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Case 44 

Case 44
Chapter:
Case 44
Author(s):

Rajkumar Rajendram

, Javed Ehtisham

, and Colin Forfar

DOI:
10.1093/med/9780199556786.003.0361
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Subscriber: null; date: 16 August 2018

A 51-year-old man received a 240-V, 50-Hz alternating current electrical injury whilst trying to repair his household washing machine. He was unable to release the appliance until his wife switched off the electricity approximately 1 minute later. He then noticed a severe painful burn in his left elbow and fast irregular palpitations, but was otherwise asymptomatic. The only significant past history was of hypertension, treated with enalapril 5 mg daily. He denied any previous episodes of palpitations.

He presented to the ED 30 minutes later. He denied any previous episodes of palpitations. On examination, a 5-cm2 third-degree burn was present in the left antecubital fossa, HR was 190 bpm and BP 130/70 mmHg. Physical examination was otherwise unremarkable. An ECG was obtained (Fig. 44.1).

Intravenous metoprolol 10 mg reduced the HR to 170 bpm. Thirty minutes later flecainide 50 mg was administered intravenously. This did not restore sinus rhythm or reduce the HR. Routine blood tests, including full blood count, serum potassium, serum magnesium and thyroid function, were normal. Plain chest radiography was unremarkable.

Six hours after the onset of AF the patient reported dull central chest pain, dizziness, and sweating. His HR was 180 bpm and BP was 80/40 mmHg. There were no clinical signs of heart failure. An ECG was performed and was similar to that shown in Fig. 44.1.

Questions

  1. 1. What does the ECG (Fig. 44.1) show?

  2. 2. What is the most likely cause of this arrhythmia?

  3. 3. How is this arrhythmia classified clinically?

  4. 4. How would you manage this patient acutely?

  5. 5. 10 years later the patient was incidentally found to be in persistent AF at a preoperative assessment for a knee replacement. What is the most likely cause?

  6. 6. How can the risk of thromboembolism after elective DC cardioversion be reduced?

  7. 7. How would you assess the long-term risk of thromboembolism due to AF?

  8. 8. How would you assess the risk of haemorrhage with anticoagulation?

Answers

  1. 1) What does the ECG (Fig. 44.1) show?

    Figure 44.1 demonstrates an irregularly irregular narrow-complex tachycardia with a ventricular rate around 200 bpm. There are no P waves. The irregular baseline consists of rapid oscillations (fibrillatory waves) that vary in size, shape, and timing. The rhythm is AF.

    There is ST-segment depression and T-wave inversion in leads II, III, aVF, and V4–V6. In the absence of symptoms suggestive of ischaemia these widespread non-specific ST-segment and T-wave changes are most likely to be rate related. However, in this case myocardial ischaemia and CAD should be considered in view of the subsequent clinical deterioriation.

  2. 2) What is the most likely cause of this arrhythmia?

    Electrical injury to the heart is likely to have triggered the AF in the present case. Electrical injury to the heart often causes ECG changes and arrhythmias, the most serious of which are asystole and VF. The initiation of AF after electrical injury is rare. Table 44.1 lists some of the more common causes of AF.

  3. 3) How is this arrhythmia classified clinically?

    Classification of AF should link the presentation of AF to a suggested management strategy. The classification should therefore include symptoms, risks of thromboembolism and haemorrhage with anticoagulation as well as type of AF.

    1. 1. Patients may be asymptomatic, symptomatic, or both.

    2. 2. Risks of thromboembolism and haemorrhage may be simply estimated and be high or low.

    3. 3. The presentation may be the first detected episode or a recurrence (Table 44.2).

    Recurrent AF may be paroxysmal, persistent, or permanent.

    This case describes a first presentation with AF.

  4. 4)How would you manage this patient acutely?

    If acute AF causes haemodynamic instability, as in the present case, urgent electrical cardioversion is required, irrespective of the duration of the AF. If there is any delay in organizing electrical cardioversion, intravenous amiodarone should be administered via a central vein.

    Patients with acute AF should be started on heparin (unfractionated or LMWH) at the initial presentation unless contraindicated (or already adequately anticoagulated). This should not delay emergency cardioversion. Heparin should be continued until a full assessment has been made and appropriate antithrombotic therapy has been started, based on risk stratification (see below).

