Week 1: Cardiac arrhythmias Flashcards
Describe the conduction system of the heart
- Myocytes that spontaneously depolarise and create action potentials
- Grey - contractile myocardial cells that contract but do not generate AP
- SA node in right atrium, pacemaker, spont. depol to create AP 60-100/ min at rest
- Travels through atrium to AV node
- The AV node should be the only route of electrical activity from the atria to the ventricles
- Crosses into interventricular septum (Bundle of his into R and L bundle branch)
- There are accessory pathways which are abnormal - there may be another place in the fibrous space of the heart where electrical activity may pass from the atria to the ventricles and vice versa.
How does electrical activity in the heart begin?
What is the main node that starts the AP in the heart?
What can takeover?
What can occur if both main nodes of the heart are damaged?
Spontaneous depolarisation of the membrane of electrical myocardial cells
Slow depolarise, reach threshold, AP released (60-100 at rest via SAN, AV node slightly slower rate than AV node, therefore SAN sets pace).
Loss of sinus node –> AV node can spontaneously depol and produce AP, but at a slower rate.
If you completely lose SAN and AVN, the bundle of His will takeover with HR of only 15-30 bpm.
Describe the pacemaker potential in the SA node
How does this relate to the AVN?
- Cells within SA node - primaru pacemaker site within the heart
- No true resting potential, generate regular, spontaneous action potentials
- Depolarising current carried into the cell primarily by slow Ca2+ currents instead of fast Na+ currents
- SA node action potentials divided into three phases:
- Phase 4 - end of repolarisation when Vm ~ -60mV get spontaenous depolarisation due to “funny currents”, slow depolarising Na+ currents.
- Cause spontaneous depolarisation initiating phase 4 - Vm reaches -50mV opening transient T type Ca2+ channels.
- Ca2+ enters depolarising the cell more, once Vm reaches around -40 mV second L type Ca2+ channels open –> reach AP threshold (between -40mV and -30mV).
- Phase 0 - depolarisation primarily caused by increase Ca2+ conductance through L type channels
- Phase 3 - repolarisation as K+ channels open, outward directed hyperpolarising K+ current. L type Ca2+ channels close. Brings Vm closer to equilibrium potential for k+ (around -96mv).
- Pacemaker activity is spontaenous but rate can be modified by autonomic NS, hormones, drugs, ions, ischemia and hypoxia.
- AVN action potential is very similar to SAN, involves slow Ca2+ and K+ currents. Have intrinsic pacemaker activity.
Describe the cardiac action potential
- Occurs in non pacemaker cells - atrial myocytes, ventricular myocytes, purkinje cells
- AP undergo very rapid depolarisation
- Non pacemaker cells have a true resting membrane potential remains near equilibrium potential for K+ around -90mV, as k+ channels are open
- Phase 4- Cells are repolarised, K+ channels are open, fast Na+ and L type Ca2+ channels are closed.
- An action potential at an adjacent cell induces depolarisation to threshold voltage of -70mV (phase 0).
- Rapid depolarisation in phase 0 caused by transient increase in fast Na+ channel conductance
- Phase 1 represents initial repolarisation caused by opening of transient outward K+ channels, causes short lived hyperpolarising outward current.
- Phase 2- Large increase in slow inward Ca2+ occurs at the same time, repolarisation is delayed and there is a plateau phase. Via L type Ca2+ channels.
- Phase 3- repolarisation when K+ increases and Ca2+ channels inactivate.
- Effective refractory period - New action potential cannot be initated by adjacent cell undergoing depolarisation - due to inactivation of Na+ channels after their closure in phase 1.
- ERP acts as a protective mechanism by preventing multiple compounded AP’s from occurring.
What can occur with damage to myocytes?
With damage to the heart (ischaemia or electrolyte imbalance), myocytes can start producing their own AP’s, leading to extra beats produced within the ventricles.
Describe how the action potential of the heart relates to the ECG waveform
- Impulse begins in the sinus node (Y), corresponds the the very start of the P wave
- Travels via atrial muscle to the AV node - forms the bulk of the P wave.
