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.

What features would make you suspect a dissecting aneurysm?

• Pain tends to radiate to back, starts abruptly and is often intense and described as tearing.

• On examination: absent arm or leg pulses, murmur of aortic regurgitation, different BP in arms, neurological signs.

• ECG might be normal or show inferior ischaemia or MI.

• As the dissection in the aortic wall extends proximally, first it disrupts the origin of the subclavian arteries (affecting arm BP), then the carotid arteries (causing neurological sequelae), the origin of the right coronary artery – causing inferior ischaemia – and finally the aortic valve is disrupted causing aortic regurgitation.

If you clinically suspect a dissecting aneurysm you must

• Get a chest X-ray to look for mediastinal widening.

• Get a senior opinion.

• Never give thrombolytic therapy, heparin or anti-platelet therapy.

• Carefully reduce BP with IV labetolol or sodium nitroprusside.

• Discuss with a cardiothoracic centre.

• CT with contrast or an MRI with contrast: although trans-oesophageal echo (TOE) is an excellent investigation it must be done by a very senior operator and should really be done in the cardiothoracic centre with surgeons on standby.

Case history (continued)

The patient’s ECG now changes at approximately 20 min with 4 mm of convex up-sloping ST elevation in leads II, III and AVF. The diagnosis is, of course, an inferior ST elevation MI (STEMI).

Immediate medical management in A&E

All hospitals are expected to have a rapid triage for chest pain to ensure that all suspected ACS patients are seen without delay. There should be a multi-disciplinary team approach with defined guidelines. With all ACS patients:

• IV access should be gained and bloods sent for cardiac markers, biochemistry, lipid profile, FBC and clotting profile.

• Oxygen is no longer recommended in the 2008 British Thoracic Society guidelines, unless the patient is hypoxaemic (check on pulse oximeter).

• Aspirin 300 mg chewed, then 75–150 mg daily, should be given.

• Sublingual glyceryl trinitrate (GTN) 0.3–1 mg should be given for pain relief, repeated as necessary (provided BP is not compromised). This can be followed by an IV infusion of 1–10 mg/hour, which is titrated to pain whilst aiming to keep systolic BP > 100 mmHg.

• IV diamorphine 2.5–5 mg or morphine 10 mg is used as analgesia, with metoclopramide 10 mg as an antiemetic.

• IV β-blockade with metoprolol is given in 5 mg boluses (up to a total of 15 mg), provided the patient is not in cardiogenic shock and/or hypotensive, and that there are no contraindications (e.g. asthma).

• Patients with a STEMI ideally should start β-blockers on the first day, provided they are definitely haemodynamically stable. If there is any doubt, wait until they are stable, to avoid the possibility of cardiac shock developing.

• All ACS patients should be transferred to a coronary care unit (CCU) for continuous monitoring and further specialist care.

• Patients with ACS should have clopidogrel 600 mg loading dose, unless PCI is not being done, in which case the loading dose should be 300 mg; thereafter 75 mg daily is given in addition to aspirin. It has been shown to reduce mortality and the occurrence of major vascular events without an increase in the risk of bleeding in STEMI ACS. Prasugrel 60 mg is an alternative

• N.B. Proton pump inhibitors, particularly omeprazole, reduce the antiplatelet effect of clopidogrel because they are inhibitors of cytochrome p450 (CYP2C19), but have only a small therapeutic effect.

• In addition, urgent reperfusion (see below) is needed.

Thrombolysis

Thrombolysis is still used in some hospitals.

You must know the indications for thrombolysis:

• A history of typical ischaemic chest pain, which started within the last 12 h.

• A 12-lead ECG that shows at least one of:

• 1 mm or more of ST elevation in two or more limb leads or

• 2 mm or more of ST elevation in two or more adjacent precordial leads or

• New-onset left bundle branch block.

Thrombolytic therapy

Alteplase (‘accelerated’ recombinant tissue-type plasminogen activator; rtPA) 1 mg/kg over 60 min (remember you must give concomitant IV heparin or LMWH for the first 24 h with rtPA).

Remember the other thrombolysis drugs that are available. For example, some hospitals use tenecteplase, which is an easy-to-administer single bolus thrombolysis agent of proven benefit in large trials. If a patient has any type of contraindication to thrombolysis you must discuss the case with a cardiologist immediately.

Don’t forget pericarditis!

ST changes in pericarditis are often widespread, involving inferior as well as anterior leads (Fig. 10.8) but the ST changes are concave with peaked T waves and there is often associated widespread PR depression (a feature specific to pericarditis).

Figure 10.8 ECG changes in pericarditis and myocardial infarction.

Also beware

• LBBB: if this is known to be old, the diagnosis will rest on the history and cardiac enzymes; it can be difficult to distinguish acute changes on a background of LBBB. If it is known to be new it can be used to support the diagnosis.

• Other (non-ischaemic) causes of ST elevation:

• High S-T take-off is seen more commonly in certain racial groups, e.g. Afro-Caribbean

• There are other causes you should be aware of such as the ST elevation seen in leads V1–3 in patients with Brugada’s syndrome.

Cardiac markers in the early assessment of a patient with chest pain (Fig. 10.9)

Troponins start to be released within minutes of myocardial damage and are very useful. But, apart from the patient with known LBBB, they rarely play a role in the initial management decisions at the time of admission in patients with acute coronary syndromes. They should, however, be measured both at admission and at 24 h in all patients with a suspected acute coronary syndrome. Most other cardiac markers take several hours to rise, might be misleading and are now used much less, given the availability of troponin assays.