    In this case, LMWH was administered and sinus rhythm restored by a single 200-J biphasic shock under general anaesthesia. A 12 lead ECG performed after cardioversion was normal. Serum troponin I taken 12 hours after the onset of haemodynamic compromise was not raised and echocardiography was normal. The patient was monitored in the CCU for 24 hours. The AF did not recur and the patient was transferred to a burns unit for skin grafting.

    On review 3 months later, the patient remained well and denied any recurrence of palpitations. ECG confirmed normal sinus rhythm and exercise tolerance testing was unremarkable.

Table 44.1 Cardiac and non-cardiac causes of AF

Cardiac causes of AF

Hypertension

Ischaemic heart disease

Valvular heart disease (particularly mitral stenosis)

Sick sinus syndrome

Pre-excitation syndromes (e.g. WPW syndrome; see Case 2)

Cardiomyopathy

Pericardial disease (including effusion and constrictive pericarditis)

Atrial septal defect

Cardiothoracic surgery

Atrial myxoma

Non-cardiac causes of AF

Electrolyte depletion (particularly K+ and Mg2+)

Excessive alcohol or caffeine consumption

Sepsis, particularly respiratory tract

Pulmonary embolism

Intrathoracic pathology (eg lung cancer, pleural effusion)

Thyrotoxicosis

Table 44.2 Classification of AF

First presentation

Management strategy

Initial event (first detected episode) – may or may not recur

Rhythm control

Symptomatic

Asymptomatic (first detected)

Onset unknown (first detected)

Recurrent AF (two or more episodes)

Paroxysmal AF1

Spontaneous termination within 7 days and usually within 48 hours

Rate or rhythm control

Persistent AF

Not self-terminating

Rate or rhythm control

Lasting more than 7 days or required cardioversion

Permanent AF

Not terminated

Rate control

Terminated but relapsed

No attempt at cardioversion

1 Use of pharmacological or DC cardioversion to reduce time to conversion does not change the classification of paroxysmal AF to persistent as AF would have terminated on its own.

Arrhythmia management

Atrial fibrillation is both the most common sustained arrhythmia and the most common cause of presentation to hospital due to arrhythmia. The prevalence of AF increases with age from 0.5% at 50–59 years to almost 9% at 80–89 years. It causes substantial mortality and morbidity due to stroke, thromboembolism, heart failure, reduced quality of life, and impaired cognitive function.

Rapid atrial stretch shortens the refractory period and can cause acute AF. This is often associated with ACS or LV failure. Management includes volume unloading and rate slowing. This may increase the atrial refractory period, improving the chance of cardioversion.

AF can be managed by either restoring and maintaining sinus rhythm (rhythm control) or ventricular rate control (rate control). There are no significant differences between these management strategies in relief of symptoms or mortality. Aggressive rhythm control is most appropriate for first presentations of AF or if symptoms persist despite control of the ventricular rate. Rhythm control increases admission to hospital and treatment-related side effects so rate control is recommended for the elderly and the minimally symptomatic.

Pharmacological therapy for rate control

AF is considered rate controlled if the resting ventricular response is 60–80 bpm and 90–115 bpm on moderate exertion. In the elderly, conduction disease is common so medication may not be required for rate control.

Beta blockade directly prolongs the refractory period of the AVN and antagonises sympathetic activity. Although beta-blockers are the first-line therapy, caution is required in patients with asthma, COPD, or heart failure.

The Calcium channel blockers CCBs verapamil and diltiazem prolong the refractory period of the AV node. These are commonly used for rate control, reducing heart rate at rest and during exercise. However, CCBs are negatively inotropic, so caution is required in patients with acute heart failure.

Digoxin is commonly used for rate control in patients with heart failure or limited activity. It blocks parasympathetic effects on the AV node but has little effect in terminating AF. It is less effective if AF is driven by sympathetic stimulation (e.g. sepsis, exercise, and hyperthyroidism). However, the combination of digoxin and beta-blockers is more effective than the combination of digoxin and diltiazem.

Amiodarone is sympatholytic and antagonises calcium, which therefore depresses AV conduction. Amiodarone is used in acute AF when conventional drugs have failed to control the ventricular rate. Rhythm control can be achieved in a significant number of cases.

