rhythms Flashcards
1st-degree heart block
PR interval > 200ms (five small squares)
2nd-degree heart block Morbitz I or wenckbench
Progressive prolongation of the PR interval culminating in a non-conducted P wave.Malfunctioning AV node cells tend to progressively fatigue until they fail to conduct an impulse. This is different to cells of the His-Purkinje system which tend to fail suddenly and unexpectedly
2nd-degree heart block Morbitz II
Intermittent non-conducted P waves without progressive prolongation of the PR interval (compare this to Mobitz I). The PR interval in the conducted beats remains constant. The P waves ‘march through’ at a constant rate. The RR interval surrounding the dropped beat(s) is an exact multiple of the preceding RR interval
Mobitz II is usually due to failure of conduction at the level of the His-Purkinje system (i.e. below the AV node).
Mobitz II is more likely to be due to structural damage to the conducting system (e.g. infarction, fibrosis, necrosis).
3rd-degree heart block
In complete heart block, there is complete absence of AV conduction – none of the supraventricular impulses are conducted to the ventricles.
Perfusing rhythm is maintained by a junctional or ventricular escape rhythm. Alternatively, the patient may suffer ventricular standstill leading to syncope (if self-terminating) or sudden cardiac death (if prolonged).
Junctional rhythm
A junctional rhythm with a rate of 40-60 bpm.
60-100 accelerated by adrenaline
100+ is tachycardia junctional
QRS complexes are typically narrow (< 120 ms).
No relationship between the QRS complexes and any preceding atrial activity (e.g. P-waves, flutter waves, fibrillatory waves).
inverted p waves before and after
fired from a bundle of his
short Pr
accelerated
no p wave
Ventricular escape or idioventricular rhythm
Ventricular Escape Rhythm: A ventricular rhythm with a rate of 20-40 bpm. QRS complexes are broad (≥ 120 ms) and may have a LBBB or RBBB morphology.Also known as Idioventricular escape rhythm
usually no p waves
VF
The ventricles suddenly attempt to contract at rates of up to 500 bpm. This rapid and irregular electrical activity renders the ventricles unable to contract in a synchronised manner, resulting in immediate loss of cardiac output.
VT sustained and unsuatined /polymorphic and monomorphic
150-300
Ventricular Tachycardia = 3 or more VEB at a rate of > 130 beats/min If > 30 seconds = sustained
Monomorphic -A regular wide QRS complex (≥120 milliseconds) tachycardia at a rate greater than 100 beats per minute. ●The consecutive beats have a uniform and stable QRS morphology
Polymorphic- disorganised but slightly is lol
VT that occurs in the setting of QT prolongation is considered as a distinct arrhythmia, known as torsades de pointes.
VT patho
The mechanism for ventricular tachyarrhythmias includes enhancement of normal automaticity or abnormal automaticity, activity triggered by early or late afterdepolarizations, and reentry.[10] In acute myocardial infarction, the transient ischemia results in an increased concentration of extracellular potassium, which causes partial depolarization of the resting membrane potential.[10] This creates injury currents between the infarcted tissue and healthy myocardium that may trigger spontaneous activity.
LBBB
the normal direction of septal depolarisation is reversed (becomes right to left), as the impulse spreads first to the RV via the right bundle branch and then to the LV via the septum.
This sequence of activation extends the QRS duration to > 120 ms and eliminates the normal septal Q waves in the lateral leads.
produces tall R waves in the lateral leads (I, V5-6) and deep S waves in the right precordial leads (V1-3)
RBBB
In RBBB, activation of the right ventricle is delayed as depolarisation has to spread across the septum from the left ventricle.
The left ventricle is activated normally, meaning that the early part of the QRS complex is unchanged.
The delayed right ventricular activation produces a secondary R wave (R’) in the right precordial leads (V1-3) and a wide, slurred S wave in the lateral leads.
Delayed activation of the right ventricle also gives rise to secondary repolarization abnormalities, with ST depression and T wave inversion in the right precordial leads.
AVRT
Wolff-Parkinson-White (WPW) Syndrome is a combination of the presence of a congenital accessory pathway and episodes of tachyarrhythmia by bundle of kent .Delta wave – slurring slow rise of initial portion of the QRS.
During tachyarrythmias the features of pre-excitation are lost as the accessory pathway forms part of the reentry circuit.
AVRT often triggered by premature atrial or premature ventricular beats.
AVNRT
AVNRT is typically paroxysmal and may occur spontaneously or upon provocation with exertion,Patients will typically complain of the sudden onset of rapid, regular palpitations. between 140-280 bpm and is regular
The slow pathway (alpha): a slowly-conducting pathway with a short refractory period.
The fast pathway (beta): a rapidly-conducting pathway with a long refractory period.
The impulse transmitted down the fast pathway enters the distal end of the slow pathway and the two impulses cancel each other out.
However, if a premature atrial contraction (PAC) arrives while the fast pathway is still refractory, the electrical impulse will be directed solely down the slow pathway (1).
By the time the premature impulse reaches the end of the slow pathway, the fast pathway is no longer refractory (2) — hence the impulse is permitted to recycle retrogradely up the fast pathway.
May respond to vagal maneuvers with reversion to sinus rhythm.
The mainstay of treatment is adenosine.
Orthodromic AVRT
In orthodromic AVRT anterograde conduction occurs via the AV node with retrograde conduction occurring via the accessory pathway through bundle of kent . This can occur in patients with a concealed pathway.vagal manoeuvres may be successful, followed by adenosine or calcium-channel blockers, and DC cardioversion may be considered if non-repsonsive to medical therapy.
PR interval short Qrs complex is longer of 0.12 and normal AV node hols for 0.1second 240 beats a min no p waves
Antidromic AVRT
n antidromic AVRT anterograde conduction occurs via the accessory pathway with retrograde conduction via the AV nodeMistaken for VT. amiodarone, procainamide or ibutilide, but may require DC cardioversion
opposite direction topic beat fires electrify and fires through the accessory pathway and to ventricles no p waves wide qrs VT look duration 0.12 longer