Figure 10.9 Enzyme and troponin profile in acute myocardial infarction.

Progress.

This 73 year old lady with a STEMI was given thrombolysis with alteplase. She was seen by the coronary rehabilitation team.

The classification of acute coronary syndromes

The term ‘acute coronary syndrome’ covers the spectrum from unstable angina to MI. This has been a rapidly evolving area (Table 10.5). With this in mind, the decisions to make, using this definition, are:

1. Is this an ST elevation MI (STEMI) or a non-ST elevation MI (NSTEMI)?

2. Or is this unstable angina?

This helps you direct your therapy; patients with an STEMI should receive PCI or thrombolysis. It is easy to appreciate from the pathogenesis (Fig. 10.10) how failure to treat unstable angina can allow progression to an MI. All the patients should initially be admitted to CCU for management.

Table 10.5 Definition of myocardial infarction (MI)

Both the following definitions satisfy the diagnosis of an acute, evolving or recent MI.

1. Typical rise and gradual fall of troponin with at least one of the following:

Ischaemic symptoms (chest pain)

ECG changes indicative of ischaemia (e.g. ST depression or elevation, T wave changes)

Development of pathological Q waves on the ECG

Following coronary artery intervention, e.g. angioplasty

2. Pathological findings of an acute MI (usually dead patient)

Figure 10.10 The pathology of unstable angina (UA) versus acute myocardial infarction (MI).

Symptoms suggestive of an acute coronary syndrome

• Angina occurring at rest, at night or on minimal effort.

• The pain might require escalating doses of GTN.

• It might be associated with sweating, nausea or breathlessness, especially in an MI.

• There might be a background of worsening exertional symptoms prior to the admission episode of pain.

Case history (2)

You are about to finish your shift when a casualty officer asks you ‘while you are here’ to look at the ECG of a patient who is about to be sent home. The patient is a 44-year-old male smoker who has had anterior central chest pain on and off at rest for the past 2 days. The first ECG shows some subtle T wave changes in the anterior leads but his repeat ECG is normal and he is now pain free, having had the GTN. The casualty officer has told him he can go home with a GTN spray and come back to clinic in 6 weeks. The patient is pleased and is sitting, fully dressed, waiting for his GTN spray, because he is keen to get home to watch the football. Can he go home?

What do you say and do?

• This patient absolutely cannot go home! He needs admission, treatment for unstable angina and risk stratification. This is exactly the type of patient who, if sent home, will go on to have an MI. Admit him to CCU.

Remember

Management of MI depends on a fast-track approach: ‘time is muscle’.

• Therapy:

– Aspirin 300 mg loading dose then 75 mg daily thereafter; in addition to this give him 300 mg loading dose of clopidogrel and 75 mg daily thereafter (CURE trial).

– Start the patient on SC low molecular weight heparin (LMWH), usually Enoxaparin (1 mg/kg × 2 daily).

– Start him on a beta blocker, such as metoprolol 25 mg × 3 daily (unless contraindicated); patients with a sinus tachycardia or hypertension will benefit most from this and should be given early IV beta blockade.

– Put him on an IV GTN infusion (0–10 mL/h, titrate according to pain and BP).

– Assess and correct risk factors (smoking, lipids, hypertension, diabetes).

– Ensure a troponin is sent at the time of admission and the following day.

Remember

• If the initial ECG is normal: do not discharge the patient. It is possible to have a normal ECG in an acute coronary syndrome

• Repeat the ECG every 20 min for at least 1 h

• Consider other causes of chest pain.

His further management will depend on risk stratification using his troponin (at 24 h), symptoms and ECG. If his symptoms settle:

• If he is troponin positive (high risk) he should be referred for immediate inpatient PCI.

• If he is troponin negative, low risk requiring further investigation, e.g. coronary artery imaging, he can be managed medically initially but will need discussion with the cardiology department.

Remember

There are many other causes of a raised troponin, e.g. pericarditis, pulmonary embolism, myocarditis.

If his symptoms do not settle:

• He will need urgent inpatient angiography; in the meantime his medical therapy should be increased.

• If he is troponin positive and has dynamic ECG changes he should be started on an IV glycoprotein IIb/IIIa antagonist infusion and referred for angiography that day.

Note: IIb/IIIa antagonist infusions have not been proven to be of benefit as medical therapy alone. A GP IIb/IIIa antagonist, e.g. abiciximab, should be given before PCI and for 12 hours post PCI. If a patient does not go straight away for a PCI, he should receive an infusion of either tirafibam or eptifibatide. The dosing is complex and you need to look it up (e.g. in a National Formulary).

A brief note on glucose and statins

Any patient with an abnormal admission glucose should be started on an IV insulin sliding scale (see p. 424); there is evidence that this improves outcome. High-dose statins (e.g. atorvastatin 80 mg daily) should be started on admission because there is evidence that they improve prognosis above and beyond their lipid-lowering effects, by stabilising the acute plaque.

Remember

• Do not miss an aortic dissection! Giving such a patient thrombolysis is dangerous and likely to be fatal

• If in doubt about whether to give thrombolysis discuss the patient with a cardiologist immediately; if thrombolysis is contraindicated coronary intervention may well be a viable option.

Progress.

In this patient the troponins were normal. As his symptoms had settled he was sent home with medication for an angiogram as an outpatient.

