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Ettinger Cardiology > 248 Cardiac Arrhythmias > Flashcards

248 Cardiac Arrhythmias Flashcards

1
Q

What is an escape rhythm? What is a junctional escape rhythm?

A

Escape rhythm = the N region of the AV node assumes role of pacemaker for the heart if sinus impulse do not reach it. A mechanism activated only if needed. Junctional escape rhythm = an escape rhythm originating from N region; i.e. originates from AV junction not His-purkinje system in ventricles

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2
Q

What is a vagal maneuver?

A
  • Diagnostically - slow HR and increase nodal refractories through vagal manoeuvres may slow rapid tachycardia, allowing some features to be more apparent and facilitate ECG diagnosis - Therapeutically - increase vagal tone interrupts macro reentrant circuits occasionally terminating arrhythmia
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3
Q

What are 3 types of vagal manoeuvre?

A

Carotid sinuses massage - digital pressure to both carotid sinuses (caudal to dorsal aspect of larynx) for 5-10 s Ocular pressure - firm pressure to both globes through closed eyelids. Immersing patients face or limb in small bucket of ice water

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4
Q

What is the atropine response test?

A

0.04 mg/kg IV administer to evaluate bradycardia - differentiate physiologic bradycardia that is purely vagal origin - atropine increases heart rate, and pathological bradycardia caused by intrinsic disturbances of impulse formation or conduction (atropine has no effect).

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5
Q

What 8 factors of a cardiac arrhythmia impact a patient hemodynamically?

A
  1. Ventricular rate 2. Duration of abnormal rhythm 3. Temporal relationship between atria and ventricles 4. Sequence of ventricular activation 5. Inherent myocardial and valvular function 6. Cycle length 7. Drug therapy 8. Extra cardiac influences
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6
Q

What is a respiratory sinus arrhythmia?

A
  • vagal and hemodynamic effects occur in thorax during each respiratory cycle. - normal not require treatment - cats can get it when sleeping
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7
Q

What is ventriculophasic sinus arrhythmia?

A
  • an uncommon phenomenon - consists of variation in P-P interval in patients with high-grade second-degree or third-degree AV block. - the p-p interval that flanks the QRS complex is shorter than the P-P interval during the block - not clinically important other than mistaking it for atrial arrhythmia
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8
Q

What is a wandering pacemaker?

A
  • normal, physiologic phenomenon in dogs requiring no treatment - origin of depolarisation in heart moves within RA, or between SA or AV node. - p wave amplitude may be high or very low (isoelectric) Differentiate from premature atrial contractions : - degree of prematurity, heart rate, p wave morphology, series of paroxysm (beats coupled)
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9
Q

What is sinus bradycardia? What might it indicate? What are common causes?

A

= abnormally low heart rate - indicated physiologic (e.g. brachycephalic) or pathologic ( e.g. intoxication) predominance of parasympathetic system - tx = atropine iv and underlying cause - causes = hypothermia, deep anaesthetic plane, high vagal tone (GI, resp, neuro, ophalmic), - exception is SSS, where SB can be primary, pathologic bradycardia, accompanied by AV block and/or extrasystole

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10
Q

What is sinus tachycardia?

A

= abnormally high heart rate - STach = >160 bpm but from SA nodal origin (PQRST complexes present) - hard to diagnose as everything blends on ECG - vagal manoeuvre may temporarily slow heart rate and seperate P and T waves.

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11
Q

How is STach treated?

A
  • prevent STach in patients with structural heart disease -NOTE: tachycardia increases myocardial oxygen consumption, and reduces the duration of diastole (when coronary perfusion of myocardium occurs) - lifestyle management = low intensity walks, avoid chasing, and intense game play with cats. - preclinical/asymptomatic/compensated heart disease treatment has involved beta-blockers, calcium channel blockers, and Na+/K+ funny current blockers. Non have shown to prolong survival. - Atenolol can be given to cats with subclinical HCM and dogs with sub-aortic stenosis. But no benefit observed or better outcome and not many prospective studies
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12
Q

What 5 features would you use to determine if a PAC is occurring?

