Treatment of Life-Threatening Arrhythmias
British Small Animal Veterinary Congress 2008
Simon G. Dennis, BVetMed, MVM, CertVC MRCVS
The Royal Veterinary College
North Mymms, Hatfield, Hertfordshire

The Origin of Arrhythmias

The heartbeat is determined by an electrical impulse that arises from the sinoatrial node (SAN), rapidly depolarises both atria (collecting chambers of the heart), is slowly conducted through the atrioventricular node (AVN), then very rapidly depolarises both ventricles (muscular pumping chambers of the heart). This pattern of sequential activation has evolved to allow the mammalian heart to pump blood in the most effective manner. Circulation of blood is essential to deliver nutrients (such as oxygen (O2) and glucose) to body tissues and to remove harmful waste products (such as carbon dioxide (CO2), hydrogen ions (H+) and lactate) via the lungs and kidneys. Cardiac arrhythmias (or dysrhythmias) are defined as any abnormality of rate, regularity or origin of the heartbeat (rhythm). This may occur by disruption of the normal pattern of activation of the heart, or by causing the heart to beat at an unacceptable rate, either too quickly (tachyarrhythmias) or too slowly (bradyarrhythmias). Both an abnormal pattern or activation and an unacceptable rate are present in many arrhythmias.

The Effects of Arrhythmias

Arrhythmias can therefore adversely affect normal circulatory haemodynamics. Failure of the heart to provide effective circulation results in either forward (output) failure or backward (congestive) failure. Output heart failure (OHF) is characterised by failure of the heart to pump an adequate volume of blood to properly perfuse the body and lung tissues. Congestive heart failure (CHF) is characterised by an accumulation of fluid within the body (e.g., ascites, pleural effusion) or lungs (pulmonary oedema). OHF can be life threatening when it results in insufficient perfusion of vital organs (brain, cardiac and ventilatory muscles), causing irreversible organ damage and death. This usually occurs in severe OHF, which results in cardiopulmonary arrest. CHF can also be life threatening.

Identification of Arrhythmias

The spectrum of clinical signs that may accompany arrhythmias is diverse and depends upon the severity and type of haemodynamic compromise. Signs include weakness, lethargy, exercise intolerance, ataxia, syncope, seizure, behavioural changes, collapse and dyspnoea. Unfortunately none of these signs are pathognomonic for an arrhythmia; many accompany other cardiac, respiratory, metabolic or neurological conditions. Furthermore, in some animals with life-threatening arrhythmias, there may be no accompanying clinical signs; sudden death may be the first, and therefore only, symptom. Some clues may be ascertained from cardiac auscultation and palpation of peripheral pulses, such as an irregular rhythm, variable pulse quality and pulse deficits. However the presence or absence of these findings does not diagnose a life-threatening arrhythmia. Therefore, the surface electrocardiogram (ECG) is the only reliable method of diagnosing a life-threatening arrhythmia.

Classification of Life-Threatening Arrhythmias

Arrhythmias that are immediately life-threatening in any patient include the following:

 Ventricular fibrillation (VF)

 Pulseless ventricular tachycardia (PVT)

 Ventricular asystole

 Pulseless electrical activity (electromechanical dissociation)

It is of vital importance that these arrhythmias are identified and rapidly corrected, as they invariably cause severe OHF and cardiopulmonary arrest.

Arrhythmias that are potentially life-threatening include the following:

 Ventricular tachycardia (VT)

 Ventricular premature complexes (VPCs)

 Atrial standstill (hyperkalaemia)

 Third-degree atrioventricular (AV) block

These arrhythmias may exert various adverse haemodynamic effects, but a major concern is that they can be electrically unstable arrhythmias, potentially progressing to an immediately life-threatening arrhythmia.

The following arrhythmias are usually only life-threatening when concurrent heart disease is present, under which circumstances they can easily precipitate CHF:

 Atrial fibrillation (AF)

 Atrial flutter

 Paroxysmal supraventricular tachycardia (PSVT)

Conditions That Predispose to Arrhythmias

The most important aspect to treatment of life-threatening arrhythmias is early recognition and prevention. Knowledge of the diseases and mechanisms that cause arrhythmias is therefore essential for identification and treatment of patients at risk of arrhythmogenesis. Conditions that predispose to arrhythmias include: primary cardiac disease (cardiomyopathy, valvular heart disease, neoplasia, congenital, primary electrical disease); thoracic trauma (blunt, penetrating, electrical); hypoxia (respiratory disease, anaemia, thromboembolic disease, anaesthesia, hypoperfusion); electrolyte/acid-base disorders (potassium imbalance, calcium imbalance, magnesium imbalance, acidosis); endocrine disease (hypoadrenocorticism, hyperthyroidism, hypothyroidism, phaeochromocytoma, diabetic ketoacidosis); abdominal organ disease (splenic disease, gastrointestinal disease, end-stage renal failure); autonomic imbalance (catecholamine excess, central nervous system (CNS) disease, vagal stimulation); temperature (hypothermia, hyperthermia); inflammation (infection, sepsis, systemic inflammatory response syndrome (SIRS), immune-mediated disease); drugs (anti-arrhythmic drugs, positive inotropic agents, anaesthetic agents, sedatives).

Patients at High Risk for Life-Threatening Arrhythmias

The patients that should be recognised as having the highest risk of developing life-threatening arrhythmias are the anaesthetised patient, the critically ill patient requiring intensive care and the patient with primary heart disease. Anaesthesia may cause arrhythmias by a combination of hypoxia, hypothermia, hypovolaemia, pro-arrhythmic drug administration and autonomic imbalance. Furthermore, patients undergoing anaesthesia for surgical procedures have the additional risk factors of pain-induced catecholamine excess, surgical trauma and inflammation secondary to tissue manipulation. It is important to recognise that the risk for arrhythmogenesis also extends into the post-anaesthetic period.