Pharmacological therapy for rhythm control

The duration and type of AF should guide drug therapy for pharmacological cardioversion. Acute AF is associated with normal atrial refractory periods and relatively short excitable gaps. Slowing of conduction by drugs such as flecainide (class IC) is effective. Prolonged AF and strongly remodelled dilated atria rarely respond to classical antiarrhythmics. However, rhythm control may still be possible with class III drugs (e.g. amiodarone) or prolonged drug administration. Newer agents such as dronaderone, structurally related to amiodarone, may offer efficacy with less risk of side effects compared to amiodarone.

A consequence of AF-induced electrical remodelling is that the efficacy of secondary prophylaxis after cardioversion may depend on the type of recurrence. To prevent immediate recurrence of AF, class IC drugs and amiodarone are most effective. Amiodarone reduces all types of postcardioversion recurrence.

Electrophysiological and surgical techniques

Reducing atrial size or confining atrial electrical activity may eliminate re-entrant AF by reducing the volume of muscle in which re-entry can occur and thus reducing the number of circulating wavelets below a critical number. This is the principle of the Maze operation and of linear catheter ablation (left-atrial circumferential ablation).

Curative treatment of AF, such as ablation and surgery, requires understanding of the underlying mechanism. In patients with AF and atrial flutter or other supraventricular arrhythmias, including WPW syndrome, radiofrequency ablation or cryoablation aimed at these arrhythmias may also cure the AF. Furthermore, if focal AF is proven, ablation of the foci may be curative.

  1. 5) 10 years later the patient was incidentally found to be in persistent AF at a preoperative assessment for a knee replacement. What is the most likely cause?

    Hypertension is the most common cause of AF. Structural change to the left atrium often develops long before AF. The 5-year risk of chronic AF in hypertensive subjects is highest in those with the greatest LV mass and largest LA diameter. Management of hypertension is important to reduce the incidence of AF. Medical treatment of hypertension is important in the primary prevention of AF.

  2. 6) How can the risk of thromboembolism after elective DC cardioversion be reduced?

    The risk of thromboembolism is increased after cardioversion. The cause is complex. Pre-existing thrombus may embolize from the endocardial wall. Furthermore, thrombus may form after sinus rhythm is restored because the mechanical function of the atria is impaired.

    If AF has been present for over 48 hours full anticoagulation is usually required for at least 4 weeks before and after elective cardioversion. Thromboembolism occurs in up to 2% of cardioversions despite these precautions.

TOE-guided cardioversion

The need for adequate anticoagulation prior to urgent cardioversion can be avoided if TOE excludes LA thrombus. TOE can reveal thrombus within the left atrium and appendage and identify indicators for thrombus formation. If thrombus is seen the patient is at high risk of postcardioversion thromboembolism. The safety and applicability of TOE-guided cardioversion is reasonably established. After exclusion of thrombus, LMWH anticoagulation should start. Anticoagulation is still required for a minimum of 4 weeks after cardioversion so warfarin is generally started at the same time. After that time risk persists in patients with typical stroke risk factors so anticoagulation should be continued even if sinus rhythm is maintained and particularly if the risk of recurrence is high (Table 44.3).

Table 44.3 Factors indicating a high risk of AF recurrence

Previous failed cardioversion

Structural heart disease (mitral valve disease, LV dysfunction or large LA)

Long duration of AF (>12 months)

Previous recurrence

A TOE-guided cardioversion may also be used to minimize precardioversion anticoagulation to reduce bleeding risk or reduce delays to other treatments, for example surgery.

  1. 7) How would you assess the long-term risk of thromboembolism due to AF?

    The relative risk of thromboembolism is increased around five-fold by non-rheumatic AF. Non-rheumatic AF impairs atrial mechanical function by electrical and mechanical remodelling, which can occur within days. Subsequent structural remodelling further impairs atrial function, promoting blood stagnation and increasing the risk of thrombus formation. Long-term thromboprophylaxis is therefore required in persistent AF. The risk of thromboembolism is affected by age and coexisting disease. The CHADS2 score (Table 44.4) is a validated clinical prediction score for estimating the risk of stroke in non-rheumatic AF (Table 44.5).

