Cardiovascular Module 2 Flashcards
Explain what PQRST denotes
P: Atrial depolarisation
QRS: Ventricular depolarisation
T: Repolarisation
What are the 4 mechanisms of arrhythmias?
- Enhance normal Automacity
- Normal pacemaker becomes more rapid and
overtakes SA node
- DDx: drugs, toxins, acquired heart disease - Abnormal Automacity
- Normal pacemaker cell is suppressed (drugs,
toxins, vagal tone) and non-pacemaker cells gains
ability to depolarise (acquired heart disease) - Re-entrant Currents
- Short circuit forms between atrial and ventricles -
congenital arrhythmia
- Short circuit forms between ischaemic or fibrous
tissue (acquired heart disease) - Blocks
- AV nodes or other sites - congenital, acquired,
drugs, toxins
What are the causes of arrhythmias?
- Congenital
- AV conduction pathways
- GSD - congenital tachycardia (either die in their
sleep of grow out of it)
- Alternative pathways bypassing AV node:
labradors (supreven. tachy) - Acquired Primary Cardiac Disease
- Ischaemia, fibrosis and other damage from DCM,
HCM, MVD - Secondary to Non-cardiac disease
- Sepsis
- T4
- Splenic mass
- Anaesthesia
- Abnormal autonomic tone
How to read an ECG?
- What is the heart rate?
- 50mm/s page speed- Number of complexes in 3 secs x20
- 15cm = 3secs
- 25mm/s page speed - number of complexes in 6secs x10
- 15cm = 6 secs
- Regular rhythm or irregular
- P-QRS relationship
- Rhythm diagnosis - does this need tx? clinical
signs? If incidental is it primary heart? or
secondary?
What is a normal heart rate? Brady v. Tachy?
70-140BPM
<55 BPM - bradyarrhythmia
>180 - tachyarrhythmia
Types of tachyarrhythmias?
- Supraventricular origin
A. regular v. irregular
a. Regular - SVT atrial flutter
b. Irregular - sinus + APCs - A-fib - Ventricular origin
A. Regular v. Irregular
a. Regular - VT
b. Irregular - Sinus + VPCs
What are VPCs?
Ventricular premature complexes
- May have pulse deficits
- Originates from ventricles
What are APCs?
Atrial premature complexes
- Looks like a p-wave
- May be deficits but doesn’t always need tx
What is caused by Atrial Fibrillation?
Most common tachyarrhythmia in dogs - structural and chemical remodelling of the atrium
- Loss of atrial kick leading to decrease of 20% output
- Loss of exercise capacity and dependance on HR increase to generate a cardiac rhythm
- Tachycardia lasting over 24 hours can result in heart remodelling, ischaemic changes and fibrosis - reversible if rhythm controlled
Caused by lots of random circuits bombarding the AV node and AV node trying to make sense of it
What does A-fib look like on ECG?
- No discernable P-waves
- Irregular R-R intervals
- Supraventricular complexes
- Undulating baseline
A-fib treatment options?
Digoxine +/- diltiazem
Amiodorone protocol
Sotalol
Cardioconversion - need to make sure patients are carefully selected
What causes atrial flutter?
Area in the right atrium where re-entry circuits occur
- Big dogs
- Can burn the tissue in RA to stop in the circuit
What does R on T phenomenon mean?
Very unstable rhythm
Means repolarisation and depolarisation are happening at the same time
What are non-pharmocological treatment options for tachyarrhythmias?
- Vagal manoeuvre
- Shock - shock on the r-wave, needs to be
anaesthetised to get at the right time - Pre-cordial thump - cause a VPC to break rhythm
What are the pharmacological treatments for tachyarrhythmias?
No Body Kills Cats
Class 1 = Na channel blockers (important for
depol/repol of ventricles)
- Lidocaine/quinodine
Class 2 = Beta-blockers (heart bathed in SNS with
beta receptors)
- Atenolol/Esmolol
Class 3 = Potassium channel blockers (important for
generating action potential within atria)
- Sotalol (class 2 as well)
- Amiodarone (1+2+3)
Class 4= Calcium channel blockers (important for
generating action potential within atria)
- Diltiazem
Digoxin: Cardiac glycoside
- Affected by hypo/hyperkalaemia
- Inhibits Na/K ATPase and competes with K+ at
binding sites
- Dirty drug
