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Cardiac care: 2. Electrocardiogram interpretation - atrial 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 second of a three-part cardiac care series comprising: - February 2003: Interpretation of electrocardiogram rhythm strips. - March 2003: Atrial arrhythmias. - April 2003: Ventricular arrhythmias
 
In this paper we examine the interpretation of electrocardiograms (ECGs) in patient with atrial arrhythmias.


Sinus rhythm
Normal sinus rhythm (Figure 1) is the term used when the SA node stimulates contraction 60-100 times per minute without interruption (Goldberger, 1999). On the ECG a QRS complex in a regular rhythmic pattern follows each P wave. The SA node initiates each impulse, thus facilitating atrial depolarisation, which is followed sequentially by ventricular depolarisation.


Sinus bradycardia is defined as having a rate of less than 60 beats per minute (bpm) and can be a normal rhythm with no haemodynamic changes, especially in fit and healthy individuals (Hand, 2002).


Extreme bradycardia is a rate of less than 35bpm and will usually cause haemodynamic disturbances, including hypotension and reduced cardiac output, leading to confusional states (related to less oxygen delivery to the brain) and tissue hypoxia and may be caused by hypoxia, vagal stimulation or hypovolaemia (Goldberger, 1999).


Sinus tachycardia is defined as having a rate of more than 100bpm and may be caused by hypovolaemia, pain, anxiety and hyperthermia (Docherty and McIntyre, 2002; Hand, 2002). There is no specific treatment for sinus tachycardia. Practitioners must look at presenting physical signs and symptoms with the patient’s history and aim to find the cause of the problem before instigating therapeutic remedies. Patients who are in pain or anxious may also present initially with hypertension (similar to a flight-or-fight response) (Docherty, 2002).

Atrial ectopics
Premature atrial ectopics/contractions (see Figure 2) occur when an ectopic focus within the atria fires before the next sinus node impulse is expected. If the AV node has repolarised, this impulse is able to conduct through the AV node in the normal fashion (Paul and Hebra 1998).


Atrial ectopics have the following features:


- Atrial depolarisation is premature, occurring before the next normal P wave is due. After the ectopic a slight pause generally occurs before the next normal sinus beat to regain rhythmicity (Figure 2)


- The QRS complex of the ectopic is often preceded by a visible P wave that usually has a slightly different morphology/shape and/or different PR interval (see Figure 2)


- The QRS complex of the ectopic is usually identical or very similar to the QRS complex of the preceding beats. Remember that, with atrial ectopics, the abnormality lies within the atria but the ventricles are usually depolarised in the normal way (see Figure 2).


Atrial ectopics are very common (Docherty and Roe, 2001). They may occur with a normal heart or virtually any type of organic heart disease. The presence of atrial ectopics does not imply that an individual has cardiac disease. They may be seen in times of stress, hyperthyroidism or excessive caffeine intake and may produce palpitations (Jowett and Thompson, 1996). Frequent ectopics may herald the onset of atrial fibrillation, but generally they are benign (Goldberger, 1999).


Atrial fibrillation
Atrial fibrillation (AF) is one of the most commonly seen arrhythmias (see Figure 3) and is common in the elderly population as their ‘normal’ heart rhythm. It is often chronic with no clinical significance (Docherty and Roe, 2001).


The atria are depolarised at a very rapid rate, up to 600bpm. This fibrillation produces a characteristically irregular wavy pattern in place of the normal P waves. If every stimulus penetrated the AV junction the ventricles would beat at a rate of up to 600bpm. Fortunately the AV junction is refractory to most of these impulses and allows only a fraction to reach the ventricles (Palazzo and Prinkley-Briggs, 1999). Consequently the ventricular rate is haphazardly irregular but usually between 120 and 140bpm (Goldberger, 1999). AF has two characteristics:


- An irregular wavy baseline produced by the rapid fibrillation waves


- A ventricular rate that is usually quite irregular with differing R-R intervals (see Figure 3).


