Cardiac arrhythmias

Question 1

Describe the 5 phases of electrical conduction through the myocardium

Answer 1

• Phase 0
  
  • Initial upswing of the action potential
• Phase 1
  
  • Potential may repolarise slightly before the plateau
• Phase 2
  
  • Plateau phase
• Phase 3
  
  • Repolarisation
• Phase 4
  
  • Diastolic membrane potential

Question 2

Describe the electrical activity during phase 0 of myocardium depolarization

Answer 2

• Activation of Na+ channels (depolarization)
• Na+ channels are open and Na+ flows into the cell until threshold is reached
• Results in a rapid positive change in voltage across the cell membrane (from -70 mV to +50 mV)

Question 3

Myocardial Action Potential

Phase 1

Describe the changes in ion movement during Phase 1

Answer 3

• Initiated by the rapid inactivation of the Na+ channels
• Inward Na+ current is stopped
• At the same time, potassium channels open and close rapidly
• Brief flow of K+ ions out of the cell

Question 4

Myocardial Action Potential

Phase 2

Describe ion movements during the plateau phase of the action potential

Answer 4

• Plateau phase - membrane potential remains almost constant
• Delayed rectifier potassium channels allow K+ to leave the cell
• L-type calcium channels open and allow Ca++ into the cell
  
  • These are activated by the influx of Na+ during phase 0
• Calcium binds to and open Ca++ channels on the SR releasing calcium from the SR
  
  • These calcium ions are responsible for the contraction of the heart
• Calcium also actives Cl- channels allowing Cl- into the cell
• Calcium increases the activity of the Na+:Ca++ exchanger
• Increase Na+ entering the cell increases the activity of the Na-K pump

Question 5

Describe the net ion movements occuring during phase 2 (plateau phase) of myocardial depolarisation

Answer 5

• K+ leaves the cell
• Ca++ enters the cell
  
  • Ca++ liberated from the SR further increases intracellular Ca++
• Chloride enters the cell
• Na+ enters the cell (via Na Ca exchanger)
• The net ion exchange during phase 2 results in a stable membrane potential
• The long duration of phase 2 is important in prevention of arrhythmia

Question 6

Myocardial Action Potential

Phase 3

Describe the movement of ions during the rapid repolarization phase

Answer 6

• The L-type Ca++ channels close
• Slow potassium channels remain open, addition potassium leak channels open
• Na Ca exchanger pumps out intracellular calcium
• Na K pump helps restore ions back to pre-AP balanced states
• The delayed rectifier K+ channels close once the membrane potential is restored to resting (-85 to -90 mV)

Question 7

Myocardial Action Potential

Phase 4

Describe to movement of ions within the cardiac myocyte during diastole (phase 4)

Answer 7

• Ventricular diastole
• K+ can leak into or out of the cell via leak channels.
  
  • The inwardly rectifying leak channel remains open during phase 4
• The resting membrane potential remains constant due to the energy dependent action of Na Ca exchanger and the Na K pump.
  
  • Na Ca exchanger - 1 Ca++ out, 3 Na+ in (net + in cell)
  • Na K pump - 2 K+ into cell, 3 Na+ out (Net - in cell)

Question 8

Describe the pacemaker potential

Answer 8

• The pacemaker potential is Phase 4 of the action potential within the pacemaker cell
• The pacemaker cells slowly become more positive during this phase due to the net movement of both K+ and Na+ into the cell.
• Na+ and K+ move into the cell via HCN channels
  
  • Hyperpolarization-activated cyclic nucleotide gated channels
  • HCN channels open at the very negative voltages generated immediately after phase 3
    
    • These negative voltages are the resting potential for non-pacemaker cells (-90 mV)
• Increased activation of the Na Ca exchanger due to calcium leak from the SR also contributes to the slow increase in cell membrane potential towards - 40 mV, predominantly at the end of the pacemaker potential
• Once the membrane potential reaches - 40 mV, depolariastion occurs.

Question 9

Describe the phases of the cardiac action potential and their relevance to the generation of the normal ECG waveform

Answer 9

• Phase 0: depolarisation
  
  • Initiation of the Q wave
• Phase 1: Transient efflux of K+ - occurs during systole or the QRs segment
• Phase 2: Plateau phase - ST segment represents the period when the ventricles are depolarised. Marks the end of systole
• Phase 3: rapid repolarisation - Represented on the ECG by the T wave
• Phase 4: ventricular diastole - end of the T wave through to the start of the next P wave.

