Cardiology

Arrhythmias

Supraventricular rhythms

Sinus Rhythm

  • Each P wave followed by QRS. QRS Rate 60-100. Normal.

Sinus arrhythmia

  • Each P wave followed by QRS and rate increases with inspiration due to increased vagal tone. Will be lost in those with with autonomic neuropathy or in a cardiac transplanted heart

Sinus Bradycardia

  • P wave followed by QRS; QRS rate < 60/min.
  • Normal in athlete. Hypothyroidism, Sinus node ischaemia, Raised Intracranial pressure, Obstructive jaundice, physiological. Check Thyroid function

Sinus Tachycardia

  • P wave followed by QRS. QRS rate > 100/min.
  • Normal response to exercise, anxiety, stress, pathological states, shock, hyperthyroidism, Sepsis. Assess TFT, BP. Identify and treat cause.

Sinus pauses

  • Normal P QRS T wave then nothing for 3 seconds or longer
  • Not uncommon but needs paced if symptomatic.

Atrial ectopics

  • P' wave early with normal width QRS < 0.12 sec unless BBB.
  • P morphology may be different

Atrial Fibrillation

introduction

Atrial fibrillation is perhaps the most important arrhythmia that you will have to deal with. It is not the effect that AF has on the heart that is the issue but its effect on the brain. The brain receives a very high proportion of cardiac output for its size and is extremely sensitive to even momentary episodes of ischaemia. The head and neck vessels are the first to come of the aorta. The main risk of AF is that of cardioembolism from thrombus in the left atrium and atrial appendage

Classification

First detected - only one diagnosed episode. Paroxysmal - recurrent episodes that self-terminate in less than 7 days. Persistent - recurrent episodes that last more than 7 days. Permanent - an ongoing long-term episode

Risks and causes

There is a long list of causes. AF is commonest in the elderly. It is also associated with heard disease which is ischaemic, hypertensive, valvular and congenital or with all forms of cardiomyopathy. It is seen with thyrotoxicosis, with alcohol misuse (post acute binge or chronic or post cardiac surgery or with chest infection or even a pulmonary embolism. Sometimes no cause is found "Lone AF".

Investigations

The ECG shows an absence of P waves and the presence of an irregular baseline. Classically the QRS is random and irregularly irregular. Loss of normal atrial systole.The atria fibrillate at 400-500 bpm with loss of any atrial component to augment ventricular filling. FBC U&E LFT. CXR, ECG, TFTs, Echocardiogram, Troponin done if ACS suspected, Dimer if PE suspected

Management

Anticoagulation is vitally important to prevent stroke in those at high risk of embolism who should receive warfarin. Those at lower risk may get Aspirin or if intolerant clopidogrel. Assess using CHADS2 score

  • Congestive heart failure + 1
  • Hypertension +1
  • Age > 75 +1
  • Diabetes +1
  • Stroke or TIA + 2

Generally those with CHADS 0 or 1 should be on aspirin. Those 2 or over consider warfarin.

Rhythm control - Some patients where the AF is new onset or there is no underlying structural cause then attempts at restoration of SR should be attempted. This can be either chemical or electrical cardioversion. Some patients will spontaneously revert once the underlying cause has passed e.g. alcohol binge, chest infection resolved. DC Cardioversion - Synchronised DC shock of 100-200 J given to a sedated patient. Patient should be anticoagulated for 4-6 weeks before and 4 weeks after even if successful. Chemical Cardioversion involves the use of drugs such as flecainide which is not to be used if there is any suggestion of structural cardiac disease. Atrial fibrillation can be transient and recurrent - Paroxysmal and is treated as if the AF was continuous in terms of anticoagulation. Ablation can be considered in some patients, which involves ablating an area around the pulmonary veins. More useful to prevent Paroxysmal AF.

Rate control - if restoration of SR is felt to be unlikely to be successful or has repeatedly failed then rate control usually with either a beta blocker, Digoxin or Diltiazem can be tried. Amiodarone and other antiarrhythmics may be used

Atrial Flutter

Introduction

Atrial flutter shares a lot in common with AF but is easier to treat. It is a more organized arrhythmia at 300 bpm. There is a re-entry circuit in the right atrium. There are sawtooth flutter waves on ECG and the QRS may be totally irregular or at a rate that is a divisor of 300 e.g. 75/100/150 bpm. Causes and precipitants are similar to AF and TFT and other tests should be done as suspected.

Management is for chronic A flutter to treat as AF. Defibrillation requires only small energy level settings. Much easier to treat and revert to SR. Warfarinise those with increased CHADS2 scoring.

Pre-excitation syndromes/Wolff Parkinson White syndrome

Introduction

The AV node is the traffic calming speed hump of the heart and prevents fast atrial rhythms from becoming fast ventricular rhythms by only allowing a maximal rate of conduction from atria to ventricle (usually around 160-180 bpm) . If there is a bypass around this safety mechanism this can lead to unwanted behaviour. This is seen in WPW and similar syndromes. They are called pre-excitation syndromes as the ventricle is depolarised "excited" before it actually should be. One is born with WPW but it can present at any age. Conduction pathways and their refractoriness and conducting properties can vary with age, drugs and other factors. Despite an accessory pathway the characteristics can mean that only the AV node route is used.