A
  1. Prematurity of PQRST 2. QRS complex supraventricular appearance - narrow, 3. P wave with different amplitude - negative, biphasic, or positive p wave but also preceding qrs complex 4. P-R interval different from sinus P-R interval - shorter or longer 5. Postextrasystolic pause that is noncompensatory
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13
Q

What is the pathogensis of PACs?

A
  • commonly a structural (atrial) lesions. - Distension of atrial is main cause of ectopic foci - but atrial tumours (hemangiosarcoma), hyperthyroidism in cats, digitalis toxicosis, or other systemic disturbance can cause PACs
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14
Q

What is treatment of PAC?

A
  • Unless multiple related bursts occur, usually minor clinical repercussions - atrial disease-> so treat underlying cause
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15
Q

What is atrial tachycardia?

A
  • Any tachycardia originating from SA node, atrial myocardium, AV node/junction, or veins entering the atria Includes: sinus tachycardia, sinus node re-entrat tachycardia, automatic atrial tachycardia, intra-atrial reentrant tachycardia, atrial flutter, atrial fibrillation, AVNRT, OAVRT, and automatic junctional tachycardia.
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16
Q

What short term treatment is used for atrial tachycardia ( >200/min in dogs, >260 in cats)?

A

Patients should have: normal systolic and diastolic function and no. Evidence of CHF (or tx is hemocompromising) - Diltiazam 0.05-0.1 mg/kg slow IV blouses, repeated to effect or cumulative max dose 0.25 -0.35 mg/kg - propranolol 0.02 mg/kg IV PRN, 2-10 m; 3 doses over 2 hours in 1 case report -

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17
Q

What causes atrial tachycardia? What is the clinical impact?

A
  • same causes as for PAC - impact depends on duration, age, and underlying cardiac lesions - if prolonged (no intermittent AV block) then need to avoid long term complications (like tachycardia-mediated cardiomyopathy)
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18
Q

What is the treatment of atrial tachycardia

A

Oral treatment is low end and only after CHF is resolved Beta-blocker: atenolol 0.3-1.5mg/kg PO q 12h Calcium channel blocker: diltiazem (regular) 0.8-1.5 mg/kgPO q 8h +/- digoxin 0.005 mg/kg PO q 12h

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19
Q

What is atrial flutter?

A

1) rapid, rhythmic flutter (f) waves at a high rate (280-400 bpm) 2) no return to baseline between F waves (sawtooth appearance) 3) QRS complex of normal, supraventricular appearance 4) irregularly irregular R-R interval if some atrial impulse blocked

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20
Q

What is atrial fibrillation?

A
  • 14% of all canine arrhythmia, including 50% prevalence in DCM and can trigger overt hemodynamic changes = complete electrical disorganisation at atrial level, leading chaotic, rapid series of atrial depolarisations (400-1200 per minute)
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21
Q

What are the 3 ECG characteristics of AFib?

A

1) supraventricular appearing QRS complexes: narrow, upright, and slightly variable amplitude in lead II 2) irregularly irregular rhythm (variable R-R interval), and a rate than can be low, normal, or higher 3) no visible P waves - replaced with f waves

22
Q

What are the treatments of AFib?

A
  1. Conversion to NSR (rhythm control) or accept AFib persist and focus on optimising resultant ventricular heart rate 2. Medications: - sustained release diltiazem 3mg/kg PO q 12h and digoxin 0.005mg/kg PO q 12h In one study biphasic defibrillation converted 92% of dogs with median duration of NSR of 120 days thereafter: amiodarone 12-15. mg/kg PO q 12h X 2 weeks, then 5-7 mg/kg PO q 12h
23
Q

What are PVCs/extrasystoles? What is their ECG appearance?

A

= Premature depolarisations generated by an ectopic focus located in the ventricular tissue. - Short R-R intervals, wide QRS complex with bizarre morphology (>0.07s in dog), with no p wave, and large different T wave.

24
Q

What is ventricular bigeminy?

A
  • 1:1 alternation between sinus beats and PVC’s - Multiples of two PVC’s = pair - 3 or more is ventricular tachycardia
25
Q

What causes PVCs?

