54. Palpitations/abnormal heart rhythm Flashcards
Assessment of new palpitations/abnormal ecg
ABCDE
A
B
C - IV access, VBG for electrolytes, ECG
D
E
when assessing someone with tachy or brady, what life threatening features do you need to check for?
Shock: SBP <90, pallor, sweating, cold, clammy, confused, <GCS
Syncope
Myocardial ischaemia
Severe HF
Management of tachycardia with life-threatening features
- Synchronised DC shock up to 3x, with sedation or anaesthesia if conscious
- If unsuccessful: amiodarone IV 300 mg over 10-20 mins, repeat DC shock
Management of bradycardia with lifethreating fetaures
Atropine 500 mcg IV
Hitsory taking palpitations
PC: palpitations? Associated with syncope?
Anxiety?
DHx: sympathomimetics eg amphetamines, beta-agonists eg salbutamol
SHx: caffeine, alcohol, stress?, RECREATIONAL DRUGS
what is normal sinus rhythm
Regular rhythm at a rate of 60-100 bpm (or age-appropriate rate in children)
Each QRS complex is preceded by a normal P wave
Normal P wave axis: P waves upright in leads I and II, inverted in aVR
The PR interval remains constant
QRS complexes < 100 ms wide (unless co-existent interventricular conduction delay present)
Pacemaking impulses arise from the sino-atrial node and are transmitted to the ventricles via the AV-node and His-Purkinje system
what is sinus arrythmia
sinus rhythm with a beat-to-beat variation in the P-P interval (the time between successive P waves), producing an irregular ventricular rate
management sinus tachycardia
treat cause eg pain, fear, infection
management SVT
- Vagal manourvres
- adenosine 6mg –> 12 –> 18
- Verapamil or beta blocker (control rate eg it might be atrial flutter)
- synchronised DC 3x
causes of narrow complex tachycardia
sinus tachycardia
SVT (AVNRT, AVRT)
atrial flutter
fast AF
who shouldn’t be given adenosine
Asthma
COPD
Heart failure
Heart block
Severe hypotension
Potential atrial arrhythmia with underlying pre-excitation
what does SVT look like on ECG
Due to an area around the AV node causing depolarisation – results in p waves very close to the QRS, or no p waves visible.
On an ECG, SVT looks like a QRS complex followed immediately by a T wave, QRS complex, T wave and so on.
management options for SVT recurrent
Long-term medication (e.g., beta blockers, calcium channel blockers or amiodarone)
Radiofrequency ablation
what is WPW
congenital accessory pathway (AP) and episodes of tachyarrhythmias
evidence of the accessory pathway can be seen on an ECG performed while in normal rhythm
The term is often used interchangeablely with pre-excitation syndrome
what tachyarrythmias can occur in WPW
Atrial fibrillation or flutter. Due to direct conduction from atria to ventricles via an AP, bypassing the AV node
Atrioventricular re-entry tachycardia (AVRT). Due to formation of a re-entry circuit involving the AP
ECG features of WPW during normal sinus rhythm
WPW
Wide qrs
PR narrow
Wave = delta wave : slurring slow rise of initial portion of the QRS
PR interval < 120ms
Delta wave: slurring slow rise of initial portion of the QRS
QRS prolongation > 110ms
Discordant ST-segment and T-wave changes (i.e. in the opposite direction to the major component of the QRS complex)
Pseudo-infarction pattern in up to 70% of patients — due to negatively deflected delta waves in inferior/anterior leads (“pseudo-Q waves”), or prominent R waves in V1-3 (mimicking posterior infarction)
commonest cause of palpitations in patients with structurally normal hearts
AVNRT
triggers AVNRT
exertion, caffeine, alcohol, beta-agonists (salbutamol) or sympathomimetics (amphetamines)
what drugs should people with WPW not have
should not have adenosine, verapamil or a beta blocker, as these block the atrioventricular node, promoting conduction of the atrial rhythm through the accessory pathway into the ventricles, causing potentially life-threatening ventricular rhythms.
