Arrhythmias + conduction defects Flashcards
1
Q
What is an arrhythmia?
A
- any deviation from the normal cardiac rhythm
- due to abnormal electrical activity of heart
- arise from disturbance of generation or conduction of normal cardiac impulses
- can be intermittent or continuous
2
Q
What are cardiac causes of arrhythmias?
A
- Ischaemic heart disease
- Structural changes
- Cardiomyopathy
- Pericarditis
- Myocarditis
- Aberrant conduction pathways
3
Q
What are non-cardiac causes of arrhythmias?
A
- Caffeine
- Smoking
- Alcohol
- Pneumonia
- Drugs (beta blockers, digoxin, tricyclics)
- Metabolic imbalance (eg. hyperkalaemia)
- Phaeochromocytoma
4
Q
What are the various types of ECG monitoring?
A
- ECG → simple 12-lead, snapshot of heart, may miss
- Telemetry → inpatient, signals shown on screen and watched continuously, reserved for high risk dangerous arrythmias
- Exercise ECGs → pts exercise, BP and ECG monitored looking for changes (eg. delta waves) and arrhythmias
- Holter monitors → pt wears monitor, records rhythm for 24h-7d whilst they go about normal life, analysed later
- Loop recorders → record only when activated, planted under skin and useful in pts w/ infrequent episodes
- Pacemakers & ICDs → record details of cardiac electrical activity, also therapeutic
5
Q
Disturbances of cardiac rhythm are common, often benign, often intermittent and occasionally severe.
What are the two main types of arrhythmia?
A
- bradycardia - HR slow, <60 during day or <50 during night
- tachycardia - HR fast, >100
6
Q
What are the bradycardias?
A
- Sinus bradycardia
- 1st degree (AV) block
-
2nd degree (AV) block
- Mobitz I / Wenkebach
- Mobitz II
- Complete (AV) heart block
7
Q
What are causes of sinus bradycardia?
A
- normal - esp in athletes + elderly
- inc vagal tone - cushing’s reflex*
- drugs - bblockers, ccbs, digoxin, etc
- ischaemia/infarction - right coronary artery
*cushing’s reflex is bradycardia, hypertension and irregular RR - caused by a raised ICP, inc pressure in skull -> inc vagal tone
8
Q
What is 1st degree heart block?
A
- prolonged PR interval (> 200ms / 0.2s)
- Every atrial depolarisation is followed by conduction to the ventricles, but with delay
- eg. if AVN or bundle of His damaged -> prolonged PR interval
- common in healthy adults, asymptomatic
- no specific treatment required
9
Q
What is Mobitz type 1?
A
- Type 1 (2o) AKA Wenkebach
- Progressive PR interval prolongation, until a P wave fails to conduct
- No treatment required
- Where the QRS is dropped, the PR interval after is short but the one before is much longer
10
Q
What is Mobitz type 2?
A
- PR interval is constant but the P wave is often not followed by a QRS complex
- Signifies block at an infranodal level such as the bundle of His
- There is a greater risk of this type to progress into complete heart block
- Consider pacemaker due to risk of developing CHB
11
Q
What is complete heart block?
A
- No synchrony between P and QRS AKA complete atrioventricular dissociation
- Regular P waves, regular QRS complexes but NO associated between the two
- By chance, the atria and ventricles may contract at same time → atrial blood occurs against a closed tricuspid → blood refluxes back up the jugular veins → cannon waves
- Ventricles can pace themselves
- Rx: permanent pacemaker
- URGENT specialist referral!
12
Q
What are the clinical features of complete heart block?
A
- Syncope
- Heart failure
- Regular bradycardia (30-50 bpm)
- Wide pulse pressure
- JVP: cannon waves in neck
- Variable intensity of S1
13
Q
What 4 adverse clinical presentations are important to recognise in severe bradycardia and what should be the management if any of these arise?
A
Manage based on adverse signs:
- shock
- syncope
- myocardial ischaemia
- heart failure
If any of these 4 arise -> TREAT -> atropine 500mcg x 6
- ?betablocker overdose —-> glucagon
14
Q
The diagram shows typical features of left bundle branch block (LBBB).
