Bradyarrhythmias and Bundle brand blockages

Bradyarrhythmia
Bradycardic disorders arise either by a sinus node disorder or by blocking the conduction of atrial excitement into the ventricles. The most common is sinus bradycardia.

Sinus bradycardia
This is a slowing of the heart rate < 60 / min. Physiologically, it occurs in situations where vaginal activity ( sleep ) predominates. We find normal value in athletes, when it reaches 40 beats per minute. Among possible causes includes, for example.: hypothyroidism, hypothermia, intracranial hypertension, AIM bottom walls, sick sinus syndrome. It is also often induced iatrogenically beta blockers, verapamil, digitalis, amiodarone.

Therapy - in symptomatic individuals atropine 0.5-1 mg i.v.

Sick sinus syndrome
It is permanent or bounty sinus bradycardia, up to the arrest of the sinus node ( sine arrest ). Seizures may be alternated flutter/atrial fibrillation. There is a failure of the formation of excitement, which can be functional / anatomical and transient / permanent.

Ethiology:

 * idiopathic degenerative damage in the area SA node,
 * coron,
 * cardiomyopathy,
 * increased vagotonia,
 * endocrinopathy,
 * farm,
 * direct damage to the sinus node.

Clinical picture
Most patients are asymptomatic, otherwise palpitations, dizziness, confusion, presyncope, syncope, ↓ MSV.

Diagnostics:
On ECG we observe a slow or irregular sinus action, various surrogate rhythms or, conversely, paroxysms tachycardia. Negative effect autonomic nervous system confirms the ability of the sinus node to increase SF at physical load ( we confirm by ergometry ). Holter ECG shows the variability of SF during the day and night, episodes of sinusoidal pauses or the occurrence of other severe arrhythmias.

Therapy:
Asymptomatic patients do not require treatment. In bradycardia with haemodynamics disorder, we indicate implantation pacemaker.

Sinus arrest ( sine arrest )
This is a different length of outage in the SA node. If there is a longer pause, a junctional or idioventricular contraction may occur. It may manifest itself clinically syncope.

Therapy - in symptomatic individuals atropine 0.5-1 mg i.v.

Sinoatrial blockade
It has three levels, but only III is of clinical significance. degree at which the pulse is not converted from the sinus node to myocardium atrium → failure of one cardiac contract. The entire P-QRS-T complex is missing on the ECG.

Therapy - in symptomatic individuals atropine 0.5-1 mg i.v.

Atrioventricular blockages
This is a fault in the transfer of the depolarization wave to the chambers. The blockade is most often in the AV node ( suprahisal ), but it can also occur in His bundle ( intrahisally ) or infrared.

Ethiology

 * AIM ( especially the lower AIM at the closure ACD),
 * inflammation - viral myocarditis, borreliosis, Chagas disease,
 * trauma,
 * bradycardicizing drugs - digoxin, beta blockers,
 * idiopathic fibrosis,
 * cardiomyopathy.

1st degree:
Extended AV line of excitement, therefore PQ > 0.2 s. Carditis in acute rheumatic fever, digoxin intoxication, β blockers. Clinically non-binding, it must be taken into account when medication with the above drugs.

2nd degree:
Intermittent line failures from atria to chambers ( some excitement is not converted to chambers ), on ECG there are P waves not followed by the QRS complex.

A-V block II °, Mobitz type I ( Wenckebach period ):
With each resurgence transferred, the fault escalates and the time of conduction of the atrium from the ventricles is extended. The line failure eventually escalates so that the excitement from the atria does not convert to chambers. A temporary complete blockage of the A-V transmission is created. Failure conversion will allow „ recovery “ of the conversion system and recovery of the A-V transmission. This process is repeated periodically. The interval from one complete A-V blockade to another complete A-V blockade is called the Wenckebach period.

