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Cardiac care 3: ECG interpretation - ventricular arrhythmias

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Brendan Docherty, MSc, RN, PGCE; Martina Douglas, BSc (Hons), RN, DMS.

Brendan-Clinical Manager - Cardiology and Critical Care, Queen Elizabeth Hospital NHS Trust, London, and Honorary Fellow, Healthcare Research Unit, City University, London; Martina-Senior Sister, Practice Development, Coronary Care Unit/Cardiology Ward 12, Queen Elizabeth Hospital NHS Trust, London


This is the third of a three-part cardiac care series comprising: - February 2003: Interpretation of electrocardiogram rhythm strips. - March 2003: Atrial arrhythmias. - April 2003: Ventricular arrhythmias

A ventricular ectopic (Figure 1), often called a premature ventricular contraction (PVC), arises from an ectopic focus from within the ventricles. It initiates abnormal depolarisation and delayed conduction through the ventricles. Therefore the QRS complex is prolonged and looks bizarre. Ventricular ectopics have two major characteristics:

- They are premature and occur before the next normal beat is expected. There is also a compensatory pause to help regain autorhythmicity

- They are aberrant in appearance. The QRS complex is abnormally wide (greater than 0.12 seconds - three small squares of ECG paper) and the T wave and QRS complexes are discordant - that is, point in opposite directions.

The wide complex (termed intra-ventricular delay) is caused by depolarisation across the ventricle walls, which increase the time it takes for contraction to occur, as opposed to the normal HIS-Purkinje mechanism (Goldberger 1999).

It is the frequency of ventricular ectopics in each minute with which practitioners should be most concerned: 6-10 PVCs should cause concern and investigation into the cause of the ventricular activity (Paul and Hebra, 1998). Three or more PVCs in a row are by definition ventricular tachycardia (Hand, 2002), although an isolated short burst of three to five PVCs is often referred to as a salvo of ventricular tachycardia and is indicative of an unstable myocardium.

A ventricular ectopic is always followed by a compensatory pause that is usually longer than that following an atrial ectopic. Frequent ventricular ectopics can be associated with excessive caffeine intake and the effects on the heart of many drugs, including epinephrine (adrenaline) and aminophylline (BMA and RPSGB, 2002). They may also be attributed to digoxin toxicity or electrolyte imbalance - specifically hypokalaemia and hypomagnesaemia (Paul and Hebra, 1998). Any underlying pathology needs to be fully investigated.

A patient may experience PVCs that are increasing in frequency, in the following manner:

- Salvos or increased frequency of ectopic activity

- Bigemeny, which is when every second beat is an ectopic beat

- R on T ventricular ectopics - when the R wave of the ventricular ectopic occurs on the T wave (repolarisation period of the cardiac cycle) of the preceding beat.

Such a patient may experience transient hypotension that can then lead to pulmonary congestion and chest pain; and may be more likely to have a ventricular arrhythmia leading to cardiac arrest (RCUK, 2000; Docherty, 2002).

Anti-arrhythmic drug treatment for the suppression of frequent ventricular ectopics or even short runs of VT/salvos has not been shown to improve survival (Goldberger, 1999). Apart from the obvious correction of electrolyte disturbances (potassium and magnesium) for patients with compromising palpitations (RCUK, 2000), beta-blocker therapy is sometimes used in patients with coronary artery disease and certain types of cardiomyopathy (Goldberger, 1999).

Ventricular tachycardia

Ventricular tachycardia (VT) is present when more than three ventricular ectopics occur in a row at a rate of 120-250 beats per minute (bpm) (Goldberger, 1999). It is also sometimes termed broad complex tachycardia (RCUK, 2000). The QRS complexes are wide and bizarre during VT and similar to those of ventricular ectopics.

There are three types of VT:

- A VT with the same ectopic focus (that is, all complexes look the same), called monomorphic VT (Figure 2)

- A VT in which the ectopic focus changes frequently (that is, the complexes all look different), called polymorphic VT (Figure 3) (Docherty and Roe, 2001). An example of this is torsade de pointes

- A monomorphic VT with a rate greater that 200 in which the complexes take on a saw-toothed appearance. This can be called ventricular flutter, but is synonymous with VT. Sustained VT is usually a life-threatening arrhythmia for two major reasons:

- Most patients are not able to maintain an adequate blood pressure due to both the very rapid ventricular rate causing reduced ventricular filling time and aberrant conduction across the ventricle walls causing inadequate ventricular emptying

- The condition may degenerate into ventricular fibrillation, causing immediate cardiac arrest (Hand, 2002).

Despite pharmacological treatment with anti-arrhythmic agents some patients are at high risk of life-threatening recurrences (Goldberger, 1999). For these patients insertion of an implantable cardioverter defibrillator (ICD) is required. This has been developed to deliver an electric shock directly to the heart during a life-threatening tachycardia, which has been demonstrated to be clinically effective and to have improved the quality of life for this patient group (NZHTA, 1997).