A
  • any cardiac or systemic disorder - valvular heart disease - Congenital heart disease - Endocarditis - Hypokalemia - Anemia - Hypoxemia - Blunt trauma - GDV - Abdominal masses - Intoxication - Acidosis
26
Q

What 2 heart diseases exclusively are primarily arrhythmogenic? Hint: produce PVCs and VT

A
  1. arrhythmogenic right ventricular cardiomyopathy - familial in boxer dogs 2. Inherited sudden cardiac death of German shepherd dogs
27
Q

What is accelerated idioventricular rhythm (AIVR)?

A
  • intermediate rate ventricular rhythm - Appears as VT - ECG: wide and bizarre QS complexes but between 70 - 160 beats/min - Treat underlying cause
28
Q

What is VT? How does it appear on ECG?

A
  • 3 or more ventricular extrasystoles at a high rate. - sustained or paroxysmal - one or several QRS complexes that are wide (>0.07s in dog, >0.04s in cat), does not resemble sinus QRS complex, associated with giant T waves, no p waves, and may have capture beat (normal sinuse P-QRS after paroxysm of VT) and fusion beats (QRS complex morphology that is intermediate, between sinus QRS complexes ad ectopic QRS complexes due to interventricular electrical collision)
29
Q

How is VT treated?

A
  1. Eliminate causes of VT 2. Eliminate according to algorithm: Lidocaine IV Or oral sotalol, mexiletine + beta blocker, tocanimide + beta blocker, amiodarone
30
Q

What is ventricular flutter?

A
  • often prefibrillatory stage of VT
  • ECG: identical, tall, tight, sinusoidal waves,
  • immediately treat- 2mg/kg IV bolus and defibrillate
31
Q

What is ventricular fibrillation?

A
  • terminal, disorganised, chaotic pattern of desynchronised ventricular activity - hemodynamically= circulatory collapsible and arrest - to determine on ECG 1) rule out artefact 2) look at multiple leads 3) feel for pulses 4) assess patient consciousness - as there is inadequate cerebral perfusion
32
Q

What is Torsades de Pointes ? How does it appear on ECG?

A
  • arises from prolongation of q-T interval
  • rotation of peaks of QRS on horizontal axis on ECG due to changing geometry of reentrant circuit, oscillates within ventricles
    1. Rhythm is slow prior to TdP onset
    2. Onset involves R-on-T extrasystole
    3. Rapid >180 beats/min ventricular rhythm. Has QRS complexes more regular than VF, but are continuously changing in amplitude and polarity
33
Q

What causes TdP? How can it be treated?

A

Usually self resolving paroxysm (5-10s), otherwise lethal if longer Caused by any disorder prolonging q-T interval: - congenital long QT syndrome (Dalmatian), hypokalemia, hypocalcemia, and overdose toxicosis due to antiarrhthmic drugs, particularly class 1A antiarrhythmics such as quinidine Treatment: - Discontinue all antiarrhythmic drugs - IV magnesium surface (20-60 mg/kg slow IV bolus)

34
Q

What is ventricular parasystole?

A

= two heart beats as one

  • 1) ventricular focus with independent automaticity at a rate greater than escape focus
    2) unidirectional block that shields the focus from sinus depolarisations
  • benign and no treatment as it is refractory to antiarrhythmic therapy
35
Q

What is isorhythmic atrioventricular dissociation?

A
  • atria and ventricles are driven by independent pacemakers at equal or nearly equal rate.
36
Q

What is 1st degree AV block?

A
  • delay in AV conduction; normal QRS complexes and prolonged P-R interval
  • not usually clinical signs or need treatment
37
Q

What is 2nd degree AV block?

A

= complete interruption of AV conduction

Mobitz type I - progressive lengthening of P-R interval until P wave is blocked (aka wenckebach phenomenon)

Mobitz type II - perfectly regular P-R intervals until P wave is blocked.

  • more guarded prognosis
  • can produce CS similar to 3rd degree block: weakness, syncope, lethargy, Adams hypoxic-anoxic seizures
38
Q

What is 3rd degree AV block?

A
  • Complete block of AV conduction
  • ventricular escape rhythm.

** DO NOT treat escape QRS complexes as they prevent asystole.

ECG:

  • constant P-P interval, no repeatable P-R interval, and slow, regular R-R rhythm.
  • QRS complex is wide and bizarre
39
Q

What are the typical causes of AV block?