Question 10

Describe the vagal manouvers that can be used in dogs and cats?

Note when these vagal manoeuvers may be beneficial.

Answer 10

• Carotid sinus massage
  
  • Sustained digital pressure to one or both carotid sinuses for 5-10 seconds.
  • Carotid sinus sits immediately behind the larynx.
  • May elicit a gag reflex, but shoudl not be uncomfortable
• Digital ocular pressure
  
  • Gentle but firm pressure to both globes over closed eyelids
  • Contraindicated if there is ocular disease present
• Vagal manoeuvers increase AV nodal refractoriness and may enhance visualisation of specific causes of supraventricular tachycardia as seen on ECG
• Particularly useful to interrupt an AV nodal re-entrant tacycardia or reciprocating tachycardia.

Question 11

Describe the atropine response test?

When is the atropine response test indicated?

Answer 11

• Atropine is administered at 0.04 mg/kg IV
  
  • Atropine should abolish vagal tone and cause an increase in the basal heart rate
• A response should be observed on ECG within minutes to 15 minutes.
• The atropine response test is used clinially to assess the cause of a bradycardia
• The test allow differentiation of vagally mediated bradycardia and pathological bradycardia caused by an intrinsic decrease in impulse formation or conduction.

Question 12

Describe the 3 major groupings of cardiac arrhythmias.

Provide examples of each and include examples of arrhythmias that do not readily fit into one group.

Answer 12

1. Disturbances of impulse formation
   
   • Sinoatrial arrest
   • Atrial fibrillation
2. Disturbances of impulse conduction
   
   • AV block
   • AV nodal reentrant tachycardia
3. Complex disturbances of both impulse formation and condution
   
   • Sick sinus syndrome

• A junctional escape rhythm is a disturbance of impulse generation secondary to a condution disturbance.

Question 13

List the factors that contribute to the clinical significance of a cardiac arrhythmia to the patient (arrhythmia and patient specific).

Answer 13

1. The ventricular rate
2. The duration of the abnormal rhythm
3. The temporal relationship between atrial and ventricular contraction
4. The sequence of ventricular activation
5. Inherent myocardial and valvular function
6. Cycle length irregularity
7. Drug therapy
8. Extra cardiac influences - eg. co-morbidities

Question 14

Describe the 5 point assessment of an ECG

Answer 14

1. Cursory check of entire trace
   
   • assess rate, QRS complexes of same morphology, R-R interval consistent or variable
2. R-R interval assessment
   
   • Regular, regularly variable and irregularly irregular
3. QRS complex morphology
   
   • Narrow - generally normal
   • Wide - due to assynchronous ventricular depolarisation either due to an ectopic beat or BBB
4. P wave assessment
   
   • Present, absent, positive, negative, variable
5. Basic underlying rhythm or any secondary rhythms
   
   • Intermittent AV block, ventricular extra-systoles

Question 15

Describe the underlying mechanisms contributing to a respiratory sinus arrhythmia.

Why is RSA rarely observed in cats?

Answer 15

• In the resting dog, parasympathetic input predominates over sympathetic inputs
• Increased cardiovascular return to the left atrium during inspiration (due to reduced left atrial pressures) triggers baroreceptors.
• Baroreceptor triggering causes a reduced vagal tone.
• Combination of increased vascular return and reduced vagal tone contributes to an increased heart rate during inspiration
• RSA is not seen with heart rates > 150 per minute due to increased sympathetic tone.
• In most cats in the hospital setting, sympathetic tone is increased and predominates.

Question 16

What is a ventriculophasic arrhythmia

Answer 16

• An unusual phenomenon that causes a variation in the P-P interval in patients with high second degree or third degree block.
• P-P interval that flanks a QRS complex is reduced

Possible explanations:

• Increased perfusion to the SA node after ventrciular systole
• Triggering of the Bainbridge reflex with atrial filling following a ventricular systole.

Question 17

Describe the pysiological mechanisms that contribute to a wandering pacemaker.

Answer 17

• The normal heart beat is generated in the pacemaker cells of the sinoatrial node.
• In the dog, the electrical impulse generates from the middle or cranial regions of the node.
• Under high parasympathetic tone, the impulse can arise from the more ventral segment of the node or the perinodal tissues
• The variation in site of impulse formation results in a variation in the P wave appearance on ECG
• This variation is often seen in conjunction with RSA as high vagal tone triggers both phenomenon.
• WP is rarely seen in cats.

