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ANTIARRHYTHMICS
Some Block Potassium Channels
Class I: Sodium (SOME) Lidocaine/Mexilitine

Class II: Beta Blocker (BLOCK) Ventricular Arrhythmia
Class III: Potassium Channel Blocker
Class IV: Calcium Channel Blocker Atenolol/Propranolol
Class V: Work by unknown mechanism V tach, Feline HCM
Class I: Lidocaine, Mexilitine Sotolol, amiodorone

Class II: Atenolol, Propranolol A fib, Vtach
Class III: Sotolol, Amiodorone Diltiazem
Class IV: Diltiazem SVT
Class V: Digoxin
Digoxin
A fib
Medical Uses
Lidocaine:
blocks Na channel to prolong the action potential and slow the HR.
Atenolol:
Beta 1 block er that causes the heart to beat slower and less forefully
Sotolol, amiodorone:
Prolongs refractory period of action potential.
Diltiazem:
Prevents calcium infux into cardiac cells to inhibt cardiac contractions.
Digoxin:
slows AV node.
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BLOOD PRESSURE
REDUCTION
Vasodilators
Nitroprusside
Sildenafil
Pimobendan
Hydralazine
Calcium Channel Blocker

Amlodipine
Alpha 1 Receptor Blockers

Prazosin
Phenoxybenzamine
Ace Inhibitors and ARBs

Enanlapril
Benazepril
Telmisartan
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ACE INHIBITORS
End in -pril
• Reduce formation of angiotensin II

• Inhibit aldosterone action
• Reduce blood pressure
• Reduce protein loss thru kidneys
angiotensin I
ACE
angiotensin II
aldosterone
Na+ retention,
increased
blood volume
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ARB
End in -sartan
Angiotensin II receptor blocker
Displace angiotensin II from the receptor to cause:
• Vasodilation
• increase Na+,fluid loss, decrease K+ loss
• Very effective at reducing protein loss thru kidneys
angiotensin I
ACE
angiotensin II
(-)
ARB
aldosterone
ARBs cause low
Na+ and elev K+,
vasodilation
in kidney
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ALPHA BLOCKERS
End in: -osin, -ine
Non-selective alpha blockers
Phenoxybenzamine
Selective alpha-1 blockers

Prazosin
Selective alpha-2 blockers

Mirtazapin
Yohimbine
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DIURETICS
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ECG FLASH CARDS

Heart Arrhythmia Classification
Arrhythmias due to faulty conduction in the AV node
Partial or complete blockage of electrical activity at the AV node is AV Block
(Types 1-3).
Junctional escape beats are started at the AV node.
Supraventricular arrhythmias
SVT (Supraventricular tachycardia)
Atrial Fibrillation
Ventricular Arrhythmias
Junctional escape beats arise from a high ventricular location
V Tach
Left and Right BBB
VPC’s: monomorphic, (all look the same, so they come from the same
hyper-exciteable focus in the ventricle) polymorphic (VPC’s are differently
shaped, meaning they come from different locations in the ventricle= more
sinister arrhythmia) fusion, bigeminy, trigeminy.
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ECG Interpretation
Six basic questions to help with
electrocardiogram interpretation:
• What is the heart rate (slow, normal,
fast)?
• What is the rhythm (regular, regularly
irregular, irregular)?
• Is there a QRS complex for every P
wave?
• Is there a P wave for every QRS
complex?
• Are they consistently and reasonably
related?
• What is the morphology of the QRS
complex
• (narrow and upright = supraventricular
• or wide and bizarre= ventricular)?
Heart Conduction
Conduction starts at the SA node

in the right atrium and propagates
to the AV node, down through the
bundle of His and finally to the
Purkinge fibers of the Ventricles.
Partial or complete blockage of
electrical activity at the AV node is a
form of AV Block (Types 1-3).
Junctional escape beats are started
at the AV node.
Premature ventricular complexes
occur at various locations in the
ventricles.
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Class I: Sodium (SOME) Lidocaine/Mexilitine

Class I: Lidocaine, Mexilitine Sotolol, amiodorone

Calcium Channel Blocker

Alpha 1 Receptor Blockers

Ace Inhibitors and ARBs

• Reduce formation of angiotensin II

Selective alpha-1 blockers

Selective alpha-2 blockers

ECG FLASH CARDS

Conduction starts at the SA node

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