Cardiovascular disease

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12 Cardiovascular disease

Cardiac arrhythmias

Approach to the patient

Investigations

Twelve-lead electrocardiogram (ECG)

This test provides a three-dimensional snapshot of the electrical activity of the heart and is a useful screening tool. The sum of the depolarization (activation) and repolarization (recovery) potentials of the atrial and ventricular myocardium gives rise to the ECG waveform (Fig. 12.1).

Potentials are recorded in the frontal or coronal plane by the six limb leads and in the transverse plane by the six chest leads. Deflections on the ECG are positive if the depolarization wavefront spreads towards the positive pole of a lead. The converse is true if the wavefront spreads towards the negative pole. If the wavefront is orthogonal to the lead’s axis, the deflection will be equally positive and negative, i.e. biphasic.

Atrial depolarization spreads from the sinus node inferiorly and to the left, producing a P wave that is usually positive in lead II and negative in aVR. Ventricular activation begins with depolarization of the interventricular septum from left to right, producing a small, positive R wave in lead V1 and a small, negative Q wave in lead V6. Depolarization of the remaining ventricular mass is usually dominated by the more massive left ventricle and therefore directed to the left and posteriorly. This results in a negative S wave in lead V1 and a positive R wave in lead V6. The normal transition from leads V1 to V6 is marked by a progressive increase in R wave amplitude and a simultaneous decrease in S wave amplitude. QRS duration is usually 100 ms or less. Ventricular repolarization usually proceeds in the reverse direction to depolarization, i.e. apex to base and epicardium to endocardium, producing a deflection of similar polarity called the T wave. See Fig. 12.1 and Box 12.1.

PR interval. The PR interval (Fig. 12.1 and Box 12.1) is measured from the start of the P wave to the start of the QRS complex. It is the time taken for electrical activity beginning in the sinus node to pass through to the ventricles.

Box 12.1 Normal ECG intervals

P wave duration 120 ms or less
PR interval 120–200 ms
QRS duration 100 ms or less
Corrected QT interval 440 ms or less in males
  460 ms or less in females

Electrophysiology study (EPS)

This is an invasive test used to detect suspected arrhythmias when the above techniques are equivocal. Electrode catheters are advanced, usually from the femoral veins, and placed at specific locations within the heart under fluoroscopic guidance. Intracardiac electrograms from each location are recorded and displayed simultaneously on a monitor, together with the surface ECG. Each electrode catheter can also be used to pace the heart from different locations. This permits the analysis of the electrical activation of the heart during both sinus rhythm and a tachyarrhythmia.

Table 12.1 The basic electrophysiology study

Action Measurements Note
Sinus rhythm Basic intervals (PA, AH, His duration, HV, QRS and corrected QT) Is there pre-excitation or evidence for slowed conduction?
Single ventricular extra-stimulus testing Retrograde AV node effective refractory period (AVNERP) Is there VA conduction? If so, is it via the AV node and decremental, or an accessory pathway?
Incremental ventricular pacing Retrograde Wenckebach cycle length (WCL)
Single atrial extra-stimulus testing Anterograde AVNERP Is there AV conduction? If so, is it via the AV node and decremental, or an accessory pathway? Is there evidence for dual AV node physiology?
Incremental atrial pacing Anterograde WCL
Arrhythmia induction pacing from the atrium Atrial effective refractory period (AERP)
Coupling interval(s) for arrhythmia induction
Extra-stimulus testing with 2 or more extra-stimuli, burst pacing and 2 or more premature beats during sinus rhythm
Wellen’s protocol Ventricular effective refractory period (VERP)
Coupling interval(s) for arrhythmia induction
Used to induce ventricular tachycardia. Ventricular extra-stimulus testing with up to 3 extra-stimuli

Pathophysiology of arrhythmias

Mechanisms and diagnosis of bradyarrhythmias

Sinus node-dependent arrhythmias

These include sinus bradycardia and sinus pauses with or without an escape rhythm.

Atrio-ventricular node-dependent arrhythmias

Second-degree block

This is when one or more, but not all, atrial electrical impulses fail to conduct to the ventricles. This encompasses both physiological and pathological variations in AV node conduction. The normal AV node exhibits the property of decrementation, which prevents excessive ventricular rates. Hence, increasingly premature atrial electrical impulses either are conducted to the ventricles more slowly or are blocked. This is due to the refractory properties of the AV node and is associated with changes in the PR intervals.

Wenckebach AV block (Mobitz type 1 block). This is a benign form of second-degree block in which the PR interval progressively lengthens until an atrial electrical impulse fails to conduct to the ventricles (Fig. 12.3). However, successive PR intervals change in smaller increments, producing a progressive decrease in the RR intervals. The longest RR interval during Wenckebach periodicity incorporates the non-conducted P wave. Anatomically, this usually occurs at the level of the AV node. Patients are usually just monitored. If symptomatic, give atropine 0.5 mg IV every 2 mins, maximum dose 0.04 mg/kg.