What is the most common way to remember the difference (on ECG) between LBBB and RBBB?
A
WiLLiam vs MaRRow
- LBBB → ‘W’ in V1 and ‘M’ in V6
- RBBB → ‘M’ in V1 and ‘W’ in V6
15
Q
What are causes of LBBB?
A
- Ischaemic heart disease
- HTN
- Aortic stenosis
- Cardiomyopathy
- Rare → idiopathic fibrosis, digoxin toxicity, hyperkalaemia
New LBBB is always pathological + may be sign of MI. Diagnosing MI for pts with existing LBBB is tricky. The Sgarbossa criteria can help with this.
16
Q
What are the causes of RBBB?
A
- Normal variant - more common w/ increasing age
- Right ventricular hypertrophy
- Chronically increased right ventricular pressure eg. cor pulmonale
- Pulmonary embolism
- Myocardial infarction
- Atrial septal defect
- Cardiomyopathy or myocarditis
17
Q
Tachyarrhythmias are when the heart is beating >100bpm. How can tachyarrhythmias be classified?
A
-
Broad complex (QRS >120ms) -> Ventricular tachycardias
- arise from ventricles
- reflect disorganised, delayed depolarisation (hence broad QRS)
-
Narrow complex (QRS <120ms) -> Supraventricular tachycardias
- arise from atrium or atrioventricular junction
- reflect organised efficient electrical activity originating above AV node (hence narrow QRS)
18
Q
What is atrial fibrillation?
A
- Technically an SVT
- Characterised by uncoordinated atrial activity on surface eCG
- With fibrillatory waves of varying shapes, amplitudes and timing
- Associated with an irregularly irregular ventricular response when AV conduction is in tact
- Cardiac output drops by 10-20% as ventricles aren’t primed reliably by atria
- AF is common in elderly (~9%)
- Main risk = embolic stroke
19
Q
What are the cardiac causes of AF?
A
- Heart failure (24%)
- IHD (33%)
- Hypertension (26%)
- Valvular heart disease (7%)
- MI
- Cardiomyopathy
- Sick sinus syndrome
- Constrictive pericarditis
20
Q
What are non-cardiac causes of AF?
A
- Alcohol intoxication or withdrawal
- Hyperthyroidism
- PE
- Electrolyte abnormalities (hypokalaemia)
- Pneumonia
- Caffeine
- Lone AF (no cause, probably genetic)
21
Q
What are clinical features of AF?
A
- May be asymptomatic
- Chest pain
- Palpitations
- Dyspnoea
- Faintness
- Signs → irregularly irregular pulse, apical pulse rate greater than radial, signs of LVF (pulm oedema)
22
Q
What investigations can be done for AF?
A
- Bedside → ECG looking for absent P waves, irregularly irregular QRS complexes
- Bloods → FBC, U+Es, TFTs, cardiac biomarkers, CRP
- Imaging → CXR (HF, pulm oedema), Echo (left atrial enlargement, mitral valve disease, poor LV function)
23
Q
AF can broadly categorised into different types.
When is a ‘first detected episode’ of AF diagnosed?
A
Irrespective of whether it is symptomatic or self-terminating
24
Q
What is persistent AF?
A
- Recurrent episodes of AF
- Not self-terminating
- Typically last greater than 7 days
25
What is **paroxysmal** AF?
* Recurrent episodes of AF
* **Spontaneously terminate**
* Episodes last **less than** 7 days (typically \<24 hrs)
* Can sometimes occur in fit athletes
26
What is **permanent** AF?
* **Continuous** AF
* _Cannot_ be cardioverted or if attempts to do so are deemed inappropriate
27
There are **two key parts** of managing patients with AF: 1) Rate/rhythm control and 2) reducing stroke risk.
What is meant by **rate** vs **rhythm** control?