The more severe the fault, the sooner the complete A-V block occurs and the shorter Wenckebach's period will be. The usual ratio of A-V conversion is 5: 4, 4: 3 and 3: 2. In the last case, Wenckebach's period can be shortened so that a complete A-V block occurs after each successful A-V conversion. The conversion system can handle one transmission of excitement from the atria to the chambers, but it can no longer handle another A-V transmission. This disorder is called fixed Wenckebach period. There is an A-V ratio of 2: 1 ( conversion, each second P wave ) is converted.

Fixed Wenckebach period, unlike A-V blockages Mobitz II, is not a clear indication for pacemaker implantation. An exception is symptomatic bradycardia in the fixed Wenckebach period. For example, if the frequency of a sick S-A node drops to 60 / min, then with a 2: 1 A-V conversion, the frequency of QRS and chamber systems will be 30/min and this usually causes a significant decrease in the minute cardiac output. If the function of the S-A node is OK, the sympathetic system of the A-V blockade 2: 1 solves by stimulating the S-A node to a higher node frequency, eg to 120/min to maintain QRS frequency ( chamber system ) 60 / min.

ECG finding:
It's on the ECG in front of everyone QRS complex wave P, the rhythm is sinusoidal and the QRS complex lasts maximum 0.12 s. With each new P-QRS complex, it gradually lengthens more and more PQ interval as the A-V transmission failure escalates. When a complete A-V blockage is created, the P wave ( evidence of atrial depolarization ) is displayed on the ECG, which is not followed by the QRS complex ( evidence of complete A-V blockade ). After a pause, it appears on the ECG P-QRS complex, usually with a normal P-Q interval ( proof of a restored A-V line ).

Lesion localization
The lesion in the transmission system is located mainly in the A-V node, less often in His bundle. The location of the fault cannot be determined from a surface ECG, but only during invasive electrophysiological examination.

A-V block II °, Mobitz type II:
At normal heart rate, the damaged area cannot convert all control pulses from the A-V node to the chambers. Each transferred pulse induces a complete blockade of the A-V ( conversion of both Tawar arms do not lead to ). The site of failure needs some recovery time to allow for further A-V conversion. At the mildest degree of failure, control pulses from the supraventricular area are converted to chambers in a ratio of 2: 1 ( P-P-QRS ). At a higher degree of failure, the A-V ratio of the conversion increases to 3: 1, 4: 1, etc. During further progression, Tawar's arm completely stops leading excitement and a complete A-V blockade III ° ( is a line block in both Tawar arms ).

This type of A-V blockade is unstable and usually progresses to complete A-V blockade III ° with ventricular bradycardia, in the worst case with asystole and syncope ( Adams-Stokes syndrome ). Therefore, the finding is Mobitz II on ECG very importantand is an indication to place the patient on a monitored bed and to early implant a pacemaker. For the above reasons, the name Mobitz II should not be used for A-V blockade with a 2: 1 conversion and a QRS complex shorter than 0.12 s. Reversible causes of conduction A-V disorder must be ruled out before indicating for pacemaker implantation: unstable coronary heart disease ( beta-blockers, verapamil or diltiazem, digoxin ), hyperkalaemia and hypothyroidism. About 20% of patients with 2: 1 A-V blockade have intermittent lesions in the His bundle and a pre-existing permanent blockade of conduction in one of Tawar's arms ( P-P-QRS...; and QRS wider than 0.12 with ). In terms of lesion localization, this is a fixed Wenkebach period with a 2: 1 A-V conversion, and this disorder usually does not have the risk of significant bradycardia as the A-V blockade Mobitz II °.However, these faults cannot be distinguished from a normal ECG record. In both cases, the QRS complex will be wider than 0.12 s, each QRS complex will be preceded by 2 P waves and the P-Q interval will be constant.

ECG finding
It's on the ECG more P waves per QRS complex ( P-P-QRS ... P-P-P-QRS ... P-P-P-QRS ). Interval PQ is constant ( chambers are controlled from the supraventricular region and if it is an S-A node, the sinus rhythm remains. QRS is wider than 0.12 s ( is a ventricular conduction failure – Tawar arm block ).

