In the absence of any abnormal investigations, the most likely diagnosis is vasovagal syncope (see Table 15.8, Features of fits and faints). You should be aware of some other specific forms of vasovagal syndrome:

• Carotid sinus syncope: on turning head or shaving the chin. Due to carotid sinus hypersensitivity, usually in the elderly.

• Cough syncope: after a paroxysm of coughing, usually in a patient with obstructive airways disease.

• Micturation syncope: more common in men. Usually occurs in the night when going to pass urine or during micturation itself.

What is the differential diagnosis?

There are many other causes of syncope and all might need to be excluded.

• Cardiac:

• Arrhythmia: associated with either profound bradycardia or tachycardia. Symptomatic palpitations can be a pointer but are often not present.

• Structural: e.g. outflow obstruction (notably aortic stenosis or hypertrophic cardiomyopathy), ischaemia, tamponade, pulmonary embolism.

• Neurological: seizures, cerebrovascular disease (TIA, CVA or vertebrobasilar ischaemia) are the most common causes. A good eye-witness account is key to the diagnosis. Note: Some jerky movements of the limbs, and even incontinence, can occur in a prolonged vasovagal attack, especially if the patient remains upright.

• Metabolic:

• Hypoglycaemia: well known in diabetics. Spontaneous hypoglycaemia from an insulinoma is a rare cause

• Hypoxaemia

• Drugs/alcohol.

• Hyperventilation/anxiety (if suspected, symptoms can often be readily reproduced by voluntary hyperventilation): usually associated with a tachycardia. The patient often has symptomatic palpitations and might feel light-headed, a feeling of being distanced from the surroundings, chest pain and/or paraesthesiae with numbness in arms, hands or lips. Pallor and peripheral cyanosis can be striking in a full-blown attack. Circumstances provoking an attack can often be the same as for a faint (e.g. warm room, stressful situation).

• Orthostatic hypotension: especially in elderly patients. This is often caused by drugs, e.g. for hypertension, but don’t forget autonomic neuropathy and Parkinson’s disease.

A cardiac cause of syncope should be sought in all patients with known structural heart disease.

Progress.

This man was sent home, having made a full recovery from his ‘faint’.

Case history (2)

A 68-year-old man passed out suddenly at the wheel of his car and ran into the car in front. His wife reports that he was pale and sweaty but that loss of consciousness was brief and he recovered quickly.

On examination in A&E, pulse 78/min, BP 140/85, no abnormality found on examination.

His ECG showed left bundle branch block (LBBB).

Practice points

• Sudden loss of consciousness without warning must be assumed to be a cardiac arrhythmia until proved otherwise.

• Altered consciousness when driving has important legal implications and the patient must be warned not to drive again until the diagnosis is established.

Investigation

The history of the event is the key to further investigation and blanket investigations are unrewarding without some clinical pointers as to the cause.

Generally, a single faint requires no further investigation but if there is some diagnostic doubt the symptoms can be reproduced by a tilt test. This is usually carried out with a mechanised tilt table giving a head-up tilt of 60° for 45 min, with continuous ECG and BP monitoring. Although false positive results can occur, if the prodrome before the faint reproduces the symptoms it provides strong support for the diagnosis.

This patient required further investigation as the LBBB indicates cardiac disease.

Diagnosis.

This man’s echocardiogram (echo) showed no abnormality. However, his ambulatory ECG monitoring subsequently showed periods of asymptomatic Mobitz type II second-degree heart block.

Progress.

A pacemaker was implanted and he had no further problems.

Case history (3)

JR is a 26-year-old physiotherapist. Her first episode of unconsciousness occurred when she was at a party with her medical team. A nursing colleague thought that she was pulseless at the time of the collapse; the possibility of excess alcohol was considered. On arrival in A&E at a nearby hospital she was intubated and ventilated, and kept ventilated overnight. The next day she was well and therefore discharged. She had two further similar episodes requiring overnight admission to hospital.

Investigations

A 12-lead ECG and cardiac enzymes were normal on all three admissions. She was investigated with 24- and 48-h ECG tapes, echo and CT scanning of the head but no abnormalities were found.