Haemodynamically the most significant effect of AF is decreased cardiac output due to irregularly fast (and therefore inadequate) ventricular emptying and reduced filling times; and, less significantly, the loss of atrial contraction (Docherty and Roe, 2001). This would be apparent in the patient demonstrating the haemodynamic symptoms of a fast and irregular thready pulse, a reduced systolic blood pressure (BP) and poor fluid movement related to reduced left ventricular emptying resulting in breathlessness, reduced oxygen saturations and possibly pulmonary oedema (Docherty, 2002).


Most of the blood flow to the ventricles is passive due to the pull pressure created during ventricular repolarisation (Tortora and Grabowski, 2001). Thromboembolism (for example pulmonary embolism, stroke or myocardial infarction) is also a serious threat in AF (Palazzo and Prinkley-Briggs, 1999) and should always be considered in these patients.


AF can be treated pharmacologically with beta-blockers, calcium channel blockers, electrolyte correction or, more commonly, amiodarone or digoxin (BMA and RPSGB, 2002). Alternatively, a new onset of AF (that is, after less than 48 hours) can be treated by synchronised cardioversion for those patients who fail to respond to initial drug therapy or who are seriously compromised - with a rate greater than 140bpm, systolic BP less than 90mmHg, chest pain or heart failure (RCUK, 2000) regardless of anticoagulation status (Prystowsky, 2000a). AF present for more than 48 hours should be treated with anticoagulates and conventional pharmacological methods (Prystowsky, 2000a; RCUK, 2000).


Atrial flutter
Atrial flutter (see Figure 4) is an arrhythmia with rapid atrial activity in which some impulses are blocked at the AV node. The waveforms that are produced as a result of flutter are identical and regular and have the appearance of being saw-toothed (Paul and Hebra, 1998).


The atrial flutter is very regular but not all of the impulses pass through to the ventricles. Most commonly the ventricular rate is:


- 150 beats per minutes: 1:1 flutter


- 100 beats per minutes: 2:1 flutter


- 75 beats per minutes: 3:1 flutter (Paul and Hebra 1998).


A combination of these on one rhythm strip would be described as variable block. Atrial flutter is rarely seen in people with normal hearts (Goldberger, 1999). It is not specific to any particular type of heart disease but can occur in patients with valvular heart disease, acute myocardial infarction (AMI), chronic ischaemic heart disease, cardiomyopathy, hypertension and lung disease (Paul and Hebra, 1998). Drug treatment includes beta-blockers, calcium channel blockers and digitalis initially (BMA and RPSGB, 2002). A second drug, for example amiodarone or procainamide, can be added to try to convert the flutter. As for AF, synchronised cardioversion can be attempted if drug therapy is unsuccessful, but atrial flutter is less likely to cause cardiorespiratory compromise due to its slower and more regular nature (Docherty and Roe, 2001). Fortunately atrial flutter responds very well to pharmacological agents and synchronised electrical cardioversion.


It is rare for the patient to have haemodynamic consequences related to atrial flutter, unless the high QRS rate is causing inadequate filling and emptying time, leading to hypotension. Breathlessness is related to reduced fluid movement in the left ventricle leading to pulmonary congestion (Docherty, 2002).


Atrial tachycardia
Atrial tachycardia (see Figure 5) occurs when an ectopic focus within the atria begins rapidly depolarising and overrides the normal pacemaker function of the SA node (Docherty and Roe, 2001). This ectopic focus usually contracts at a rate of between 150 and 250bpm. These patients should be continuously monitored in lead II as this lead gives the clearest picture of the ‘P’ wave activity (Goldberger, 1999). This arrhythmia is sometimes referred to as narrow complex tachycardia or supraventricular tachycardia (SVT) (RCUK, 2000). The patient with this arrhythmia will usually present with hypotension related to inadequate ventricular filling and emptying; breathlessness related to pulmonary congestion caused by reduced left ventricular efficiency; possible chest pain; anxiety; and disorientation due to cerebral hypoxaemia in severe cases (Docherty, 2002).


