Bradyarrhythmias and Bundle brand blockages
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Bradyarrhythmia

Heart

Bradycardic disorders are caused either by a disorder in the sinus node or by a blockage of the conduction of excitement from the atria to 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 vagal activity predominates (sleep). Normally, this kind of value can be found in athletes, in which it reaches 40 beats per minute. Possible causes include for example: hypothyroidism, hypothermia, intracranial hypertension, Myocardial Infarction of the lower wall, sick sinus syndrom. It is also often induced iatrogenically by Beta-blockers, verapamil, digitalis or amiodaron.

Therapy - in symptomatic individuals atropine 0.5-1 mg iv

Sick sinus syndrome

It is a permanent or paroxysmal sinus bradycardia, until the sinus arrest. It can be alternated with flutter / atrial fibrillation . Excitement disorder occurs, which may be functional / anatomical and transient / permanent.

Ethiology

  • Idiopathic degenerative damage in the area of ​​the SA node
  • Ischemic heart disease,
  • cardiomyopathy,
  • increased vagotonia,
  • endocrinopathy ,
  • medications
  • direct damage to the sinus node.

The clinical picture

Most patients are asymptomatic. Otherwise they experience palpitations, dizziness, confusion, pre-syncopies, syncope and they can also suffer from a lower minute cardiac output.

Diagnosis

On the ECG we observe a slow or irregular sinus action, various surrogate rhythms or, conversely, paroxysms of tachycardia.The negative effect of the autonomic nervous system confirms the ability of the sinus node to increase heart frequency during exercise (confirmed by ergometry). Holter ECG shows the variability of heart frequency during the day and night, episodes of sinus pauses or the occurrence of other severe arrhythmias.

Therapy

Asymptomatic patients do not require treatment. In bradycardia with a hemodynamic disorder, we indicate a pacemaker implantation.

Sinus arrest

This is an outage of various lengths in the SA node. With a longer pause, junctional or idioventricular contraction may occur. It may be clinically manifested bt syncope.

Therapy - in symptomatic individuals atropine 0.5-1 mg iv

Sinoatrial blockade

It has three degrees, but only the III. degreeis clinically significant. In this case, a pulse is not transferred from the sinus node to the atrial myocardium → loss of a single heartbeat. The entire P-QRS-T complex is missing from the ECG.

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

Atrioventricular block

6:14CC
Video in English, definition, pathogenesis, symptoms, complications, therapy

This is a disorder in the transfer of the depolarization wave to the ventricules. Blockade is most often in the AV node (suprahisally), but can also occur in the His bundle (intrahisally) or infrahisally.

AV-Blocks:


Etiology

  • Myocardial Infarction (especially of the lower wall with closure of the coronary artery),
  • inflammation - viral myokarditis, borreliosis, Changeas disease
  • trauma,
  • bradycardizing drugs - digoxin , beta-blockers,
  • idiopathic fibrosis,
  • cardiomyopathy.

Degrees

1st degree

Prolonged AV conduction of excitement, therefore PQ> 0.2 s. Carditis in acute rheumatic fever , digoxin intoxication, β blockers. Clinically insignificant, it must be taken into account when medicating with the above drugs.

2nd degree

Intermittent outages from the atrium to the ventricles (some excitations do not pass to the ventricles), P waves not followed by the QRS complex occur on the ECG.

AV block II, Mobitz type I (Wenckebach)

With each excitation transmitted, the disorder escalates and the conduction time of the excitation from the atria to the ventricles increases. Eventually, the conduction failure escalates so that the excitement from the atria to the ventricles is not transferred. A temporary complete blockage of the AV transfer occurs. Failure to convert the excitement will allow the transmission system to "recover" and resume the AV transmission. This process repeats periodically. The interval from one complete AV block to another complete AV block is called the Wenckebach period.

The more severe the disorder, the sooner a complete AV block will occur and the shorter the Wenckebach period. The usual ratio of AV conversion is 5: 4, 4: 3 and 3: 2. In the last case, the Wenckebach period can be shortened so that a complete AV block occurs after each successful AV conversion. The transfer system can handle one excitation transmission from the atrium to the ventricles, but can no longer handle another AV transmission. This disorder is called the fixed Wenckebach period . There is an AV conversion ratio of 2: 1 (every second P wave is converted).

The fixed Wenckebach period , unlike Mobitz II AV block , is not a clear indication for pacemaker implantation. The exception is symptomatic bradycardia in a fixed Wenckebach period. For example, if the patient's SA node frequency drops to 60 / min, then with AV conversion 2: 1, the QRS and ventricular systolic frequency will be 30 / min, and this will usually cause a significant decrease in cardiac output. If the SA node function is OK, the sympathetic system resolves the 2: 1 AV block by stimulating the SA node to a higher node rate, such as 120 / min to maintain a QRS (ventricular systole) rate of 60 / min.

ECG findings

On the ECG, there is a P wave in front of each QRS complex , the rhythm is sinusoidal and the QRS complex lasts a maximum of 0.12 s . With each new P-QRS complex, the PQ interval gradually lengthens as the AV transmission failure progresses . When a complete AV block occurs, a P wave (evidence of atrial depolarization) is displayed on the ECG, which is not followed by a QRS complex (evidence of a complete AV block). After a pause, a P-QRS complex appears on the ECG , usually with a normal PQ interval (evidence of renewed AV conduction).

