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Palpitations and Dysrhythmias Flashcards

1
Q

Explain pathophysiology of Atrial fibrilation?

A
  • Disorganised electric activity in the atria
  • Signals are not systematically triggered via the SA node,
  • Instead, are generated from all over the atria, resulting in a quivering or fibrillating (don’t contract properly) and uncoordinated atrial activity.
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2
Q

What are some common causes of AF in the patient in the ED?

A

Reversible/secondary causes of AF (PIRATES)

  • Pulmonary embolism
  • Ischemia (IHD/MI/heart failure)
  • Respiratory disease (including trauma)
  • Atrial enlargement/myxoma
  • Thyroid (hyper)
  • Ethanol (holiday heart
  • Sepsis/sleep apnoea

*can also get ectopic beats

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3
Q

What is paroxysmal AF? Is it concerning?

A

-Paroxysmal AF is when there is fibrillation but it is transient
-This is more concerning because clots form and then can be thrown off when heart beats normally again
(leading to PEs/strokes)

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4
Q

Explain these types of AF

Acute AF
Recurrent AF
Paroxysmal/intermittent AF
Persistent AF
Permanent AF
A
  • Acute AF -onset within last 48hrs
  • Recurrent AF- 2+ episodes
  • Paroxysmal/intermittent AF- resolves spont in 7 d
  • Persistant >7 days, terminates with cardioversion
  • Permanent > 7 days cannot resolve w/ cardioversion
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5
Q

What other investigations should you do in a patient with probable AF? (3)

(bedside, bloods, imaging)

A

Investigations for AF

  1. ECG
    - 24-hr ambulatory ECG monitor if asymptomatic or symptomatic episodes < 24hrs apart
  2. Bloods
    - FBC (anemia)
    - TFTs (↑T4 = thyrotoxicosis)
    - U+E,
    - LFT (gGT-alcohol)
    - HbA1c
    - lipids
  3. Imaging Echo
    - Atrial enlargement (left common)
    - May see mitral valve prolapse
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6
Q

How do we predict risk in AF?

A

CHA2DS2VASc score - calculates the risk of stroke in AF

o Congestive HF/LVSD 1
o Hypertension 1
o Age 65+ 1point.....75+ 2points
o Diabetes mellitus 1
o Stroke/ TIA/ thromboembolism Hx 2
o Vascular disease 1
o Sex category (female) 1

anti-coagulation medication if 2+ women, or 1+ men

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7
Q

When should you treat with anti coagulation?

What are your options and how do they differ?

A

Anticoagulation in atrial fibrillation

  • treat men with chadsvasc 1+ or women with 2+
  • give normal VTE prophylaxis until assessment is made

DOAC (e.g. rivaroxaban, apixaban, dabigitran)

  • do not use if egfr<30
  • can’t miss a dose

Warfarin (monitor for INR 2-3)
-can reverse and can also miss dose

Aspirin alternative

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8
Q

How do we assess someone’s bleeding risk once they have been put on anti-coagulant therapy?

A 
HASBLED 
Hypertension
Abnormal liver function (clotting fx)
Stroke 
Bleeding
Labile INR 
Elderly 
Drugs and alcohol (aspirin, clopidogrel, NSAIDS)
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9
Q

What is the 1st line managment of AF (both acute and chronic)?

A

ALWAYS ASSESS FOR ANTICOAGULATION

  • DOACS (direct thrombin: dabigatran/ factor Xa: rivaroxaban, apixaban, edoxaban )
  • vitamine K antagonist (warfarin)

RATE CONTROL IS 1ST LINE (unless unstable) (aim for <110)

  • 1st line: BB or rate limiting CCB (non:hydro dil/vera)
  • Digoxin (only consider in sedentary patients and heart failure)-beware of vomiting ↓K+ (this will increase risk of toxicity)
  • 2nd line: combine any combo of 2 above

** don’t use sotalol as BB

RHYTHM CONTROL IS SECOND LINE

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10
Q

When would you do RHYTHM control in someone with AF?

A

RHYTHM control in AF

  • 2nd line if rate control not worked (chronic and acute)
  • if heamodynamically UNSTABLE (syncope/shock/acute HF/MI)
  • New onset AF <48 hours
  • AF with reversible cause (e.g. infection)
  • Clinical judgment e.g. active young patients (want to avoid rate control)
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11
Q

What are the options for RHYTHM control in AF?

What do you need to bare in mind with medical conversion?