- impulse then travels via the common bundle and L/R bundle branches (end of P but before QRS)
- travels via purkinje fibres (just before QRS)
- Then via ventricular muscle - forms the QRS complex = ventricular depolarisation.
- T wave represents ventricular repolarisation
Timing of sq’s on ECG?
1 large sq = 0.2 secs
5 large sq’s 1 sec
What are the key things to look for on an ECG?
Reference normal figures and abnormal
Rate: 60 -100 bpm
Rhythm –> reg/ irreg?
P wave –> P wave present means AP comes from sinus node, travels in normal conduction system to the ventricles. Is it present before each QRS? Sinus rhythm.
PR interval (from beginning of p wave to start of QRS): normal within 0.12- 0.2 s (3-5 small sq’s)
1st degree heart block > 0.2s
QRS complex –> normally < 0.12 s
(<3 small sq’s) –> narrow complex
(> 3 small squares) –> broad complex
If the QRS complex shape is abnormal, means that the impulse is not travelling in the ventricles along the normal route. Might mean AP originates from somewhere in ventricle.
What can variations in a normal looking ECG be due to?
- Rate and rhythm may vary with respiration - sinus arrhythmia
- may increase during respiration and decrease during expiration
Define arrhythmia
Arrhythmia –> Any variation from the normal rhythm or rate of the heart beat
OR
a disturbance in the electrical activity of the heart due to a disorder of impulse formation and/or impulse conduction which may be paroxysmal or continuous.
How can arrythmias be classified?
Arrhythmias may be classified on the basis of:
- Rate - tachycardia or bradycardia
- Site of origin - Supraventricular or ventricular
- Mechanism (e.g. re-entry)
- ECG appearance (e.g. long QT)
Describe broadly the two main causes of arrhythmia and the two main defects this can cause in heart rate.
- Two main causes of arrhythmia within the heart are either 1) altered impulse FORMATION (SAN) or altered impulse CONDUCTION (often the AVN or other conductive pathways).
- Altered formation or conduction can lead to two main defects in heart rate either 1) Tachycardia (above 100 bpm) or bradycardia (below 60bpm).
- With altered impulse formation –> either reduced automaticity –> reduced HR OR enhanced automaticty –> increased HR.
- Triggered activity –> may have abnormal impulse formation, where you get an after depolarisation post a normal Action potential. If delayed after depolarisation you may trigger a new AP or allow sustained triggered activity. If early afterdepolarisation (before full repolarisation) you may initate a continued AP which fails to repolarise.
- With altered impulse CONDUCTION –> may have conduction BLOCK (damage to conductive pathways) or RE-ENTRY –> where the impulse choses not to travel via the normal physiological route but travels into ventricles and back into the atrium forming a loop –> re-rentry tachcardia.
What two things can cause tachy/ brady
Bradycardias:
Altered impulse FORMATION –> reduced automaticity
Altered impulse CONDUCTION –> Conduction block
Bradycardia –> SAN dysfunction or AV conduction disturbance
Tachycardia:
Altered impulse FORMATION –> Enhanced automaticity or triggered activity
Altered impulse CONDUCTION –> re-rentry (loop, unidirectional block).
Causes of bradycardia?
Causes may be CARDIAC or SYSTEMIC
E.g. cardiac –> age related degen, fibrosis, infection, ischaemia, cardiomyopathy, congenital)
Systemic –> drugs, hypo thyroid, electrolyte abnormality, hypothermia, autonomic dysfunction
What are two main sites of dysfunction that can induce a bradycardia?
What conditions are included in these two categories of dysfunction?
-
SAN dysfunction —> sick sinus syndrome
- sinus bradycardia
- sinus pause/ arrest
- others –> e.g. sinus node exit block
-
AVN conduction disturbance –> heart or AV blocks
- First degree (delayed conduction)
- Second degree (intermittent conduction)
- mobitz type 1 (wenckebach)
- mobitz type 2
- Complete/ third degree (complete conduction block)
What is the diagnosis?
Fill in the blanks
Sinus bradycardia
300/ 6 squares —> rate 50 bpm
Note: This may be a normal finding at rest/ athletes/ during sleep
What is the diagnosis?