Localization of lesions

The lesion in the transmission system is located predominantly in the AV node, less often in the His bundle . The location of the disorder cannot be determined from the surface ECG, but only by invasive electrophysiological examination.

AV block II, Mobitz type II.

At normal heart rate, the damaged area fails to transfer all control pulses from the AV node to the ventricles. Each converted pulse induces a complete blockage of the AV transmission (both Tawara branches do not conduct). Místo poruchy potřebuje určitou dobu na zotavení k tomu, aby mohlo dojít k dalšímu A-V převodu.The fault location needs some recovery time for further AV conversion to occur. At the mildest degree of disturbance, the control pulses from the supraventricular region are converted to chambers in a 2: 1 ratio (PP-QRS). At a higher degree of failure, the AV conversion ratio increases to 3: 1, 4: 1, etc. As the Tawar arm progresses, it completely stops the excitement and a complete III ° AV block occurs (there is a conduction block in both Tawar arms).

This type of AV block is unstable and usually progresses to a complete III ° AV block with ventricular bradycardia, or worse, asystole and syncope (Adams-Stokes syndrome). Therefore, the finding of Mobitz II on the ECG is very important and is an indication for the patient to be placed on a monitored bed and for early implantation of a pacemaker. For the above reasons, the name Mobitz II should not be used for AV block with a 2: 1 ratio and QRS complex shorter than 0.12 s. , verapamil or diltiazem, digoxin), hyperkalaemia and hypothyroidism. About 20% of patients with 2: 1 AV block have an intermittent His-bundle lesion and a pre-existing permanent conduction block in one of the Tawar arms (PP-QRS ...; and QRS wider than 0.12 s). In terms of lesion location, it is a fixed Wenkebach period with AV transmission 2: 1 and this disorder usually does not have the risk of significant bradycardia as AV block Mobitz II °. However, these disorders cannot be distinguished from normal ECG recording. 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 PQ interval will be constant.

ECG findings

There is a larger number of P waves per QRS complex on the ECG (PP-QRS… PPP-QRS… PPPP-QRS). The PQ interval is constant (ventricles are controlled from the supraventricular area and if it is the SA node the sinus rhythm remains. QRS is wider than 0.12 s (there is a ventricular conduction defect - blockage of the Tawara branch).

Localization of lesions

In 80% of these disorders, the lesion in the transmission system is located in one of the Tawara branches . The lesion is distal to the bifurcation of His's bundle in a situation where the second Tawara branch does not conduct at all (at the same time a complete blockage of conduction in the contralateral Tawara branch).

3rd degree

Permanent complete AV block. None of the supraventricular excitations reach the ventricules.

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

AV block III ° with ventricular rhythm is a clear indication for pacemaker implantation. Implantation is postponed in reversible causes of AV conduction block (acute diaphragmatic myocardial infarction, bradycardic drugs, hyperkalemia, hypothyroidism, infectious endocarditis). In contrast, pacemaker implantation is not postponed in the onset of III ° AV block in acute anteroseptic myocardial infarction. Severe bradycardia usually does not occur in III ° AV blocks with a QRS complex shorter than 0.12 s (40% of AV blocks) (the alternative ventricular control center is supraventricular). If the surrogate center has a frequency greater than 40 rpm, this complete AV block is not an indication for pacemaker implantation.

ECG findings

P waves appear on the ECG independently of QRS complexes wider than 0.12 s (there is a junctional or idioventricular rhythm, usually SF <40 / min). There is AV dissociation in which P waves have a higher frequency than QRS complexes.

Localization of lesions

In 61% of all III ° AV blocks, the lesion is located in one of the Tawara branch with the current previous conduction block in the contralateral Tawara branch..

Therapy

1st degree

  • not treated.

2nd degree

  • elimination of potential cause - antiarrhythmic treatment, digoxin, hyperkalemia, myocardial ischemia, hypotension
  • type I:
    • atropine: 0.02 mg / kg iv, io, et, i.e. 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 acute myocardial infarction

3rd degree

  • elimination of potential cause - antiarrhythmic treatment, digoxin, hyperkalemia, myocardial ischemia, hypotension
  • atropine or temporary cardiostimulation
  • continuous cardiostimulation in chronic symptomatic AV block with heart failure.

Principles of pacemaker implantation


Cardiostimulators
Diagnosis Stimulation mode
Optimál Possible Inappropriate
Sick sinus syndrome DDD(R) AAI(R) VVI, VDD
AV blockade DDD DD AAI, DDI, VVI + VA conduction
SSS + AV block or branch block DDDR, DDIR DDD, DDI AAI, VVI
Permanent atrial fibrillation or atypical atrial flutter VVI(R) VVI AAI, DDD
SSS or AV block + paroxysmal atrial arrhythmias DDDR + AMS DDIR, DDDRP + AMS VDD, AAI
Heart Failure DDD BiV VVIR BiV AAI, VDD
Hypertrophic cardiomyopathy DDD + optimalized AV delay VDD, DDDR + optimalized AV delay AAI, VVI
BiV: biventricular stimulation, DDDRP: dual-cavity rate-responsive pacing using preventive atrial pacing algorithms in patients with paroxysmal atrial fibrillation
taken from [2]


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

__ Blokáda pravého Tawarova raménka

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

Division:

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

Therapy

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.

Shoulder blockades:

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

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:

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.


Links

Related articles

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 ]
  1. ↑
  2. ↑
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