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Small animal > 10) electrocardiography, cardiac arrythmias in cats and dogs > Flashcards

10) electrocardiography, cardiac arrythmias in cats and dogs Flashcards

1
Q

what is a cardiac arrythmia?

A

❖ 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

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2
Q

electrocardiograph

A
  • 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
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3
Q

P-wave?

A

depolarization of the atria

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4
Q

P-R wave?

A

impulse through AV node and bundle of His

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5
Q

QRS complex?

A

ventricular depolarization

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6
Q

R wave

A

depolarization of left ventricle

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7
Q

Q wave

A

depolarization of septum

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8
Q

S wave?

A

depolarisation of right ventricle

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9
Q

S-T segment?

A

interval of ventricular systole

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10
Q

T wave ?

A

repolarization of ventricles

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11
Q

Q-T interval=

A

ventricle depolarization and repolarization

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12
Q

indications for ECG

A

arrythmia, bradycardia, tachycardia

monitoring during anaesthesia

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13
Q

limitations of ECG

A

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

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14
Q

technique of ECG

A
  • 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
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15
Q

Red

A

right forelimb

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16
Q

yellow

A

left forelimb

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17
Q

green

A

left hindlimb

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18
Q

black

A

RIGHT hindlimb

19
Q

evaluation of the ECG

A
  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?
20
Q

attributes of physiological ECG

A
  • 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)
21
Q

These alterations occur simultaneously: arrythmias?

A
  • 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
22
Q

impulse formation disorders

A
  • Slow conduction and block
    1. Enhanced/depressed normal automacity
    2. Triggered activity (early, late after-depolarization)
    3. reentry
23
Q

sinus arrest

A

➢ Long pause following a normal complex

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

24
Q

Atrial extrasystole/ atrial premature complexes (APCs)

A

➢ 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

25
Q

Atrial tachycardia

A

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

26
Q

Atrial fibrillation

A

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

27
Q

Atrial flutter

A

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

28
Q

Junctional extrasystole / AV junctional premature complexes

A

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

29
Q

Junctional tachycardia

A

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

30
Q

Ventricular extrasystole / ventricular premature complex (VPCs or PCVs)

A

➢ 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

31
Q

Ventricular tachycardia

A

➢ 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

32
Q

Ventricular fibrillation:

A

➢ 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

33
Q

Ventricular flutter

A

➢ 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!

34
Q

Sinoatrial (SA-) block

A

➢ 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

35
Q

Atrial standstill

A

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

36
Q

AV block

A

➢ 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

37
Q

Causes for arrhythmias:

A
  • 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
38
Q

consequences of arrythmias

A
  • 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
39
Q

treatment of arrhytmias

A
  • 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
40
Q

arrythmias we don’t treat?

A
  • Nonfrequent atrial or ventricular extrasystoles
  • Slow idioventricular or junctional rhythms
  • Lone atrial fibrillation
  • I-degree and Mobitz-I II-degree AV-blocks
41
Q

rules for first steps in arrythmia causes:

A
  • 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
42
Q

treatment options of arrythmias

A
  • 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
43
Q

supraventricular arrythmias treatment

A
  • 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
44
Q

ventricular arrythmia arrythmia

A
  • Causative treatment

- Lidocaine, mexiletine, amiodarone

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