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Flashcards in Periarrest arryhtmia Deck (23):

Patient with arrhythmia

Assess condition of the patient
Nature of arrhythmia


Adverse features

Heart failure
Myocardial ischaemia
Extremes of heart rate


Broad complex
No adverse features

With adverse features:

Patient is unstable-see algorithm page 107

If cardioversion fails give amiodarone 300mg over 10-20mins then after this loading dose give 900mg over 24hrs

Synchronised cardioversion under general anaesthesia-shock is delivered at R waves (unsync shock at T waves can cause VF)


Broad complex
No adverse features

If no adverse features:

Broad complex: SVT or VT
Regular and VT-amiodarone 300mg IV over 20-60mins then 900mg over 24hrs

Irregular and VT:
AF with BBB
WPW syndrome
Polymorphic VT (Torsades de pointes): stop all drugs that prolong QT, correct electrolyte anomalies esp hypokalaemia. Give magnesium sulfate 2g IV over 10mins


Narrow complex
Adverse features

Sinus tachycardia
AVRT due to WPW
Atrial flutter

Sinus tachy: Treat cause

AVNRT or AVRT: Usually benign

Atrial flutter: Regular AV conduction (2:1 block)
Usually 150 bpm

If adverse features: sync cardioversion post vagal manouvres and adenosine


Narrow complex
No adverse Features

No adverse features:
1) Vagal manouvres: carotid sinus massage
2) adenosine 6mg rapid IV bolus (ensure it is not atrial flutter)
3) No response give 12mg bolus
4) Give one further 12mg bolus if again no response

Almost all AVNRT and AVRT is terminated within secs

If no success of atrial flutter consider verapamil 2.5-5mg over 2mins


Rapid narrow complex tachycardia with no pulse

Start CPR
Sync shock will treat so this is an exception to the nonshockable algorithm.


Irregular narrow complex tachycardia
No adverse features:
- Rate control with drug therapy
- Rhythm control with chemical cardioversion
- Rhythm control with sync cardioversion
- Anticoagulation

AF with rapid ventricular response
Atrial flutter with variable AV conduction

If adverse features-sync cardioverson
Start anticoag-LMWH

If AF >48hrs high risk of clot so no cardioversion until 3 weeks of anticoagulation given or TOE confirms no thrombus

If cardioversion is urgent give LMWH therapeutic dose or infusion of unfract heparin and keep APTT at 1.5-2

If controlling heart rate use beta blocker-diltiazem or digoxin in heart failure.



Drug therapy

See page 111

Adverse features:
Atropine 500mcg IV rpt every 3-5 mins up to 3 mg (6 times)
Use with care in IHD

if persists use pacing

Second line drugs: IV glucagon
Theophylline 100-200mg slow IV
No atropine to cardiac transplant patients
isoprenaline 5mcg per min
Adrenaline 2-10mcg per min
Dopamine 2.5-10mcg per kg per min)


Cardiac pacing

No response to atropine then transcutaneous pacing immediately

Severe bradycardia use percussion pacing


AF and anticoag

In general, patients who have been in AF for longer than 48 hours should not be treated by cardioversion (electrical or chemical) until they have been fully anticoagulated for at least 3 weeks, or unless transoesophageal echocardiography has detected no evidence of atrial thrombus.

If the clinical situation dictates that cardioversion is needed more urgently, you should give:

Either regular low-molecular-weight heparin in therapeutic dose
Or an intravenous bolus injection of unfractionated heparin followed by a continuous infusion to maintain the activated partial thromboplastin time (APTT) at 1.5 – 2.0 times the control value
You should then continue heparin therapy and commence oral anticoagulation after successful cardioversion. It is important to seek expert advice on the duration of anticoagulation, which should be a minimum of 4 weeks, but substantially longer treatment is required in many cases.


First degree atrioventricular block

Extreme bradycardia may sometimes precede cardiac arrest and this may be prevented by prompt and appropriate treatment. In this context the most important bradyarrhythmia is complete heart block.

First degree atrioventricular block

The PR interval is the time between the onset of the P wave and the start of the QRS complex (whether this begins with a Q wave or R wave). The normal PR interval is between 0.12 and 0.20 s (or 3-5 small squares).

First degree atrioventricular (AV) block is present when the PR interval is > 0.20 s and is a common finding. It represents a delay in conduction through the AV junction (the AV node and immediately adjacent myocardium).

First degree AV block rarely causes any symptoms and as an isolated finding rarely requires treatment.


Second degree atrioventricular block

Second degree atrioventricular block

Second degree AV block is present when some, but not all, P waves are conducted to the ventricles, resulting in absence of a QRS complex after some P waves. There are two types.

