BLS and ACLS Surveys

Foundational to every ACLS Algorithm is the BLS survey. The BLS Survey is the first step that you will take when treating any emergency situation, and there are 4 main assessment steps to remember. These for steps are designated by the numbers 1, 2, 3, and 4.This is an outline of the 4 steps in the BLS Survey :(1) Check responsiveness by tapping and shouting, “Are you all right?” Scan the patient for absent or abnormal breathing (scan 5-10 seconds).(2) Active emergency response system and obtain a AED. If there is more than one rescuer, have the second person activate emergency response and get the AED/Defibrillator.(3) Circulation: Check for a carotid pulse. This pulse check should not take more than 5-10 seconds. If no pulse is palpable begin CPR.(4) Defibrillation: If there is no pulse, check for a shockable rhythm with the AED or defibrillator as soon as it arrives. Follow the instructions provided by the AED or begin ACLS Protocol.For a more in-depth review of BLS refer to the American Heart Association’s BLS Provider Manual. Remember to assess first then perform appropriate actions, and after each action…reassess.

The ACLS Survey uses the ABCD model to systematize the ACLS process. The ABCD’s of the ACLS Survey are:(A) Airway: Maintain airway and use advanced airway if needed. Ensure confirmation of placement of an advanced airway and secure the advanced airway device.(B) Breathing: Give bag-mask ventilation, provide supplemental oxygen, and avoid excessive ventilation. Also, adequacy of ventilation and oxygenation should be monitored during this step.(C) Circulation: Obtain IV access, attach ECG leads, identify and monitor arrhythmias, giving fluids if needed, and use defibrillation if appropriate.(D) Differential diagnosis: Look for reversible causes and contributing factors for the emergency.First Degree Heart BlockDefinition

PR interval > 200ms (five small squares)

‘Marked’ first degree block if PR interval > 300msExamplesFirst degree heart block (PR interval > 200 ms)

Marked first degree heart block (PR interval > 300 ms, P waves are buried in the preceding T wave)

Causes Increased vagal tone Athletic training Inferior MI Mitral valve surgery Myocarditis (e.g. Lyme disease) Hypokalaemia AV nodal blocking drugs (beta-blockers, calcium channel blockers, digoxin, amiodarone) May be a normal variant

Clinical significance Does not cause haemodynamic disturbance No specific treatment is required

AV Block: 2nd degree, Mobitz I (Wenckebach Phenomenon)

Definition Progressive prolongation of the PR interval culminating in a non-conducted P wave The PR interval is longest immediately before the dropped beat The PR interval is shortest immediately after the dropped beat

Other Features The P-P interval remains relatively constant The greatest increase in PR interval duration is typically between the first and second beats of

the cycle. The RR interval progressively shortens with each beat of the cycle. The Wenckebach pattern tends to repeat in P:QRS groups with ratios of 3:2, 4:3 or 5:4.

Example of a typical Wenckebach ECG

The first clue to the presence of Wenckebach AV block on this ECG is the way the QRS complexes cluster into groups, separated by short pauses (This phenomenon usually represents 2nd-degree AV block or non-conducted PACs; occasionally SA exit block).

At the end of each group is a non-conducted P wave; the PR interval progressively increases from one complex to the next.

The Wenckebach pattern here is repeating in cycles of 5 P waves to 4 QRS complexes (5:4 conduction ratio).

The increase in PR interval from one complex to the next is subtle. However, the difference is more obvious if you compare the first PR interval in the cycle to the last.

The P-P interval is relatively constant despite the irregularity of the QRS complexes.Thanks to Dr Harry Patterson, FACEM, for providing this ECG. Mechanism

Mobitz I is usually due to reversible conduction block at the level of the AV node. Malfunctioning AV node cells tend to progressively fatigue until they fail to conduct an impulse.

This is different to cells of the His-Purkinje system which tend to fail suddenly and unexpectedly (i.e. producing a Mobitz II block).

Causes Drugs: beta-blockers, calcium channel blockers, digoxin, amiodarone Increased vagal tone (e.g. athletes) Inferior MI Myocarditis Following cardiac surgery (mitral valve repair, Tetralogy of Fallot repair)

Clinical significance Mobitz I is usually a benign rhythm, causing minimal haemodynamic disturbance and with low

risk of progression to third degree heart block.

Asymptomatic patients do not require treatment. Symptomatic patients usually respond to atropine. Permanent pacing is rarely required.

AV Block: 2nd degree, Mobitz II

Definition Intermittent non-conducted P waves without progressive prolongation of the PR interval

(compare this to Mobitz I). The PR interval in the conducted beats remains constant. The P waves ‘march through’ at a constant rate. The RR interval surrounding the dropped beat(s) is an exact multiple of the preceding RR interval

(e.g. double the preceding RR interval for a single dropped beat, treble for two dropped beats, etc).

Example of Mobitz II

Arrows indicate “dropped” QRS complexes (i.e. non-conducted P waves)Mechanism

Mobitz II is usually due to failure of conduction at the level of the His-Purkinje system (i.e. below the AV node).

While Mobitz I is usually due to a functional suppression of AV conduction (e.g. due to drugs, reversible ischaemia), Mobitz II is more likely to be due to structural damage to the conducting system (e.g. infarction, fibrosis, necrosis).