Sinus pause/ arrest –> failure of SA node to fire, the next P wave doesn’t occur at the expected time–> missed beat, then resets.
N p wave, No QRS.
Sinus node recovers, produces an AP, get QRS complex.
This may present asymptomatically or it may present with patients “skipping beats” –> always ECG
What is the diagnosis?
Fill the blanks
Prolonged PR interval, delayed conduction between SAN to AVN, slows the rate down.
Often seen in patients with Beta blocker
Other causes: ischaemia and electrolyte abnormalities
What is the diagnosis and why?
Fill the blanks on the ECG
Diagnosis: Second degree heart block (type 1)
PR interval gets longer and longer with each beat until eventually P wave fails to produce QRS complex, leading to a missed beat.
Key: PR interval “resets” after each dropped beat and the cycle repeats.
Known as Wenckebach phenomemnon - Mobitz Type 1.
What is the diagnosis and why?
Fill in the blanks
Constant PR interval but failure of P wave to produce QRS everytime. Missed beats after normal beat.
Intermittent failure of conduction.
May give “regularly irregular” rhythms - dudumdudumdu…dudumdudumdu…
consistent pattern of dropped beats
What is the diagnosis and why?
What are the distingushing features of this ECG?
Complete dissocation between p waves and QRS complexes, conduction between atria and ventricles is completely blocked.
Instead you get escape rhythm.
Escape rhythm –> myocytes in ventricles spont. depol at slow rate which keeps pt. alive, narrow QRS complexes in this ECG means escape rhythm most likely from the septum.
Patient case: What is the diagnosis of this ECG?
Case: 63 yr old male attending GP for well man check
PMH: BPH, HTN
Drug hx: Tamsulosin, amlodipine
NKDA
SHX: independent, lives with wide, retired council worker, no alc or smoking
O/E: HR 45 bpm BP 140/78
- First degree heart block due to prolonged PR interval ( 7 small squares - 0.28 seconds) (should be 3-5 small squares (0.12-0.2)
Patient case 2: 84 yr old male presents after syncopal episode while out shopping.
Complaining of dizziness and lethargy which started last week.
PMH: type 2 diabetes, HTN, hypercholesterolaemia
Dhx: lantus, metformin, amlodipine, simvastatin
SHx: ex smoker (40 pack yrs); social drinker, mobilised with walking stick.
O/e: bp 110/68, HR 45 bpm, pulse irregular
Second degree heart block - Mobitz Type 2
Twice as many P waves as QRS complexes. Every other P wave does not conduct - fixed block of 2: 1.
Case 2 continued –>
As an inpatient awaiting pacemaker the patient develops:
1) profound bradycardia - HR drops to 30bpm
2) confusion
3) signs of HF –> SOB, hypotension, sacral oedema
What is the diagnosis on ECG?
- Complete heart block –> complete dissociation between P waves and QRS complex
What is the role of a pacemakers?
- Used for bradycardias only
- two leads are inserted via subclavian vein into the right side of the heart
- Right atrium +/- ventricle
- pulse generator placed in a “pocket” under the skin near the clavicle.
How does a pacemaker ECG look?
- Atrial pacing spike followed by a ventricular pacing spike
- Wide QRS complex and an abnormal ST segment/ T wave due to impulse arising OUTSIDE usual conducting system
What is shown on the ECG?
what are the defining features of this condition?
- Rate > 100 bpm
- Increased firing rate of the SA node
- usually an appropriate response to an underlying condition
- wide range of causes –> exercise, pain, anxiety, fever, drugs, anaemia, hypoxaemia, hypovolaemia, PE…
What is shown on the ECG?
What are the defining features of this condition?
Paroxysmal/ re-entrant SVT
- usually due to re-entry circuit within the AV node (AVNRT) –> activates both the atria and the ventricles
- May be caused by re-entry circuit using AV node and accessory pathway (AVRT)
- Key feature: Retrograde conduction –> P wave merged with QRS/T
What are the two types of re-entrant supraventricular tachycardias?