Case history (3)

A 62-year-old man with type 2 diabetes was admitted to hospital with a 6-h history of central chest pain radiating to both shoulders and to his jaw. The ECG in A&E showed 2 mm of ST segment depression in the inferior leads. His troponin T was elevated at 0.9. The diagnosis was a NSTEMI. The pain settled with medical therapy and he was referred for PCI.

His angiogram showed a single tight mid-right coronary artery stenosis but no other significant disease. He went on to have a successful angioplasty and a stent, with excellent results.

Acute myocardial ischaemia – who needs acute intervention?

This is a very rapidly evolving field because of constant advances in techniques and biomechanical engineering, i.e. stent technology. As a result, there is a lot of clear evidence from numerous large trials showing improved outcome with percutaneous intervention in certain groups of patients (FRISC II, Tactics-TIMI 18, GUSTO IV ACS, RITA III – to name just a few). Broadly speaking, these can be put into one of three groups:

1. ST elevation MI (STEMI):

i. Primary intervention: there is now clear evidence that percutaneous coronary intervention (PCI) is better than thrombolysis for acute STEMI. There is no doubt that, given appropriate resources, infrastructure and staff, this is the treatment of choice. In the UK thrombolysis is still used although PCI is becoming more readily available.

ii. Secondary intervention: patients who are reinfarcting, in whom thrombolysis has failed to resolve the ECG findings and symptoms, have post-infarct angina or have VT after the first 24 h should be discussed urgently with a cardiologist with a view to urgent PCI.

2. Non-ST elevation MI (NSTEMI): these patients should be referred for immediate PCI. If PCI is not available, give fondapurinox 2.5 mg sc daily with aspirin 75 mg as they represent a high-risk group for further subsequent events.

3. Unstable angina: patients with ongoing symptoms despite medical treatment with evidence of ischaemia should be discussed with a cardiologist for consideration of PCI.

In the long term, the value of revascularisation – whether by surgery or PCI – in relieving persistent symptoms is beyond doubt. Revascularisation should be considered in all outpatients taking into account their symptoms, lifestyle and investigation results. Generally, bypass surgery is used in: left main stem disease, three-vessel disease, diffuse disease with a poor ventricle and diabetics.

Cardiogenic shock

Information

Definition: persistent hypotension (< 90 mmHg systolic) associated with reduced end organ perfusion due to low cardiac output.

This is usually the result of acute myocardial infarction and is manifested by poor peripheral perfusion and low urine output, often associated with clinical/radiological evidence of LVF. Mortality approaches 80% with treatment and is much higher without. Predisposing factors include:

• Old age

• Previous MI

• Large anterior MI

• Prior hypertension/diabetes

• Inadequate or late thrombolysis.

Case history

You are called at 2 a.m. to see a 68-year-old diabetic woman who was admitted with a 12-h history of chest pain and ECG changes of an extensive anterior MI. She was treated with alteplase at 2 p.m. the previous day. She has previously had an inferior myocardial infarct. She has remained hypotensive with a poor urine output since admission and is now feeling very unwell. Her current CXR is clear. What do you do?

Management (Fig 10.11)

• Get a repeat ECG to look for evidence of reperfusion or continuing ischaemia.

• Check that patient is not volume depleted; this must be done using at least a CVP line and preferably a Swan–Ganz catheter on CCU.

• Check that there is no structural cause: get an urgent transthoracic echo:

• Ventricular septal rupture (murmurs at left sternal edge – may be inaudible if large) usually occurs after 2–3 days

• Papillary muscle rupture giving severe mitral regurgitation (usually murmur but might be silent).

Figure 10.11 Algorithm for the management of acute heart failure with systolic dysfunction.

From Nieminen MS, Böhm M, Cowie MR et al. European Heart Journal 2005; 26: 364–416, Fig. 6, with permission from Oxford University Press and the European Society of Cardiology.

Remember

An urgent echocardiogram should be performed in every patient with cardiogenic shock.

• Give inotropes intravenously if there is no response to volume replacement:

• Dobutamine and/or low dose dopamine

• If possible, try and avoid adrenaline (epinephrine) or noradrenaline (norepinephrine) because they will worsen any ischaemia.

• Discuss with cardiologists immediately with a view to transfer for PCI:

• This is particularly appropriate in the patient with an anterior MI and no previous history of IHD where cardiac stunning might be present.

• In the SHOCK trial, patients referred for early intervention (within 24 h of onset) had an improved prognosis – time counts.

• Insert an intra-aortic balloon pump (IABP), if available: this is a highly effective way of improving cardiac perfusion, and should be used in any patient in whom there is a reasonable prospect of further definitive treatment (e.g. revascularisation/repair VSD). Cannot be used in the presence of significant aortic regurgitation.

Progress.

This patient was treated with intravenous dobutamine with some initial improvement in BP and peripheral perfusion, but 24 h later she remained anuric and developed acute pulmonary oedema and shock unresponsive to increasing inotropic support. By the time she was discussed with the cardiologists she had been anuric and shocked – with a systolic BP of 65 despite inotropes – for 36 h. She was too unstable to transfer and she died shortly after.

Remember

Do not go to bed when you have a patient in cardiogenic shock (who is appropriate for aggressive treatment). Stay up, get on the phone to the cardiologists quickly and sort it out. It is hopeless referring a patient 36 h later: by this time he or she will not be treatable.

Remember

• There is never a role for renal dose dopamine in any patient with renal failure

• In patients on prior beta blockers, competitive blockade may persist for 24 h or more and will require much higher doses of dobutamine/dopamine

• It is probably simpler in this situation to use milrinone/enoximone, which bypasses the beta adrenoceptor.