Mechanism

There are two main problems. Firstly the abnormal connection brings into existence a small circuit for depolarisation from atria to ventricle across the AV node and back to the atria via the accessory bundle or vice versa. This can set up a fast narrow complex tachycardia called a Atrioventricular nodal reentrant tachycardia (AVNRT). If the pathway goes down through the AV node it is orthodromic. If it travels up the AV node it is antidromic. This can be triggered by an atrial ectopic. These arrhythmias though troublesome are usually benign. The second problem is that conduction from atria to ventricles can be unregulated and if the patient gets AF then this can stimulate very fast ventricular rates which can cause VT or VF. This is potentially life threatening.

Various types of PES include Wolff Parkinson-white syndrome with a Bundle of Kent (conducting tissue) between atria and ventricles. The location of the accessory pathway can be in different places giving different surface ECG appearance. Lown Ganong levine has an accessory pathway between atria and conducting tissues resulting in an ECG finding with a short PR but no delta wave

Investigations

The ECG is key and this may actually be normal if the AVN is always used and this is called a "concealed pathway". Both pathways may be used and this shows a normal P wave and shortened PR interval with a delta wave. AV re-entrant tachycardia - Narrow complex with inverted p waves seen buried in the QRS. Fast AF conducting to the ventricles via accessory pathway with an irregular fast wide complex rhythm with delta wave can lead to VT and even degenerate to VF.

Clinical

Clinically the patient experiences palpitation associated with episodes of AVRT. In some patients they have no symptoms and the diagnosis is made on a routine ECG. Some patients have years of recurring episodes of palpitation. There may be polyuria after palpitations due to ANP release.

Management

If the PES found on ECG is causing no symptoms then nothing needs to be done at all. For those presenting with AV reentrant tachycardia this can be treated by either vagal stimulation e.g. Carotid sinus massage or by using adenosine. Other choices include flecainide or IV beta blockers. If this fails then DC cardioversion should be tried. This should terminate the AVRT. If this recurs often then the patient may be a good candidate for ablation of the accessory pathway. In those with pre excited AF conducted to the ventricles management should be defibrillation. Digoxin or verapamil should be avoided as this can encourage conduction via the accessory pathway. If ablation is not possible or successful long term flecainide or propafenone or even amiodarone have been used.

Ventricular Arrhythmias

Ventricular ectopics

Wide QRS complex earlier than expected. Compensatory pause after. Do not treat. Look for causes e.g. ischaemia. Correct electrolytes. Manage any case found. Suppression of ectopics has not been shown to be beneficial.

Idioventricular Tachycardia

This is a benign arrhythmia seen usually in the setting post MI. The ECG shows wide complex regular tachycardia which looks very much like VT but the rate is less than 120 bpm. Assess the patient and if stable and pain free and electrolytes are normal then observe and avoid treatment. It may be a good sign suggesting reperfusion and patency of a culprit vessel in a STEMI. It will usually resolve.

Ventricular Tachycardia

Introduction

This is a wide complex regular tachycardia arising in the ventricle with a rate > 120 pm. It can be divided into sustained (> 30 seconds) and non sustained VT. VT is potentially life threatening and needs rapid assessment and appropriate treatment. As with all tachyarrhythmias DC cardioversion must be considered if patients are unstable.

Causes

Causes of VT include Ischaemic heart disease, Cardiomyopathy, Drug overdose, Electrolyte disturbance. Long QT due to drugs or Congenital.

Clinical

VT may present with cardiac arrest and pulseless VT or with only the mildest symptoms. I have had patients drive considerable distances to the hospital in VT. Patients may have syncope, be hypotensive or in crushing pulmonary oedema. Much depends on rate and underlying myocardial function.

Investigations

Check Electrolytes, Troponin, ECG and clinical Features of VT - QRS > 0.12 seconds (3 small squares), Regular, History of IHD or structural cardiac disease, LBBB pattern, Fusion beats, Capture beats.

Management

Treat all regular broad complex tachycardias as VT unless you have very convincing senior evidence to the contrary. There are lists of ECG clues to differentiate VT and SVT with aberration but this is for post hoc analysis. It's VT until a senior person says otherwise. The concern is always that VT degenerates to VF which is lethal. VT is a potentially fatal arrhythmia. Treatment is immediate synchronised DC cardioversion. If the patient is stable Amiodarone IV is a reasonable choice of antiarrhythmic. Alternatively IV Lidocaine. Ensure electrolytes and magnesium and acid base balance are normal. If the VT is in the setting of acute coronary syndrome with ongoing chest pain then urgent PCI to establish re perfusion should be the main focus. Long term management is often antiarrhythmic and in high risk cases an ICD may be inserted. Surgery or catheter ablation may be appropriate in selected cases.

Torsades de pointes

Introduction

A Form of VT where the axis constantly changes. It is precipitated by anti-arrhythmic drugs or any drug that causes prolongation of the QT (repolarisation) interval and any cause of QT prolongation, congenital or acquired.

Causes

These include Amiodarone Erythromycin, terfenadine, TCA, quinidine, Class I and III antiarrhythmics, Lithium, phenothiazines

Management

Avoid amiodarone or other anti-arrhythmics if possible - can make it worse by prolonging QTc. Stop any drugs which may be to blame. Correct K and Mg. Temporary atrial pacing may well be useful to increase ventricular rate which can often stop or reduce the episodes of torsade until the QT normalises

Ventricular fibrillation

VF is a lethal but easily treatable arrhythmia. The underlying aetiology is complex with circuits or reentry and increased automaticity. The causes are Myocardial infarction/Ischaemia, drug overdose, cardiac trauma, cardiomyopathy and hyperkalaemia. Management is fundamentally early defibrillation.