What is the underlying pathophysiology underlying these two conditions?
-
Atrioventricular nodal re-entrant tachycardia (AVNRT)
- Most common type of supraventricular tachycardia
- narrow complex rates 120-240 bpm
- patients have dual atrioventricular nodal physiology and the ability for re-entrant arrhythmia to occur involving the AVN and perinodal tissue
- Unidirectional block occurs in the fast pathway after a premature atrial contraction–> conduction then proceeds down the flow pathway intil it reaches the point of lower ocmmon pathway fusion where two pathways join. Conduction wavefront then proceeds back up the fast pathway in retrograde fashion and re-entry ensues.
-
Atrioventricular re-entrant (reciprocating) tachycardia (AVRT)
- Prescence of an accessory pathway to bypass the regular conduction system.
- Electrical signal passes in normal manner from AVN to ventricles, then passes back into the atria via accessory pathway causing atrial contraction, returns to AVN to complete re-entrant circuit.
What is shown on this ECG?
What are the defining features of this condition?
Preexcitation
- Part of the ventricles are activated too early, caused by an abnormal accessory pathway between/ within the cardiac chambers
- Early activation of ventricles as impulses bypass AVN via accessory pathway
- Features: short PR interval and often broad QRS due to delta wave
- Note: short PR internal and “slurring” into QRS complex (delta wave)
- may give rise to AVRT
- symptomatic patients have Wolff-Parkinson-White syndrome –> individuals born with accessory pathway that may also transmit electrical impulses from the ventricles back to the atria.
What condition is shown on this ECG?
What are the defining features?
Atrial flutter
-
Characteristics:
- Saw toothed pattern of atrial activity –> flutter waves
- P wave not seen - flutter waves
- PR interval is immeasurable
- QRS - normal (under 0.12 secs)
- Ventricular rate depends on the rate of the AVN conduction (flutter waves often ~300/min)
- Caused by re-entry circuit within the atria (often right atrium)
What condition is shown on this ECG?
What are the defining features?
Atrial fibrillation
- Uncoordinated atrial activity giving fibrillatory waves rather than P waves
- intermittent conduction through the AVN leads to irregular rhythm
- may be acute, paroxysmal (sudden occurence or exacerbation of preexisting sx), persistent or permanent
- NOTE: Thromboembolism risk
- Rhythm - irregular
- P waves - absent
What condition is shown and what are the defining features?
Premature ventricular complex (PVC)
Also known as ventricular ectopics or extrasystoles
spontaenous early discharge from ectopic pacemaker in ventricle
similar process can occur in atria
- Rate set by SAN still
- Rhythm is irregular
- P wave - absent for the PVC
- PR interval not measurable for the PVC
- QRS tends to be broad and different morphology
- compensatory pause after ectopic beat
What condition is shown and what are the defining features?
Ventricular tachycardia
- Rate is fast (100-250 bpm)
- rhythm is regular
- No p waves
- PR interval not measurable
- QRS –> broad complexes
- may be monomorphic (most common) or polymorphic
- NOTE: may impair cardiac output –> pulseless VT
What conditions is shown and what are the defining features?
Torsade de pointes
- “twisting of peaks” –> specific type of abnormal heart rhythm that can lead to sudden cardiac death
- specific form of polymorphic ventricular tachycardia
- characterised by gradual change in amplitude and twisting of the QRS complexes around the isoelectric line
- is associated with a prolonged QT interval
- usually terminates spontaneously but frequently recurs and may degenerate into ventricular fibrillation.
- Rate: 200- 250 bpm
- rhythm: irregular
- P WAVE - not seen
- PR interval immeasurable
- QRS - broad with changing morphologies
What condition is shown
What are the defining features
Ventricular fibrillation
Medical emergency –> rapid uncoordinated irregular ventricular contractions
incompatible with adequate cardiac output –> pulseless
Rate - immeasurable (150-500 bpm)
Rhythm: irregular
P wave : absent
PR interval: absent
QRS : no organised ventricular activity
What is the tachycardia treatment algorithm?
Talk it out step by step.
