Ecg, Mhu, Mbbs Iv

Rapid heart rate that originates from above or within the AV node. Encapsulates many different rhythms

Originates from a single point in the atrium or AV node that is firing at a faster rate than the SA node (can also be the SA node in sinus tachy).

There is organised atrial contraction so a (normal or modified) P wave will be present

Different focus in the atrium takes over from the SA =>ABNORMAL P waves preceding QRS complexes.

- Often in px w chronic lung disease.

- Normally > 100 bpm + reg .

- P waves have diff morphologies as the atrial focus changes from beat to beat.

- Similar to atrial tachycardia in all other respects.

Problem with SA node (high vagal tone, sick sinus), AV node is next most autonomic tissue, takes over

- Impulses propagated to ventricles + atria simultaneously

- P waves hidden in QRS

- Inappropriate tachy: b blockers or ivabradine (selective sinus node blocker) but is usually best left alone

- APPROPRIATE: (eg d/t sepsis / anaemia / thyrotoxicosis/pain) should be left alone and the underlying trigger treated.

- Atrial tachys can usually be rate controlled with b blockers or ca channel blockers.

- Saw tooth

- Single large re-entry circuit around the atrium=>AV node every time it passes

- Typical AF runs anti clockwise around the right atrium and across the cavotricuspid valve isthmus

- Sawtooth best in inferior leads, caused by the circuit alternately heading towards the inferior leads and away as it speeds around the atrium.

- Fixed circuit=> constant rate

- Clockwise in the right atrium, in the left atrium or around sites of prev surg

- Lack sawtooth pattern

- Suspect flutter in any reg tachy ~150bpm

-Irreg irreg d/t disorganised activity

- Rate depends on the degree of AV block

- Tiny fibrillatory baseline reflects lots of tiny circuits in A

- Within AVnode=>activates vents +atria almost simultaneously

- Two anatomical pathways next to the AV node (slow +fast pathways) form a circuit w v rapid conduction =>rapid regular tachycardia

=>‘Pseudo R wave’ =retrograde P wave superimposed on the QRS complex

- Requires AV pathway + accessory pathway (AP)

- Antegrade (A to V - pre-excitation delta wave on ECG (scoop up on QRS) or retrograde (V to A)

- Down accessory path and up normal AV path.

- As the impulse goes down the AP, the vent contraction starts in an abnormal way (pre-excitation).=>delta waves! + wide QRS

- Down the AV node and up AP

- Narrow QRS as it propagates from normal AV

- Spreads slowly across V => reaches access path=> propagates to atrium=>delay in atrial contraction=> LONG RP interval

- PR interval >200ms

- Marked block >300ms (p wave will be buried in preceeding T wave)

Increased vagal tone, sport, Inferior MI, Mitral valve surgery, Myocarditis, Electrolyte disturbances (e.g. Hyperkalaemia), AV nodal blocking drugs (beta-blockers, calcium channel blockers, digoxin, amiodarone), May be a normal variant

- Progressive prolongation of the PR interval culminating in a non-conducted P wave

- PR interval is longest immediately before the dropped beat, shortest immediately after the dropped beat

- Usually asymptomatic, does not need tx. Symptomatic respond to atropine

- P-P interval remains relatively constant

- Greatest increase in PR interval duration is typically between beats 1&2

- RR interval progressively shortens with each beat

- The Wenckebach pattern tends to repeat in P:QRS groups with ratios of 3:2, 4:3 or 5:4.

- Mobitz I is usually due to reversible conduction block at AV node.

- 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 (i.e. producing a Mobitz II block).

- Drugs: b-blockers, ca chan blockers, digoxin, amiodarone

- Increased vagal tone (e.g. athletes)

- Inferior MI

- Myocarditis

- Following cardiac surgery (mitral valve repair, Tetralogy of Fallot repair)

- PR interval in the conducted beats remains constant.

-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 (e.g. double the preceding RR interval for a single dropped beat, treble for two dropped beats)

- Anterior MI (septal infarct w necrosis bundle branches)

- Idiopathic fibrosis of the conducting system (Lenegre’s or Lev’s disease)

- Cardiac surgery

- Inflammatory conditions (rheumatic fever, myocarditis, Lyme disease)

- Autoimmune (SLE, systemic sclerosis)

- Infiltrative myocardial disease (amyloidosis, haemochromatosis,sarcoidosis)

- Hyperkalaemia

- Drugs: b-blockers, ca channel, digoxin, amiodarone.

- Block below AV node, his/purkinje

- Usually due to structural damage

- May be no pattern, or may be fixed ratio

- Usually have LBBB or bifasicular block and Mobitz II is caused by intermittent failure of the remaining fasicle

- ~75% of cases, block distal to Bundle of His, =>broad QRS

- ~25%, block within His Bundle=> narrow QRS

- Causes haemodynamic comp, severe bradycardia, progression to 3rd degree heart block.

- Onset of haemodynamic instability may be sudden=>syncope or sudden cardiac death.

- The risk of asystole is around 35% per year

- Needs permanent pacemaker.

- Complete absence of AV conduction

- Perfusing rhythm is maintained by - a junctional or ventricular escape rhythm.

- Ventricular standstill can cause syncope/sudden cardiac death

- Severe bradycardia with independent atrial and ventricular rates

The atrial rate is approximately 100 bpm.The ventricular rate is approximately 40 bpm.The two rates are independent; there is no evidence that any of the atrial impulses are conducted to the ventricles.

