Collapse, weakness and exercise intolerance dysrhythmias

• Anatomy of the conduction system

  • Impulse originates from SA node.
  • Spreads across atria to cause atrial contraction.
  • Can only pass through AVN to reach ventricular myocardium.
  • AVN delays impulse to allow for ventricular filling.
  • Spreads rapidly through bundle of his, bundle branches and Purkinje network to cause ventricular contraction.
• What is an electrocardiogram?

  The recording of cardiac electrical activity bu measuring the amplitude and direction of the flow of electricity between a positive and negative electrode.
• Genesis of electrocardiagram in lead II

  1. Impulse starts at SA node and travels across atria towards positive electrode (p-wave).
  2. Pauses as reaches AV node and usually small negative deflection of impulses towards right ventricle (away from the positive electrode) when first crosses AV node; (Q-wave).
  3. Impulse moves rapidly across ventricular myocardium towards atria and away from positive electrode leading to negative deflection (S-wave).
  4. Ventricular depolarisation is seen and this results in small positive deflection (T-wave).
• What is a sinus rhythms?

  Rhythms originating from the sino-atrial node following the correct conduction pathways.

  
• What is the definition of dysrhythmias?

  An abnormal heart rhythm caused by a disturbance in the hearts electrical conduction system.
• History and presentation of dysrhythmias

  History:

  Syncope, lethargy/weakness, exercise intolerance, ’funny turns’, known cardiac disease.

  Physical examination:

  Abnormal heart rate, audible irregular rhythm, pulse deficits, evidence of underlying cardiac disease (e.g. murmur).
• Causes of dysrhythmias

  • Structural cardiac disease.
  • Drugs
  • Toxins
  • Metabolic diseases/ electrolyte imbalance
  • Systemic disease - sepsis, neoplasia (anything that causes wide spread inflammation).
  • Primary issue with the hearts inherent conduction system.
• Treatment options for dysrhythmias

  • Anti-dysrhythmias drugs
  • Pacemaker
  • Ablation with catheters
  • Implantable cardiovertors.
• What types of dysrhythmias are there?

  Bradyarrhythmia:

  Leads to a reduction in heart rate.

  Tachyarrhythmia:

  Leads to an elevation in heart rate when present.

  Supraventricular (above the ventricles)

  Ventricular (from the ventricles)
• What are bradyarrhythmias?

  Markedly increased vagal tone - sinus bradycardia: consider giving atropine (parasympathetic) and check for resolution.

  Abnormal generation of an impulse at the sino-atrial node.

  Abnormal conduction of the impulse at the AV node.

  Also consider underlying primary causes: electrolyte imbalances (especially Hyperkalemia), primary cardiomyopathy/ valvular disease, drug toxicity/effect.
• What is sinus arrest?

  SAN fails to discharge.

  Pause noted on ECG with no P-QRS-T complex.

  Pause can be terminated by either a sinus complex (sinus pause).

  If SAN doesn’t fire then next fastest pacemaker takes over.

  AV node then ventricular cells.
• What is persistent atrial standstill?

  SAN not working at all.

  Complete absence of p-waves.

  Next fastest pacemaker takes over.

  Heart rate is usually lower but regular.

  QRST usually appears normal if AVN takes over.

  Wide/ bizzare QRS if ventricualr myocardial cells take over.

  
• Atrioventricular blocks

  Type 1: delay in the transmission of the impulse; prolonged P-R interval: p-waves always eventually conducted.

  Type 2: occasional block; p-wave not conducted.

  Mobitz type I: conduction through the AVN progressively slower and then leads to a blocked beat - progressively longer P-R intervals until non-conducted P-wave.

  Mobitz type II: occasionally blocked beats but P-R interval constant.

  Type 3: complete block - p-waves and QRS complexes not related to each other.