An electrophysiological study was therefore performed, to exclude the possibility of tachyarrhythmia. During this study she spontaneously became bradycardic and hypotensive but no arrhythmias were induced.

A tilt table test performed the following day produced profound bradycardia, hypotension and syncope on 60° head-up tilting.

Remember

In a tilt test, syncope is often accompanied by 10–20 s of asystole. This recovers as soon as the patient is returned to the flat; for this reason a doctor should always be present.

Diagnosis

Neurally mediated syndromes are due to a reflex (called Bezold–Jarisch) that may result in both bradycardia (sinus bradycardia, sinus arrest and AV block) and reflex peripheral vasodilatation. These syndromes usually present as syncope or presyncope (dizzy spells).

Treatment and progress

A DDD pacing system (see p. 278) was implanted and programmed to produce a tachycardic response to counter any detected bradycardia of sudden onset. So far she has had no more syncopal attacks.

A clinical approach to patients with tachycardia

The main reason people have difficulty assessing tachyarrhythmias is that they concentrate on the ECG changes without thinking about the patient to whom the ECG belongs.

Case history (1)

A 35-year-old man presents with a tachycardia at a rate of 180 per minute. He is not seriously compromised by his tachyarrhythmia and the BP is 128/64. The ECG shows narrow complex tachycardia.

There are three simple questions you need to ask yourself as you approach a patient with an acute tachyarrhythmia:

1. What is the heart rate? – i.e. 180 beats/min in this man

2. Has the patient collapsed?

In other words, is the patient clinically compromised by the tachycardia or not? In assessing the degree of cardiovascular collapse take the heart rate into account. Remember that the maximal heart rate you would expect a patient to achieve on the treadmill is 220 minus age.

Someone with a heart rate at this level (180 bpm) is going at the same rate you would expect if they had just hurried up several flights of stairs.

This man is not compromised by the tachycardia so it is likely that he has a good ventricle. People with heart rates substantially above their predicted maximum who tolerate the situation well are more likely to be suffering from a primary electrophysiological problem than from an arrhythmia secondary to LV disease.

3. Are the ECG complexes broad or narrow?

Divide tachycardias into broad complex (QRS complex of > 120 ms or three small squares on the standard ECG) or narrow complex, rather than try to split them into supraventricular tachycardia (SVT) and ventricular tachycardia (VT) at the first glance. If you follow this approach you will not treat VT as an SVT, which is the error to avoid.

Having answered these questions, you should decide who needs admission to hospital (Table 10.1).

Table 10.1 Patients with tachycardia: who to admit to the Medical Assessment Unit?

	Broad complex	Narrow complex
Collapsed	Usually need immediate cardioversion and must be admitted from A&E. Do not give verapamil or other negatively inotropic drugs	Usually need admission into hospital, especially if the patient is in heart failure
Did not collapse	The most difficult category to sort out	Can probably go home if tachycardia stops on treatment (Case 1)
	Probably need admission to sort out diagnosis	Need outpatient assessment
	Irregular tachycardia in this group may be due to WPW with AF, so do not give verapamil	If this is a recurrent problem they need to be referred to a cardiologist to be considered for EPS, as they may benefit from radiofrequency ablation of their pathway or their arrhythmia focus

AF, atrial fibrillation; EPS, electrophysiological studies; WPW, Wolff–Parkinson–White syndrome.

Take a 12-lead ECG of the arrhythmia: this is essential to sort VT from the SVT. It is also valuable in sorting out the mechanisms in narrow complex tachycardias; the retrograde P waves can be seen in the ST–T segments in re-entrant tachycardias, but they may be seen only in some leads. Do not be fooled into thinking you can diagnose and manage arrhythmias with rhythm strips alone.

Remember

Think about the underlying state of the ventricle.

To be safe:

• Always assume a broad complex tachycardia is VT until proved otherwise.

• If in doubt use DC cardioversion rather than drugs.

• Seek advice if your first drug does not work.

• Beware of verapamil (which should not be used as first-line therapy) and other negatively inotropic drugs.