- Vent rhythm w rate 20-40 bpm.

- QRS complexes are broad (≥ 120 ms) and may have a LBBB or RBBB morphology

- Junctional+vent escape rhythms arise when the rate of supraventricular impulses arriving at the AV node or ventricle is less than the intrinsic rate of the ectopic pacemaker.

- Severe sinus bradycardia

- Sinus arrest

- Sino-atrial exit block

- High-grade second degree AV block

- Third degree AV block

- Hyperkalaemia

- Drugs: beta-blocker, calcium-channel blocker or digoxin poisoning

- Rate of 40-60 bpm.

- 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).

- AF with reg rhythm

- Indicates that none of the atrial impulses are conducted to the ventricles, i.e. complete heart block is present.

- Often seen as a consequence of digoxin toxicity

- Normal direction of septal depolarisation is reversed (becomes right to left), impulse spreads first to RV via RBB then to LV via septum.

- => broad QRS, > 120 ms+eliminates normal septal Q waves in lateral leads.

- Depolarisation from R to L=> tall R waves in lat leads (I, V5-6) + deep S waves in R precordial leads (V1-3), + usually leads to L axis dev.

-Vents activated sequentially(R then L)=> broad or notched (‘M’-shaped) R wave in lat leads

- QRS duration of > 120 ms

- Dominant S wave in V1

- Broad monophasic R wave in lateral leads

- Absence of Q waves in lateral leads (except avL)

- Prolonged R wave peak time > 60ms in L praecordial leads (V5-6)

- R wave height ≤ 3 mm in V3.

- Causes:

- Prior anteroseptal MI

- LV hypertrophy

- Inaccurate lead placement (e.g. transposition of V1 and V3)

- Dilated cardiomyopathy

- May be a normal variant

- Aortic stenosis - IHD - HTN

- Dilated cardiomyopathy

- Anterior MI

- Primary degenerative disease (fibrosis) of the conducting system (Lenegre disease)

- Hyperkalaemia

- Digoxin toxicity

- LV act=normal=>norm first part of QRS

- Delayed RV act =>secondary R wave in R praecordial leads (V1-3)+wide, slurred S in lat leads

- Also causes secondary repolarisation abnormalities. eg. ST depression+T wave inversion R praecordial leads.

- In isolated RBBB cardiac axis is unchanged, as left ventricular activation proceeds normally via the left bundle branch.

- Broad QRS > 120ms

- RSR’ pattern in V1-3 (‘M-shaped’ QRS)

- Wide, slurred S wave in the lateral leads (I, aVL, V5-6)

- ST depression and T wave inversion in the right precordial leads (V1-3)

- Sometimes rather than an RSR’ pattern in V1, there may be a broad monophasic R wave or a qR complex.

- Right ventricular hypertrophy/cor pulmonale

- PE

- IHD

- Rheumatic heart disease

- Myocarditis or cardiomyopathy

- Degenerative disease of the conduction system

- Congenital heart disease (e.g. atrial septal defect)

GIT: Nausea, vomiting, anorexia,diarrhoea

Visual: Blurred vision, yellow/green discolouration, halos

CVS: Palpitations, syncope, dyspnoea

CNS: Confusion, dizziness, delirium, fatigue

- Digoxin can cause a multitude of dysrhythmias, due to increased automaticity (increased intracellular calcium) and decreased AV conduction(increased vagal effects at the AV node)

- Classic is combo of a SVT (d/t inc. automaticity) w slow ventricular response (d/t dec AV conduction), e.g. ’atrial tachycardia with block’.

- SVT w slow vent response

- Frequent PVCs (the most common abnormality), including ventricular bigeminy and trigeminy)

- Sinus bradycardia or slow AF

- Any type of AV block

- Regularised AF = AF with complete heart block and a junctional or ventricular escape rhythm

- VT, including polymorphic and bidirectional VT

- Pacing spike precedes the p wave

- Short vertical spikes

- Morphology of p wave dependent of lead placement but may appear normal.

- Pacing spike precedes the QRS complex.

- RV pacing lead=>QRS morphology similar to LBBB.

- Left epicardial lead=>similar to RBBB

- ST segments and T waves should be discordant with the QRS complex i.e. the major terminal portion of the QRS complex is located on the opposite side of the baseline from the ST segment and T wave.

- Peak p waves > 2.5 mm in the inferior leads (II, III and AVF) > 1.5 mm in V1 and V2

- Indicates r atrial enlargement

- d/t pulmonary htn

Combination of the presence of a congenital accessory pathway and episodes of tachyarrhythmia.

- Incidence 0.1 – 3.0 per 1000.

- Associated with a small risk of sudden cardiac death.

- Accessory pathways formed in cardiac development

- Can conduct anterograde (rare), retrograde (15%) or both ways (most common)

- Tachyarrythmia facilitated by the formation of reentry circuit involving the accessory path, (atrioventricular reentry tachycardias AVRT) or by direct conduction from A to V via the accessory pathway, bypassing the AV node, seen with atrial fibrillation or atrial flutter in conjunction with WPW

- PR interval <120ms

- Delta wave – slurring slow rise of initial portion of the QRS

- QRS prolongation >110ms

- ST Segment and T wave discordant changes – i.e. in the opposite direction to the major component of the QRS complex

- Pseudo-infarction pattern can be seen in up to 70% of patients – due to negatively deflected delta waves in the inferior / anterior leads (“pseudo-Q waves”), or as a prominent R wave in V1-3 (mimicking posterior infarction).