* **Rate control** → accept that the pulse will be irregular, but slow the rate down to avoid negative effects on cardiac function
* **Rhythm control** → try to get pt back into, and maintain, normal sinus rhythm. This is termed cardioversion. Drugs (pharm cardioversion) and synchronised DC electrical shocks (electrical cardioversion) may be used for this purpose
For many years, predominant approach was to maintain pt in sinus rhythm - changed in early 00s and now majority of pts are managed with a rate control strategy. NICE advocate using a rate control strategy except in a number of specific situs eg. coexistent heart failure, firs tonset AF or where there is an obvious reversible cause
28
Factors favouring rate control include being older than 65yrs and a history of IHD. What are the options for **rate control**?
* **First line** → beta-blocker eg. **bisoprolol**
* **Second line** → rate-limiting calcium channel blocker eg. **diltiazem**
* If one drug does not control rate adequately, NICE recommend combo therapy with any 2 of: beta-blocker, diltiazem & **digoxin**. Use digoxin only if pt sedentary.
29
Factors favouring rhythm control include being younger than 65y, symptomatic, first presentation, lone AF or 2o to a correct precipitant (eg. alcohol), and congestive heart failure.
What are the options for **rhythm control**?
* *If AF \< 48 hrs:*
* pts should be heparinised
* immediate cardioversion can take place
* electrical → **DC cardioversion**
* pharm → **amiodarone** (structural heart disease) or **flecainide**/amiodarone (without structural heart disease)
* *If AF \> 48 hrs / timing uncertain*
* **anticoag** required **3wks prior** to cardioversion, or
* perform TOE to exclude thrombus → then heparin + DC cardioversion immediately
* continue anticoag for 4 wks after DC
30
When **cardioverting**, why do patients need to have presented with \<48 hrs of symptoms or to be anticoagulated before?
When considering cardioversion it is very important to remember that the **moment** a patient switches from **AF** to **sinus rhythm** presents the highest risk for **embolism** leading to **_stroke_**. Imagine the thrombus formed in the fibrillating atrium suddenly being pushed out when sinus rhythm is restored. For this reason patients must either have had a short duration of symptoms (less than 48 hours) or be anticoagulated for a period of time prior to attempting cardioversion.
31
**When** do you _acutely_ treat AF and **what** needs to be done?
* If the patient has adverse signs (_shock, MI, syncope, heart failure_):
* **ABCDE**
* **Get senior help**
* **DC Cardioversion** (synchronised shock, start at 120-150J) +/- amiodarone if unsuccessful
* If pt _stable_ and AF started **\<48hrs ago** → rate or rhythm control; rhythm control @ SGH:
* **IV** **flecainide** (1-2 mg/kg over 10 mins; max dose 150mg)
* In presence of HF or acute ischaemia, **amiodarone** should be used (300mg bolus via large bore cannula in large vein or centrally, then a 900mg 24hr infusion)
* If pt stable and AF started **\>48hrs** ago or **unclear** time of onset → **RATE control** (eg. w/ bisoprolol or diltiazem). If rhythm control chosen, the patient MUST be _anticoagulated_ for \>3wks first!
32
How is **paroxysmal** AF **managed**?
**'Pill in the pocket'** (eg. Sotalol or flecainide PRN) may be tried if:
* Infrequent AF
* BP \>100 mmHg
* No past LV dysfunction
Anti-coagulate if needed and consider ablation of symptomatic or frequent episodes
33
How is **anticoagulation** used in acute AF?
* Use **HEPARIN** until full risk assessment for emboli made
* E.g: AF started \<48hr ago and elective cardioversion planned, if \>48hr, ensure \>3wks of therapeutic anticoagulation before elective cardioversion
* Use **DOAC** (eg. apixaban) or **warfarin** (target INR 2-3) if high risk of emboli (eg. past ischaemic stroke, TIA or emboli, high BP and \>75yrs, coronary disease)
34
How is **anticoagulation** used for **chronic** AF?
* May be paroxysmal, persistent or permanent
* In all cases, need for anticoag should be assessed using the **CHA2DS2-VASC** score to _assess embolic stroke risk_ and balancing this against _risk of anticoagulation_ to the patient, assessed with the **HAS-BLED** score
35
How do **DOACs** work?