Question 18

Define sinus bradycardia (SB)

Discuss the clinical relevance of sinus bradycardia

Answer 18

• Sinus bradycardia is a sinus or regular rhythm in which the heart rate is abnormally low.
• The P wave and QRS morphology are normal and there is a normal P-R interval with a 1:1 ratio.
• SB indicates the physiological or pathological predominance of parasympathetic tone
• When clinical signs are present in conjunction with SB, SB is typically secondary and not the cause of clinical signs.
• Asphixiation or upper airway obstruction can trigger SB
• Hypothermia and deep anaesthesia are common causes
• GIT, respiratory, opthalmic and neurological conditions can all cause SB
• SSS is the major exception, however SB only comprises one distinct arrhythmia in this complex problem which does require more definitive and direct treatment.

Question 19

Define Sinus tachycardia

Describe the clinical causes and implications of sinus tachycardia.

Answer 19

• ST is a sinus rhythm that occurs at an elevated rate from normal.
• As with normal heart rates, the definition of ST varies with species, breed, age and body weight.
• In dogs, a rate of >160 per minute is used as a defining rate
• ST is triggered by a predominance of sympathetic tone
• ST is typically a result of rather than a cause of a patient’s clinical signs.
• The causes of ST are diverse and include: CHF, anaemia, pain, hyperthermia, hypovolaemia
• As ST is a result of an underlying process, treatment directed at reducing the heart rate primarily can be catastrophic.
• Prevention of ST in animals with preclinical heart disease has been investigated without a convincing benefit

Question 20

List the various arrhythmias that can arise from atrial excitability disturbances

Answer 20

1. Premature atrial complex
2. Atrial tachycardia (paroxysmal or sustained)
3. Atrial fibrillation
4. Atrial flutter
5. Macroreentrant tyachycaridia
   
   • AVN reentrant tachycardia
   • orthodromic AV reciprocating tachycardia

Question 21

List the specific arrhythmias typically grouped together as Atrial Tachycardia (AT)

Answer 21

Micro-reentrant tachycardia

1. sinus node reentrant tachycardia
2. intra-atrial reentrant tachycardia

Spontaneous automaticity

1. automatic atrial tachycardia
2. junctional tachycardia

Question 22

List the various pharmacological treatments for AT in the acute setting

Note: patients need to have normal systolic function and no CHF

Answer 22

• Diltiazem
  
  • 0.05-0.1 mg/kg IV bolus repeated to effect (max 0.25-0.35 mg/kg)
  • Oral 0.5-1 mg/kg PO q 8 hours
• Propranolol
  
  • 0.02 mg/kg IV PRN, typically q 2-10 mins
• Esmolol
  
  • 25 mcg/kg/min IV CRI
  • some reports up to 100-500 mcg/kg/min
• edrophonium
• phenylephrine
  
  • 0.004-0.01 mg/kg IV

Question 23

List the oral treatment options for clinical AT

Answer 23

Note: all signs of CHF should be controlled prior to commencement of these rate control medications. Start at low end of dose range and up-titrate as necessary

• Beta blocker
  
  • Atenolol: 0.3-1.5 mg/kg PO q 12 hours
  • Metoprolol: 0.2-0.4 mg/kg PO q 12 hours
  • Carvedilol: 0.2-0.3 mg/kg PO q 12 hours
• Diltiazem
  
  • 0.5-1.5 mg/kg PO q 8 hours (not sustained release)
• Digoxin
  
  • 0.005 - 0.011 mg/kg PO q 12 hours
  • 0.22 mg/m2 for dogs > 20 kgs, not exceeding 250 ugm/dog

Question 24

Atrial Flutter

What is the cause of atrial flutter

Describe the classical ECG characteristics

What is the definitive treatment for spontaneous or paroxysmal atrial flutter?

Answer 24

Atrial flutter is caused by propgation of the electrical impulse through a macro-rentrant circuit contained within the right atrium. This causes self-perpetuating triggering of the SAN

A “saw tooth” baseline is the classical appearance of AF caused by rapid repeating atrial depolariation (rtare 280-400). There is usually a rapid tachycardia and normal QRS complexes. The R-R interval may be irregularly irregular due to variable AV block.

Atrial flutter can be abolished with radiofrequency catheter-based interruption of the flutter circuit.

