10) electrocardiography, cardiac arrythmias in cats and dogs

Question 1

what is a cardiac arrythmia?

Answer 1

❖ 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

Question 2

electrocardiograph

Answer 2

• 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

Question 3

P-wave?

Answer 3

depolarization of the atria

Question 4

P-R wave?

Answer 4

impulse through AV node and bundle of His

Question 5

QRS complex?

Answer 5

ventricular depolarization

Question 6

R wave

Answer 6

depolarization of left ventricle

Question 7

Q wave

Answer 7

depolarization of septum

Question 8

S wave?

Answer 8

depolarisation of right ventricle

Question 9

S-T segment?

Answer 9

interval of ventricular systole

Question 10

T wave ?

Answer 10

repolarization of ventricles

Question 11

Q-T interval=

Answer 11

ventricle depolarization and repolarization

Question 12

indications for ECG

Answer 12

arrythmia, bradycardia, tachycardia

monitoring during anaesthesia

Question 13

limitations of ECG

Answer 13

just temporal, but can use holter monitoring
distorting effects of extracardiac factors
needs specialized knowledge

Question 14

technique of ECG

Answer 14

• 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

Question 15

Red

Answer 15

right forelimb

Question 16

yellow

Answer 16

left forelimb

Question 17

green

Answer 17

left hindlimb

Question 18

black

Answer 18

RIGHT hindlimb

Question 19

evaluation of the ECG

Answer 19

1. Assess quality and look for artefacts
2. Determine the heart rate
3. Determine the heart rhythm
   ➢ Regularity of R-R and P-P intervals
   ➢ P waves
   ➢ QRS complex characteristics
   ➢ P-QRS relations
4. 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?

Question 20

attributes of physiological ECG

Answer 20

• 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)

Question 21

These alterations occur simultaneously: arrythmias?

Answer 21

• 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

Question 22

impulse formation disorders

Answer 22

• Slow conduction and block
  1. Enhanced/depressed normal automacity
  2. Triggered activity (early, late after-depolarization)
  3. reentry

Question 23

sinus arrest

Answer 23

➢ Long pause following a normal complex

➢ Due to high parasympathetic tone, e.g. surgical stimulation, neoplasia on vagus nerve, respiratory disease

Question 24

Atrial extrasystole/ atrial premature complexes (APCs)

Answer 24

➢ 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

Question 25

Atrial tachycardia

Answer 25

➢ Differentiate from sinus tachycardia (physiologic) ➢ Episode of atrial tachycardia usually initiated by APCs → can see those as well ➢ Often secondary to atrial enlargement

Question 26

Atrial fibrillation

Answer 26

➢ No P waves → instead many fine f waves (fibrillation waves) ➢ Often secondary to atrial enlargement

Question 27

Atrial flutter

Answer 27

➢ No P waves → instead many F waves, which are much bigger than in atrial fibrillation → “saw-toothed” appearance

Question 28

Junctional extrasystole / AV junctional premature complexes

Answer 28

➢ Early P waves and often negative ➢ Due to abnormal impulse formation at or near the AV junction ➢ E.g. due to digitalis toxicity

Question 29

Junctional tachycardia

Answer 29

➢ Increased rate, regular rhythm throughout episode ➢ Absent, negative or buried P wave ➢ Due to abnormal impulse formation at or near the AV junction

Question 30

Ventricular extrasystole / ventricular premature complex (VPCs or PCVs)

Answer 30

➢ 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

Question 31

Ventricular tachycardia

Answer 31

➢ 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

Question 32

Ventricular fibrillation:

Answer 32

➢ 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

Question 33

Ventricular flutter

Answer 33

➢ 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!

Question 34

Sinoatrial (SA-) block

Answer 34

➢ 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

Question 35

Atrial standstill

Answer 35

➢ Absence of P wave ➢ Persistent: fibrosis of the atrium prevents proper conduction ➢ Temporary: hyperkalaemia → alters atrial transmembrane resting potential

Question 36

AV block

Answer 36

➢ 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

Question 37

Causes for arrhythmias:

Answer 37

- 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

Question 38

consequences of arrythmias

Answer 38

- 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

Question 39

treatment of arrhytmias

Answer 39

- 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

Question 40

arrythmias we don't treat?

Answer 40

- Nonfrequent atrial or ventricular extrasystoles - Slow idioventricular or junctional rhythms - Lone atrial fibrillation - I-degree and Mobitz-I II-degree AV-blocks

Question 41

rules for first steps in arrythmia causes:

Answer 41

- 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

Question 42

treatment options of arrythmias

Answer 42

- 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

Question 43

supraventricular arrythmias treatment

Answer 43

- 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

Question 44

ventricular arrythmia arrythmia

Answer 44

- Causative treatment | - Lidocaine, mexiletine, amiodarone