Critically ill patients often have severe underlying single or multisystemic disease, as well as a myriad of electrolyte, acid-base, perfusion, hydration and inflammatory abnormalities. Symptomatic arrhythmias occur in approximately 20% of human patients in intensive care units.

Patients with structural heart disease may have arrhythmias from atrial or ventricular damage. These commonly include cardiomyopathies, chronic valvular disease and severe congenital diseases. Some arrhythmias may present in the absence of obvious structural disease. These include patients with primary electrical disease of the heart (e.g., third-degree AV block). Patients in heart failure may be given drugs that are pro-arrhythmic (e.g., digoxin) or that predispose to arrhythmias as a result of electrolyte loss (e.g., hypokalaemia with furosemide). Furthermore, the effects of any arrhythmia are more marked in the already compromised (diseased) heart.

Patients identified as being at high risk for arrhythmogenesis should therefore be monitored appropriately. Such monitoring may include regular cardiac and respiratory auscultation, evaluation of mucous membranes and peripheral pulses, electrocardiography, blood pressure and central venous pressure measurement, pulse oximetry, end-tidal CO2, measurement of packed cell volume and haemoglobin, arterial and venous blood gas and electrolyte analysis. The level of monitoring will depend upon the individual circumstances of the patient, availability of equipment and expertise of the operator. Nevertheless, it is intuitive that the identification of, and response to, the development of a life-threatening arrhythmia is more rapid and effective in the patient that is more closely monitored.

Specific Treatment for Life-Threatening Arrhythmias

In the circumstance of an immediately life-threatening arrhythmia, cardiopulmonary resuscitation (CPR) should be instigated immediately. This includes basic cardiac life support (BCLS) initially (airway, breathing, circulation), followed by evaluation of cardiac rhythm and advanced cardiac life support (ACLS) with the use of fluids, anti-arrhythmic drugs, vasopressors, positive inotropic agents, anticholinergic drugs and electrical defibrillation/ cardioversion as appropriate. Patients with immediately life-threatening arrhythmias will generally be unresponsive with absent pulses. Although these signs are readily identifiable in the conscious animal, they can be easily overlooked in the anaesthetised animal that is not properly monitored.

In the circumstance of a potentially life-threatening arrhythmia, the most effective treatment is one that is aimed at the specific underlying condition(s) causing the arrhythmia. Such treatment can be as diverse as the underlying disease process, with indicated treatment for one condition possibly contraindicated for another. For example, high-rate intravenous fluid therapy and urinary catheterisation are indicated in the cat with urinary obstruction and hyperkalaemic atrial standstill. Such treatment would be deleterious for the animal with tachyarrhythmia and congestive heart failure, for which oxygen therapy, diuretics, vasodilators and negative chronotropic agents would be indicated. If no underling condition can be identified, the decision of whether to treat a life-threatening arrhythmia becomes a judgment call. This decision depends upon the likelihood of acute progression to an immediately life-threatening arrhythmia and the haemodynamic status of the animal. Treatment usually involves use of one (or more) anti-arrhythmic agent. These drugs, which are classified by mode of action, are presented in Figure 1.

Therefore, when deciding to treat with an antiarrhythmic agent, it must be remembered that despite best intentions, any treatment can have potentially harmful effects. This is particularly true for anti-arrhythmic agents, as all have the potential to cause or worsen arrhythmias (pro-arrhythmia), even when the intention is to treat. Furthermore, many anti-arrhythmic agents are ineffective in the presence of certain metabolic or systemic abnormalities (e.g., lidocaine in the patient with hypokalaemia). The underlying tenet of veterinary medicine is 'First, do no harm', and to this regard, once an arrhythmia has been identified, it is essential that every effort is made to correct any underlying cause, rather than the blanket use of anti-arrhythmic agents.

Figure 1. Classification of anti-arrhythmic drugs.

Classification

Examples

Action

Indications

Class Ia

Procainamide, quinidine

Na+ channel blocker

Refractory ventricular arrhythmias
Effective in some PSVTs

Class Ib

Lidocaine, mexiletine

Na+ channel blocker

Ventricular arrhythmias (lidocaine first-line drug in acute VT)
Effective in some PSVTs

Class Ic

Flecainide, encainide

Na+ channel blocker

Rarely used in veterinary medicine

Class II

Atenolol, propranolol

β-adrenergic blocker

Refractory ventricular arrhythmias
Supraventricular tachyarrhythmias (mainly for rate control)

Class III

Sotalol, amiodarone

Prolong repolarisation (K+ channel blocker)

Effective in many supraventricular and ventricular arrhythmias

Class IV

Diltiazem, verapamil

Ca2+ channel blocker

Supraventricular tachyarrhythmias (both conversion and rate control)

References

1.  Bonagura JD, Muir III WW. Antiarrhythmic therapy. In: Tilley, LP. ed. Essentials of canine and feline electrocardiography (third edition). London: Lea & Febiger, 1992; 320-364.

2.  Martin MWS. Small animal ECGs: an introductory guide (second edition). Oxford: Blackwell, 2007.

3.  Reising S, Kusumoto F, Goldschlager N. Life-threatening arrhythmias in the intensive care unit. Journal of Intensive Care Medicine 2007; 22: 3-13.

Speaker Information
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Simon G. Dennis, BVetMed, MVM, CertVC, MRCVS
The Royal Veterinary College
Hatfield, Hertfordshire , UK


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