Question 25

Define Atrial Fibrillation

Answer 25

AF is characterised by complete electrical disorganisation at the atrial level, leading to a chaotic, rapid series of atrial depolarisations.

Question 26

Describe the ECG characteristics of Atrial Fibrillation

Answer 26

1. Absence of P waves
   
   • may see fibrillation waves - fine variable undulation of the baseline
2. Normal appearance to the QRS complexes
3. Variable R-R interval - irregularly irregular

Question 27

Describe the cardiovascular consequences of rapid atrial fibrillation

Answer 27

• Atrial contraction becomes chaotic and variable AVN block or transmission occurs
• Reduced contribution to ventricular filling by synergistic atrial contraction (up to 30% of total ventricular filling)
• There is a marked reduction in diastolic filling times
• The above all leas to reduced and variable diastolic filling prior to systole
• The results is reduced and variable systolic outflow
• The combination of intermittent transmission of the electrical impulse through the AV node and variable diastolic filling leads to variable and irregular pulses and potentially markedly reduced cardiac output.

Question 28

Discuss the prognosis in the following scenarios:

1. Atrial fibrillation in a large breed dog
   
   • Lone AF
   • AF with subclinical structural disease
   • AF and CHF
2. MMVD and CHF: with and without AFib
3. AFib in cats with structural heart disease

Answer 28

1. Lone AFib - median 40 months survival
2. AF with structural disease - 32 months
3. AF and CHF - median survival of 5 months
4. MMVD and CHF
   
   • With AFib - median survival 142 days
   • Without AFib - median survival 234 days
5. AFib in cats: Median survival of 165 days in 50 cats, 33% survived to 1 year (8 of 24).

Question 29

Discuss the pharmacological treatment options for dogs with atrial fibrillation

Answer 29

• Lone AFib without structural disease and a slow heart rate (< 140) does not require treatment
• Manage structural underlying heart disease - pimobendan for subclinical DCM and Stage B2 MMVD
• Adequately treat CHF with diuretics as needed

From a baseline ventricular response rate of 194 bpm (Geltzer JVIM 2009)

• Diltiazem alone - VR median 158 per minute
• Digoxin alone - VR median 164 per minute
• Combination diltiazem and digoxin - VR 126 per minute. Heart rate also remained below 140 per minute for 85% of 24 hour Holter recording period

Question 30

List the various rhythm abnormalites caused by ventricular excitability disorders

Answer 30

1. Premature ventricular complexes
2. Accelerated idioventricular rhythm
3. Ventricular tachycardia - sustained or paroxysmal
4. Ventricular flutter
5. Ventricular fibrillation
6. Torsade de Pointes (TdP
7. Ventricular Parasystole
8. Isorhythmic Atrioventricular dissociation (IAVD)

Question 31

VPCs

Descirbe the typical ECG changes

Answer 31

• Prematurity - shortened R-R interval
• Not associated with a preceding P wave
• Wide QRS morphology - typically a different shape to the normal sinus QRS complex
• Different and often large associated T wave
• Single VPCs are often followed by a compensatory pause

Question 32

List the major differentials for abnormally wide QRS complexes.

Note how each of the differentials vary in appearance to a VPC

Answer 32

1. Bundle branch block
   
   • Associated with a P wave
2. Changes due to cardiomegaly or axis shift
   
   • Consistent change to all QRS complexes should be present
3. Artifact - motion or otherwise
4. Ventricular escape beats
   
   • These are not premature and appear after a prolonged pause.
5. Wide complexes seen with severe hyperkalaemia
   
   • Associated with a P wave (if still present). Atrial arrest may be seen. Prolonged PR interval expected. Sustained abnormality, not paroxysmal or solitary.

Question 33

Discuss the releavence or association of VPCs with underlying cardiac disease in:

1. Dogs
2. Cats

Answer 33

VPCs can be caused by almost any cardiac or systemic disorder. Systemic diseases include hyperkalaemia, hypoxaemia, trauma, GDV, abdominal masses (esp splenic or hepatic), intoxication, acidosis.

1. Underlying cardiac disease is present in ~ 69% of dogs with VPCs
2. Cardiac disease is present in ~96% of cats with VPCs

In both species, treatment of any underlying trigger should first and foremost. Treatment of single VPCs is rarely required (ARVC is the notable exception).