• Check the electrolytes and correct them appropriately before using drugs, but do not delay treatment in a patient who is compromised because you are waiting for results. Remember in an emergency, K⁺ levels can be roughly measured using blood gas machines in A&E and used to guide replacement therapy.

The ECG and classification of tachycardias

Broadly speaking, tachycardias are classified as either supraventricular (SVT) or ventricular (VT) in origin.

SVT

These are narrow complex tachycardias (Fig. 10.1), unless there is bundle branch block. Adenosine is very useful for their diagnosis and will terminate some SVTs:

• Atrial tachycardia: an SVT from a focus in the atrium, rather than due to re-entry.

• Atrial flutter (Afl): look for regular rhythm, often with a rate of 150. Adenosine will help in the diagnosis, often revealing underlying flutter waves.

• Atrial fibrillation (AF): look for lack of P waves, irregular rhythm and baseline; this can be very hard to see with very fast rates, in which case adenosine will help.

• Re-entrant tachycardias:

• Wolff–Parkinson–White (WPW) is the classic example of a re-entrant tachycardia. The depolarisation wavefront ‘re-enters’ the atrium through the bundle of abnormal conducting tissue between ventricle and atrium. In some cases a bundle is present but is not visible on the resting ECG so that it is a ‘concealed pathway’. Never treat AF in WPW with digoxin or verapamil – this can lead to dangerous retrograde conduction down the accessory pathway leading to VF.

• AV nodal re-entry tachycardia (AVNRT).

Figure 10.1 Narrow complex tachycardia.

Features suggesting that a tachycardia might be an SVT

• Normal LBBB or RBBB morphology but be careful: VT from RV outflow tract with LBBB morphology can look like SVT. A small stubby R wave in V1–2 is characteristic of VT.

• You might be able to see evidence of both atrial and ventricular activity. A constant relationship between the P waves and the QRS complexes suggests a supraventricular origin.

• The frontal and horizontal QRS axes are in the same general direction as that in sinus rhythm.

• It slows with manoeuvres designed to increase vagal tone, e.g. carotid sinus massage.

• If the onset is witnessed you might see a P wave that is premature.

Diagnosis.

Narrow complex supraventricular tachycardia.

Management

This rhythm responded to adenosine (see below), 3 mg IV going up in 3-mg aliquots to a maximum of 12 mg. Intravenous beta blockade (Esmolol has a very short half-life of seconds and can be very useful) is also used. Synchronised DC cardioversion (start with 50 J) should be used if medication fails.

Case history (2)

A 57-year-old woman presents with a tachycardia at a rate of 132 per minute.

On examination she is hypotensive (90/50), looks pale and distressed and has bibasal crackles.

The 12-lead ECG shows an axis of –120° and the complexes are predominantly positive across the chest leads (regular broad complex tachycardia).

Ventricular tachycardia (VT)

This causes a broad complex regular tachycardia (Fig. 10.2), often called monomorphic VT. However, a broad complex pattern can be caused by any tachycardia if there is a pre-existing abnormality of the conduction system (usually bundle branch block). So, for example, AF with bundle branch block can cause a broad complex tachycardia that is irregular. Although adenosine (see below) can be useful for diagnostic purposes, do not waste time using it if the patient is compromised.

Figure 10.2 Broad complex tachycardia after three normal beats.

Features suggesting that a tachycardia might be a VT

• A QRS duration of > 140 ms strongly suggests a ventricular origin.

• The frontal and horizontal axes are grossly discordant with that seen in sinus rhythm. Most people are used to looking at the frontal QRS axis in the limb leads. The horizontal axis is estimated by seeing where the predominantly negative QRS complexes become equiphasic as you look across from V1 towards V6. This equiphasic point is called the zone of transition and is usually at V3 or V4. In VT there might be no transition zone or it might be far to the right, or left, of V4.

• QRS morphology: the pattern is not typical of LBBB or RBBB. These are specific appearances that strongly suggest VT, e.g. concordance; seek help if unsure.

• Fusion beats: these are beats where there is simultaneous activation of the ventricles from a focus of arrhythmia and from the atria via the AV node at the same time. These beats will look like a cross between the standard VT complex and the patient’s normal complexes in sinus rhythm.

