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cardiology > supraventricular tachycardias > Flashcards

supraventricular tachycardias Flashcards

1
Q

where do Supraventricular tachycardias arise

A

atrium of the atrioventricular junction

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2
Q

what are the ECG features of sinus tachycardia

A
  • P wave morphology similar to that of sinus rhythm

- P wave always precedes QRS

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3
Q

what are the ECG features of atrioventricular nodal reentrant tachycardia

A
  • no visible P wave
  • most common cause of palpitations in patients with normal hearts
  • normal regular rhythm
  • rate of 140-240 bpm
  • sometimes will show bundle branch block
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4
Q

what are the ECG features of atrioventricular re-entrant tachycardia complexes

A
  • P wave visible between QRS and T wave

- Due to an accessory pathway: if pathway conducts in both directions, ECG during sinus rhythm may be pre excited

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5
Q

what are the ECG features of atrial fibrillation

A
  • irregularly irregular RR intervals and absence of organised atrial activity
  • most common tachycardia in patients above 65
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6
Q

what are the ECG features of Atrial flutter

A
  • visible flutter waves at 300bpm usually with 2:1 AV conduction
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7
Q

what are the ECG features of atrial tachycardia

A
  • organised atrial activity with P wave morphology different from sinus rhythm preceding QRS
  • usually occurs in patients with structural heart disease
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8
Q

what are the ECG features of multifocal atrial tachycardia

A
  • multiple P wave morphologies and irregular RR intervals

- rare arrhythmia most commonly associated with significant chronic lung disease

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9
Q

what are the ECG features of accelerated junctional tachycardia

A
  • ECG similar to that in AVNRT

- rare in adults

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10
Q

what is inappropriate sinus tachycardia

A

Is a condition in which an individual’s resting heart rate is abnormally high – greater than 100 beats per minute or rapidly accelerating to over 100 beats per minute without an identifiable cause; although small amounts of exercise, emotional or physical stress are triggering

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11
Q

what are features of AV nodal re-entrant tachycardia

A
  • sticks suddenly without obvious provocation

- emotion, exercise, emotional stress etc may provoke it

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12
Q

what are the 2 pathways of within the AV node

A
  1. slow = short effective refractory period and a slow conduction period
  2. fast = longer effective refractory period and a faster conduction phase
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13
Q

what are features of atrioventricular re-entrant tachycardia

A
  • macro re-entry circuit and each part of the circuit is activated sequently
  • atrial activation occurs after ventricular activation and the P wave is usually seen clearly between the QRS and T waves
  • the AV node and ventricles are activated normally usually resulting in a narrow QRS
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14
Q

what are the Kent bundles

A

The bundle of Kent is an abnormal extra or accessory conduction pathway between the atria and ventricles

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15
Q

what is Wolff Parkinson’s white syndrome

A

Condition that causes the heart to beat abnormally fast for periods of time. The cause is an extra electrical connection in the heart.

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16
Q

what is orthodromic AVRT

A

In orthodromic AVRT, anterograde conduction occurs via the AV node, with retrograde conduction occurring via the accessory pathway. This can occur in patients with a concealed pathway.

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17
Q

what is antidromic AVRT

A

In antidromic AVRT anterograde conduction occurs via the accessory pathway with retrograde conduction via the AV node. Much less common than orthodromic AVRT, occurring in ~5% of patients with WPW.

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18
Q

what does anterograde mean

A

towards the ventricle

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19
Q

what does retrograde mean

A

away from the ventricle

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20
Q

what are clinical features of AVNRT and AVRT

A
  • rapid regular palpitations usually with an abrupt onset and sudden termination
  • termination by Valsalva manoeuvres ie a breathing method that may slow your heart when it’s beating too fast.
  • in patients with depressed ventricular function, uncontrolled atrial fibrillation can reduce cardiac output and cause hypotension and congestive heart failure
  • anxiety, dizziness, dyspnoea, neck pulsation, central chest pain
  • syncope
21
Q

what is the acute management for AVNRT and AVRT

A
  • patients presenting with SVTs and haemodynamic instability require emergency cardioversion
  • patients that are haemodynamically stable, vagal manoeuvres, including right carotid massage the Valsalva manoeuvre and facial immersion in cold water can be successfully employed
  • if physical manouvres are not successful then IV adenosine should be tried - it is highly effective at termination AVNRT and AVRT or unmasking underlying atrial activity , but rarely affects ventricular tachycardia.
22
Q

what is long term management for AVNRT and AVRT

A
  • refer to cardiologist for electrophysiological evaluation and long term management
  • verapamil, ditiazem and beta blockers, potassium depolarisation current blockers and multichannel blockers may also prevent tachycardia
23
Q

What are some types of atrial tachycardia

A
  • atrial fibrillation
  • atrial flutter
  • atrial tachycardia
  • atrial ectopic beats
24
Q

what may cause atrial fibrillation

A
  • any condition that results in raised atrial pressure, increased atrial muscle mass, atrial fibrosis, or inflammation and infiltration of the atrium
  • hypertension
  • heart failure
  • alcohol intoxication
  • hyperthyroidism
  • rheumatic heart disease
25
Q

what is atrial fibrillation

A

a chaotic irregular atrial rhythm at 300 to 600bpm, the AV node responds intermittently, hence an irregular rhythm. cardiac output drops as the ventricles aren’t primed reliably by the atria