Information

Myocardial stunning and hibernating myocardium

• When heart muscle is subjected to acute ischaemia it might cease to contract but remain viable. This is a potentially reversible cause of haemodynamic problems in acute MI.

• Myocardial stunning. If the blood supply to the relevant area is restored as a result of natural recanalisation of occluded arteries, pharmacological thrombolysis or angioplasty, the functional capacity might return relatively quickly – over a matter of a few hours. Such myocardium is called stunned myocardium.

• Hibernating myocardium. A similar state of affairs might occur on a more chronic basis, usually in severe three-vessel disease. In this case, the cellular ultrastructure might become seriously deranged even though the ischaemic myocytes are still potentially viable. This is known as hibernating myocardium; such myocardium can be restored by revascularisation.

These major changes, which have occurred at the cellular level, mean that the period of recovery might be over weeks or even months. PET scanning, stress echocardiography and radionuclide myocardial perfusion scanning can all be used to identify hibernating myocardium.

Right ventricular infarction

Right ventricular infarction is often associated with volume-dependent hypotension that responds well to fluid replacement.

Case history

A 58-year-old man is admitted with an inferior MI (Fig. 10.12) and is given successful thrombolysis within 2 h of the onset of pain. Although ST elevation and pain largely resolve within 1 h, he remains hypotensive with a systolic BP of 70–80 mmHg associated with a low urine output.

Figure 10.12 An acute inferior wall myocardial infarction. Note the raised ST segment and Q waves in the inferior leads (II, III and AVF).

A further ECG with right-sided chest electrodes (Fig. 10.13) suggests right ventricular infarction with ST elevation in V3R–V4R. A fluid challenge of one litre of 5% glucose, given over half an hour IV, restores the BP to 110 systolic with a good urine output.

Figure 10.13 Right ventricular infarct.

Intravenous fluids in an acute MI should be given using an appropriate measure of the patient’s filling status, such as CVP (via a central line) or using Swan–Ganz (pulmonary artery) catheter readings.

Right ventricular infarction is:

• Diagnosed readily by elevation of ST segment in V3R–V4R on right-sided ECG

• Associated with volume-dependent hypotension

• Often associated with elevation of JVP without other evidence of heart failure

• Associated with a higher incidence of all post-MI complications, e.g. arrhythmias, cardiac rupture.

Heart failure and cardiogenic shock usually reflect extensive cardiac damage but cardiac ‘stunning’ might be present, and active treatment can save lives.

Progress.

He was given medical therapy with aspirin, clopidogrel, β blockers and LMWH and was stable after 5 days. He was referred for urgent PCI.

Heart failure following an MI

Case history

A 63-year-old man has been on CCU for 5 days following his second myocardial infarction. He has been managed with percutaneous coronary intervention and on this occasion has had two eluting stents in his left anterior and circumflex arteries.

You are asked to see him because he has felt breathless over the last hour.

On examination he is tachypnoeic with a pulse of 90/min and a BP of 140/80. His venous pressure is raised and he has a gallop rhythm and basal crackles. You diagnose acute heart failure.

The presence of heart failure, even if transient or only evident on CXR or echo, places the patient with an MI in a far worse prognostic group.

Acute heart failure in the context of an acute MI is associated with a very high inpatient mortality.

Treatment

• IV diamorphine boluses 2.5–10 mg.

• An IV nitrate infusion (0–10 mL/h), titrated to blood pressure and symptoms.

• Boluses of IV furosemide 40–80 mg, although an infusion is better in severe heart failure.

• Invasive monitoring to help to guide therapy.

• IV inotropes if patient remains hypotensive despite the above measures.

Treatment of underlying poor ventricle

• Introduce ACE inhibitor (or angiotensin receptor antagonist) as soon as possible: ACE inhibitors have been shown to reduce the mortality of this high-risk group by 20–30%. Initiate this therapy as soon as the patient is off inotropes, haemodynamically stable and has stable renal function. Ramipril (1.25 mg initially) is a good choice given its simple dosing regime. A slight deterioration in renal function (up to 30%) might be seen, and if this happens do not increase the dose. If, despite this, renal function continues to worsen, withdraw the ACE inhibitor and reconsider at a later date.

• The introduction of a beta blocker as soon as it is safe: there is a wealth of evidence supporting the use of beta blockers in heart failure to improve prognosis. Evidence from the CAPRICORN and COPERNICUS trials showed that even patients with severe heart failure benefit from the cautious introduction of beta blockers, (provided the patients are not on IV inotropes or vasodilators) e.g. carvedilol, starting at 3.125 mg × 2 daily or bisoprolol, starting at 2.5 mg daily).

• Spironolactone 12.5–25 mg daily (if the heart failure is moderate to severe).

• Consider further revascularisation: remember patients will benefit from revascularisation if part of their poor ventricular function is due to viable stunned or hibernating myocardium. All patients with post-infarct cardiac failure should be seen by a cardiologist.

Progress.

The patient was treated intensely with diuretics, an ACE inhibitor and a β blocker. He made a very slow recovery but was able to be discharged in 2 weeks and followed up by the cardiologists.