• Capture beats: occasionally the atria ‘captures’ a normal complex in the midst of a tachycardia.

• You might be able to see evidence of both atrial and ventricular activity. If there is no constant relationship between the P waves and the QRS complexes it suggests a ventricular origin and this is called atrioventricular dissociation.

A word about torsade de pointes

Torsade de pointes is an uncommon form of VT with a characteristic ECG pattern (often called polymorphic VT (Fig. 10.3)). The complexes appear to twist around the baseline by virtue of their changes in amplitude. It is particularly associated with syndromes involving a long QT interval. Correct diagnosis of torsade de pointes is necessary because the treatment is very different from VT and treating the underlying cause can often have a marked effect.

Figure 10.3 Torsade de pointes showing the complexes twisting around the baseline.

The acute treatment of arrhythmias

Remember

Always think about the underlying state of the ventricle when treating an acute arrhythmia.

Problems with the use of any anti-arrhythmic drugs:

• Many arrhythmias arise as a result of pre-existing LV disease. You need to be aware of any drugs that you give which could further suppress LV function and make matters worse.

• A drug that is ineffective for the rhythm in question might also depress ventricular function without alleviating the rate-related stress on the ventricle.

• The final catch when you are treating arrhythmias with drugs (Fig. 10.4) is that ischaemia might alter the electrophysiological activity of drugs. This means that drugs that are anti-arrhythmic under normal circumstances become pro-arrhythmic in ischaemic myocardium.

This limits the use of drugs in many patients because it is often difficult to exclude the possibility of coexisting ischaemia. Because of these problems it is often safer to use DC cardioversion than drugs.

Figure 10.4 Drugs used to treat arrhythmias. The numbers in brackets refer to the Vaughan–Williams classification.

Remember

Both digoxin and verapamil can be dangerous in WPW; if uncertain it is safer to cardiovert.

A word on adenosine

Intravenous adenosine has revolutionised the diagnosis and management of acute tachycardias. It should be used in most SVTs and is safe because of its very short half-life. The major limitation is that is should not be used in asthmatics. It will not usually cardiovert AF or flutter but will slow the rate transiently (often for only one or two complexes – have the ECG running) and enable you to see the baseline, helping you make the diagnosis. It will cardiovert most other SVTs. Although it is safe to give adenosine to patients in VT, it will not usually cardiovert the problem, although it might slow the rate. Remember to give it as a rapid bolus, warn the patient he or she will feel terrible transiently and remember that he or she might become transiently asystolic.

Management of this patient (Case 2)

This patient has a ventricular tachycardia with severe hypotension and pulmonary oedema. She requires emergency DC cardioversion. Measure and correct any electrolyte abnormality while preparing for DC cardioversion. If in doubt, give empirical intravenous magnesium sulphate, 8 mmol over 10–15 min (it is not appropriate to give K⁺ because hypo- or hyperkalaemia can be arrhythmogenic, so you must know serum K⁺ before treating it). The arrhythmia did not settle with the DC shock, and IV amiodarone was started with a view to repeat DC cardioversion.

This patient has clinical evidence of poor LV function but in a patient who has a good LV, a beta blocker such as sotalol might be used. Finally, in patients refractory to treatment, remember the possibility of torsade de pointes, with low magnesium and potassium levels.

Progress.

This lady settled after the repeat DC cardioversion but as she is at risk of sudden death she was referred to the cardiologist for further management. She was given an implantable cardioverter defibrillator.

Atrial fibrillation

Prevalence and risks

Atrial fibrillation (AF) remains one of the most common and challenging of arrhythmias. It is estimated that 10% of the population will suffer from AF at some stage of their lives. Patients who remain in AF after their hospital admission face a long-term risk of embolism and stroke. This is reduced by the use of anti-coagulation, but long-term anti-coagulation also carries a risk. In an ideal world, all patients would be cardioverted to sinus rhythm but this might not be possible when there is underlying heart disease.

Case history (1)

A 76-year-old woman with a history of hypertension presents with a 6-week history of worsening palpitations accompanied by breathlessness.