A

Electrical conversion

  • DC current shock
  • Preferred if heamodynamically unstable (syncope/shock/acute HF/MI)
  • If not anti coagulated give LMWH first but dont delay shock
Medical conversion (bolus then infusion) 
-If symptoms are milder or if electrical conversion not available
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12
Q

What are the options for medical cardioversion for AF?

A

Medical conversion for AF (bolus then infusion)
-If symptoms are milder or if electrical conversion not available

1st line = IV Flecainide (if no structural abn)
AMIODARONE (central line) IF STRUCTURAL ABNORMALITY or IHD (300mg 10-20min, 900mg 24hr)

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13
Q

What are the risks of cardioversion for AF?

How do you minimise risk?

A

Risks of cardioversion for AF
-risk of stroke when cardioverted because coordinated contraction with throw off clots formed in static blood> thrombophylaxis 3 weeks prior if elective

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14
Q

Differential for AF?

What things would be seen in those differentials?

A

Wolf-Parkinson white syndrome – Δ waves, short PR, broad QRS
Atrial flutter – 150bpm, saw tooth

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15
Q

Complications of AF?

A
  • Stroke/TIA (INR< 2)
  • Bleed (if INR>4)
  • Mesenteric ischemia (abdo pain)
  • Paroxysmal AF: terminates spontaneously < 7 d, usually 48 h
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16
Q

What is a supra ventricular tachycardia? (SVT)

Narrow or broad?
Whats the rate?

A

Supra ventricular tachycardia

  • Occurs above ventricles
  • Narrow complex tachycardias (unless BBB = broad complex)
  • Rate >100 and QRS complex <120ms in width (3 squares)
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17
Q

What are some symptoms of SVT?

A

Symptoms of SVT

  • Chest pain
  • Palpitations
  • Dizzyness
  • Sweating
  • SOB
  • Feeling faint

Worrying signs: ‘2s and 2 hearts’

  • Cardiogenic shock (hypotension)
  • Syncope
  • acute MI
  • acute Heart failure
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18
Q

What are 4 main types of SVT?

A

Causes of SVT

  • Atrial fibrillation
  • Atrial flutter
  • Paroxysmal SVT
  • WPW syndrome
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19
Q

What is atrial flutter?

What will the pulse normally be?

A

Atrial flutter

  • the atria contract at 300bmp
  • this is too fast for the AV node to conduct
  • the ventricles contract at a slower rate most common is 2:1 (pulse 150)
  • can also be 3:1 (100) or 4:1 (75)
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20
Q

Explain the ECG in atrial flutter?

  • narrow vs wide
  • irregular vs regular
  • p waves vs no p waves (discrete or continuous)
A

ECG atrial flutter (saw soothed baseline no visible p wave)

  • Narrow QRS (its an SVT)
  • Regular
  • P waves present and continuous
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21
Q

Risk factors for atrial flutter?

A

Atrial flutter risk factors

  • M>F
  • ↑age
  • CAD/HTN/obesity
  • valve dysfunction
  • alcohol
  • COPD/sleep apnoea
  • drugs (NSAIDs)
  • thyrotoxicosis
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22
Q

What is the ACUTE managment of atrial flutter (<48 hours)?

  • if adverse features
  • if no adverse features
A

Adverse features? (shock, syncope, MI, HF)

  • if so SHOCK (up to 3 attempts) GET HELP
  • then give amiodarone 300mg IV over 10-20 mins
  • repeat shock
  • amiodarone 900mg over 24 hours

If no adverse features (treat as regular narrow tachy)

  1. Vagal manoeuvres
  2. Adenosine 6mg → 12 mg → 12 mg (reduce tachycardia and may reveal flutter)
  3. If sinus rhythm not achieved, possible atrial flutter then… Rate control e.g. BB or rate limiting CCB (dil or vera)
23
Q

What is the managment of atrial flutter if they’ve had it for over 48 hours?

A

Atrial flutter lasting >48 hours

  • catheter ablation is 1ST LINE
  • electric cardio version (with anticoag) and chemical cardio version can also be used
24
Q

Explain the ECG in Atrial fibrillation?

  • narrow vs wide
  • irregular vs regular
  • p waves vs no p waves (discrete or continuous)
A

Atrial fibrillation

  • Narrow complex (SVT)
  • irregular (irregularly irregular QRS)
  • no p waves
25
Q

Explain the ECG in AVRT/AVNRT?