Question 34

Descirbe the ECG characteristics of accelerated idioventricular rhythm

Answer 34

• AV dissociation
• Wide and bizarre QRS complexes - sustained
• May see capture and fusion beats
• QRS rate of beteen 70-160 beats / minute
  
  • <70 beats per minute = idioventricular escape rhythm
  • > 160 beats per minute = ventricualar tachycardia

Note: causes are similar as for VPCs and treatment is generally aimed at any underlying systemic or cardiac disease. Anti-arrhythmic therapy is not typically required.

Question 35

Ventricular Tachycardia

Describe the ECG charateristics of VT

Answer 35

• Wide and bizarre QRS complexes
• AV dissociation
• 3 or mote abnormal beats with a QRS rate > 160 per minute
• Can be sustained or paroxysmal
• May see fusion beats or capture beats
  
  • Capture - first normal P-QRS complex after a run of VT
  • Fusion - intermediate QRS comples caused by collision of the electrical activity of normal and ectopic QRS complexes

Question 36

Discuss the treatment algorithm for VT

Answer 36

1. Define that VT is present - ECG required - appropriate elevated heart rate present
2. Are there clinical signs attributable to the arrhythmia (eg. syncope, presyncope - lightheadedness, weakness, ataxia, malaise, hypoxic seizures)
   
   • If present, commence treatment with IV Lidocaine or oral sotolol, oral mexiletine,oral amiodarone
   • If absent, then identify and address any underlying cause
3. If VT remains present despite appropriate management of underlying causes, then treatment may become indicated.

Question 37

Describe the ECG characteristics of TdP

Note the causes for this rare arrhythmia

What is the treatment for TdP?

Answer 37

• Ventricular arrhythmia that arises secondary to prolongation of the Q-T interval
• Polymorphic ventricular tachycardia
• The QRS complexes vary in amplitude around the isoelectric line.

Causes include:

• Congenital long QT syndrome (seen in dalmation dogs)
• hypokalaemia
• hypocalcaemia
• hypomagnesemia
• toxicosis - especially class 1A antiarrhythmics eg. quinidine

Definitive treatment involves intravenous infusion of magnesium sulfate at 20-60 mg/kg slow IV.

In humans, the TpD can be managed with an automated implantable cardioverter defibrillator

Question 38

Define Ventricular parasystole

Answer 38

• Ventriocular parasystole is a complex arrhythmia that results from the concurrent and independent activity of two pacemakers
• There is typically a normal supraventricular pacemaker and a second, protected ventricular pacemaker - there is a uni-directional entry block that protects the ectopic focus from sinus depolarisation
• The ventricular focus has an independent automaticity that is greater than an ectopic focus.

Question 39

Define isorhythmic AV dissociation

What are the ECG characteristics?

What are the clinical implications?

Answer 39

• The atria and ventricles are driven by independent pacemakers at nearly equal rates
• The P waves and QRS complexes are dissociated.
• P wave may drift in and out of the QRS complex and at times may appear in normal relationship to the QRS complex (variable PR interval)
• There are no known clinical implications and the condition is usually identified incidentally. May be over-represented in the Samoyed breed.

Question 40

Define the 3 degrees of AV block

Answer 40

1. First degree AV block involves slower than normal impulse conduction through the AV node with a subsequent prolongation of the PR interval.
2. Second degree AV block is a transient but complete disruption to AV nodal impulse transmission
   
   • Mobitz type I - progressive lengthening of the PR interval prior to a blocked P wave
   • Mobitz type II - regular PR interval with a variable number of blocked P waves
3. Third degree AV block is a complete and sustained interruption of AV nodal conduction

Question 41

Describe the causes of AV block

Describe the clinial impact of AV block

Discuss treatment options for high grade second degree and third degree AV block

Answer 41

• First degree AV block and Mobitz type I second degree block can be caused by:
  
  • high vagal tone
  • anti-arrhythmic drugs
  • structural disease high in the AV node.
• There is no clinical impact and treatment is not required.
• Mobitz type II and third degree AV block can be functional secondary to:
  
  • hyperkalaemia
  • digitalis toxicosis
  • alpha 2 receptor antagonists - eg medetomidine
• Mobitz type II and third degree AV block are more commonly associated with structural disease that is irreversible in ~ 95% of cases. Examples include:
  
  • Myocarditis
  • Endocarditis
  • Cardiomyopathy, endocardiosis, fibrosis

Treatment of mobitz type II and third degree AV block involves pacemaker implantation.