On examination she is breathless getting undressed, she has a raised JVP, bibasal crackles, BP is 116/70 and her heart rate is 160. The ECG is compatible with atrial fibrillation (AF).

Management

This woman has AF in association with heart failure. The CXR shows evidence of pulmonary oedema. You need to treat the heart failure (e.g. diuretics, ACE inhibitors) and control her ventricular rate with digoxin. Remember that a tachycardia might be an indication of poorly controlled failure or the AF might have tipped her into heart failure. Occasionally, poor LV function is secondary to poor rate control but more commonly poor rate control is secondary to poor control of CCF. In such cases where digoxin fails to control the rate (as in this patient), use amiodarone, which will improve rate control and the chance of cardioversion.

Progress.

She was anti-coagulated and proceeded to cardioversion as an outpatient. She converted to sinus rhythm but had to continue anti-coagulation for a further 3 months.

Remember

AF alone, without evidence of heart failure, can cause breathlessness.

Case history (2)

A 70-year-old woman with a history of hypertension presented to the hospital with a history of 6 h of palpitations. She had been taking 75 mg of aspirin prescribed by her GP for 2 years. The ECG showed atrial fibrillation at a rate of 132 beats per minute. The patient looked well and had a BP of 142/78 and there was no cardiomegaly on X-ray. She was clear that the symptoms started acutely 6 h previously so anticoagulation was not required.

Management

This patient reverted to sinus rhythm in response to a single DC shock (200 J). She remained in sinus rhythm at follow-up 6 months later.

The choices facing clinicians with a patient in AF are:

Should I cardiovert?

Yes, generally DC cardioversion is always worth trying at least once, provided there are no contraindications. Cardioversion can also be achieved with drugs but do not forget there is nearly as much of a risk of a thromboembolic event as with DC cardioversion, so these patients should be appropriately anti-coagulated. Amiodarone (200 mg × 3 daily for 1 week then 200 mg maintenance per day) and class 1c drugs (e.g. flecainide) both promote cardioversion. Figure 10.4 shows the sites of action of drugs on the heart but do not use flecainide in the presence of ventricular disease.

DC conversion (using a biphasic defibrillator) reverts AF to sinus rhythm in 80% of patients. This is the best treatment for AF of less than 24 h duration (see Case history 2, above).

What precautions should I take to prevent embolism at the time of cardioversion?

The risk of cerebral embolism can be markedly reduced by anticoagulation and patients who have been in AF for more than 24 h should be adequately anti-coagulated (INR > 2) for a minimum of 3 weeks before and 4 weeks after elective cardioversion.

With a trans-oesophageal echo (TOE)-guided approach, patients do not need formal anti-coagulation prior to the cardioversion but should be covered with a full therapeutic dose of SC heparin before and during the procedure. If this is successful, they need another 4 weeks formal anti-coagulation with warfarin (or dabagatrim) post-procedure.

Remember, a patient suffering a stroke because of lack of anticoagulation in AF is negligent. A common misconception is that aspirin is as effective as warfarin, but this is not true. You need to make a careful risk–benefit analysis of the use of warfarin in elderly patients but in most of them the benefits will outweigh the risks.

Chads 2 score

How to assess the risk of thromboembolism in atrial fibrillation

What should be done to promote good rate control in the long term if cardioversion fails?

Digoxin alone is often not effective in rate control and a second drug often needs to be added – beta blockers and verapamil are usually effective. There is no good evidence that digoxin promotes conversion to sinus rhythm and it should not be used in paroxysmal atrial fibrillation. The only good way to assess rate control is with a 24-h tape.

If this strategy fails, amiodarone is an excellent second-line treatment: it helps with rate control, makes cardioversion more likely and can be used with poor LV function, but remember that it does have long-term side effects. However, it can sometimes be effectively used at a lower dose (100 mg daily), with a lower risk of side effects, especially in the elderly.

Should I give prophylactic medication to prevent AF if sinus rhythm is achieved?

This depends on numerous clinical factors; the best drug is sotalol. You should discuss this with the cardiologist.

Which patients should I refer to an electrophysiologist (EP)?