  • narrow vs wide
  • irregular vs regular
  • p waves vs no p waves (discrete or continuous)
A

AVRT/AVNRT

  • narrow
  • regular
  • no clear p waves seen before QRS (may be immediatly before/after QRS or seen inverted after QRS)
26
Q

What investigations should you do in a patient with SVT?

A

ECG

Bloods – investigate associated causes
-TFTs (↑T4), FBC, ESR, U+E, LFT, Coagulation screen

CXR – check for signs of heart failure or valvular defects

Echo – evaluate underlying cardiac function, structural abnormalities, evidence of CAD or pericardial fluid

27
Q

Explain the ECG in Sinus tachycardia?

  • narrow vs wide
  • irregular vs regular
  • p waves vs no p waves (discrete or continuous)
A

Sinus tachycardia

  • Narrow complex
  • Regular
  • P waves (not continuous)
28
Q

How should you treat tachycardias?

A

Via the tachycardia algorhythm

  1. Adverse features? (shock, syncope, MI, HF)
    - if so SHOCK (up to 3 attempts) GET HELP
    - then give amiodarone 300mg IV over 10-20 mins
    - repeat shock
    - amiodarone 900mg over 24 hours
  2. Figure out whether broad or narrow and then treat condition
29
Q

What is AV nodal re-entry tachycardia (AVNRT)

A

AV nodal re-entry tachycardia (AVNRT)

  • circuits form WITHIN the AVN causing narrow complex tachycardias
  • very common (most common cause of regular palpitations for people with no structural heart abnormalities)
30
Q

How do you treat AVNRT?

A

Treating AVNRT
Adverse features? (shock, syncope, MI, HF)
-if so SHOCK (up to 3 attempts) GET HELP
-then give amiodarone 300mg IV over 10-20 mins
-repeat shock
-amiodarone 900mg over 24 hours

If no adverse features (treat as regular narrow tachy)

  1. Vagal manoeuvres (valsalva manœuvre-blow into syringe, positioning, carotid massage if not CI)
  2. IV Adenosine 6mg → 12 mg → 12 mg (reduce tachycardia and may reveal flutter)
  3. If sinus rhythm achieved probably re-entry paroxysmal SVT (if not think atrial flutter>BB or CCB)
31
Q

What is atrioventricular re-entry tachycardia?

Definitive management?

A

-anatomical accessory pathway (Bundle of Kent)
(atria>AVN>ventricles>accessory pathway>atria)
-E.g. wolf parkinson white

Definitive management is ablation of the pathway

32
Q

What ECG changes would you see in WPW syndrome?

A

WPW (form of AVRT)

  • Short PR interval <3 squares (<120ms)
  • narrow QRS complex (most common). Can have wide complex in antidromic
  • Delta waves (upstroke) before the QRS complexes
33
Q

What drugs should be avoided in WPW?

A

Be wary of rate control drugs e.g. BB, CCB , digoxin adenosine

34
Q

Explain what VT is

A

Ventricular tachycardia

  • Ventricular pacemaker cells to overtake rate of SAN
  • Monomorphic (common)
  • Polymorphic/Toursaads (more likely to be assosiated with electrolyte abnormalities or toxicities) (give 2g IV magnesium in 10 mins)
35
Q 
What does the ECG look like in VT?
(rate)
(narrow or broad) 
(regular or irregular) 
(p waves?)
A

Ventricular tachycardia

  • Tachycardia >150bpm
  • Broad complex QRS (>3 small squares)
  • Regular
  • No P waves or T waves
36
Q

Investigations for VT?

A

Full A to E
Bloods
-Urgent U&E: esp. ↓K+ & Mg+, Ionised Ca2+, PO4-
-Therapeutic drug levels e.g. digoxin or TCA
-Troponin/CK/myoglobin – screen for complications
-CXR – element of congestive heart failure (might also hear fine crackles and raised JVP)

37
Q

What is the treatment of VT WITH pulse?

A

(Think about that sim you did)

Adverse features? (shock, syncope, MI, HF)

  • if so SHOCK (up to 3 attempts) GET HELP
  • then give amiodarone 300mg IV over 10-20 mins
  • repeat shock
  • amiodarone 900mg over 24 hours

If no adverse features (treat as VT)

  • amiodarone 300mg IV over 10-20 mins
  • amiodarone 900mg over 24 hours

*if ↓Mg (due to alcohol, diuretics) give IV magnesium

38
Q

What is the treatment of VT WITHOUT pulse?