Bundle branch blocks and hemiblocks

These are due to delayed conduction within the His–Purkinje system, producing QRS complex durations > 120 ms. Causes include ischaemic heart disease, idiopathic fibrosis of the conduction system, cardiomyopathies, aortic stenosis, hypertensive heart disease, recurrent pulmonary emboli, cor pulmonale, congenital lesions, infective endocarditis and myotonic dystrophy.

Left bundle branch block (LBBB). In LBBB depolarization of the left ventricle is delayed, giving a deep QS pattern in lead V1 and tall R waves in leads 1 and V6 (Fig. 12.5). This is usually associated with heart disease and causes a reverse split of the second heart sound. In some patients with poor LV function this can result in dyssynchronous ventricular contraction that requires biventricular pacing.

Mechanisms and diagnosis of tachyarrhythmias

Atrial origin

Atrial fibrillation (AF)

AF is the commonest arrhythmia globally, with a prevalence of 0.5–1% of the general population and 5–10% of the population over 65 years. It is characterized by rapid (300–600 bpm), irregularly irregular contractions of the atria. The 12-lead ECG shows no regular atrial activity (Fig. 12.7) and the ventricles beat in an irregularly irregular fashion at rates of up to 150–200 bpm. The mechanisms underlying AF are thought to be a combination of triggering atrial ectopics usually originating within the pulmonary veins, and progressive electrical changes within the atrial myocardium (remodelling) that allow it to be sustained. AF is a consequence of a wide range of pathologies but it can exist independently in a structurally normal heart (lone AF).

Clinically, patients either are asymptomatic or complain of palpitations, breathlessness, dizziness and, less commonly, syncope. AF is a spectrum ranging from infrequent episodes (paroxysmal), to those requiring termination with drugs or DC cardioversion (persistent), to permanent AF.

Management of AF consists of either restoring rate and rhythm or, if this is not possible in the long term, controlling rate and preventing complications.

Chronic AF

Atrio-ventricular junction origin

Atrio-ventricular node re-entry tachycardia (AVNRT)

This is one of the commonest causes of a paroxysmal supraventricular tachycardia, occurring in up to 60% of cases. It is more frequently found in females and most patients have structurally normal hearts.

Accessory pathway-dependent tachycardias

Accessory pathways (APs) are myocardial bundles that electrically couple the atria and ventricles, at one or several points across the AV junction, in addition to the AV node and His–Purkinje system. Most APs do not exhibit decremental conduction and are therefore able to conduct rapidly between atria and ventricles. APs may conduct both antegradely and retrogradely, or only retrogradely. The former are seen in the Wolff–Parkinson–White syndrome and the latter are known as concealed APs. A rare form of AP is the atrio-fascicular or Mahaim connection between the right atrium and the right bundle branch. These APs usually conduct in the antegrade direction only and exhibit decrementation.

Wolff–Parkinson–White syndrome (WPW) has a prevalence of 0.1–0.4% and typically presents during infancy or in the second and third decades. Antegrade conduction via the AP causes ventricular pre-excitation, characterized by a PR interval of < 0.12 secs and a slurred initiation to the QRS complex called a delta wave (Fig. 12.9). During sinus rhythm, the extent of pre-excitation is determined by the relative conductions through the AP and the AV node–His–Purkinje system. AP conductivity and location, as well as the effects of autonomic tone on AV nodal conduction, are significant factors. Several detailed ECG algorithms have been devised for identifying AP location. Orthodromic AV re-entry tachycardia (AVRT) is seen in 84% of cases of WPW, AF in 51%, antidromic AVRT in 10% and ventricular fibrillation in less than 1%.

Orthodromic AVRT is usually initiated by a premature ventricular or atrial beat establishing the macro re-entry circuit shown in Fig. 12.10a. The 12-lead ECG shows regular, narrow QRS complexes with retrograde P waves (Fig. 12.10b). However, functional delay in one of the bundle branches can produce broad QRS complexes. Orthodromic AVRT usually terminates with block in the AV node, although any limb of the circuit may be responsible. This is also the re-entry circuit seen with concealed AP tachycardias.
Antidromic AVRT has a re-entry circuit that is the reverse of that for orthodromic AVRT (Fig. 12.11a). The ventricles are fully pre-excited and the 12-lead ECG demonstrates regular, broad QRS complexes similar to those in ventricular tachycardia (Fig. 12.11b). Antidromic AVRT usually terminates with block in the AV node. Atrio-fascicular or Mahaim APs produce a characteristic antidromic AVRT with LBBB morphology and left axis deviation.