Post-infarction arrhythmias and heart block

Case history (1)

A nurse on CCU calls you at 5 a.m. A 56-year-old man without previous heart disease was admitted with an inferior MI and had had successful thrombolysis at 11 p.m. the previous evening. The nurse had been looking at the monitor and noticed that the patient kept having ectopics and has had two short five-beat bursts of non-sustained VT. The nurse wants you to ‘review’ the patient. When you arrive the patient is lying flat, fast asleep with a heart rate of 50 (sinus rhythm) and haemodynamically stable. He was given a beta blocker on admission and when you look at his results all his electrolytes (including Mg²⁺ and Ca²⁺) are normal. You reassure the nurse who, however, is ‘just not happy’ and wants you to prescribe something.

What do you do?

• Reassure the nurse that anti-arrhythmics are not indicated. In the CAST trial, post-MI patients with asymptomatic ventricular arrhythmias were randomised to anti-arrhythmic drugs or placebo; the patients given anti-arrhythmics had a worse outcome.

• There is no role for giving empirical IV Mg²⁺ to all patients with an acute MI, as shown by the MAGIC trial.

Arrhythmias – atrial and ventricular – are common in the first 24 h after an MI and might be life threatening. For this reason, all these patients must be in monitored beds on CCU. Late arrhythmias (after the first 24 h) are of more prognostic significance and will require specialist evaluation.

Early ventricular arrhythmias

• Ectopics and non-sustained VT are very common, particularly in the 1–2 h after thrombolysis (‘re-perfusion arrhythmias’) and usually require no treatment. Check K⁺, Mg²⁺ and Ca²⁺ and correct if needed.

• Sustained VT or after VF: Standard practice is IV bolus 100 mg over 5 mins, then infusion of 2-4 mg/min) for 24 hrs after cardioversion. Amiodarone is also used.

• Early use of IV beta blockers, e.g. metoprolol, often reduces incidence of ventricular arrhythmias.

Progress.

This patient’s arrhythmias settled without the need for anti-arrhythmics. He was discharged with an outpatient appointment with the cardiologist.

Case history (2)

A 72-year-old woman with diabetes was admitted with an anterior MI and received thrombolysis 8 h after the onset of pain. The CXR showed pulmonary venous congestion. The ECG after thrombolysis is shown in Figure 10.14.

Figure 10.14 ECG following thrombolysis in this patient.

During the night, nurses observed isolated non-conducted P waves but no action was taken. The next morning the patient collapsed with a heart rate of 28/min and complete heart block; she had not passed urine since admission. A wire was passed via the internal jugular route and she was successfully paced. Despite this, she developed increasing heart failure and died 2 days later.

Heart block

Management is usually very different for inferior and anterior MI. In inferior infarcts a conduction disturbance is common and, provided the patient is not haemodynamically compromised, temporary pacing is usually not required and the problem resolves within 2 weeks; permanent pacing is rarely required. However, heart block in anterior infarcts invariably represents extensive myocardial damage and nearly always needs pacing (temporary and permanent).

Information

Indications for temporary pacing post-MI

• Mobitz II heart block with anterior MI.

• Third-degree (complete) heart block (CHB) with inferior MI if hypotensive or cardiac failure, always with anterior MI.

• Bifascicular block (RBBB with left or right axis deviation): usually anterior MI and at risk of CHB.

• Trifascicular block (long PR interval and either LBBB or RBBB with axis deviation): usually anterior MI and at risk of CHB.

• Alternating LBBB and RBBB: usually extensive myocardial injury and high risk of CHB.

Note: Do not use the subclavian route after thrombolysis – instead use either the jugular or femoral route because there is less risk of haemorrhagic complications.

Management of late arrhythmias

• Atrial fibrillation/SVT: commonly associated with pericarditis or heart failure. Usually self-limiting or responds to digoxin. Consider cardioversion if this fails or the patient is compromised. Treat pericarditis or cardiac failure actively.

• Ventricular tachycardia: as a late event carries a bad prognosis.

• Beta blockers: all patients should be on these unless contraindicated.

• IV amiodarone: if recurrent VT that has not settled with beta blockers.

• All patients must be referred for early inpatient angiography and appropriate electrophysiological investigations and management as necessary (usually implantation of an internal defibrillator).

• Avoid other anti-arrhythmics, especially those that are negatively inotropic, e.g. flecainide.

Remember

Ventricular ‘escape’ rhythms are common in bradycardia due to increased vagal tone, and usually respond to atropine.

Information

Anterior MI and complete heart block carry a very high in-hospital and 1-year mortality.

Myocardial infarction – secondary prevention

The greatest concern of patients who have recovered from a heart attack is whether they will have another. As well as lifestyle changes, there are a wide range of drugs available for secondary prevention, with strong evidence to support their use. The following should be undertaken:

• Stop smoking

• Strict control of blood pressure

• Diet modification with a view to appropriate weight loss: low fat, low salt, fish oils, high vegetable content

• Exercise

• Drug therapy.

Drug therapy

Antiplatelet therapy

Summary of drugs required for secondary prevention

• Aspirin for all

• Statins for all

• Beta blockers for all, unless contraindicated or not tolerated

• ACEI for all, unless contraindicated or not tolerated

• Calcium antagonists for selected patients, e.g. intolerance to beta blockers.

• Anti-coagulation for selected patients.

Heart failure recognition and acute management

Differentiating heart failure from lung disease as a cause of breathlessness can be difficult because there is often coexisting cardiac and respiratory disease. In the case of smokers, this usually consists of ischaemic heart disease and COPD. There is thus a tendency to give a concoction of therapy to cover both cardiac failure and an exacerbation of COPD, often with antibiotics being added in to cover infection, especially in the elderly. This section will attempt to provide a diagnostic route to clarify the problem and seek therapeutic solutions.

