Module 5: Rhythm recognition Flashcards
How do you identify normal Atrial, AV, and Ventricular electrical activity?
Atrial activity = P wave
Depolarisation begins at the SAN (specialist pacemaker cells). Atria contract.
Normal AV activity = isoelectric PR.
Electrical activity reaching the AVN is conducted slowly. From the AVN, it rapidly conducts down the Purkinje fibres to the ventricles.
Normal ventricular electrical activity = QRS
Depolarisation moves down Purkinje fibres in the Bundle of His, Left & Right bundle bracnhes, and throughout the ventricles. This coordinated depolarisation of the BoH, bundle branches & ventricular myocardium is the QRS.
ECG for SR?
A&V contract at the same rate, around 60 beats min-1.
Myocardial activity is coordinated.
ECG for VF?
Electrical activity is chaotic, there is no coordinated activity in the A/V.
ECG for pVT?
V contract at a much faster rate than the A. There may or may not be a pulse rhythm. Confirmation of cardiac arrest will dictate the action taken.
HR around 240 min-1.
ECG for asystole?
Neither the A or V exhibit any electrical or mechanical activity
How to read a rhythm strip
Stage 1: Is there any electrical activity?
No electrical activity + no signs of life → begin CPR
No electrical activity + signs of life → continue to stage 2 of rhythm recognition
Stage 2 - What is the ventricular (QRS) rate?
Calibrated to 25 mm s-1.
and obviously 1 large square = 5 mm.
5 large squares (25 small sq) = 25mm = 1sec.
Ventricular rate = how many QRS occur in 6s (30 large squares) x10
Stage 3: Is the QRS rhythm regular or irregular?
Measure and compare each R-R
If irregular, is it:
- Totally irregular
- Basic regular rhythm with intermittent irregularity
- Recurring cyclical variation in R-R
Stage 4 - Is the QRS width normal (narrow) or broad?
- Upper limit for QRS = 0.12 s (3 small squares)
<0.12s = rhythm originates from above bundle of His bifurcation (atrial, SAN, AVN)
≥0.12s = rhythm is ventricular OR supraventricular with aberrant conduction
Stage 5 - Is atrial activity present?
(Is so, - are they sinus P waves? AF? Flutter? Abnormal P waves?).
Normal ECG P waves are:
- Positive in Lead II and
- Biphasic in V1
Ectopic atrial rhythm
= P waves of different morphology which arise from another part of the atria
Sustained VT with rapid QRS rate
= atrial activity may not be visible between QRS complexes
AFib
= Waves of depolarisation are travelling in different directions through both atria, best seen in V1 as irregular electrical activity which varies in amplitude & frequency
= Irregularly irregular rhythm
= Normal P waves are absent
AFlutter
= An SVT caused by a re-entry circuit within the RA which occurs at a fairly predictable atrial rate of ~300 bpm (260–300 min-1)
= Regular pattern of ‘saw-tooth’ waves
= Best seen in inferior leads (II, III, aVF)
Stage 6 - How is atrial activity related to ventricular activity?
Examine a strip for PR intervals – look carefully as variations may be subtle!
E.g. 1:1 conduction, 2:1 conduction, no relationship
Consistent PRs = ventricular depolarisation is likely triggered by atrial depolarisation
Variations in PR, QRS rate is slower than atrial rate = indicates a degree of heart block
No relationship = atrioventricular dissociation
= ventricular depolarisation arises independently
Summary of the 6 stage ECG approach.
- Any electrical activity?
- Ventricular rate?
- Rhythm (R–R interva)
- Narrow or broad QRS (0.12s)
- Atrial activity (P)
- Relationship between P:QRS (PR)
What are the cardiac arrest rhythms (these need rapid identification to enable safe and effective treatment!)
- VF
- pVT
- PEA
- Asystole
Ventricular fibrillation (VF)
In a collapsed pulseless patient, VF is usually easy to confirm from a study of the ECG rhythm strip.
Once VF is confirmed: defib asap + treat according to ‘shockable’ rhythm algorithm
The rhythm abnormality that is most likely to be mistaken for VF is polymorphic VT (torsades de pointes VT). Patients may be pulseless and lose consciousness during this rhythm; it may terminate spontaneously, or may degenerate into VF. But in TSP with cardiac arrest the appropriate treatment is still defibrillation, so don’t worry about giving inappropriate treatment.
Ventricular tachycardia (VT)
- May generate a detectable cardiac output (pulse)
- Or may cause loss of cardiac output, resulting in arrest (pVT)
- May degenerate into VF
VT QRS morphology may be
- Monomorphic (regular rhythm strip pattern)
- Polymorphic (QRS complexes vary from complex to complex)
One form of polymorphic pVT is Torsades de Pointes pVT (sinusoidal pattern of variation in QRS amplitude).
Aystole
- Pulseless patient AND
- No electrical activity
Absent electrical activity indicates asystole in atria as well as ventricles.
NB: important to differentiate from ventricular standstill – ventricular asystole with continued P wave activity in the atria –arial contraction alone will not maintain cardiac output, so cardiac arrest will be present – but essential to identify as cardiac pacing may restore ventricular contraction.
What if you can’t distinguish Asystole from very fine VF?
- Do not waste time!
- If you think VF, shock
- If you think asystole, continue CPR
…Avoid excessive interruptions off the chest.
Pulseless electrical activity (PEA)
- PEA does not refer to a specific cardiac rhythm.
- = Clinical absence of CO despite electrical activity that would normally be expected to produce a CO.
Treatable causes include:
- Large MI (poor prognosis)
- Massive PE
- Tension pneumothorax
- Cardiac tamponade
- Acute severe blood loss
Atrial fibrillation ECG
Is the ventricular (QRS) rate normal?
Is the QRS rhythm regular?
Is the QRS complex width normal?
Is atrial activity present?
Is atrial activity related to ventricular activity?
- No (fast e.g. 200 min-1)
- No (irregularly irregular)
- Yes (<0.12s)
- Yes -but abnormal, with fibrillation waves present
- No -completely irregular, no relationship between atrial & irregular ventricular rhythm that results from it.
Second degree AV block, Mobitz 1 (Wenckebach)
Is the ventricular (QRS) rate normal?
Is the QRS rhythm regular?
Is the QRS complex width normal?
Is atrial activity present?
Is atrial activity related to ventricular activity?
- No -bradycardia
- No -irregularity due to progressive lengthening of PR followed by a non-conducted P wave
- Yes -a narrow-complex bradycardia
- Yes
- Yes -The PR interval becomes progressively longer with each cycle until a P wave is not conducted to the ventricles, and then the PR interval becomes shorter again after the non-conducted P wave.
Types of heart block?
1st Degree =PR >0.2s
2nd Degree
* Mobitz I = progressive PR + dropped beat
* Mobitz II (Wenkenbach) = intermittent dropping of ventricular conduction
* 2:1 = alternate p waves not conducted
3rd degree = complete dissociation (complete)
Branch blocks
* LPFB
* LAFB
* LBBB
* RBBB
* Bifascicular
* Trifascicular
Management of heart blocks
- 1st degree = nothing unless Sx
- 2nd degree MI = nothing unless Sx
- 2nd degree MII = pacemaker
- 3rd degree = pacemaker
- Branch blocks
- Nothing unless Sx or progresses
- If symptomatic -> pacemaker
- Trifascicular -> pacemaker
- May need temporary pacing wire or external pacing
- If rate too slow & unresponsive to drugs -> pace
Emergency management of bradycardia
- Check BP
- Atropine 25mcg/kg
- glycopyrolate 0.2mg
- isoprenaline 1-10mcg/min
- Adrenaline 0.1-1.0mcg/kg/min
- Temp pacing (TT, TO, TV)
VT
Is the ventricular (QRS) rate normal?
Is the QRS rhythm regular?
Is the QRS complex width normal?
Is atrial activity present?
Is atrial activity related to ventricular activity?
- No –very rapid
- Yes
- No – difficult to measure but very prolonged (i.e. broad QRS)
- No –not possible to see atrial activity with any confidence
- N/A due to above
What else may appear as a regular broad-complex tachycardia other than VT?
SVT with BBB, but it is safer to manage as VT unless proven to be supraventricular in origin
Complete AV block
Is the ventricular (QRS) rate normal?
Is the QRS rhythm regular?
Is the QRS complex width normal?
Is atrial activity present?
Is atrial activity related to ventricular activity?
- No –bradycardia
- Yes
- No –broad
- Yes
- No –no relationship
Atrial flutter with 2:1 conduction
Is the ventricular (QRS) rate normal?
Is the QRS rhythm regular?
Is the QRS complex width normal?
Is atrial activity present?
Is atrial activity related to ventricular activity?
- No
- Yes
- Yes –a narrow-complex tachy
- Yes – saw-tooths
- Yes –atrial:ventricular relationship of 2:1, gives a very fast QRS rate
ECGs in acute MI.
Patients p/w ACS symptoms require a 12-lead ECG asap.
ECG may be normal in ACS, including acute MI, so serial ECGs may be needed.
12-lead ECGs look at electrical activity in 3 dimensions. Those leads with ST-segment or T wave abnormalities will indicate the part of the LV myocardium which is affected.
