10) electrocardiography, cardiac arrythmias in cats and dogs Flashcards
what is a cardiac arrythmia?
❖ Any cardiac rhythm falling outside of the sinus rhythm (abnormalities in rate, regurgitation, site of cardiac impulse) → auscultable during clinical examination
When any arrhythmia is heard an ECG should be performed for better evaluation
electrocardiograph
- measurement in amplitude and time of potential differences of electrical current
- electrical current generated through depolarization and repolarization of cardiac structures
- types of recording:
➢ intracardial
➢ epicardial
➢ on the surface of the body → bipolar leads placed
according to the Einthoven triangle → Einthoven triangle placements no longer used for ECG
P-wave?
depolarization of the atria
P-R wave?
impulse through AV node and bundle of His
QRS complex?
ventricular depolarization
R wave
depolarization of left ventricle
Q wave
depolarization of septum
S wave?
depolarisation of right ventricle
S-T segment?
interval of ventricular systole
T wave ?
repolarization of ventricles
Q-T interval=
ventricle depolarization and repolarization
indications for ECG
arrythmia, bradycardia, tachycardia
monitoring during anaesthesia
limitations of ECG
just temporal, but can use holter monitoring
distorting effects of extracardiac factors
needs specialized knowledge
technique of ECG
- Right lateral recumbency, sternal recumbency, standing
- Attaching the leads (wetted alligator clips)
➢ Red → right forelimb
➢ Yellow → left forelimb
➢ Green → left hindlimb
➢ Black → right hindlimb - Consider disturbances due to: movement, respiratory, and electrical artifacts
- Paper speed 25 or 50 mm/sec
- Sensitivity 10, 20, 5 or 2.5 mm/mV
Red
right forelimb
yellow
left forelimb
green
left hindlimb
black
RIGHT hindlimb
evaluation of the ECG
- Assess quality and look for artefacts
- Determine the heart rate
- Determine the heart rhythm
➢ Regularity of R-R and P-P intervals
➢ P waves
➢ QRS complex characteristics
➢ P-QRS relations - Determination of wave morphology and electric axis
- Always do a physical exam at the same time and check for:
o Tachycardia
o Dogs > 180 bpm
o Cats > 220 bpm
o Can be due to: fear, stress, pain, fever, hyperthermia, shock, hypovolemia, anaemia, heart failure, gastric dilation etc….
o Bradycardia
o Dogs < 60-70 bpm
o Cats < 140 bpm
o Can be due to: sinus node disease or impulse conduction
o Arrhythmia
o Palpate the pulse
o Jugularis pulse?
attributes of physiological ECG
- Sinus originated (normotopic)
- Heart rate according to species, breed, physical needs
- Respiratory arrhythmia or sinus rhythm
- Escape beat if heart rate drops
- Sometimes atrioventricular blocks (horse, dog)
These alterations occur simultaneously: arrythmias?
- Reduced resting potential
- Alteration in the slope of phase 0 polarization
- Decreased conduction
- Repolarization alterations
- Changes in the refractory state of the cells
- Abnormal automacity
2 types of arrhythmias: impulse formative disorders or impulse conductive disorders
impulse formation disorders
- Slow conduction and block
1. Enhanced/depressed normal automacity
2. Triggered activity (early, late after-depolarization)
3. reentry
sinus arrest
➢ Long pause following a normal complex
➢ Due to high parasympathetic tone, e.g. surgical stimulation, neoplasia on vagus nerve, respiratory disease
Atrial extrasystole/ atrial premature complexes (APCs)
➢ Ectopic beat – impulse originates in the atrial tissue rather than from sinus node
➢ quite common
➢ Abnormally shape, premature P wave → submerged or superimposed in T wave
➢ Treatment usually unnecessary if they occur infrequently and only after exercise
➢ Atrial bigeminy → APC followed by normal sinus complexes
Atrial tachycardia
➢ Differentiate from sinus tachycardia (physiologic)
➢ Episode of atrial tachycardia usually initiated by APCs → can see those as well
➢ Often secondary to atrial enlargement
Atrial fibrillation
➢ No P waves → instead many fine f waves (fibrillation waves)
➢ Often secondary to atrial enlargement
Atrial flutter
➢ No P waves → instead many F waves, which are much bigger than in atrial fibrillation → “saw-toothed” appearance
Junctional extrasystole / AV junctional premature complexes
➢ Early P waves and often negative
➢ Due to abnormal impulse formation at or near the AV junction
➢ E.g. due to digitalis toxicity
Junctional tachycardia
➢ Increased rate, regular rhythm throughout episode
➢ Absent, negative or buried P wave
➢ Due to abnormal impulse formation at or near the AV junction
Ventricular extrasystole / ventricular premature complex (VPCs or PCVs)
➢ Abnormally wide QRS complex and unusual in shape, without preceding P wave, Q wave very deep
➢ Due to abnormal impulse formation distal to the AV junction
➢ Occasional VPC is normal → pathologic if frequently
Ventricular tachycardia
➢ Multiple QRS complexes with no P waves → looks like many VPCs
➢ Also due to abnormal impulse conduction causing an ectopic rhythm
➢ Primary concern here: inadequate CO
Ventricular fibrillation:
➢ Irregular pattern of high and low-amplitude waves → cannot be differentiated into QRS complexes or T waves
➢ Serious arrhythmia → immediate treatment!! → electrical defibrillation often indicated
➢ Cardiac arrest often preceded by ventricular fibrillation
Ventricular flutter
➢ High ventricular rate with regular rhythm
➢ No P wave and QRS complexes indistinguishable from T wave
➢ May precede ventricular fibrillation (ventricular tachycardia → ventricular flutter → ventricular fibrillation → cardiac arrest)
➢ Severe and needs immediate treatment!