A

Pulseless VT or VF-cardiac arrest algorhythm
-CRP and attach defibrillator pads
UNSYNCHRONISED DEFIBRILATION

39
Q

Whats the definitive treatment for VT?

A

Ventricular tachycardia

  • may be legible for radiofrequency ablation (remove ventricular tissue responsible for rate
  • implantable cardioverter defibrillators (ICDs) – if sustained VT causing syncope or ejectraction fraction < 35%, prev cardiac arrest due to VT/VF, MI
40
Q

Complications of VT?

A

Complications of VT

  • Ventricular fibrillation or pulsless VT (cardiac arrest pathway)
  • Torsades (give IV Mg)
  • Congestive heart failure or cariogenic shock (increased ventricular rate>↓preload>↓blood flow to vital organs
41
Q

What is the PR interval?

How long should the P-R interval be?

A
  • PR interval is from beginning of P to beginning of QRS

- PR interval is 3-5 small sqaures (120-200)

42
Q

what is heart block?

What are some causes?

A

Heart block
-Conduction abnormality (AVN has delayed response to SAN)

Causes

  • INFERIOR MI (will present as narrow QRS)
  • aging/scarring/IHD
  • well trained athletes
  • lyme disease/SLE
  • medication (flecainide, BB, CCB, digoxin, magnesium)
43
Q

What are the types of heart block?

What is complete heart block?

A

1st degree- constant prolonged PR (>1 big square/200ms)

2nd degree mobitz type 1: progressive lengthening PR , then drop, then back to normal WENKEBACK
2nd degree mobitz type 2: Fixed prolonged PR with regular dropping of QRS (ratio 2:1 or 3:1)

3rd degree: complete block between SAN and AVN
-contract independently

44
Q

How will the different types of heart block present?

A

1st degree-asymptomatic

2nd degree- Dizzy, syncope, fatigue, chest pain, SOB palpitations

3rd degree-same but may have confusion. STOKE ADAMS ATTACK- sudden syncope without warning, loss of consciousness

45
Q

What is the most common cause of heart block? How does this look on ecg?

A

Cardiac ischaemia is most common cause of heart block

  • SPECIFICALLY inferior wall MI
  • Will often lead to narrow QRS complex
46
Q

What tests should be done in someone who has heart block

A 
ECG (look for previous ischemic changes) 
Bloods
-FBC
-U+Es 
-Mg
-Ca
-TFTs

Drug history and PMH of cardiac problems

47
Q 
What does an ECG look like in complete heart block?
(brady/tachy?
pr interval length?
p waves regular or irregular?
QRS regular or irregular?
QRS narrow or broad?
relationship of P to QRS?)
A 
Complete heart block 
(men dont deal well with brake ups) 
-bradycardia usually 30-40bpm 
-prolonged PR interval 
-p waves regular
-QRS irregular 
-QRS broadened (if proximal) or narrow (if distal/near AVN)
-no connection to QRS complex
48
Q

How do you acutely manage bradycardia if adverse features?

A

BRADYCARDIA PATHWAY
-A to E assessment attach DEFIB and lay flat

  1. If ADVERSE features (shock <90, syncope, acute HF/MI)
    - 500mcg IV atropine
    - repeat Atropine every 2-3 mins until maximum of 3mg

AND

-TRANSCUTANEOUS pacing (central line)

AND

  • isoprenaline/adrenaline infusion titrated to response
  • aminophylline or dopamine or glycopyrolate
  1. if no response do TRANSVENOUS PACING (central line)
49
Q

What is the chronic managment of heart block?

A

Chronic managment of heart block

-if MOBITZ TYPE 2 or COMPLETE they need PERMANENT PACEMAKER

50
Q

What medication can you give for heart block in BB or CBB OD

A

Glucagon

51
Q

In AF when would you use a Holter monitor?
In AF when would you use an external loop recorder?
In AF when would you use an event recorder?

A
  • Palpitations should first be investigated with a Holter monitor after initial bloods/ECG
  • If normal, still with symptoms do an external loop recorder
  • Event recorder ECG if symptomatic eps. > 24hrs apart
52
Q

When giving Adenosine what should you remember?

A

Adenosine has short half life

  • Best given with 20ml saline flush to hurry it along
  • Give in ACF (as central as poss)
53
Q

What can torsades be caused by?

A

Hypokalaemia and Hypomagneseamia (you give IV mag sulfate)

54
Q

When do you use synchronised and when do you use desynchronised shock?

A

unsynchronised shock=pulseless

synchronised shock= with pulse

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