* Examples: **Rivaroxaban**, **apixaban**
* **Factor Xa inhibitors**
* Do _not_ require regular monitoring and dose adjustment, just a quarterly assessment and annual blood test
* They offer an attractive alternative to warfarin
* **CIs**: severe renal/liver impairment, active bleeding, reduced clotting factors
36
How does **warfarin** work?
* Inhibits reductase enzyme responsible for regenerating active form of Vit K
* Produces a state analogous to Vit K deficiency
* In UK, warfarin tablets are 0.5mg (white), 1mg (brown), 3mg (blue) or 5mg (pink)
37
What is **atrial flutter**?
* Form of **SVT** characterised by a succession of **rapid atrial depolarisation waves**
* Generally results from **structural** or **functional** **conduction** abnormalities of _atria_
* It can be precipitated by **toxic** and **metabolic** conditions such as thyrotoxicosis or pericarditis
* Patients taking anti-arrhythmics for **AF** may convert to atrial flutter
38
What are **ECG** findings for atrial flutter?
* Classic '**_sawtooth_**' appearance
* As underlying rate is often around **300/min**, the ventricular or HR is dependent on the degree of AV block
* For example, if there is a 2:1 block the ventricular rate will be 150bpm
* **Flutter waves** may be visible following carotid sinus massage or adenosine
39
What is the **management** of atrial flutter?
* Similar to AF although meds may be less effective
* Atrial flutter is more sensitive to **cardioversion**, **DC** \> pharm; start with **70-120J**
* Recurrence rates are high so **radiofrequency** **ablation** often recommended for long-term management
40
Whilst strictly speaking the term **supraventricular** **tachycardia** (SVT) refers to any tachycardia that is _not_ **ventricular** in origin, the term is generally used in the context of **paroxysmal** **SVT**. Episodes are characterised by the **sudden** **onset** of a **narrow complex tachycardia**, typically an atrioventricular nodal re-entry tachycardia (**AVNRT**). Other causes include atrioventricular re-entry tachycardias (**AVRT**) and **junctional** **tachycardias**.
What is **AVNRT**?
* Most **common** cause of SVT (~80%)
* Caused by small **re-entry circuit** involving AVN and surrounding atrial tissue
* 2x common in **women**
* Often strikes suddenly w/out obvious provocation
* **Triggers** → coffee / alcohol / exertion
41
What are the **two** **pathways** in **AVNRT**?
Both predominantly within AV node:
* **Short** effective refractory period and **slow** conduction
* **Long** effective refractory period and **fast** conduction
In sinus rhythm, the atrial impulse that depolarises the ventricle usually conducts through the **fast** pathway. If the atrial impulse occurs **early** when the fast pathway is **still** **refractory**, the **slow** pathway takes over. It then travels back through the **fast** pathway which has **already** **recovered** excitability, thus initiating the most common '**slow-fast**', or typical AVNRT.
42
**AVRT** occurs when electrical signal conducts abnormally between the atria and ventricles usually by accessory pathways.
Which **condition** is AVRT almost always seen in?
* **Wolff-Parkinson-White syndrome** (WPWS)
* Most of the time, pts w/ WPWS have a **normal** sinus rhythm
* Tendency for pre-excitation is apparent in the form of **delta** waves → slow depolarisation preceding the R wave
* This represents spread of action potential 'leaking down' accessory pathway, where it's conducted more slowly than action potentials carried by bundle of his
* **Type A** → left-sided pathway, dominant R wave in V1
* **Type B** → right-sided pathway, no dominant R wave in V1
43
What are **associations** of **Wolff-Parkinson-White**?
* HOCM
* Mitral valve prolapse
* Ebstein's anomaly
* Thyrotoxicosis
* Secundum ASD
44
What are the **two** **types** of **AVRT**?
* **Orthodromic** AVRT → 95% cases
* **Antidromic** AVRT → 5% cases
45
For **management** of AVNRT and AVRT, how can **AVN** **blockade** be achieved?
* **Vagal manoeuvres** → carotid sinus massage / valsalva manoeuvre
* **IV adenosine** if vagal manoeuvres don't work: 6mg → 12mg → 12mg
* verapamil preferred in asthmatics
* **Electrical cardioversion**
Can _prevent_ episodes with **beta-blockers** and **radiofrequency ablation**
46
How are **broad-complex tachycardias** identified on ECG?