Question 42

Define bundle branch block

Describe the ECG characteristics of a bundle branch block

Answer 42

• BBBs are a slowing or interruption to conduction along one or more of the bundles of His.
• The BBB can be functional or structural
• The QRS complexes are wide and bizzare and monomorphic
• There is a normal sinus rhythm
• There is a normal and regular P-R interval
• Left BBB - positive in lead II
• Right BBB - negative in lead II

Question 43

Describe the clinical implications of both left and right bundle branch blocks in dogs and cats

Answer 43

• BBBs can be caused by a large array of pathological changes, so definitive treatment is often directed at the underlying cardiac disease. Accurate identification of the underlying cardiac disease is essential
• In dogs, right bundle branch block is usually an incidental and clinically silent problem
• In both dogs and cats, left bundle branch block is almost always associated with left ventricular enlargement. Note that left BBB (left anterior fascicle) block is very common in cardiomyopathic cats.
• Note that a LBBB may be the first indicator of underlying cardiac disease, so should serve as a trigger for further diagnostic investigation.

Question 44

Define atrial standstill and the associated ECG findings

What are the differential diagnoses for atrial standstill

Answer 44

• Atrial standstill is defined by the total absence of atrial depolarisation
• The characteristic ECG finding is an absence of P waves and a junctional or ventricular escape rhythm. Most often the QRS complexes are of a normal morphology (ie of junctional origin). The heart rate is low normal to low.
• Atrial standstill can be caused by severe hyperkalaemia (> 7.5 mEq/L), atrial myopathy or as an artifact (P waves too small to see).

Question 45

List the various CAUSES of complex arrhythmias

an arrhythmia with both a disorder or impulse generation and conduction

Answer 45

1. Hypokalaemia
2. Hyperkalaemia
3. Hypocalcaemia
4. Hypercalcaemia
5. Pre-excitation and macro-reentrant syndromes
6. Sinus node dysfunction / sick sinus syndrome

Question 46

Describe the effects of hypokalaemia on the electrical activity of the heart.

Answer 46

1. Low serum potassium makes the resting membrane potential increasingly negative
   
   • This decreases membrane excitability
2. Repolarization is delayed due to reduced potassium transport through the delayed rectifier channels
3. Normal repolarization is rapid during which time, resting membrane potential is near threshold
   
   • Delayed repolarization extends the window of excitability and predisposes to ectopic activity

• Clinically, increased excitability (arrhythmogenic effect) dominates over the suppressive effects

Question 47

Give examples of the ECG characteristics of hypokalaemia

Answer 47

ECG characteristics:

• Increased chance of atrial or ventricular ectopy (APCs or VPCs).
• U waves (small deflection after T) can be seen
• Prolongation of the QT interval
• AV dissociation

Question 48

Describe why lidocaine administration may be ineffective in the hypokalaemic patient with a ventricular arrhythmia.

Answer 48

• Hypokalaemia can contribute to ventricular ectopy due to prolongation of the refractory period and increased myocyte time near threshold potential
• Lidocaine acts on the sodium channels. These channels need normal serum potassium concentrations to function
• Low serum potassium increases the risk of lignocaine refractoriness, thus increasing the risk of toxicity

Question 49

Describe the effects of hyperkalaemia on the cardiac cycle

Answer 49

• Mild hyperkalaemia increases membrane permeability to potassium. This effect is most evident during repolarisation
• More rapid repolarisation has a stabilising effect on the heart rhythm
  
  • May see reduced QT interval +/or a tall, narrow T wave.
• Decreased activity of the normal pacemaker cells may lead to sinus bradycardia, however this is rarely seeen clinically
• Mild to moderate increases start to slow propogation of the AP in the ventricles - widening of the QRS complex and reduced R wave amplitude
• Moderate to severe hyperkalaemia can cause prolongation of the PR interval and absence of P waves
  
  • A sinoventricular rhythm is seen. Impulse is generated in the SA node and crosses the atria along internodal tracts, but does not spread to the atrial myocardium.
• Severe hyperkalaemia > 8.5 mEq/L can be fatal. Widening of the QRS and T waves can lead to a sine-type wave or a ventricular escape at a low rate and non-functional rhythm

Question 50

Describe the effects on cardiac myocytes due to hypocalcaemia

Note the ECG changes that may be seen with hypocalcaemia

Answer 50

• Hypocalcaemia lowers the threshold of a myocytes action potential.
• As a result of a lower threshold, propogation of depolarisation is facilitated
• The effect is much more evident on skeletal muscle cells, and cardiac myocytes are relatively resistant to hypocalcaemia
• The initial phase of repolarisation is delayed
• A prolonged QT interval is the most likely ECG abnormality

Question 51

When is intravenous calcium infusion considered cardioprotective?