Lesion localization
The lesion in the transmission system is located in one of 80% of these faults Tawar arms. The lesion is distal from the bifurcation of the His bundle in a situation where the second Tawar arm does not lead at all ( the currently complete blockade of the line in the contralateral Tawar arm ).

3rd degree
Permanent complete A-V blockade. None of the excitement of the supraventricular chamber can reach the chambers.

It occurs either as the progression of a Mobitz II ° blockade or as sudden damage to the transmission system, for example in acute myocardial infarction.

A-V block III ° with a ventricular rhythm is a clear indication for pacemaker implantation. Implantation is expected for reversible causes of block A-V conduction ( acute diaphragmatic myocardial infarction, bradycardic drugs, hyperkalaemia, hypothyroidism, infectious endocarditis ). In contrast, cardiostimulator implantation is not delayed when A-V blockade III ° occurs in acute anteroseptal myocardial infarction. For A-V blocks III ° with a QRS complex shorter than 0.12 with ( 40% A-V blockade ) there is usually no severe bradycardia ( the chamber control replacement center is supraventricular ). If the replacement center has a frequency higher than 40 / min, this complete A-V blockade is not an indication for pacemaker implantation.

ECG finding:
They appear on the ECG record P waves independent of QRS complexes wider than 0.12 s ( is a junctional or idioventricular rhythm, usually with SF < 40 / min ). There is an A-V dissociation in which P waves have a higher frequency than QRS complexes. A-V dissociation and A-V block can be reliably demonstrated by strolling R-R intervals from the ECG onto a free piece of paper. When comparing plotted R-R intervals, we show a mismatch with P-P intervals and shorter P-P intervals than R-R intervals.

Lesion localization
In 61% of all A-V blocks III °, the lesion is located in one of Tawar's arms at the current previous block of line in the contralateral Tawar arm

1st degree

 * not being treated.

2nd degree

 * elimination of potential cause - antiarrhythmic treatment, digoxin, hyperkalaemia, myocardial ischemia, hypotension
 * type I:
 * atropine: 0.02 mg / kg i.v., i.o., e.t., ie 0.1 mg / 5 kg ( 0.2 ml ) in symptomatic individuals;
 * type II:
 * alternatively isoprenaline 0.02 mg / kg;
 * implantation of a permanent pacemaker
 * temporary cardiostimulation in symptomatic and asymptomatic with AIM ( especially front walls ) with 2nd degree AV block, RBBB or LBBB;

3rd degree

 * elimination of potential cause - antiarrhythmic treatment, digoxin, hyperkalaemia, myocardial ischemia, hypotension
 * atropine or temporary pacemaker during AIM with AV blockade
 * permanent paceimulation in chronic symptomatic AV blockages with symptoms heart failure.

Blockade of the real Tawar arm
Complete BPRT: wide QRS complex, image rSR´ve V1, deep wide oscillation S with positive P wave in V6. BPRT and AV block I. degree Physiological propagation of the wave of depolarization Wool propagation of depolarization at BPRT

Blockade of the real Tawar arm ( BRPRT, English right bundle branch block, RBB ) is a failure of myocardial infarction due to disability cardiac conduction system and resulting in delayed depolarization ( and therefore the activity ) of the right ventricle.

Types
We distinguish according to the width of the QRS complex 2 BPRT types:


 * 1) complete BPRT ( QRS longer than 0.12 s, blockade of the proximal part of the right Tawar arm );
 * 2) incomplete BPRT ( QRS shorter than 0.12 s, distal blockade of the right Tawar arm ).

The normal width of the QRS complex is 0.06 – 0.11 s.

Ethiology
BPRT itself is hemodynamically insignificant. However, it can signal damage true heart. BPRT often occurs in:


 * pulmonary chronicum ( right heart pressure overload );
 * pulmonary acutum (embolism a. Pulmonalis, right heart pressure overload );
 * atrial septal defect ( real heart overload );
 * ischemic cardiomyopathy;
 * cardiomyopathy due to a valve defect;
 * congenital or idiopathic cardiomyopathy.