* **Rate \> 100**
* **QRS \> 120ms**
If no clear QRS complexes → VF or asystole
47
**_Monomorphic_** **ventricular** **tachycardia** is very common. What **symptoms** may it present with?
* **Moderate** **discomfort** (haemodynamically stable tachycardia)
to. ..
* **Profound** **collapse** or **arrest** (haemodynamically unstable tachycardia)
48
What are the **commonest** **causes** of monomorphic ventricular tachycardia?
* Acute infarction / ischaemia
* Chronic LV scarring after infarction
49
**Monomorphic VT** - first get the diagnosis correct and identify the underlying rhythm, if this cannot be obtained bc of collapse then urgent DC shock is required.
What are the ECG **features** of VT?
* **Wide QRS complexes** (\>0.14s or \>3.5 small sq)
* AV dissociation sometimes w/ capture and fusion beats
* **capture beat** → normal QRS complex between abnormal beats
* **fusion beats** → 'normal beat' fuses w/ VT complex to create an unusual complex
* A **leftward axis shift** compared to sinus rhythm
* Any **previous history of IHD** (MI, PTCA, CABG)
Most instances of VT can be correctly diagnosed but if in doubt treat broad complex tachycardia as VT
50
What is the **management** of **VT**?
* Connect pt to **cardiac monitor** + have **defib** to hand
* O2 sats, if \< 90% → supplemental **oxygen**
* Correct **electrolyte** **abnormalities**, esp K+ and Mg+
* Check for **adverse** **signs** (shock, MI, syncope, HF)
* Obtain **12-lead ECG** and obtain IV access
51
How do you treat **haemodynamically** **unstable** **VT**?
* Synchronised DC shock
* Follow arrest protocol
52
How do you treat **VT** if **haemodynamically** **stable**?
* **Lidocaine** **1.5mg/kg IV** → if this terminates tachycardia continue as an infusion at 2mg/min for up to 24hrs (use w/ caution in severe left ventricular impairment)
* If tachycardia continues → additional lidocaine bolus of 0.5-0.75 mg/kg
* Otherwise consider giving **amiodarone** (300mg bolus via large bore cannulae in large vein or centrally, then a 900mg 24hr infusion)
* If drug therapy fails, or pt has poor cardiac fxn → **DC cardioversion** (150-200L biphasic) under **sedation** is the best therapy
53
How is **polymorphic** VT different to **monomorphic** VT?
* _Less_ common than monomorphic VT
* Causes **presyncope**, **syncope** or cardiac arrest
54
What is **Torsade de pointes**?
* 'Twisting of the points'
* Polymorphic VT assoc w/ **long QT interval**
* Causes: **acquired** vs **congenital**
55
What is the **management** of Torsade de pointes?
* Congenital → high dose **beta-blockers**
* Acquired → stop all predisposing drugs, correct hypokalaemia and give **magnesium sulfate** (2g IV / 10 mins)
56
What is **long QT syndrome** (LQTS)?
* Inherited condition associated w/ **delayed repolarisation of ventricles**
* May lead to ventricular tachycardia / TdP → **sudden death**
* Most common variants caused by defects in alpha subunit of slow delayed rectifier potassium channel
* Normal corrected QT interval is less than 430 ms in males and 450 ms in females
57
What are the **causes** of a prolonged QT interval?
* **Long QT 1** → exertional syncope, often swimming
* **Long QT 2 →** syncope following emotional stress, exercise or auditory stimuli
* **Long QT 3** → after night or at rest
Tx → avoid drugs which prolong QT interval and other preciptants; beta-blockers; implantable cardioverter defibs in high risk cases
58
What is **ventricular** **fibrilation**?
* **Life-threatening** cardiac arrhythmia
* Most often associated w/ **coronary artery disease**
* VF can result from **acute MI**/ischaemia, or from myocardial scarring from an old infarct
* Ventricular tachycardia may degenerate into VF
* Most common cause of death following MI