    Anticoagulation with warfarin reduces the relative risk of stroke by 66%. However, the risk of haemorrhagic stroke and significant extracranial bleeding is increased, therefore in the lower risk groups aspirin, which provides a 33% relative risk reduction, is more appropriate. Recommended strategies for anticoagulation are listed in Table 44.6.

    Other independent risk factors for stroke in AF include structural heart disease and previous MI. The relative risk of thromboembolism is increased 17 times if AF is associated with rheumatic mitral valve disease so warfarin is strongly recommended.

    In the present case, the patient was anticoagulated with warfarin for 4 weeks before and after elective DC cardioversion. Thereafter he was treated with aspirin 75 mg daily as the CHADS2 score was 1. The knee replacement was performed 3 weeks later without complication.

  2. 8) How would you assess the risk of haemorrhage with anticoagulation?

    Anticoagulation is associated with an increased risk of spontaneous and traumatic haemorrhage. Assessment of bleeding risk is an important part of the clinical assessment and must be discussed with the patient before starting anticoagulation therapy.

    The annual rate of major haemorrhage (defined as intracranial haemorrhage, requiring transfusion of at least two units of blood, or requiring hospital admission) was 1% in controls and 1.3% in warfarin-treated patients. The annual risk of intracranial haemorrhage increases from 0.1% in control to 0.3% in warfarin-treated groups (excess of two intracranial bleeds per annum per 1000 patients treated). Factors that increase the risk of haemorrhage in patients on warfarin therapy are listed in Table 44.7

    To provide adequate thromboprophylaxis and minimize the risk of bleeding, aim for INR 2.5 (acceptable range 2.0–3.0). INR >3.0 is associated with increased bleeding and INR <2.0 with increased stroke risk.

    Low-dose aspirin also increases the risk of major haemorrhage, especially if hypertension is not well controlled. The addition of aspirin to oral anticoagulation therapy does not further reduce the risk of thromboembolism but increases bleeding risk. Warfarin should not be prescribed with aspirin or clopidogrel to reduce the risk of strokes in patients with AF.

Table 44.4 CHADS2 score

Condition

Points

C

Congestive heart failure

1

H

Hypertension (or treated hypertension)

1

A

Age >75 years

1

D

Diabetes

1

S2

Prior stroke or TIA

2

Table 44.5 The association between CHADS2 score and risk of stroke in non-rheumatic AF

CHADS2 Score

Stroke risk (%)

95% CI

0

1.9

1.2–3.0

1

2.8

2.0–3.8

2

4.0

3.1–5.1

3

5.9

4.6–7.3

4

8.5

6.3–11.1

5

12.5

8.2–17.5

6

18.2

10.5–27.4

Table 44.6 Strategies for anticoagulation based on the CHADS2 score

CHADS2 score

Risk

Anticoagulation therapy

Considerations

0

Low

Aspirin

75 mg/day lower doses may be equally efficacious

1

Moderate

Aspirin or warfarin

Aspirin daily or raise INR to 2.0–3.0, depending on factors such as patient preference

≥2

Moderate or high

Warfarin

Target INR range 2.0–3.0, unless contraindicated (e.g. history of falls, clinically significant gastrointestinal bleeding, inability to monitor INR regularly)

Table 44.7 Factors that increase risk of haemorrhage with anticoagulation therapy

Age over 75 years

Polypharmacy

Antiplatelet drugs (e.g. aspirin or clopidogrel) or NSAIDs

History of poorly controlled anticoagulation therapy

Uncontrolled hypertension

History of bleeding (e.g. peptic ulcer or cerebral haemorrhage)

Further reading

National Collaborating Centre for Chronic Conditions (2006). Atrial fibrillation: national clinical guideline for management in primary and secondary care. London: Royal College of Physicians.Find this resource:

    Androulakis A, Aznaouridis KA, Aggeli CJ, Roussakis GN, Michaelides AP, Kartalis AN, Stougiannos PN, Dilaveris PE, Misovoulous PI, Stefanadis CI, Kallikazaros IE. (2007). Transient ST-segment depression during paroxysms of atrial fibrillation in otherwise normal individuals: relation with underlying coronary artery disease. J Am Coll Cardiol; 50: 1909–1911.Find this resource: