Tachycardias (see DM for more depth) Flashcards
things to look out for when determining a tachycardia (9)
context; age; PMH; FH; congenital abnormalities; development of substrate; aquired abnormality; red flags (FH and present w cardiac arrest, syncope etc.); common presentations
common tachy presentations (7)
asymptomatic; SOB; palpitations; pre-syncope; chest pain; collapse/LOC; cardiac arrest -always check what other associated symptoms there are e.g. sweating, nausea, sudden onset
what happens to CO in tachys
decreases
why does CO decrease in tachys
decreased time between contractions/incorrect contractions leads to less time for ventricular filling and therefore a decrease in the volume of blood pumped pumped out
what counts as narrow complex tachycardia
> 100bpm, QRS <120ms (1.2 squares)
what counts as broad complex tachycardia
> 100bpm, QRS >120ms
irregular narrow complex tachy (what condition)
AF
regular narrow complex tachy (5)
p waves - sinus tachy, focal atrial tachy
no typical p waves - atrial flutter, AVRT, AVNRT
irregular broad complex tachy
pre-excited AF
regular broad complex tachy (4)
p waves - atrially driven with aberration, pre-excited tachy;
independent p waves - VT
pacing spike - paced tachy
where does AF usually arise from
focal pulmonary cells (i.e. where the pulmonary veins enter)
atrial flutter ECG
“sawtooth” appearance of flutter waves (give adenosine to see more clearly) - inverted in inferior leads if anticlockwise reentry; Regular atrial activity at ~300 bpm; Loss of the isoelectric baseline; Ventricular rate depends on AV conduction ratio (usually 2:1 i.e. 150bpm)
what is atrial flutter
regular tachy of 150bpm; caused by an ectopic beat which causes a “re-entrant
rhythm” in either atrium; usually anticlockwise re-entry (90%)
common causes of atrial flutter (5)
RA dilation; ischaemic heart disease; idiopathic; normal variant; pt w history of endurance sport
treatment of Atrial flutter
rate or rhythm control (same as AF); electrical cardioversion; radiofrequency ablation can be done if chronic
what is a re-entrant circuit
in certain people the fibres in the conducting cells have different conduction speeds with different refractory times, if there are ectopic beats then these impulses may travel down the slow pathway while the fast pathway is refractory - when this impulse reaches the end of the slow pathway it then has the potential to go back up the fast pathway as it has now finished its refractory period (re-entry)
what is wolff-parkinson-white syndrome
a syndrome that arises due to a congenital accessory pathway (bundle of kent) that causes early, slow, depol of the ventricles
signs of narrow complex tachycardia (sinus, normal conduction)
abrupt rapid regular palpitations; presyncope
wolff-parkinson-white ECG
pre-excitation, slurring of the upstroke of the P wave - delta wave; short PR interval (due to pre excitation); T wave abnormalities; dominant R waves in V1/V2; inferior q waves may be present
what is AVNRT
a paroxysmal supraventricular tachycardia (ie it originates above the level of the Bundle of His) and is the commonest cause of palpitations in patients with hearts exhibiting no structurally abnormality; caused by abberant circuit within the AVN
AVNRT ECG
tachycardia of 140-280 bpmwith normal and regular QRS complexes; No visible P-waves (hidden within the QRS complex)
what is AVRT
paroxysmal supraventricular tachycardia that occurs in patients with accessory pathways, usually due to formation of a re-entry circuit between the AV node and accessory pathway; can be orthodronic or antidronic
AVRT ECG
orthodromic: Rate usually 200-300 bpm, Retrograde P waves are usually visible, with a long RP interval, delta wave may be seen;
antidromic: Rate usually 200-300 bpm, Wide QRS complexes due to abnormal ventricular depolarisation via AP
what is ventricular tachycardia
3 or more consecutive ventricular beats occurring at a rate greater than 120bpm; if > 30 seconds = sustained; can be monomorphic or polymorphic
VT ECG
broad QRS complex; extreme axis; monomorphic – uniform QRS complexes in most leads (most common form); polymorphic – QRS of varying amplitudes, axis and duration across the leads
difference between AVNRT and AVRT
with AVNRT tachy arises from near the AV node which similarly contracts the ventricle and the atria every time it goes around;
what is torsades de pointe
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; For TdP to be diagnosed, the patient must have evidence of both PVT and QT prolongation
what arrhythmia is associated w digoxin toxicity
bidirectional VT; downward sloping T wave
torsades de pointe ECG
Peaks of the QRS twist around the isoelectric line; Irregular RR intervals; Tachycardia with ventricular rates of 160 to 250 bpm; Prolonged QTc (male >0.43 s, female >0.45 s); R on T phenomenon; can trigger a run of polymorphic VT
what is brugada syndrome
an autosomal sodium channelopathy associated with sudden cardiac
deaths; . Defective
sodium channels impair influx of sodium ions, resulting in shorter action potentials
brugada syndrome ECG
brugada sign - downsloping coved ST elevation
followed by an inverted T wave - this is only present in leads V1 and V2;”
what is ventricular fibrillation
A rapid, unco-ordinated and life-threatening ventricular arrhythmia resulting in poor
myocardial contraction, eventually leading to cardiac death
VF ECG
Chaotic waveforms with varying amplitudes; Unidentifiable P-waves, QRS complexes or T waves
what is long QT syndrome
prolonged ventricular repolarisation - can be congenital or acquired
RBBB ECG
“MaRRoW” (M in V1, W in V6); Wide QRS complexes (>0.12 s); RSR’ pattern in V1
–V3 (M pattern); Long S wave duration in V6/1
LBBB ECG
WiLLiaM (W in V1, M in V6); Wide QRS complexes (>0.12 s); Deep S wave in V1 and ‘M-shaped’ R wave in V6; Poor R wave progression in chest leads; ST elevation may be seen