ECG features atrial flutter
Rate: tachycardia
Rhythm: regular (can be irregular)
P waves: flutter waves present (sawtooth appearance )
PR interval: F waves are consistent, 2 for every QRS (2:1 or 3:1 is typical
QRS: <0.12 so narrow complex tachycardia
pathophysiology atrial flutter
reentrant rhythm through sinoatrial node in atrium
PResentation symptoms AF
Asymptomatic
Symptomatic: palpitations, SOB, dizziness or syncope
Symptoms of associated conditions (sepsis, stroke, thyrotoxicosis)
ECG fetaures AF
Rate: tachycardia
Rhythm: irregularly irregular
P: absent p waves
QRS: narrow QRS complex tachycardia
pathophysiology AF
Disorganised atrial activity. This chaotic electrical activity overrides the regular, organised activity from the sinoatrial node. It passes through to the ventricles, resulting in irregularly irregular ventricular contraction.
Commonest causes of AF
SMITH
S – Sepsis
M – Mitral valve pathology (stenosis or regurgitation)
I – Ischaemic heart disease
T – Thyrotoxicosis
H – Hypertension
Alcohol and caffeine are lifestyle causes worth remembering.
what is paroxysmal AF
Paroxysmal atrial fibrillation refers to episodes of atrial fibrillation that reoccur and spontaneously resolve back to sinus rhythm. These episodes can last between 30 seconds and 48 hours.
invetsigations for patients ?paroxysmal AF with normal ECG
24-hour ambulatory ECG (Holter monitor) or
Cardiac event recorder lasting 1-2 weeks
- The device automatically detects and records any abnormal heart rhythm, but you can also ‘activate’ an ECG recording if you start to experience symptoms.
What is valvular AF
Valvular atrial fibrillation is AF with significant MITRAL STENOSIS or a MECHANICAL HEART VALVE. The assumption is that the valvular pathology has led to atrial fibrillation.
principles of treating AF
Rate or rhythm control
Anticoagulation to prevent strokes
most common combination drugs AF
Beta blocker bisoprolol for rate control
DOAC for anticoagulation
questions to ask yourself to see which approach to use treating AF
do they need immeidate cardioversion? <48 hrs, LT haemodynamic instability
do they need delayed cardioversion? reversible, HF, symptoms despite rate control
are there any CI to any of the drugs?
when should immediate cardioversion be used for AF management
- Present for less than 48 hours
- Causing life-threatening haemodynamic instability
options for immediate cardioversion in AF
Pharmacological cardioversion: flecainide or amiodarone
Electrical cardioversion
what is the drug of choice in patients with structural heart disease immediate cardioversion
amiodarone
when should delayed cardioversion be used as the treatment for AF
A reversible cause for their AF
Heart failure caused by atrial fibrillation
Symptoms despite being effectively rate controlled
how is delayed cardioversion carried out - prior, on the day, after
Prior
- rate controlled whilst waiting for cardioversion
- anticoagulated for at least 3 weeks before
On the day:
Electrical cardioversion is recommended.
After:
LT rhythm control is with:
1. Beta blockers
2. Dronedarone
3. Amiodarone is useful in patients with heart failure or left ventricular dysfunction
first line management of AF
Rate control is first line as long as they dont meet the above/below criteria:
A reversible cause for their AF
New onset atrial fibrillation (within the last 48 hours)
Heart failure caused by atrial fibrillation
Symptoms despite being effectively rate controlled
- Beta blocker first-line (e.g., atenolol or bisoprolol)
- Calcium-channel blocker (e.g., diltiazem or verapamil) (not preferable in heart failure)
- Digoxin (only in sedentary people with persistent atrial fibrillation, requires monitoring and has a risk of toxicity)
Management paroxysmal AF
- Flecainide is usual pill-in-pocket drug
+ Anticoagulation based on chadsvasc as they would with normal AF
management refractory AF
Left atrial ablation
Atrioventricular node ablation and a permanent pacemaker
how much does anticoagualtion decrease risk of stroke AF? how much does it increase risk of bleed
Anticoagulation reduces the risk of stroke by about 2/3.
patients with atrial fibrillation have around a 5% risk of stroke each year, depending on individual factors. With anticoagulation, patients with atrial fibrillation have around a 1-2% risk of stroke each year
Anticoagulation treatment carries around a 2.5-8% risk of serious bleeding each year, depending on individual factors.
interpretation of CHADSVASC score
0 – no anticoagulation
1 – consider anticoagulation in men (women automatically score 1)
2 or more – offer anticoagulation
what is part of the orbit score?
O – Older age (age 75 or above)
R – Renal impairment (GFR less than 60)
B – Bleeding previously (history of gastrointestinal or intracranial bleeding)
I – Iron (low haemoglobin or haematocrit)
T – Taking antiplatelet medication
what is part of chadsvasc score
C – Congestive heart failure
H – Hypertension
A2 – Age above 75 (scores 2)
D – Diabetes
S2 – Stroke or TIA previously (scores 2)
V – Vascular disease
A – Age 65 – 74
S – Sex (female)
anticoagulation for AF
Direct-acting oral anticoagulants (DOACs) first-line
Warfarin second-line, if DOACs are contraindicated
reversal agent apixaban and rivaroxaban
Andexanet alfa
DOAC advantages over warfarin
No monitoring is required
No issues with time in therapeutic range (provided they have good adherence)
No major interaction problems
Equal or slightly better than warfarin at preventing strokes in atrial fibrillation
Equal or slightly lower risk of bleeding than warfarin
regular broad complex tachycardia - first ddx?
assume ventricular tachycardia (unless previously confirmed SVT with bundle branch block)
regualr broad complex tachy - treatment?
assume ventricular tachycardia
loading dose of amiodarone followed by 24 hour infusion
amiodarone 300mg IV over 30-60 mins
apart from VT, what is another cuase of broad complex tachy regualr?
SVT w BBB
causes of irregualr broad complex tachycardia
atrial fibrillation with bundle branch block - the most likely cause in a stable patient
atrial fibrillation with ventricular pre-excitation
torsade de pointes
management irregualr broad complex tachycardia
seek expert help
magnesium 2g over 10 mins
what is polymorphic VT
is a form of ventricular tachycardia in which there are multiple ventricular foci with the resultant QRS complex varying in amplitude, axis, and duration. The most common cause of PVT is myocardial ischaemia/infarction.
what is torsades?
is a specific form of PVT occurring in the context of QT prolongation — it has a characteristic morphology in which the QRS complexes “twist” around the isoelectric line.
pathophysiology VT
These are caused by a foci in the ventricles discharging at a high frequency. This causes an abnormal spread of charge through the ventricles, resulting in wide and abnormal QRS complexes.
ecg features VT
QRS is broad
T waves difficult to identify
No p waves
Regular QRS (~200bpm)
how to ddx VT from BBB
supportive of BBB
- p waves
- qrs same shape as prev normal ecg
- qrs irregualr (AF w BBB)
supportive of VT
- wide qrs >160ms
- left axis deviation
what acute thing may cause VT or PVT
myocardial infarction
causes of prolonged QT
congenital
drugs
amiodarone, sotalol, class 1a antiarrhythmic drugs
tricyclic antidepressants, selective serotonin reuptake inhibitors (especially citalopram)
other
hypocalcaemia, hypokalaemia, hypomagnesaemia
acute myocardial infarction
myocarditis
hypothermia
subarachnoid haemorrhage
management long qt syndrome
avoid drugs which prolong the QT interval and other precipitants if appropriate (e.g. Strenuous exercise)
beta-blockers*** not sotalol
implantable cardioverter defibrillators in high risk cases
what is long qt syndrome
an inherited condition associated with delayed repolarization of the ventricles. It is important to recognise as it may lead to ventricular tachycardia/torsade de pointes and can therefore cause collapse/sudden death.
features long qt syndrome eg symptoms
Long QT1 - usually associated with exertional syncope, often swimming
Long QT2 - often associated with syncope occurring following emotional stress, exercise or auditory stimuli
bradycardia with life threatening symptoms. You have given atropine but not a good response, what next?
- atropine 500mcg IV repeated up to 3g
- transcutaneous pacing
- other drugs eg adrenaline infusion
bradycardia with life threatening symptoms. You have given atropine and there has been a goos response, what next?
Assess for any risk of asystole?
- recent asystole?
- mobitz type 2 AV block
- complete heart block with broad qrs
- ventricualr pause > 3 secs
If yes to risk: specialist help is indicated to consider the need for transvenous pacing
if no to risk: observe
causes sinus bradycardia
athletic training, fainting attacks, hypothermia, myxoedema, seen immediately after MI
life thretaening causes bradycardia
- hyoxia in children
- mobitz type 2 block
- complete heart block
- pause > 3s on ecg
ecg features first degree heart block
PR interval is greater than 0.2s
pathophysiology mobitz 1 vs 2
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)
what is second degree heart block
This is where there is an intermittent absence of QRS complexes – and thus an indication that there is a blockage somewhere between the AV node and the ventricles.
ecg features of mobitz 1
progressive lengthening of the PR interval followed by an absence of the QRS, then a shortened PR interval and normal QRS, and the cycle begins again. The cycle is variable in length, and the R-R interval shortens with the lengthening of the PR interval
causes 1st degree heart block
First degree heart block is not in itself very important – it can be a sign of coronary artery disease, acute rheumatic carditis, digoxin toxicity or electrolyte disturbance, but does not usually require treatment.
causes mobitz 1
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)
what is mobitz 2, ecg features?
regular rhythm, and a fairly constant PR interval, but every now and again there is an absent QRS (pictured above). basically for every QRS, there are 2 or 3 p waves.
are complexes narrow or broad in mobitz 2?
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.
causes mobitz 2
Anterior MI (due to septal infarction with necrosis of the bundle branches)
Idiopathic fibrosis of the conducting system (Lenègre-Lev 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
management mobitz 2
if causing bradycardia with LT features - atropine then transcutaenous pacing
if stable
immediate admission for cardiac monitoring, backup temporary pacing and ultimately insertion of a permanent pacemaker
what are fixed conduction ratios?
there is one normal cycle, then one cycle with an absent QRS (2:1) or there is one normal cycle, then two cycles without a QRS (3:1)
Fixed ratio blocks can be the result of either Mobitz I or Mobitz II conduction.
features complete heart block symptoms/signs
syncope
heart failure
regular bradycardia (30-50 bpm)
wide pulse pressure
JVP: cannon waves in neck
Cannon wave occurs in conditions with atrioventricular dissociation and right atrial contraction against a closed tricuspid valve.
variable intensity of S1
pathophysiology complete heart block
atrial contraction is normal, but no beats are conducted to the ventricles.
The ventricles are still excited by their own internal ‘ectopic pacemaker’ system!
ecg features complete heart block
P wave ~90/min (more p waves than QRS complexes)
QRS ~36/min
Variable PR intervals
No relationship between P wave and QRS complexes, but both are present.
Abnormally shaped QRS due to abnormal spread of conduction throughout ventricles
QRS will generally be broad (~160ms – as opposed to a maximum of 120ms in a normal heart – 4 little squares as opposed to 3 little squares)
Right axis deviation
Escape rhythms present
causes complete heart block
MI – it will occur acutely, and is often transient
Chronic – often due to fibrosis around the Bundle of His, or bundle branch block of both branches
Always indicates underlying disease – more often fibrosis then ischaemia
Management complete heart block
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
pathophysiology BBB
wave of depolarisation reaches intraventricualr septum fine = normal PR
block in the bundle branch –> the time taken for depolarisation to spread throughout the ventricles is prolonged = wide QRS
why do you get RSR in RBBB V1
right bunder branch block. left ventricular depolarisation continues as normal, and produces a normal R and a normal S wave. But after this has happened, the right ventricle then depolarises, and causes a second R wave (R1).
features ecg RBBB
MaRRoW
M in V1 RSR’
W in V6 Wide slurred S wave
features ecg LBBB
WiLLiaM
W in V1 Wide slurred S wave
M in V6 RSR’
causes RBBB
atrial septal defect
causes LBBB
Ischaemic disease - if the patient has had recent chest pain, LBBB is likely to indicated MI, and thus thrombolysis should be considered.
Aortic stenosis
If the patient is asymptomatic, then no treatment is needed
features ventric ectopic
Absence of P wave before the QRS
Wider, taller QRS complex (>120ms)
Often immediately follows a T wave
Has a discordant T wave (T wave point in opposite direction to major portion of QRS)
management vent ectopics
Rule out structural heart disease with an echo
If present – refer to cardiology
assess FHx
If all the above is normal:
Reassure
Consider beta-blocker or calcium-channel blocker
features ecg hypokalameia
U have no POT, you have no T, you have a long PR and a long QT
- prominent u waves
- T wave inversion
- long QT
- ST depression
in any pt with arrythmia, what electrolytes in particualr should be checkeD?
Check both potassium and magnesium levels in any patient with an arrhythmia
Replace potassium to ≥ 4.0 mmol/L and magnesium to ≥ 1.0 mmol/L to stabilise the myocardium and protect against arrhythmias – this is standard practice in most CCUs and ICUs
what other electrolyte abnormality is associated with hypokalaemia
hypomagnesaemia
ecg changes hypomagnesia
Prolonged PR interval
Prolonged QT interval
Atrial and ventricular ectopy
Predisposition to ventricular tachycardia and torsades de pointes
ecg features hypocalcaemia
prolonged QT and torsades