Patients typically have a pre-existing LBBB or bifascicular block, and the 2nd degree AV block is produced by intermittent failure of the remaining fascicle (“bilateral bundle-branch block”).

In around 75% of cases, the conduction block is located distal to the Bundle of His, producing broad QRS complexes.

In the remaining 25% of cases, the conduction block is located within the His Bundle itself, producing narrow QRS complexes.

Unlike Mobitz I, which is produced by progressive fatigue of the AV nodal cells, Mobitz II is an “all or nothing” phenomenon whereby the His-Purkinje cells suddenly and unexpectedly fail to conduct a supraventricular impulse.

There may be no pattern to the conduction blockade, or alternatively there may be a fixed relationship between the P waves and QRS complexes, e.g. 2:1 block, 3:1 block.

Causes of Mobitz II

Anterior MI (due to septal infarction with necrosis of the bundle branches). Idiopathic fibrosis of the conducting system (Lenegre’s or Lev’s disease). Cardiac surgery (especially surgery occurring close to the septum, e.g. mitral valve repair) Inflammatory conditions (rheumatic fever, myocarditis, Lyme disease). Autoimmune (SLE, systemic sclerosis). Infiltrative myocardial disease (amyloidosis, haemochromatosis, sarcoidosis). Hyperkalaemia . Drugs: beta-blockers, calcium channel blockers, digoxin, amiodarone.

Clinical Significance Mobitz II is much more likely than Mobitz I to be associated with haemodynamic compromise,

severe bradycardia and progression to 3rd degree heart block. Onset of haemodynamic instability may be sudden and unexpected, causing syncope (Stokes-

Adams attacks) or sudden cardiac death. The risk of asystole is around 35% per year. Mobitz II mandates immediate admission for cardiac monitoring, backup temporary pacing and

ultimately insertion of a permanent pacemaker.

AV block: 2nd degree, “fixed ratio” blocksDefinition

Second degree heart block with a fixed ratio of P waves: QRS complexes (e.g. 2:1, 3:1, 4:1). Fixed ratio blocks can be the result of either Mobitz I or Mobitz II conduction.

Examples2:1 block

The atrial rate is approximately 75 bpm. The ventricular rate is approximately 38 bpm. Non-conducted P waves are superimposed on the end of each T wave.

3:1 block

The atrial rate (purple arrows) is approximately 90 bpm. The ventricular rate rate is approximately 30 bpm. Note how every third P wave is almost entirely concealed within the T wave.

Mobitz I or II? It is not always possible to determine the type of conduction disturbance producing a fixed ratio

block, although clues may be present.

Mobitz I conduction is more likely to produce narrow QRS complexes, as the block is located at the level of the AV node. This type of fixed ratio block tends to improve with atropine and has an overall more benign prognosis.

Mobitz II conduction typically produces broad QRS complexes, as it usually occurs in the context of pre-existing LBBB or bifascicular block. This type of fixed ratio block tends to worsen with atropine and is more likely to progress to 3rd degree heart block or asystole.

However, this distinction is not infallible. In approximately 25% of cases of Mobitz II, the block is located in the Bundle of His, producing a narrow QRS complex. Furthermore, Mobitz I may occur in the presence of a pre-existing bundle branch block or interventricular conduction delay, producing a broad QRS complex.

The only way to be certain is to observe the patient for a period of time (e.g. watch the cardiac monitor, print a long rhythm strip, take serial ECGs) and observe what happens to the PR intervals. Often, periods of 2:1 or 3:1 block will be interspersed with more characteristic Wenckebach sequences or runs of Mobitz II.

AV block: 3rd degree (complete heart block)

Definition In complete heart block, there is complete absence of AV conduction – none of the

supraventricular impulses are conducted to the ventricles. Perfusing rhythm is maintained by a junctional or ventricular escape rhythm. Alternatively, the

patient may suffer ventricular standstill leading to syncope (if self-terminating) or sudden cardiac death (if prolonged).

Typically the patient will have severe bradycardia with independent atrial and ventricular rates, i.e. AV dissociation.

Example of complete heart block

The atrial rate is approximately 100 bpm. The ventricular rate is approximately 40 bpm. The two rates are independent; there is no evidence that any of the atrial impulses are

conducted to the ventricles.Mechanism

Complete heart block is essentially the end point of either Mobitz I or Mobitz II AV block. It may be due to progressive fatigue of AV nodal cells as per Mobitz I (e.g. secondary to

increased vagal tone in the acute phase of an inferior MI).

Alternatively, it may be due to sudden onset of complete conduction failure throughout the His-Purkinje system, as per Mobitz II (e.g. secondary to septal infarction in acute anterior MI).

The former is more likely to respond to atropine and has a better overall prognosis.Causes of complete heart blockThe causes are the same as for Mobitz I and Mobitz II second degree heart block. The most important aetiologies are:

Inferior myocardial infarction AV-nodal blocking drugs (e.g. calcium-channel blockers, beta-blockers, digoxin) Idiopathic degeneration of the conducting system (Lenegre’s or Lev’s disease)

Clinical significance Patients with third degree heart block are at high risk of ventricular standstill and sudden cardiac

death. They require urgent admission for cardiac monitoring, backup temporary pacing and usually

insertion of a permanent pacemaker.