-
ABCDE approach, noting the prescence of “adverse features”
- Shock - hypotension, SBP < 90 mmHg, pallor, sweating, cold clammy extremities, confusion or impaired concsciousness.
- syncope - transient loss conciousness due to global reduction in blood flow to the brain
- MI- ischaemic chest pain and/or evidence MI on 12 lead ECG
- HF - pulmonary oedema/ raised JVP
- If adverse features present and unstable –> synchronised DC shock/ cardioversion(up to 3 attempts)
- Note cardioversion = restoring normal heart rhythm during arrhytmia in patients with a pulse but haemodynamically unstable vs defibrillation used in cardiac arrest patients.
- If 3 attempts fail –> 300mgIV amiodarone over 10-20 mins, repeat shock, then amiodarone 900mg over 24 hrs
- No adverse features/ patient is stable:
- Give o2 immediately to hypoxaemic patients, adjust according to sats
- insert IV cannula
-
Record 12 lead ECG - determine the QRS duration
- if 0.12s or greater = broad complex tachycardia
- if less than 0.12s narrow complex tachycardia
- correct any electrolyte abnormalities
- If broad complex tachycardia - often ventricular in origin or a supraventricular rhythm with abberant conduction.
- unstable–> attempt synchronised cardioversion
- stable –> determine if rhythm is regular or irregular
- regular = VT or supraventricular rhythm with bundle branch block. TX = Amiodarone 300 mg IV over 20-60 mins.
- Irregular = AF with bundle branch block, or AF with pre-excitation in Wolff parkinson white or polymorphic VT
- In narrow complex:
- assess if regular or irregular
- regular - sinus tachycardia, AV nodal re-entry tachycardia, AV re-entry tachycardia, atrial flutter with regular AV conduction
- again if unstable –> cardioversion and give adenosine/ vagal manoeuvres whilst waiting
- if stable –> vagal manouevres, carotid sinus massage or valsalva will terminate paroxysmal SVT. Record ECG during manouvres. If arrhythmia persists and is not AF give adenosine 6 mg rapid bolus.
- Then treat according to underlying arrhythmia and status of patient
- CPR/ fist pacing
- pharamacological
- electrical - cardioversion for tachyarrhymia and pacing for bradyarrhythmia
- repeat ABCDE assessment and 12 lead ECG to detect any other abnormalities.
What is the diagnosis?
Atrial fibrillation - fibrillatory waves evident
Irregularly irregular QRS complexes
When should you begin rate control or rhythm control in atrial fibrillation?
What are the two methods of rhythm control?
What are the two drugs used in one form of cardioversion?
- If the onset of arrhythmia within 48 hours –> rhythm control either via electrical direct current cardioversion (DC) or chemical cardioversion.
- Electrical cardioversion is more effective but requires more resources and sedation
- Chemical cardioversion –> either amiodarone (if heart structure not known or abnormal) or flecainide (if normal heart).
- Don’t forget anticoagulation
What is the rate control pathway for atrial fibrillation?
What three drugs are used?
How do they work?
- If onset of arrhythmia is not within 48 hours then use RATE CONTROL
- this uses three drugs BCD
- Beta blocker e.g. bisprolol
- Calcium channel blocker e.g. verapamil
- Digoxin
- DO NOT FORGET ANTICOAGULATION
MOA:
Betablocker –> competitive antagonist of adrenergic B receptors, slow AV conduction, prolongs AV refractory period
CCB: depresses cardiac contractility, increases AV conduction time and refractory period, slows SA and AVN automaticity
Digoxin –> Improves contractility, depresses AV node conduction. Reduces myocardial refractory period, increases purkinje fibre refractory period and reduces conduction.
What is the diagnosis of this ECG?
Ventricular tachycardia
more than 3 consective ventricular beats with rate 100-250 bpm
How should you manage a patient in ventricular tachycardia?
- A-E assessment
- 1) if unstable –> shock/HF/confusion
- synchronised DC cardioversion
- amiodaron IV 300mg over 10 mins
- repeat DC cardioversion
- 2) If stable
- amiodarone IV 300mg over 20 mins