Digoxin toxicity should be suspected in any patient already receiving digoxin and if they are haemodynamically stable then withholding digoxin is usually the only treatment necessary, along with ensuring potassium and magnesium levels are monitored - two or three times a day until digoxin levels are reduced to a safe therapeutic level - and the administration of potassium chloride to maintain potassium at 4.0-4.5mmol and magnesium sulphate to maintain magnesium at 0.7-1.1mmol (Paul and Hebra, 1998; Docherty 2002). In patients not receiving digoxin then anti-arrhythmic agents may be added, including digoxin or amiodarone to maintain decreased AV nodal conduction (Paul and Hebra, 1998). Synchronised cardioversion can also be used if the patient becomes compromised (RCUK, 2000) but is contraindicated in patients with digoxin toxicity (Paul and Hebra, 1998).

Emergency cardioversion
For those patients with atrial or ventricular tachyarrhythmias who are compromised with a systolic BP of less than 90mmHg, chest pain, heart failure and reduced consciousness, the following should be undertaken:


- If possible and time allows, conduct a physical assessment including 12-lead ECG, potassium and magnesium levels, coagulation status, blood sugar level if diabetic and gain consent if patient is able. Potassium should be 4-4.5 and international ratio (INR) should be greater than 2.0 if possible; if INR is not greater than 2.0 then the risk of a cerebral vascular event is increased and should be identified to the patient/family if possible


- Sedate patient with light anaesthetic or sedative, usually propofol or midazolam. Even if patient appears to be unconscious, a small amount of sedation/anaesthetic should still be given


- If using a semi-automatic/hands-free defibrillator apply defibrillation self-adhesive pads to the patient in the anterior-posterior position. Alternatively, it may be easier to use the anterior-lateral position when using manual hand-held paddle machines


- Select ‘synchronise’ mode on the defibrillator machine - the R wave should be highlighted and will allow only the delivery of the electric shock on that wave (electricity delivered in the repolarisation period - T wave - may cause ventricular fibrillation cardiac arrest)


- Select energy value starting at 100kJ, and progressively increasing to 200kJ and 360kJ if unsuccessful. Begin ECG rhythm strip recording - if possible - to give a documented print out of the event


- When cardioverting, hold the deliver buttons down until the machine delivers energy selected as there is sometimes a pause while the machine awaits a highlighted R wave to deliver the shock


- Check pulse, BP, oxygen saturation and sedation level between each shock, allowing for a minute between each shock to assess the rhythm and cardiorespiratory status. Continue to oxygenate patient


- If successful, care for the sedated patient as required, being vigilant with the airway and positioning and undertake a 12-lead ECG and a full physical assessment. Consider anti-arrhythmic therapy and electrolytes to stabilise myocardium whether or not the cardioversion has been successful (Prystowsky, 2000b; RCUK, 2000; Docherty, 2002).



British Medical Association and Royal Pharmaceutical Society of Great Britain. (2002) British National Formulary (No.44). London: BMA and RPSGB. Available at: www.bnf.org


Docherty, B., Roe, J. (2001) Cardiac arrhythmias: recognition and care. Professional Nurse 16: 11, 1492-1496.


Docherty, B., McIntyre, L. (2002) Nursing considerations for fluid management in hypovolaemia. Professional Nurse 17: 9, 545-549.


Docherty, B. (2002) Cardiorespiratory physical assessment for the acutely ill: part 1. British Journal of Nursing 11: 11, 750-758.


Goldberger, A. (1999) Clinical Electrocardiography: A simplified approach (6th edn). St Louis, Mo: Mosby.


Hand, H. (2002) Common cardiac arrhythmias. Emergency Nurse 10: 3, 29-38.


Jowett, N.I., Thompson, D.R. (1996) Comprehensive Coronary Care (2nd edn). London: RCN and Bailliere Tindall.


Palazzo, M., Prinkley-Briggs, L. (1999) Atrial fibrillation: managing the most common sustained arrhythmia. American Journal of Nursing 99: 5 (supp), 2-7.


Paul, S., Hebra, J.D. (1998) The Nurse’s Guide to Cardiac Rhythm Interpretation: Implications for patient care. Philadelphia, Pa: W.B. Saunders.


Prystowsky, N. (2000a) Management of atrial fibrillation: therapeutic options and clinical decisions. American Journal of Cardiology 85: 10A.