Case history

At 3 a.m., an SHO in A&E refers you an 80-year-old man with a 4-day history of increasing breathlessness, wheeze and non-productive cough. He lives alone in a first-floor flat and smokes 10 cigarettes a day. The SHO is not sure what the diagnosis is but thinks it might be a ‘chest infection’.

Is it heart failure?

Remember that wheeze and cough occur in heart failure as well as respiratory disease. Although the onset of breathlessness is often rapid in heart failure, it can also be rapid in respiratory disease. Clinical examination might help you further differentiate the two but you often need the results of investigations to help differentiate the causes.

• In heart failure the ECG will almost always be abnormal.

• The echo will invariably show depressed systolic function (but beware of a small percentage of patients with diastolic heart failure and normal systolic function).

• The CXR will help as will respiratory function tests (but remember respiratory function tests may be of no help in the acute phase).

• Serum naturietic peptides are useful in the diagnosis of heart failure; serum BNP >200.

• Assess response to therapy.

Case history (continued)

The patient gives you a history of a sudden onset of breathlessness, preceded by dull chest pain, which started 4 days ago. On examination he is apyrexial, tachypnoeic and sitting up; he has crackles at both his lung bases, a small left-sided pleural effusion, a raised JVP and a BP of 160/95. His ECG showed an old anterior myocardial infarction.

He clearly has left ventricular failure, the aetiology of which is likely to be due to ischaemic heart disease with hypertension.

Common causes of acute cardiac failure include:

• Ischaemic heart disease

• Hypertension

• Valvular heart disease

• Profound tachy- or bradycardia

• Myocarditis

• Myocardial depression by drugs

• Cardiac tamponade.

Practice point

If you can’t identify an aetiology for the cardiac failure, and the ECG is normal, reconsider your diagnosis, but don’t forget the possibilities of constrictive pericarditis or diastolic ventricular dysfunction. This latter diagnosis is difficult to make but is more common in elderly hypertensives and can be diagnosed with echocardiography.

When cardiac failure appears, consider what has precipitated it and treat this as well as the failure itself; such precipitating factors include:

• Arrhythmia: tachy- or brady- (e.g. atrial fibrillation, complete heart block)

• Myocardial infarction

• Excess fluid intake (e.g. post-op IV fluids)

• Excess fluid retention (e.g. NSAIDs, acute kidney injury)

• Anaemia, thyrotoxicosis or any precipitating illness, such as infection in the elderly

• Either precipitating drugs or poor medication compliance in a patient on anti-failure drugs.

Rule out the above with the appropriate investigations and correct them if possible.

Case history (continued)

The patient remained breathless despite an initial bolus of furosemide 80 mg. His chest X-ray confirmed that he had pulmonary oedema.

Management

He needs rapid therapy to improve his clinical condition, with acute treatment to correct his breathlessness, followed by further therapy to maintain and improve left ventricular function.

The acute phase of therapy consists of:

• IV nitrates (e.g. glyceryl trinitrate 10–200 µg/min titrated to reduce systolic BP by 10–15% and not below 90 mmHg): these provide excellent rapid symptomatic relief by offloading the ventricle, and should be first-line therapy. Continue IV diuretics, initially boluses (e.g. furosemide 40 mg) but he might need a furosemide infusion.

• IV diamorphine (5 mg slowly): this not only relieves symptoms, by offloading the ventricle, but is an excellent anxiolytic.

• ACE inhibitor or angiotensin receptor antagonist:

• Start after acute symptoms have settled and patient is haemodynamically stable.

• Remember to watch renal function.

• Use an appropriate dose of ACEIs, or they will be ineffective.

• Beta blockers:

• There is excellent evidence to back their use (e.g. CIBIS II, MERIT) and these should be started as soon as the patient is haemodynamically stable and off IV inotropes and IV vasodilators. There is now evidence to back their use even in patients with severe heart failure. Either carvedilol or bisoprolol is the first-line drug (see starting dose, mentioned above).

• Up-titration of the drugs must be very gentle (every 2 weeks) and warn patients they might initially feel worse. If their symptoms worsen do not increase the dose; if they continue to worsen, reduce or stop the beta blockers.

• Spironolactone: 12.5–25 mg daily should be given to all patients with moderate to severe heart failure (RALES trial); check the potassium because of risk of hyperkalaemia.

• Digoxin:

• Valuable in atrial fibrillation

• Shown to reduce rate of hospitalisation in patients, not mortality (VA study).

• Non-invasive positive pressure ventilation (NIV): patients often respond very well to just CPAP alone, but might need BIPAP. You should be aware that positive pressure ventilation might cause hypotension: monitor the patient appropriately.

Other lifestyle changes

• Reduce alcohol intake

• Reduce weight

• Reduce salt intake

• Take moderate regular exercise.

His breathlessness and pulmonary oedema resolved after 2 days and plans were made to discharge him when his condition was stable.

Practice point

Patients are often left on excessively high doses of diuretics and can easily become dehydrated on discharge unless their therapy is reduced. However, patients developing heart failure while on diuretics usually require to be discharged on a higher dose than on admission.

The trend would be to increase the dose of the ACEI while reducing the diuretic dose, assessing the response by monitoring symptoms, signs and weight. Ideally this should be done by a heart failure clinic; these are often nurse led and excellent for such patients.

Selected points

• Heart failure may be difficult to diagnose – especially with diastolic dysfunction.

