyte disturbances, cardiac
arrhythmias, GI symptoms, visual
disturbances, fatigue
Heart rate must be checked prior to
digoxin administration and must be >60
bpm
Treatment is drug discontinuation and
treat symptoms. Check dig.level to be
between 0.5 to 2.0 ng/ml
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THANK YOU
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