Prystowsky, N. (2000b) Cardioversion of atrial fibrillation to sinus rhythm: who, when, how and why? American Journal of Cardiology 86: 1, 326-350.


Resuscitation Council (UK). (2000) Advanced Life Support Provider Manual (4th edn). London: RCUK. Available at www.resus.org.uk


Resuscitation Council (UK). (2001) CPR Guidance for Clinical Practice and Training in Hospitals. London: RCUK. Available at www.resus.org.uk


Tortora, G.J., Grabowski, S.R. (2001) Principles of Human Anatomy (9th edn). Chichester: John Wiley & Sons.
 
In this paper we examine the interpretation of electrocardiograms (ECGs) in patient with atrial arrhythmias.


Sinus rhythm
Normal sinus rhythm (Figure 1) is the term used when the SA node stimulates contraction 60-100 times per minute without interruption (Goldberger, 1999). On the ECG a QRS complex in a regular rhythmic pattern follows each P wave. The SA node initiates each impulse, thus facilitating atrial depolarisation, which is followed sequentially by ventricular depolarisation.


Sinus bradycardia is defined as having a rate of less than 60 beats per minute (bpm) and can be a normal rhythm with no haemodynamic changes, especially in fit and healthy individuals (Hand, 2002).


Extreme bradycardia is a rate of less than 35bpm and will usually cause haemodynamic disturbances, including hypotension and reduced cardiac output, leading to confusional states (related to less oxygen delivery to the brain) and tissue hypoxia and may be caused by hypoxia, vagal stimulation or hypovolaemia (Goldberger, 1999).


Sinus tachycardia is defined as having a rate of more than 100bpm and may be caused by hypovolaemia, pain, anxiety and hyperthermia (Docherty and McIntyre, 2002; Hand, 2002). There is no specific treatment for sinus tachycardia. Practitioners must look at presenting physical signs and symptoms with the patient’s history and aim to find the cause of the problem before instigating therapeutic remedies. Patients who are in pain or anxious may also present initially with hypertension (similar to a flight-or-fight response) (Docherty, 2002).

Atrial ectopics
Premature atrial ectopics/contractions (see Figure 2) occur when an ectopic focus within the atria fires before the next sinus node impulse is expected. If the AV node has repolarised, this impulse is able to conduct through the AV node in the normal fashion (Paul and Hebra 1998).


Atrial ectopics have the following features:


- Atrial depolarisation is premature, occurring before the next normal P wave is due. After the ectopic a slight pause generally occurs before the next normal sinus beat to regain rhythmicity (Figure 2)


- The QRS complex of the ectopic is often preceded by a visible P wave that usually has a slightly different morphology/shape and/or different PR interval (see Figure 2)


- The QRS complex of the ectopic is usually identical or very similar to the QRS complex of the preceding beats. Remember that, with atrial ectopics, the abnormality lies within the atria but the ventricles are usually depolarised in the normal way (see Figure 2).


Atrial ectopics are very common (Docherty and Roe, 2001). They may occur with a normal heart or virtually any type of organic heart disease. The presence of atrial ectopics does not imply that an individual has cardiac disease. They may be seen in times of stress, hyperthyroidism or excessive caffeine intake and may produce palpitations (Jowett and Thompson, 1996). Frequent ectopics may herald the onset of atrial fibrillation, but generally they are benign (Goldberger, 1999).


Atrial fibrillation
Atrial fibrillation (AF) is one of the most commonly seen arrhythmias (see Figure 3) and is common in the elderly population as their ‘normal’ heart rhythm. It is often chronic with no clinical significance (Docherty and Roe, 2001).


The atria are depolarised at a very rapid rate, up to 600bpm. This fibrillation produces a characteristically irregular wavy pattern in place of the normal P waves. If every stimulus penetrated the AV junction the ventricles would beat at a rate of up to 600bpm. Fortunately the AV junction is refractory to most of these impulses and allows only a fraction to reach the ventricles (Palazzo and Prinkley-Briggs, 1999). Consequently the ventricular rate is haphazardly irregular but usually between 120 and 140bpm (Goldberger, 1999). AF has two characteristics:


- An irregular wavy baseline produced by the rapid fibrillation waves


- A ventricular rate that is usually quite irregular with differing R-R intervals (see Figure 3).