• A proportion of elderly patients are on diuretics but have no objective evidence of heart failure (systolic or diastolic).

• Echocardiography should be performed in all patients to identify an aetiology.

• ACEIs should be given to all patients unless contraindicated (i.e. renal impairment, aortic stenosis, renal artery stenosis).

Information

• Systolic heart failure is associated with a decreased left ventricular ejection fraction. The heart is enlarged and there is frequently accompanying diastolic heart failure. The cause is often IHD.

• In diastolic heart failure there is normal left ventricular systolic function with a small heart and impaired left ventricular filling. It often occurs in the elderly associated with hypertension. At present there are no data from large trials on treatment of diastolic failure but the expert consensus opinion at present is that it should be treated in the same way as systolic failure.

Progress.

This 80-year-old man was treated according to the algorithm in Fig. 10.11. He made a gradual recovery but was unable to go home. He was placed in a nursing home but was readmitted with pulmonary oedema again and died.

Valvular heart disease

Aortic stenosis

In the UK, the most common cause of aortic stenosis in the elderly is degenerative calcific disease; in younger patients it is more often on the basis of a congenital bicuspid valve. Although it is now less common, do not forget rheumatic heart disease as a cause.

Case history (1)

A 75-year-old man is brought to hospital after he had blacked out when running for a bus. He had fully recovered when he reached hospital.

Cardiac examination revealed normal pulse, with normal rhythm and BP 180/90. The heart sounds were soft with an ejection systolic murmur heard all over the praecordium.

The CXR was normal and the ECG showed LBBB.

A clinical diagnosis of aortic sclerosis was made. The house officer has seen him and has asked you to review him.

Practice points

In aortic stenosis, the physical signs can be misleading and do not necessarily correlate with its severity:

• Post-exercise syncope in someone with a systolic murmur is suggestive of significant aortic stenosis.

• A diagnosis of aortic sclerosis should not be made without full echo assessment.

• Soft heart sounds in the context of an aortic murmur often suggest significant stenosis.

• Although the pulse might be useful in diagnosing aortic valve lesions (Fig. 10.15), you should note that in elderly patients the pulse might not be reduced because of loss of arterial tree elasticity.

• Severe aortic stenosis with symptoms needs referral for inpatient surgery.

• Elective aortic valve replacement of aortic stenosis is associated with a very low mortality and is excellent curative surgery for symptomatic aortic stenosis with good ventricular function.

Figure 10.15 Pulse patterns in aortic valve disease.

Aortic regurgitation (AR)

There are many causes of aortic regurgitation, including both valve and aortic root disease. Degenerative disease, rheumatic disease, congenital valvular diseases and infective endocarditis are some of the more common causes.

Remember

In acute AR (e.g. endocarditis) the murmur might become inaudible and be replaced by a third heart sound. If this happens the patient needs urgent surgical referral.

Practice points

In aortic regurgitation the physical signs do tend to correlate with its severity, i.e. the worse the lesion, the more marked the collapsing pulse, the wider the pulse pressure and the longer the murmur:

• Echocardiography to quantify the severity and left ventricular size and monitor these parameters on a regular basis thereafter.

• When the ventricle begins to dilate, referral for consideration of surgery is necessary.

• Medical therapy with an ACE inhibitor may delay the time until surgery is needed.

Mitral valve disease

Case history (2)

A 64-year-old man was admitted in heart failure with signs of mitral regurgitation. He had been in hospital 6 months earlier with heart failure and had been well since then on maintenance medical therapy including an ACE inhibitor. He had cardiomegaly on chest X-ray but the ECG showed no ischaemic changes. Echo assessment confirmed papillary muscle dysfunction causing posterior valve leaflet prolapse with resultant severe MR; the left ventricle was dilated and had some impairment of function. Cardiac catheterisation showed normal coronary arteries and confirmed the echo findings. He had an intra-operative TOE and then mitral valve repair and made a good recovery.

In mitral regurgitation, the underlying cause must be adequately treated; this alone can cause a marked improvement in the severity of the MR. Surgery should be considered in all patients with functional disability (despite adequate medical therapy) and/or worsening LV function documented by echo. The threshold for surgery is constantly dropping with improving technique. Outcome often depends on LV function, so refer early. All patients with MR should be discussed with a cardiologist to arrange appropriate follow-up, investigation and surgical referral.

When should you consider surgery in valvular disease?

• Aortic stenosis: this is usually well compensated but deterioration is rapid once symptoms have developed. Refer for operation if dyspnoea, chest pain or syncope. Note: as an inpatient if stenosis is severe.

• Aortic regurgitation: refer for operation when LV starts to dilate (end systolic dimension > 5.5 cm).

• Mitral stenosis: refer for opinion when symptoms uncontrolled on medical treatment. Remember percutaneous valvuloplasty may be a first-line option. Generally when the valve area < 1 cm² then intervention is needed.

• Mitral regurgitation: progressive symptoms despite medical therapy and/or LV dilatation.

Remember

Age is not a barrier to valvular surgery if LV function is good and no major coronary disease is present.

Prosthetic valve problems (all these should be referred to a cardiologist urgently)

• Heart failure: must be assumed to be due to valve malfunction until proved otherwise.

• Murmurs: paraprosthetic leaks common but should be formally assessed by urgent echo followed by TOE.

• Infection: blood cultures must be taken for any febrile illness before giving antibiotics. Endocarditis of prosthetic valve should be referred to cardiothoracic centre.