Atrioventricular arrhythmias

First-degree block

First-degree atrioventricular heart block (Figure 4) is recognised by a prolonged PR interval that is greater than 0.20 seconds (five small squares of ECG paper) and is constant (Goldberger, 1999). A prolonged PR interval does not produce symptoms or significant change in cardiac function (Goldberger, 1999). However, in the acute setting following an acute myocardial infarction (AMI) atrioventricular blocks are often temporary and resolve as the ischaemia resolves or reperfusion becomes more effective (Hand, 2002).

Digoxin can produce any degree of heart block; other drugs such as amidarone, beta-blockers and calcium channel blockers can also depress AV conduction (Goldberger, 1999). PR interval prolongation is also seen as a normal variant and does not require any intervention except to monitor for deterioration and haemodynamic instability (Goldberger, 1999).

Second-degree block

Second-degree atrioventricular block Mobitz Type I - often called the Wenchebach phenomena - (Figure 5) is characterised by a progressively prolonging PR interval (that is, worsening ischaemia from beat to beat) until an impulse is blocked from reaching the ventricles - that is, it appears that a beat is dropped or lost (Paul and Hebra, 1998). The blocked beat is followed by a relative recovery and temporary resolution of ischaemia and the whole cycle starts again. Common causes of this block are ischaemic heart disease and drugs such as digitalis, beta-blockers and calcium channel blockers; it is also common in acute inferior MI (Hand, 2002). It is usually transient and generally does not require treatment except observation as it can occasionally progress to complete block (Paul and Hebra, 1998).

Mobitz Type II atrioventricular block (Figure 6) is altogether more serious (Goldberger, 1999). It is characterised by a sudden non-conducted P wave without the prolongation of the PR interval. Mobitz Type II is generally the sign of severe conduction problems involving both the atrioventricular pathway and the HIS-Purkinje system (Goldberger, 1999). This type of block generally progresses to complete block and it is usually considered an indication for insertion of a permanent pacemaker due to the associated higher mortality rate should the arrhythmia persist (Paul and Hebra, 1998). The prophylactic insertion of a temporary pacing wire into the right ventricle is indicated during AMI resolution to maintain haemodynamic stability in the acute setting, unless staff have access to transcutaneous temporary pacing, which is preferable after thrombolysis to prevent excessive bleeding and myocardial irritability (RCUK, 2000). In most cases of acute onset related to AMI the patient will experience dizziness or light-headedness due to a reduced cardiac output related to the low ventricular rate Hypotension may then cause pulmonary congestion, hypoxaemia and chest pain (Docherty, 2002).

Third-degree block

Third-degree atrioventricular block (Figure 7) is also described as complete heart block because the atrioventricular junction conducts no impulses from the atria to the ventricles. Instead, they are contracting independently (Paul and Hebra, 1998; Docherty and Roe, 2001). The atria are generally still paced by the SA node but the ventricles are paced by an escape myocardial pacemaker located somewhere in the ventricles with a rate of 50 beats or fewer; or by the atrioventricular node at a rate of around 30bpm (Docherty and Roe, 2001). Therefore the ECG will show a regular atrial rate with regular P waves usually faster than the ventricular rate; it will have a slower ventricular rate, which is usually fixed and the P waves bear no relation to the QRS complexes (Paul and Hebra, 1998). Complete heart block most commonly occurs in elderly people who have chronic degenerative changes or are acutely ill post-MI (Goldberger 1999).

Complete heart block in an acute setting is a life-threatening arrhythmia and requires insertion of a temporary pacing wire. For those settings where image scanning is not possible for emergency wire insertion, or where operators are inexperienced, a Swan-Ganz flotation wire can make the process of wire insertion easier and more successful. This involves insertion of a wire into the central venous system. A balloon is inflated at the end of the wire that carries the pacemaker into the right ventricle with the blood flow. Following this, a permanent pacemaker is usually inserted (Hand, 2002).


For those patients cared for in general ward environments who experience these arrhythmias, a full physical assessment, blood analysis and 12-lead ECG should be conducted, followed by a safe transfer to a monitoring area equipped to deal with serious arrhythmias (Docherty, 2002).

Caring for patients with serious arrhythmias can take place in a coronary care unit (CCU), intensive care, accident and emergency and in ward settings with designated monitored beds. Most trusts will have a designated CCU with skilled nursing and medical staff to care for a large array of cardiac conditions. However, these designated beds often have high occupancy and therefore only complex cardiac cases will receive care in this area, emphasising the need to strengthen ward-based cardiac skills.

In ward settings, staff must ensure that the appropriate training and technology is available to support them as the lower risk patients often do not require additional staff to care for them (Thompson, 1997) but do require the staff to be more vigilant. Ward-based staff must ensure that they are familiar with monitoring devices, the alarm mechanism and basic ECG interpretation as outlined in this three-part series. 

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