Patients without evidence of underlying heart disease and who have either failed drug therapy or do not want to take any medication (usually young patients) should be referred for EP studies with a view to a definitive EP procedure to prevent further AF. However, any patient might potentially benefit from this approach, so if in doubt discuss any case with your cardiologist.

Remember

AF becomes more stable over time, and might be less easy to cardiovert the longer you wait.

Diagnosis

• Difficulties often arise in establishing arrhythmia as a cause of dizzy spells when the condition is intermittent, as it often is in the early stages.

• 24-h ECG is the best investigation but repeat tapes might be needed to demonstrate an abnormality when the history is very suggestive. Occasionally, in a patient with persistent symptoms and no findings on repeat ambulatory ECG monitoring, an implantable ECG recording device can help.

Classification of generic pacemaker code

Notation is by the following abbreviations:

• Chamber paced (0 = none, A = atrial, V = ventricular, D = both or dual).

• Chamber sensed (0 = none, A = atrial, V = ventricular, D = both or dual).

• Response to sensing (0 = none, I = inhibited, T = triggered, D = both T + I).

• Rate response (0 = none, R = rate modulation).

• Anti-tachycardia function (0 = none, P = anti-tachycardia pacing, S = shock, D = pace and shock).

For example: VVI = ventricular pacing, ventricular sensing, inhibition of pacing when beat is sensed; DDD(R) = dual pacing, dual sensing, inhibition and triggered as appropriate when beat is sensed, rate response mode available.

Pacemakers in common use

• VVI: usually for AF with slow ventricular rate and/or pauses.

• DDD: for complete heart block.

Rate response (R) is used when a patient has lost the chronotropic response, i.e. cannot increase the heart rate with exercise/stress. The cardiologist inserting the pacemaker will decide this but will need to know the patient’s usual level of activity/independence to make this decision. AAI pacemakers are not often used in practice because a small proportion of these patients go on to develop coexisting AV nodal disease, so in anticipation of this dual-chamber pacemakers are usually implanted.

Pacemaker problems

All problems with pacemakers need to be referred to the pacing clinic; they will check the pacemaker and adjust its function as necessary. They will also refer to a cardiologist when necessary.

Surgical problems

• Infection is potentially very serious. Even slight redness around the scar should be treated promptly with antibiotics, e.g. flucloxacillin 500 mg × 3 daily; if relevant, send swabs first. Usually occurs early after implantation.

• Haematoma can predispose to infection or technical problems.

Technical problems

• Fibrosis occurring around the pacemaker tip: this can cause pacemaker thresholds to rise, which can affect pacemaker function.

• Lead displacement: this will cause pacemaker malfunction, usually manifesting as failure to capture. It is most common in the first 6 weeks after implantation.

• Lead or pacemaker erosion through the skin: usually occurs long term.

• Pacemaker syndrome: vague feelings of weakness or dizziness in patients with VVI pacemakers and complete heart block. This is caused by loss of synchrony between atrial and ventricular contraction leading to episodic falls in BP and retrograde conduction of pacing impulse from ventricle to atria leading to simultaneous atrial and ventricular contraction. It is not seen with dual-chamber pacing and is treated by upgrading to a dual-chamber system.

Remember

If you suspect a pacemaker problem, always send the patient to a pacing clinic – that day – to have the function checked. The clinic will consult with a cardiologist if necessary. Out-of-hours, call the cardiologist on call.

Case history (2)

A 78-year-old man is admitted for a routine hip replacement. You are fast bleeped to the Orthopaedic ward; when you arrive the orthopaedic SHO tells you the patient is in ‘VT’. You rush to see the patient, who is sitting up reading his newspaper. His rhythm strip from his preoperative ECG is shown (Fig. 10.5). What do you tell the SHO and what do you do?

• This is a paced rhythm but there is evidence of failure to capture.

• You ask the pacing clinic to check his pacemaker; they find that the sensing threshold has risen but all other parameters are fine. They increase his pacemaker output and his pacemaker function returns to normal.

Figure 10.5 ECG showing pacing spikes (arrows) with failure to capture.