ECG the image of the blockade of the right Tawar arm can also occur in healthy people. It is mainly an incomplete BPRT with a normal QRS complex width in young endurance athletes ( in endurance sports, there is a volume load of the right chamber ).

Diagnostics
BPRT diagnostics is based on ECG. In case complete BPRT:


 * The QRS complex is extended above 0.11 s ( 3 small squares );
 * in seductions V1 – V2 ( right-hand leads, above the right ventricle ) we observe the image rSR´, decendent depression of the ST section and negative wave T ( for complete BPRT is typical that R´is higher than r);
 * in seductions V4 – V6, I and aVL ( left-hand leads, above the left ventricle ) we find deep and wide oscillation S and positive wave T.

In case incomplete BPRT takes a QRS complex of less than 0.12 s.

Differential diagnostics

 * Right ventricular hypertrophy,
 * intraventricular block,
 * non-specific conversion failure,
 * Brugado syndrome,
 * preexcitation syndrome,
 * rear myocardial infarction,
 * ventricular rhythm.

Blockade of the left Tawar arm:
Blockade of the left Tawar arm ( BLRT, English left jacket branch block, LBBB ) is a failure of myocardial infarction due to disability cardiac conduction system and resulting in delayed depolarization ( and therefore activity ) of the left ventricle. The entire left ventricle is depolarized from the right of Tawar's arm, which occurs extension and morphological change QRS complex.

Types
We distinguish according to the width of the QRS complex 2 BLRT types:


 * 1) complete BLRT ( QRS longer than 0.11 s );
 * 2) incomplete BLRT ( QRS in the range of 0.06 – 0.11 s ).

The normal width of the QRS complex is 0.06 – 0.11 s.

Ethiology:
BLRT alone is hemodynamically insignificant. However, it signals damage and / or increased load on the left ventricle, which may be due to the following conditions:


 * cardiomyopathy,
 * left heart valve defects,
 * hypertension ( hypertensive cardiomyopathy ),
 * coron ( ischemical cardiomyopathy ).

Complications
BLRT increases the risk heart failure, IM, sudden heart death, AV block II. degrees, AV block III. degrees.

Diagnostics
BLRT diagnostics is based on ECG. In case complete BLRT:


 * The QRS complex is extended above 0.11 s ( 3 small squares ) a forked, and V6 resembles a letter „ M “ ( RsR´ );
 * and V1 we observe the image QS or qRS ( qRS resembles the letter „ W “ );
 * in lateral leads ( V5, V6, I, and VL ) occurs inversion of waves T and descendent depression of ST sections ( = secondary repolarization changes );
 * the axis is normal or deviated to the left.

In the case of incomplete BLRT, the QRS complex lasts 0.06 – 0.11 s.

Attention! CAVE! BLRT prevents IM diagnostics. If we suspect an IM ( pain of coronary origin ) in a patient with left Tawar arm blockade, it is always necessary to hospitalize this patient!!

Differential diagnostics

 * Left ventricular hypertrophy,
 * lateral IM,
 * pre-excitation syndrome.

Random block therapy
It is governed by the presence and severity of the underlying organic disease. Chronic, randomly diagnosed shoulder block is not an indication for any treatment, for acute myocardial infarction, the introduction of temporary stimulation is considered.

Related articles

 * Manifestation of faults in the formation and conduction of excitement on the elctrocardiogram
 * Antiarrhythmics
 * Radiofrequency catheter ablation
 * Electrophysiological examination
 * Cardiac transmission system

Reference
1.BEAUTY, Richard. Intern. - edition. 2015

2.TÁBORSKÝ, Miloš, et al. Principles for implantation of pacemakers and implantable cardioverters-defibrillators - 19 [ online ]. [ cit. 2013-10-10 ]

3.HORKÝ, Karel. Medical repetitorium. 2nd edition. Prague: Galén, c2005.

Source

 * HAVRÁNEK, Jiří: Arrhythmia.
 * PASTOR, J. Langenbeck's medical web page [ online ]. [ cit. 2009 ]