A

Type 1 and mobitz type 1= often functional such as high vagal tone; negative dromotropic effect of digitalis, antiarrhythmic, or alpha 2- stimulating sedatives

Mobitz type II and 3rd degree = functional such as hyperkalemia, digitalis toxicosis, alpha 2 receptor agonists like Dexmedetomidin, and also structural such as inflammation (endocarditis, Lyme myocarditis, traumatic myocarditis), or degenerative(physical disruption of AV node arising from cardiomyopathy, endocarditis, or fibrosis)

40
Q

How does hyperkalemia affect the heart?

A
  • mild elevations associated with greater cell membrane permeability to potassium during repolarisation
  • faster ventricular repolarisation (shorter than normal Q-T internal and an abnormally narrow, often peaked o T wave)
  • sinus bradycardia can occur, but hyperkalemia co-occures with abnormalities so severe hyperkalemis can have unreliable heart rates. Mild-Mod increase in serum potassium (6.6-7.5 mEq/l) = interfere with cell-to-cell transmission moderate to severe hyperkalemia (7- >8.5 mEq/L) : P-R interval prolongation or absence of P waves which is characteristic Very high serum potassium (>8.5 mEq/L) can be lethal - widening of QRS complex of T wave, and blend into sine wave type of regular but poorly functional or nonfunctional rhythm, or a ventriuclar-type of escape rhythm at a very low rate.
41
Q

What causes BBB?

A
  • hypertrophy -> HCM
  • Dilation-> DCM -

inflammation -> endocarditis, traumatic myocarditis

  • RBB in dogs is not a worrying find, but LBBB is associated wth ventricular enlargement
42
Q

How is BBB treated?

A
  • treat underlying cause
43
Q

What is Atrial standstill? how is it caused?

A

= total absence of atrial depolarisation

Causes:

1) moderate/marked hyperkalemia
2) atrial myopathy - e.g. atrial stretch, or parenchyma hyperplasia
3) ECG artefact (P waves to small)

44
Q

How does hypokalemia affect the heart?

A

1) causes resting membrane potential to be increasingly negative which decreases myocyte excitability
2) prolongs repolarisation, increasing action potential duration

Hypokalemia- induced prolongation of repolarisation opens a window of increased excitability during which spontaneous ectopic activity can occur based on threshold being reached after the absolute refractory period by a slowly repolarising cell

45
Q

How is hypokalemia treated?

A
  • Class I antiarrhythmics act on sodium channels that require normal serum potassium to function. So Treatment with lidocaine during hypokalemia is unlikely to alter ventricular arrhythmia but can cause lidocaine toxicosis

Treat:- The maximum safe rate IV potassium chloride infusion is 0.5 mEq/kg/h

46
Q

How does hypocalcemia affect the heart?

A

Hypocalcemia lowers the threshold, facilitating depolarisation

  • The cardiomyocytes are not so affects. The fine skeletal muscle fasciculations progress to generalised treatment - prolongs initial phase of ventricular repolarisation, which can manifest as prolongation of Q-T interval on the ECG Treat with IV calcium gluconate (50mg/kg slow IV over 10-30 minute)
  • When infusing calcium IV, signs of hypercalcemia are sudden slow heart rate, short Q-T internal
47
Q

What effect does hypercalcemia have?

A
  • raise threshold of cardiomyocyte, and hinder depolarisation.
  • shorter ventricular repolarisation making Q-T interval shorter.
48
Q

What is sick sinus syndrome?

A
  • affects cardiac pacemaking and conductive tissues at all levels
  • disturbance of cardiac conductive tissues producing simultaneous defects in sinus activity, AV conduction disturbance, and disturbance in supraventricual and ventricual excitability.
  • unknown cause -
49
Q

How is SSS treated?

A

surgery= Pacemaker Medications:

  • propantheline 0.5-3 mg/kg PO q 8h - or hyoscyamine 0.005mg/kg PO q 8h
  • or aminophylline/theophylline 10mg/kg PO q 8h
50
Q
A

Ettinger Cardiology (11 decks)

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