26
Q

what are symptoms of atrial fibrillation

A
  • may be asymptomatic
  • chest pain
  • palpitations
  • dyspnoea
  • faintness
27
Q

what are signs of atrial fibrillation

A
  • irregularly irregular pulse - the irregular nature of AF is maintained during exercise
  • apical pulse rate is greater than the radial rate
  • 1st heart sound is of variable intensity
28
Q

what genes have been linked to genetic defects leading to atrial fibrillation

A

linked to chromosomes 10,6,5,4

29
Q

how is atrial fibrillation maintained

A

by continuous rapid activation of the atria by multiple meandering re-entry wavelets, often driven by rapidly depolarising automatic foci, located predominantly on the pulmonary veins

30
Q

what does the ECG show for AF

A
  • irregularly irregular pulse
  • atrial rhythm >300bpm
  • fine oscillations of the baseline
  • no clear P waves
  • QRS rhythm is rapid and irregular
  • ventricular rate is variable
31
Q

what is the clinical classification of atrial fibrillation

A
  • first detected - irrespective of duration or severity of symptoms
  • paroxysmal <48 hours, recurrent and can have spontaneous resolution
  • persistent >48 hours, can still be cardioverted to NSR, unlikely to spontaneously revert to NSR
  • permenant (chronic)
32
Q

what’s the acute management of atrial fibrillation

A
  • ventricular rate control, achieved by drugs the block the AV node
  • cardioversion, achieved electrically by DC shock or medically by IV infusion of an antiarrhthmic drug
33
Q

what is the long term management for atrial fibrillation

A
  • rate control (slow down AVN conduction)
    1. beta blocker or CCB
    2. + Digoxin
    ablating AF focus
  • rhythm control (arrhythmic drugs plus DC cardioversion plus oral anticoagulation)
34
Q

what is rhythm control

A
  • advocated for younger, symptomatic and physically active patients
  • recurrent paroxysms may be prevented with oral medication
35
Q

what is rate control

A

usually achieved by a combination of digoxin, beta blockers, non dihydropyridine calcium channel blockers

  • AV nodal ablation and pacemaker implantation
36
Q

what is atrial flutter

A

an organised atrial rhythm with an atrial rate typically between 250 and 350bpm. The atria depolarise regularly at very high rates appearing to flutter

37
Q

what does typical or isthmus dependent atrial flutter involve

A

macro reentrant right atrial circuit around the tricuspid annulus. The wave circulates foes the lateral wall of the right atrium, through the Eustachain ridge between the tricuspid annulus and the inferior vena cava and up the intertribal septum, giving rise to the most frequent pattern, referred to as the counter clockwise flutter

38
Q

what does the ECG of atrial flutter show

A
  • regular sawtooth like atrial flutter waves between QRS complexes - localised to leads II, III, aVF and V1
  • ventricular 150bpm
  • atrial 300 bpm
  • irregularly irregular rhythm
39
Q

what are features of atrial flutter

A
  • usually paroxysmal
  • episodes last from seconds to years
  • chronic atrial flutter usually progresses to AF
40
Q

how is atrial flutter caused

A
  • re-entrant electrical signal from either atrium. Re-enterant signal loops back on itself and overrides the normal sinus rhythm and establishes an endless loop of stimulation
  • underlying sides
  • premature atrial contraction
  • partial premature contraction, normal tissue relaxes – wave of stimulation propagates – normal tissue contracts, premature tissue recovers – change or re entrant circuit, stimulation wave double backs on itself
41
Q

what are symptoms of atrial flutter

A
  • palpitations
  • fatigue
  • chest pain
  • exercise intolerance
  • difficulty breathing at night/lying down
  • peripheral oedema
42
Q

what is the treatment of atrial flutter

A
  • unstable: DC cardioversion
  • Stable : BB, CCB, amidoarone, anticoagulant
  • long term: RF ablation
43
Q

what does the CHADS-VASc score stand for

A 
Congestive HF 
Hypertension 
Age>75
Diabetes mellitus 
Stroke 
Vascular disease 
Age 65-74
Sex (female)
44
Q

what do the CHADS-VASc scores correlate to for treatment

A

0 = aspirin and no therapy
1 = aspirin or anticoagulation
2 > oral coagulation

45
Q

what is the treatment for acute haemodynamic instability in AF

A

DC cardioversion

46
Q

what is the treatment for actue haemodynamic stable AF

A

1st line: treat reversible causes

2nd line (onset <24hr): rhythm control

  • chemical cardioversion = IV Amiodorone and Flecianide
  • DC cardioversion

3rd line (onset>24hr): rate control

  • 1st = BB or CCB (Diltiazem proffered)
  • 2nd = Digoxin if HF
47
Q

when should you give anticoagulants when a patient has AF

A

if high risk for a thromboembolism (CHADVAS)

indicated if:

  • thyrotoxicosis
  • hypertrophic cardiomyopathy
  • Valvular AF - warfarin only
48
Q

how to treat chronic AF

A

1st rate control

  • slow down AVN conduction
    1. BB or CCB
    2. + Digoxin

2nd rhythm control

  • restoration of NSR ie anti arrhythmic drugs (amiodarone)
  • maintenance of NSR ie antiarrhythmic dress, catheter ablation or atrial focus

cardiology (13 decks)

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