Remember

• Bradycardia and even transient conduction disturbance (first-degree and Mobitz type I or Wenckebach) can occur in healthy people during sleep. Great caution is needed when interpreting rhythm disturbances at night.

• Always take dizzy spells in a patient with a pacemaker seriously. Formal evaluation and an urgent pacing clinic check are required.

Cardiac arrest and basic life support

Case history

You are walking alone along an isolated corridor of your hospital. Just ahead, you observe a man collapse to the ground. As you approach you notice he is one of the hospital porters. He is lying motionless.

What should you do?

An assessment and initial resuscitation of the critically ill patient should be undertaken (ABCDE):

• Airway – remove any obstructing material and make sure airway is clear.

• Breathing – look, listen and feel for signs of breathing.

• Circulation – check carotid and peripheral pulses and start external chest compression if cardiac arrest.

• Disability – conscious level – Glasgow Coma Scale (see Table 15.3, p. 492).

• Examination/exposure. – to allow a full examination to be carried out.

Recent evidence emphasises that maintaining the circulation is the key factor overall.

The order of resuscitation should be CAB, i.e. Circulation, Airways, Breathing.

• Check for danger then shake and shout to check responsiveness.

• If there is no response shout for help.

• If no one responds to your call open the airway (Fig. 10.6).

Figure 10.6 Basic life support. With permission from the Resuscitation Council.

What two methods could you use to open the airway?

1. Head tilt, chin lift.

2. A jaw thrust in suspected cervical spine injury.

There are no signs of breathing, you remain alone. What must you do now?

You must leave the patient and go to the nearest telephone to initiate the cardiac arrest call.

You have initiated the emergency call from a telephone further along the corridor.

What should be your next action?

There are no signs of circulation after your assessment. The patient is cyanosed and motionless.

Commence basic life support (see Fig. 10.6).

Chest compressions – carefully note the following:

• Hand position: place the heel of the hand on the sternum, two fingers’ breadth above where the rib margins meet.

• Arm position: lock the elbows and lean directly over the porter.

• Rate: aim to maintain a rate of 100 per minute.

• Depth: compress the chest one-third of the resting diameter of the chest.

• CPR at a ratio of 30 : 2 (30 compressions to 2 breaths), irrespective of number of rescuers.

• Continue this until the defibrillator arrives (Fig. 10.7).

Figure 10.7 Universal advanced life-support algorithm.

Progress.

The patient showed VF on the defibrillator and was successfully brought back into sinus rhythm with DC cardioversion. He was admitted and referred to the cardiologists.

He will need investigations to rule out structural heart disease (echo and angiogram). He will then need electrophysiological studies and an automatic implantable cardioverter defibrillator (AICD; Table 10.3) implanted to prevent recurrence because he has, in effect, had an ‘out of hospital’ VF arrest.

Table 10.3 AICDs – who needs referring for consideration of implantation of one?

* Although this indication is backed up by evidence from the MADIT II trial, the healthcare cost implications are enormous and this is neither a routine indication in the UK at present nor likely to be in the near future.

Information

• The chance of survival from ventricular fibrillation is generally agreed to deteriorate by 5–10% per minute. It is therefore imperative that a defibrillator is brought as soon as possible

• Alerting the team is a priority

• Give a praecordial thump if appropriate

Chest pain (p. 336) and acute coronary syndromes

Case history (1)

You are called to assess a 73-year-old woman who gives a 40-min history of sudden-onset, tearing, severe central chest pain radiating down her left arm and through to her back. She has a history of treated hypertension and has not smoked for 15 years. How are you going to manage her?

Causes of chest pain to consider

• Aortic dissection (see later)

• Acute coronary syndrome

• Pericarditis: sharp central pain, related to posture and respiration

• Pleurisy: sharp, usually lateral, related to respiration

• Herpes zoster: nerve root distribution, rash might appear later

• Gastro-oesophageal reflux disease: retrosternal burning pain but can be very similar to angina.

Note: Many episodes of chest pain do not easily fit into any category and patients are often admitted and treated for acute coronary syndromes. Their symptoms should be assessed in conjunction with their risk factor profile. If in doubt, it is safer to admit.