Mobitz Type I AV block (also called Wenckebach AV block)

The PR interval shows progressive prolongation after each successive P wave until a P wave occurs without a resulting QRS complex. Often the cycle is then repeated.

The need for treatment is dictated by the effect of the bradyarrhythmia on the patient and the risk of developing more severe AV block or asystole.


Mobitz Type II AV block

Mobitz Type II AV block

There is a constant PR interval in the conducted beats but some of the P waves are not followed by QRS complexes.

This may occur randomly, without any consistent pattern. People with Mobitz II AV block have an increased risk of progression to complete AV block and asystole.

2:1 AV block describes the situation in which only alternate P waves are followed by a QRS complex. 2:1 AV block may be due to Mobitz I or Mobitz II AV block and it may be difficult to distinguish which it is from the ECG appearance. If bundle branch block is present (broad QRS complexes) as well as 2:1 block, this is likely to be Mobitz II block.


3:1 AV block

3:1 AV block

3:1 AV block is less common and is usually a form of Mobitz II AV block.

Immediate decisions about treatment of these rhythms will be determined by the effect of the resulting bradycardia on the patient. After identifying and providing any necessary immediate treatment, continue cardiac monitoring and arrange expert cardiological assessment.


Third degree atrioventricular block

In third degree (complete) AV block, there is no relationship between P waves and QRS complexes; atrial depolarisation and ventricular depolarisation arises independently from intrinsic ‘pacemakers’. The site of the pacemaker stimulating the ventricles will determine the ventricular rate and QRS width.

A pacemaker site in the AV node or proximal bundle of His may produce a narrow QRS complex.

A pacemaker site in the distal His-Purkinje fibres or ventricular myocardium will produce broad QRS complexes and is more likely to stop abruptly, resulting in asystole.


Agonal rhythm

Agonal rhythm occurs in dying patients.

It is characterised by the presence of slow, irregular, wide ventricular complexes, often of varying morphology. The section from an ECG rhythm strip here shows agonal rhythm.

This rhythm is seen commonly during the later stages of unsuccessful resuscitation attempts. The complexes slow inexorably and often become progressively broader before all recognisable activity is lost.


Escape Rhythm

If the normal cardiac pacemaker (SA node) fails, or operates abnormally slowly, cardiac depolarisation may be initiated from a ‘subsidiary’ pacemaker in atrial myocardium, AV node, conducting fibres or ventricular myocardium.

The resulting escape rhythm will, in most cases, be slower than the normal sinus rate.


Bradycardia: Atropine

As detailed in the bradycardia algorithm (available from the algorithm tab), where there are adverse features, give 500 mcg of atropine intravenously.

If there is not a satisfactory response, this dosage of atropine can be repeated up to a maximum total does of 3 mg.


Bradycardia: Cardiac Pacing

In some cardiac arrest or peri-arrest settings, appropriate use of cardiac pacing can be life-saving.

Non-invasive pacing may be used to maintain cardiac output temporarily while expert help to deliver longer-term treatment is obtained. Non-invasive pacing can be established rapidly and is well within the capabilities of an ALS provider.


Bradycardia: Cardiac Pacemakers

The ALS provider does not need to have a detailed technical knowledge of permanent cardiac pacemakers and implanted cardioverter defibrillators (ICDs) but needs to be able to recognise:

When one of these devices is present
When they are failing
How the presence of an implanted device may influence the management of a cardiac arrest.
Implanted devices that deliver pacing include pacemakers implanted for the treatment of bradycardia, as well as ICDs (which have pacing capacity) and biventricular pacemakers (implanted for left ventricular failure).


Bradycardia: Percussion Pacing

When bradycardia is so profound that it causes clinical cardiac arrest, percussion pacing may be used in preference to CPR because it may produce an adequate cardiac output with less trauma to the patient.

To perform percussion pacing:

With the side of a closed fist deliver repeated firm blows to the precordium lateral to the lower left sternal edge.
Raise the hand about 10 cm above the chest for each blow.
If initial blows do not produce a QRS complex try using slightly harder blows and try moving the point of contact around the precordium until a site is found that produces repeated ventricular stimulation.
If attempted percussion pacing does not achieve a cardiac output within a few seconds, start CPR.


Bradycardia: Transcutaneous Pacing

Patients requiring transcutaneous pacing are likely to need sedation. Transcutaneous pacing and drugs used in extreme bradycardia should be a bridge to definitive treatment (transvenous pacing and/or correction of the cause of the extreme bradycardia).

Once the patient is connected to the external pacemaker the output (in milliamps) should be increased until electrical capture is achieved.

Once this has occurred the patient cardiovascular status should be reassessed, starting with the pulse, to ensure electrical capture is associated with mechanical capture.

This ECG shows ventricular capture after each pacing spike.