Why is calcium infusion cardioprotective?

Answer 51

• IV Calcium infusion is cardioprotective in severe hyperkalaemia
• Hyperkalaemia raises the resting membrane potential (making it less negative), thus increasing the likelihood of depolarisation.
• Calcium supplementation increases the threshold for depolarisation.
• This combination of changes leads to normalisation of the ionic gradient across the cell membrane.

Question 52

Describe the affects of hypercalcaemia on the caridac myocyte.

Describe the cardiac consequences of hypercalcaemia.

Answer 52

• Hypercalcaemia increases the cell membrane threshold to depolarisation
  
  • Thus, high calcium could hinder depolarisation
• Hypercalcaemia also increases the rate of early repolarisation
  
  • This can be seen as a shortened Q-T interval on the ECG.
  • Monitoring of the QT interval is important during IV calcium infusion
• The cardiac conserquences of hypercalcaemia are clinically minimal, especially compared to the dystrophic mineralisation seen in the kidneys and other soft tissues.

Question 53

Discuss the cause of pre-excitation and macro-reentrant circuits

Answer 53

1. In pre-excitation, there is an abnormal pathway of rapidly conductive fibres that links the atria with the ventricles, bypassing the AV node.
2. A macro-reentrant circuit is completed when the impulse can be tramsmitted normograde and antegrade through the bypass tract.
3. The depolarisation passes from the ventricles, through the bypass tract, to the atria and AV node.
4. The impulse in orthodromic AV reentrant tachycardia passes through an ‘endless’ closed loop, with a normal passage through the AV node.

Question 54

Describe the typical ECG findings with pre-excitation.

What are the clinical consequences of pre-excitation?

How can pre-excitation conditions be managed?

Answer 54

• Due to passage of the impulse through a bypass tract, the usual delay at the AV node is not present. This causes a shortened P-R interval on the ECG, with the P often blending with the Q wave.
• Due to activation of the ventricles at the bypass tract and the AV node, a notched R wave (delta wave) may be present.
• Unless there is development of a macro-reentrant tachycardia, there is no clinical consequence to pre-excitation alone.
• If pre-excitation contributes to development of a macro-reentrant circuit and rapid tachycardia, then treatment is required.
  
  • Diltiazem can increase the refractoriness of the bypass tract and block the re-entrant circuit.
  • Radiofrequency catheter ablation of the tract is the definitive treatment of choice for tracts located in the right atrium.

Question 55

Describe the pathophysiology underlying the various ECG abnormalities seen in SSS

Answer 55

• SSS is a bradycardia / tachycardia syndrome with abnormalites noted in the all conductive tissues in the heart, namely the sinus node, AVN and both supraventricular and ventricular excitability.
• Sinus node dysfunction leads to variation in impulse generation. This can manifest as sinus block and sinus arrest
• AV nodal dysfunction can manifest as first or second degree AV block.
• Disturbances in excitability can manifest as premature atrial, junctional or ventricular ectopic beats.

Question 56

Describe the typical signalment and clinical history of a dog with SSS.

Discuss how to obtain a definitive diagnosis

What are the treatment options?

Answer 56

• Female miniature schnauzers are predisposed, but WHWT, cocker spaniels and cross breed dogs can also develop SSS.
• Median age of 11 y in Ward et al paper - 93 dogs
• Syncope, stumbling and ataxia are the most common historic findings.
• Clinical examination may reveal an arrhythmia with both bradycardia and tachycardia - prolonged auscultation may be required.
• Concurrent mitral valve endocardiosis is common
• Clinical signs are most attributed to periods of sinus arrest or AV nodal block (periods of bradycardia)
• Diagnosis requires either ECG tracing, Holter recording or use of an event monitor. SSS is defined by a complex of both brady- and tachyarrhythmias.
• Definitive treatment requires placement of a caridac pacemaker
• A positive response to atropine is predictive of medical management success
• Medical management with propantheline, hyosciamine or aminophylline/theophylline can improve and reduce clinical signs.
• ~54% of dogs were medically controlled in Ward et al, with a further 20% medically managed as a bridge to pacemaker implantation.