Haemodynamically the most significant effect of AF is decreased cardiac output due to irregularly fast (and therefore inadequate) ventricular emptying and reduced filling times; and, less significantly, the loss of atrial contraction (Docherty and Roe, 2001). This would be apparent in the patient demonstrating the haemodynamic symptoms of a fast and irregular thready pulse, a reduced systolic blood pressure (BP) and poor fluid movement related to reduced left ventricular emptying resulting in breathlessness, reduced oxygen saturations and possibly pulmonary oedema (Docherty, 2002).


Most of the blood flow to the ventricles is passive due to the pull pressure created during ventricular repolarisation (Tortora and Grabowski, 2001). Thromboembolism (for example pulmonary embolism, stroke or myocardial infarction) is also a serious threat in AF (Palazzo and Prinkley-Briggs, 1999) and should always be considered in these patients.


AF can be treated pharmacologically with beta-blockers, calcium channel blockers, electrolyte correction or, more commonly, amiodarone or digoxin (BMA and RPSGB, 2002). Alternatively, a new onset of AF (that is, after less than 48 hours) can be treated by synchronised cardioversion for those patients who fail to respond to initial drug therapy or who are seriously compromised - with a rate greater than 140bpm, systolic BP less than 90mmHg, chest pain or heart failure (RCUK, 2000) regardless of anticoagulation status (Prystowsky, 2000a). AF present for more than 48 hours should be treated with anticoagulates and conventional pharmacological methods (Prystowsky, 2000a; RCUK, 2000).


Atrial flutter
Atrial flutter (see Figure 4) is an arrhythmia with rapid atrial activity in which some impulses are blocked at the AV node. The waveforms that are produced as a result of flutter are identical and regular and have the appearance of being saw-toothed (Paul and Hebra, 1998).


The atrial flutter is very regular but not all of the impulses pass through to the ventricles. Most commonly the ventricular rate is:


- 150 beats per minutes: 1:1 flutter


- 100 beats per minutes: 2:1 flutter


- 75 beats per minutes: 3:1 flutter (Paul and Hebra 1998).


A combination of these on one rhythm strip would be described as variable block. Atrial flutter is rarely seen in people with normal hearts (Goldberger, 1999). It is not specific to any particular type of heart disease but can occur in patients with valvular heart disease, acute myocardial infarction (AMI), chronic ischaemic heart disease, cardiomyopathy, hypertension and lung disease (Paul and Hebra, 1998). Drug treatment includes beta-blockers, calcium channel blockers and digitalis initially (BMA and RPSGB, 2002). A second drug, for example amiodarone or procainamide, can be added to try to convert the flutter. As for AF, synchronised cardioversion can be attempted if drug therapy is unsuccessful, but atrial flutter is less likely to cause cardiorespiratory compromise due to its slower and more regular nature (Docherty and Roe, 2001). Fortunately atrial flutter responds very well to pharmacological agents and synchronised electrical cardioversion.


It is rare for the patient to have haemodynamic consequences related to atrial flutter, unless the high QRS rate is causing inadequate filling and emptying time, leading to hypotension. Breathlessness is related to reduced fluid movement in the left ventricle leading to pulmonary congestion (Docherty, 2002).


Atrial tachycardia
Atrial tachycardia (see Figure 5) occurs when an ectopic focus within the atria begins rapidly depolarising and overrides the normal pacemaker function of the SA node (Docherty and Roe, 2001). This ectopic focus usually contracts at a rate of between 150 and 250bpm. These patients should be continuously monitored in lead II as this lead gives the clearest picture of the ‘P’ wave activity (Goldberger, 1999). This arrhythmia is sometimes referred to as narrow complex tachycardia or supraventricular tachycardia (SVT) (RCUK, 2000). The patient with this arrhythmia will usually present with hypotension related to inadequate ventricular filling and emptying; breathlessness related to pulmonary congestion c
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