Inferior leads
II, III, aVF
Look at heart from below
Show abnormalities in inferior wall LV
Lateral leads
I, aVL, V6
Look at heart from left side
Show abnormalities which arise from lateral wall of LV
Anterior leads
V2, V3, V4
Look at front of heart
Show abnormalities in anterior wall of LV
TWI in aVR
Normal
TWI in V1
Usually normal & not inverted
QRS is also mainly a negative deflection
TWI in III
QRS is often but not always positive
If QRS is negative, T wave is usually too
A negative T wave with a positive QRS or with abnormalities in other leads more likely represents true TWI
Significance of TWI
Can be normal
Can occur in STEMIs
Can occur in NSTEMIs*
- Non-specific
- Requires supportive clinical and biochemical evidence to confirm acute MI
*TWI may be the only abnormality in NSTEMIs (as there is no ST-elevation) but must be accompanied by clinical and biochemical evidence of acute MI
TWI alone is non-specific, may be present in many people for other reason, is not evidence of acute MI unless supportive clin & biochem evidence
Significance of ST-depression
- Non-specific
- Requires supportive clinical and biochemical evidence to confirm acute MI
Significance of ST-elevation in a patient with severe chest pain
- Complete occlusion of a coronary
- Requires immediate arrangements for reperfusion therapy
Anterolateral STEMI
ST-elevation in: anterior and lateral leads e.g. I, aVL, V2–V6
STD in: III, aVF
Inferior STEMI
ST-elevation: II, III, aVF
STD: I, aVL
Posterior-wall STEMI
ST-elevation: posterior leads
ST-depression: anterior leads
STD anterior leads -> consider getting posterior ECG to look for reciprocal ST-elevation at back of heart.
Patients who DO vs DONT require cardiac monitoring?
DO
- Signs of shock (high risk sudden deterioration)
- Post MI (high risk arrhythmia)
- Syncope during exercise (high risk symptom, may indicate structural heart disease and/or life-threatening arrhythmia)
Don’t:
- Sinus tachycardia (e.g. a common physiological response to anxiety)
- Sinus bradycardia (e.g. a common physiological response to exercise training)
True/False:
A: In a patient with a tachyarrhythmia a 12-lead ECG should be recorded whenever possible.
B: In a collapsed patient monitoring through self-adhesive pads usually provides the quickest method of identifying the rhythm.
C: Electrodes for 3-lead monitoring should be attached over bone rather than muscle.
D: When ECG monitoring is indicated, single-lead monitoring is better than no monitoring at all.
E: Body hair may prevent good-quality monitoring.
A: True
B: True –True, but don’t delay monitoring if pads + defib not available and other forms of monitoring are
C: True
D: True
E: True –hair, grease, sweat
True/False when interpreting a cardiac rhythm from an ECG rhythm strip
A: The first priority is to look for atrial activity.
B: Broad QRS complexes always indicate bundle branch block.
C: Effective, immediate treatment can be chosen for all rhythms, based on the heart rate, rhythm regularity and QRS width.
D: Atrial fibrillation always causes a tachycardia.
E: Absence of electrical activity is due to asystole.
A: False =Identification of atrial activity should be attempted only when it is clearly present on the recording.
B: False =fascicular blocks?
C: True
D: False
E: False
Complete the sentences:
A: The SAN initiates ….
B: normal PR interval is up to…
C: The T wave represents….
D: The AVN connects…to…
E: Conduction through AVN is …slow/rapid…., conduction down the bundle of His and bundle branches …slow/rapid….
A: atrial depolarisation (P wave)
B: 0.2 s in duration.
C: ventricular recovery (repolarisation)
D: AVN connects atrial myocardium to the bundle of His.
E: Relatively slow …. Very rapid
True/False
A patient has had central chest pain for the last 2 hours.
True/False:
A: ST-segment depression indicates that this is unstable angina.Incorrect option
B: ST-segment-elevation in leads I and aVL suggests inferior myocardial infarction.Incorrect option
C: Negative T waves in leads V1 and aVR suggest a non-ST-segment MI.Incorrect option
D: Q waves indicate previous myocardial infarction.Incorrect option
E: A normal ECG excludes myocardial infarction.
ST-segment depression is non-specific. In a patient with ischaemic chest pain it may indicate unstable angina but may also be seen in people with NSTEMI. Leads I and aVL are lateral leads, so ST elevation in these leads indicates lateral wall MI. A negative T wave in aVR is normal and a negative T wave in V1 is also a normal finding in many people. The time at which Q waves appear in the evolution of acute myocardial infarction is very variable and they can be seen very early; in many people they persist and provide evidence of previous infarction on ECGs recorded at a later date. A few people suffer myocardial infarction without any diagnostic ECG features, or these develop over several hours or even a day or two in some cases, so if myocardial infarction is likely from the history, a normal ECG does not exclude the diagnosis.