All patients with symptomatic WPW should be assessed for curative catheter ablation of the AP. This can be performed safely and has a success rate of 95%.

Ventricular origin

Ventricular tachycardia (VT)

This tachyarrhythmia originates from the ventricles and is usually a broad-complex tachycardia (QRS > 140 msec) with rates between 150 and 200 bpm, which can cause haemodynamic compromise. In monomorphic VT the QRS complexes are identical, whereas they vary in polymorphic VT. There is frequently underlying heart disease, most commonly ischaemic heart disease with previous myocardial infarction. Other pathologies include cardiomyopathies, ion channel disorders and congenital heart disease. Rarely, VT occurs in structurally normal hearts.

Typical symptoms of VT include palpitations, chest pain, dizziness, syncope and breathlessness. In some patients the presentation is with sudden death.

Table 12.3 ECG features distinguishing ventricular tachycardia from supraventricular tachycardia with aberrant conduction

ECG criterion VT SVT with aberrant conduction
AV relationship Usually dissociated Usually associated
Capture and fusion beats Present Absent
QRS duration > 140 msec with RBBB morphology
> 160 msec with LBBB morphology
≤ 140 msec
≤ 160 msec
Mean frontal plane axis −90 to ±180° Similar to sinus rhythm
QRS transition across chest leads Usually positive or negative concordance, i.e. no transition Similar to sinus rhythm

LBBB/RBBB, left/right bundle branch block.

image

Fig. 12.15 Adult tachycardia algorithm (with pulse).

(Reproduced with permission from the Resuscitation Council (http://www.resus.org.uk/siteindex.htm.)

The only treatments to improve prognosis are β-blockers and ICDs. N.B. In patients with LV impairment, flecainide and propafenone increase mortality and should not be used.

Ventricular fibrillation (VF)

This is a cardiac arrest rhythm requiring immediate electrical defibrillation. There are advanced life support treatment algorithms that should be applied (p. 705). The underlying causes are similar to those of VT; the commonest is ischaemic heart disease with previous or acute myocardial infarction. The ECG shows disorganized electrical activity (Fig. 12.16) that is usually sustained. Unless there is an obvious reversible cause, such as acute myocardial ischaemia, all patients require ICD implantation.

Sudden cardiac death

Sudden cardiac death (SCD) is defined as a sudden collapse within the first hour after onset of symptoms. The majority of patients become unconscious within seconds to minutes. This is sometimes preceded by chest pains, palpitations, breathlessness or generalized weakness.

In the USA, the incidence of SCD is 0.1–0.2% per year and SCD is responsible for 300 000 deaths annually. Around 50% of the 700 000 deaths per year from coronary heart disease are due to SCD (American Heart Association 2003, Heart and Stroke Statistical Update).

Ion channel disorders

Long QT syndrome (LQTS)

This is another cause of potentially lethal ventricular arrhythmias in structurally normal hearts and presents with sudden death or syncope. It is characterized by prolongation of the QT interval > 440 msec due to abnormal myocardial repolarization. The underlying causes may be ion channel mutations, certain drugs and electrolyte disturbances. The prevalence is around 1 in 4000, although it is probably under-diagnosed.

Two major forms of inherited LQTS have been described. They are the Romano–Ward and Jervell–Lange–Nielson (JLN) syndromes, which have ion channel mutations. These mutations affect currents generated by sodium or potassium ions. QT prolongation is the result of overloading cells with positive ions during repolarization. They each cause variations in T wave morphology. Some have a normal corrected QT interval (15%) but QT interval prolongation during exercise testing at faster heart rates. Ventricular arrhythmias are usually caused by adrenergic stimuli such as exercise, emotion and loud noises.

The classical VT in LQTS is torsades de pointes. This is a polymorphic VT in which the amplitude of the QRS complexes constantly changes around the isoelectric line (Fig. 12.17). This causes palpitations or syncope. Most episodes are self-terminating but SCD results from degeneration into VF.

Device therapy

Pacing

Pacemakers are commonly used in the treatment of symptomatic bradycardias. Symptoms include syncope, dizziness, breathlessness and reduced exercise capacity. Pacemakers can be either temporary or permanent systems. All pacing systems usually consist of a transvenous endocardial pacing wire and a pacing generator.

Table 12.5 International pacemaker nomenclature

I Chamber paced II Chamber sensed III Response to sensing
O: None O: None O: None
A: Atrium A: Atrium T: Triggered
V: Ventricle V: Ventricle I: Inhibited
D: Dual (A and V) D: Dual (A and V) D: Dual (T and I)

DDD and VVI are most commonly used.