• Anti-coagulants: control is essential (INR 3.5). Always take specialist advice before any surgical intervention. Do not stop a patient’s warfarin or reduce the dose until he/she is fully anti-coagulated with IV heparin.

Infective endocarditis

Infective endocarditis is an endovascular infection of cardiovascular structures, including cardiac valves, atrial and ventricular endocardium, large intrathoracic vessels, and intracardiac foreign bodies e.g. prosthetic valves, pacemaker leads, and surgical conduits. The annual incidence in the UK is 6–7 per 100 000, but it is more common in developing countries. Without treatment the mortality approaches 100% and even with treatment there is a significant morbidity and mortality.

Untreated infective endocarditis is invariably fatal. Delay in the diagnosis of infective endocarditis might:

• Make medical treatment more prolonged

• Increase the risk of death

• Promote the need for surgery which might have been avoided had treatment been started earlier.

It follows that endocarditis is a diagnosis that needs to be kept in mind when dealing with any pyrexial or constitutional illness in patients with valvular or congenital heart disease.

Remember

The main problem with endocarditis is delay in the diagnosis. Never delay empirical antibiotic therapy; take the appropriate cultures and start treatment.

Diagnosis is made using the modified Duke criteria (Table 10.6).

Table 10.6 Modified Duke criteria for endocarditis *

Major criteria

← A positive blood culture for infective endocarditis, as defined by the recovery of a typical microorganism from two separate blood cultures in the absence of a primary focus (viridans streptococci, Abiotrophia species, and Granulicatella species; Streptococcus bovis, HACEK † group, or community-acquired Staphylococcus aureus or enterococcus species); or

← Persistently positive blood cultures, defined as the recovery of a microorganism consistent with endocarditis from either blood samples obtained more than 12 hours apart or all three or a majority of four or more separate blood samples, with the first and last obtained at least 1 hour apart; or

← A positive serologic test for Q fever, with an immunofluorescence assay showing phase 1 IgG antibodies at a titre >1 : 800; or

← Echocardiographic evidence of endocardial involvement

← an oscillating intracardiac mass on the valve or supporting structures, in the path or regurgitant jets, or on implanted material in the absence of an alternative anatomical explanation; or

← an abscess; or

← new partial dehiscence of prosthetic valve; or

← New valvular regurgitation.

Minor criteria

← Predisposition: predisposing heart condition or intravenous drug use

← Fever: temperature ≥ 38°C (100.4°F)

← Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial haemorrhage, conjunctival haemorrhages, Janeway’s lesion

← Immunologic phenomena: glomerulonephritis, Osler’s nodes, Roth’s spots, rheumatoid factor

← Microbiological evidence: a positive blood culture but not meeting a major criterion as noted above, or serological evidence of an active infection with an organism that can cause infective endocarditis ‡

← Echocardiogram: Findings consistent with infective endocarditis but not meeting a major criterion as noted above.

^*The diagnosis of infective endocarditis is definite when: (a) a microorganism is demonstrated by culture of a specimen from a vegetation, an embolism, or an intracardiac abscess; (b) active endocarditis is confirmed by histological examination of the vegetation or intracardiac abscess; (c) two major clinical criteria, one major and three minor criteria, or five minor criteria are met.

^†HACEK denotes haemophilus species, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae.

^‡Excluded from this criterion is a single positive blood culture for coagulase-negative staphylococci or other organisms that do not cause endocarditis. Serologic tests for organisms that cause endocarditis include tests for Brucella, Coxiella burnetii, Chlamydia, Legionella, and Bartonella species.

After Raoult D, Abbara S, Jassal DS, Kradin RL. Case records of the Massachusetts General Hospital. Case 5-2007. A 53-year-old man with a prosthetic aortic valve and recent onset of fatigue, dyspnea, weight loss, and sweats. NEJM 2007.

Case history

One of your colleagues hands over a patient who has just been admitted. He is a 28-year-old man who presented with a pyrexia and history of feeling unwell for 6 weeks. His doctor had prescribed amoxicillin for a flu-like illness 3 weeks previously. He has a pyrexia of 38.5°C and looks unwell. There is a mid-systolic murmur radiating to the neck and the apex. Careful inspection of the nail beds showed some splinter haemorrhages. Blood cultures were taken in A&E on arrival. Your colleague wants you to look these up tomorrow and, depending on the results, start antibiotics.

What do you do and what else do you want to ask the patient?

• If you have good clinical grounds for a diagnosis of endocarditis you must start empirical treatment, as soon as you have taken at least three sets of cultures (from different sites). You take blood for a full blood count and a further blood culture now so that he can have his first dose of antibiotics without delay.

• You will ask him if he has had any recent dental work, if he is an IV drug user or if he has ever been told he has a murmur (pre-existing lesion).

• You will send off baseline U&Es, CRP, ESR, urinalysis and microscopy and get an ECG.

While taking the cultures you ask him a few questions and he tells you someone mentioned he had a murmur when he was a child but nothing further was done. He also tells you he had root canal work 8 weeks ago. You start him on a slow injection of benzylpenicillin (1.2 g, to be given 4-hourly thereafter) and gentamicin (80 mg 12-hourly) for the first 2 weeks. You must subsequently discuss anti-microbial therapy with a microbiologist.

His cultures subsequently show he has Streptococcus viridans in all sets of cultures and his echo shows a vegetation on a bicuspid aortic valve but no significant gradient (stenosis) or regurgitation.