  
• Bradyarrhythmias

  Abnormally slow heart rate
• Treatment for Bradyarrhythmias

  1. Treat underlying cause (e.g. correct hyperkalaemia)

  2. If no or limited clinical signs, treatment likely not required

  3. Sinus node dysfunction may not have associated clinical signs and sudden death is very rare

  4. Type 1 and most type 2 AV blocks often a response to increased vagal tone - often noted under GA

  5. In cases of sick sinus syndrome, advanced type 2 AV block and type 3 AV block an artificial pacemaker is often the only effective treatment

  6. Parasympatholytic or sympathiomimetic drugs such as atropine or terbutaline may be attempted but are largely ineffective
• Sinus node dysfunction may not have associated clinical signs and sudden death is very rare
• Type 1 and most type 2 AV blocks often a response to increased vagal tone - often noted under GA
• In cases of sick sinus syndrome, advanced type 2 AV block and type 3 AV block an artificial pacemaker is often the only effective treatment
• Parasympatholytic or sympathiomimetic drugs such as atropine or terbutaline may be attempted but are largely ineffective
• Types of tachyarrythmias

  Supreaventricular tachycardia (SVT)

  • originating from above the ventricles.
  • Therefore ventricular impulse conduction normal and QRS normal in appearance - tall and narrow.

  Ventricular tachycardia (VT):

  • all rhythm disturbances originating from within the ventricles.
  • Ventricular conduction abnormal leading to wide and bizarre QRS complexes.
• What are premature beats?

  Any beat that occurs before it is expected, generally happens when you have a damaged cell. It is an ectopic beat not originating from sinus node. Can occur when normal Leo cardiac cells develop ability ti become pacemaker cells (ischaemic damage) or a short-circuit is created in the myocardium.

  Common example is secondary atria enlargement in dogs with mitral valve disease.
• What are the types of supraventricular tachyarrhythmia?

  Atrial tachycardia:

  • occurs when there is an ectopic pacemaker in atria that is able to ire at a high rate.

  Accessory pathway mediated tachycardia:

  • rare, very high heart rates; there is a gap in insulation between the atria and the ventricles so impulses can bypass the AVN.

  Atrial flutter:

  • Rare.

  Atrial fibrillation:

  • Common especially in conditions that cause significant left atrial enlargement.
• What is atrial fibrillation?

  Most common SVT; chaotic rhythm as a result of concurrent activation of different areas of atrial myocardium, likely atrial enlargement.

  ECG characteristics:

  • HR normal (lone AF) to tachycardia
  • Rhythm: irregular
  • F-waves: P-waves not seen instead fluctuations of baseline.
  • QRS: normal as ventricular activation via normal pathways (can have concurrent ventricular issues in some cases).

  Treatment: if high rate then slow conduction through AVN; combination treatment with Diltiazem and Digoxin often effective.
• What are the types of ventricular tachyarrhythmia?

  Ventricular premature beat:

  • Same causes as premature beats; wide and bizarre QRS, can occur in couplets and triplets.

  Ventricular tachycardia (VTAC):

  • Sequence of or >4 ventricular beats with a rate >160bpm - often fast and unstable rhythm.

  Ventricular flutter:

  • A very rapid VTAC in which T-waves and QRS are no longer distinguishable; DANGER - often precedes death.

  Base your decision on whether or not to treat on clinical signs and nature of ECG findings, consider Holter monitor to look for underlying cause.
• Antiarrhythmic drugs

  Not benign, can promote other arrhythmia, reduce cardiac output
• Treating underlying causes

  1. Correction of electrolyte abnormalities

  2. Treating systemic illness/neoplasia

  3. Withdrawal of medication

  4. Treating congestive heart failure
• Arrhythmia present

  Treatment will likely lead to a reduction of clinical signs/improve quality of life or reduce risk of sudden death
• Not all arrhythmia require treatment if having minimal impact on patient
• If in doubt contact cardiologist for advice and consult drug formulary
• Ensure owners informed of potential risks of medications
• Types of antiarrhythmic drugs

  • Lidocaine
  • Sotalol
  • Diltiazem
  • Digoxin
• Lidocaine

  Class 1b, blocks Na+ channels, enhances repolarisation, commonly used for ventricular arrhythmias
• Sotalol

  Class III, blocks K+ channels, commonly used for SVT and ventricular arrhythmias
• Diltiazem

  Class IV, effects Ca channel blockers, commonly used for heart rate control of SVT by reducing conduction through AV node
• Digoxin

  Class V, has a narrow therapeutic index, and severe effects common, measure animals serum levels, blocks Na+/K+ ATPase, commonly used for atrial fibrillation (best results when combined with Diltiazem; don't use for ventricular arrhythmias)