Sinoatrial (SA-) block
➢ Impulse of SA node is blocked when exiting the SA node → no conduction reaches the cardiac tissue → results in a pause in the ECG
➢ Looks like Sinus arrest → in SA block the pause is as long as a normal complex would be! Because SA node forms impulse on time and regularly, it is just not conducted properly
➢ Can be clinically insignificant
Atrial standstill
➢ Absence of P wave
➢ Persistent: fibrosis of the atrium prevents proper conduction
➢ Temporary: hyperkalaemia → alters atrial transmembrane resting potential
AV block
➢ I.-degree AV block
o Delay of the impulse conduction in the AV node region
o P wave for every QRS complex, prolonged but constant P-R interval
➢ II.-degree AV block
o Impulse is not just delayed but can also be blocked → some P waves followed by QRS and some not
o Mobitz type I: P-R intervals gradually lengthen until QRS is missing
o Mobitz type II: P-R intervals constant between missing QRS
➢ III-degree AV block
o Impulse is completely blocked
o There is no association between P waves and QRS → QRS are not formed by AV node conduction but by escape rhythm → if escape rhythm is adequate and the patients CO is not compromised, therapy might not be necessary → but under anesthesia there is no escape rhythm!! → needs aggressive and immediate treatment
➢ Possible causes for AV-blocks:
o Physiologic, functional
o Drug induced, toxicosis
o Increased vagal tone
o hyperkalemia
o Hypothyroidisms
o Inflammation, neoplasia, amyloidosis, fibrosis (Lyme, autoimmune?)
o Congenital
Causes for arrhythmias:
- Structural heart disease (cardiac remodeling, neurohormonal changes, inflammatory mediators, free radicals, hypoxia) (40%)
➢ Atrial fibrillation, ventricular arrhythmias in congestive heart failure - Systemic disease (hypoxia, vegetative tone, temperature, ions (K, Ca), drugs, toxicosis) (50%)
➢ Many different causes possible: e.g. renal failure, hyperthyroidism, digoxin toxicosis, sepsis, trauma, shock, etc. - Primary (congenital or acquired) arrhythmias (channelopathies, fibrosis, infarcts, amyloidosis) (10%)
➢ Boxer, bulldog and cat → arrhythmogenic cardiomyopathy
➢ Miniature Schnauzer, westi → sick sinus syndrome SSS
➢ Cocker Spaniel → AV block
➢ Labrador, boxer→ atrioventricular accessory pathways SVT
consequences of arrythmias
- Innocent abnormality without clinical consequences → most common
- Weakness
- Syncope
- Sudden death
- Heart failure
➢ Worsening of preexisting cardiac disease
➢ Tachycardiomyopathy or heart failure due to bradyarrhythmias
treatment of arrhytmias
- Assessing whether treatment is beneficial:
➢ No signs, no severe hemodynamic changes → don’t treat, but search for the cause
➢ Most antiarrhythmic also work as proarrhythmic → harms can be greater than benefit
arrythmias we don’t treat?
- Nonfrequent atrial or ventricular extrasystoles
- Slow idioventricular or junctional rhythms
- Lone atrial fibrillation
- I-degree and Mobitz-I II-degree AV-blocks
rules for first steps in arrythmia causes:
- ECG
- Exclude heart disease
- Diagnostic work up (electrolytes!)
- Atropine response test in bradyarrhythmias
- First oxygen, symptomatic treatment (fluids or diuretics) before antiarrhythmics are administered → except for very fast potentially lethal rhythms
treatment options of arrythmias
- Causative treatment
- Physical maneuvers → stimulate vagal nerve (e.g. ocular pressure, carotic massage
- Drug therapy
➢ Class I Sodium-channel blockers e.g. lidocaine, mexiletine
o Reduce phase 0 slope and peak of action potential
➢ Class II Beta-blockers e.g. atenolol, propranolol, esmolol
o Block sympathetic activity, reduce rate and conduction
➢ Class III potassium-channel blockers e.g. amiodarone, sotalol
o Delay repolarization and thereby increase action potential duration and effective refractory period
➢ Class IV calcium-channel blockers e.g. verapamil, diltiazem
o Block calcium-channels
o Most effective at SA and AV nodes → reduce rate and conduction
➢ Class V unclassified drugs e.g. digoxin, adenosine, anticholinergic, sympathomimetic drugs - Artificial pacemaker
- Electric cardioversion
- Radiofrequency catheter ablation
➢ A line of block that interrupts the flutter circuit→ in the right atrium
supraventricular arrythmias treatment
- Goal: restore sinus rhythm
- Vagal maneuvers
- Diltiazem (calcium-channel blocker) IV
- Decrease ventricular rate → slow own AV conduction
➢ Digoxin, calcium-channel blockers, beta blockers amiodarone
ventricular arrythmia arrythmia
- Causative treatment
- Lidocaine, mexiletine, amiodarone
