Расположение дельта-волны

тип WPW	I	III	V1	V6
A	–	+	+	+	парасептально или заднебазально
B	+	–	–	+	правосторонне
AB	+	–	+	+	правосторонне или заднебазально
C	–	+	+	–	левосторонне

1.На педовом этапе рационально оказывать медицинскую помощь лишь при возникновении таких аритмий, при которых нарушается системное кровообращение - в большинстве случаев это приступы желудочковой тахикардии.

2. Диагностика (санинструктором и фельдшером):

Определяется частый (от 100 до 240 в мин), малого наполнения пульс или пульс вообще не определяется, на фоне чувства стеснения в груди, сжимающих болей за грудиной, одышки, резкого головокружения, общей слабости, тошноты(может быть рвота).

3. Медицинская помощь:

а) первая:

- горизонтальное положение больного;

- удар кулаком по грудине;

- лидокаин 6 мл 2% раствора подкожно медленно (в виде капельницы);

- дальнейшая помощь невозможна, так как необходимые препараты для купирования недопустимо вводить на поле боя.

б) доврачебная:

- повторное введение лидокаина в той же дозе и тем же способом (это является минимальным обьемом медпомощи);

- новокаинамид 5 мл 10% раствора + 0,3 мл 1% раствора мезатона, внутривенно медленно (за 5 мин) (оптимальный обьем медпомощи на данном этапе).

Комбинация этих препаратов позволяет сохранить высокий антиаритмический эффект новокаинамида при купировании как желудочковых, так и наджелудочковых тахикардий, и избежать его основного побочного эффекта - снижения артериального давления.

5.1Заключение:

Таким образом, эффективность ААП зависит от правильного их выбора на основе знаний фармакодинамики, фармакокинетики ААП и их побочных эффектов, рационального комбинирования препаратов. Выбор во многом определяется также характером нарушений ритма, изменениями гемодинамики, сопровождающими пароксизм аритмии, и задачами последующего лечения, наравленного на профилактику нарушений ритма. Антиаритмические препараты устраняют НСР в конечном итоге за счет изменения электрофизиологических свойств миокарда и ЧСС. Однако на практике часто подбор ААТ проводится без острых лекарственных тестов, методом проб и ошибок с предварительным определением относительной вероятности участия тех или иных аритмогенных механизмов и целесообразной последовательности тестирования препаратов.

В целом, сегодня проблема медикаментозного лечения НСР характеризуется определенным равновесием представлений, основанных на данных теоретических, экспериментальных и клинических исследований. Это способствует более осознанному применению ААП в клинической практике с реальной оценкой возможностей ААТ и предохраняет от крайностей - чрезмерного энтузиазма и неоправданного нигилизма.

6.Литература

I.Использованная при подготовке лекции:

1. Бойцов С.А., Захарова А.И., Захарова И.М., Кучмин А.Н. Электрокардиографические симптомы и синдромы /Под ред. В.П.Андрианова, Л.Л.Боброва.- Санкт-Петербург, 1996.

2. Болезни сердца и сосудов /Под ред. Е.И.Чазова, М.,1992.

3. Дощицин В.Л. Лечение аритмий сердца. – М.: Медицина, 1993.

4. Кушаковский М.С. Аритмии сердца (причины, механизмы, электрокардиографическая и электрофизиологическая диагностика, клиника, лечение). Руководство для врачей.— Санкт-Петербург: Гиппократ, 1992.

5. Лепахин В.К., Белоусов Ю.Б., Моисеев В.С.Клиническая фармакология с международной номенклатурой лекарств, М.,1988.

6. Терапевтический справочник Вашингтонского университета.— Boston: Little, Brown, and Company, 1992.

7. Интенсивная терапия / Под ред. А.И.Мартынова, А.М.Москвичева, В.В.Яснецова. – М.: Гэотар Медицина, 1998. – 639 с.

8. Руксин В.В. Основы неотложной кардиологии. – Санкт-Петербург: Политехника, 1995. – 303 с.

9. The Sicilian Gambit. A new Approach to the Classification of Antiarrhythmic Drugs Based on Their Actions on Arrhythmogenic Mechanisms. Task Fors of the Working Group on Arrhythmias of the European Society of Cardiology //Circulation. – 1991. – Vol.84. – P.1831-1851.

10. The Sicilian Gambit. A new Approach to the Classification of Antiarrhythmic Drugs Based on Their Actions on Arrhythmogenic Mechanisms. Task Fors of the Working Group on Arrhythmias of the European Society of Cardiology //European Heart Journal. – 1991. – Vol.12. – P.1112-1131.

11. Schwartz P.J., Zaza A.The Sicilian Gambit – Theory and Practice //European Heart Journal. – 1992 (supplement F). – Vol.13. – P.23-29.

II.Рекомендуемая слушателям для самостоятельной работы:

1. Бойцов С.А., Захарова А.И., Захарова И.М., Кучмин А.Н. Электрокардиографические симптомы и синдромы /Под ред. В.П.Андрианова, Л.Л.Боброва.- Санкт-Петербург, 1996.

2. The Sicilian Gambit. A new Approach to the Classification of Antiarrhythmic Drugs Based on Their Actions on Arrhythmogenic Mechanisms. Task Fors of the Working Group on Arrhythmias of the European Society of Cardiology //Circulation. – 1991. – Vol.84. – P.1831-1851.

3. The Sicilian Gambit. A new Approach to the Classification of Antiarrhythmic Drugs Based on Their Actions on Arrhythmogenic Mechanisms. Task Fors of the Working Group on Arrhythmias of the European Society of Cardiology //European Heart Journal. – 1991. – Vol.12. – P.1112-1131.

4. Schwartz P.J., Zaza A.The Sicilian Gambit – Theory and Practice //European Heart Journal. – 1992 (supplement F). – Vol.13. – P.23-29.

НАГЛЯДНЫЕ ПОСОБИЯ

1.Таблицы:

• классификация ААП,

• сравнительная характеристика ААП,

• ААП для купирования пароксизмальных нарушений ритма,

• ААП для предупреждения нарушений ритма (при приеме внутрь),

• схема «сицилианского гамбита»;

• взаимодействие ААП.

2.Диапозитивы.

7.Vol. 4, No. 3 January 1999 . Article No. 99010001. http://www.heartweb.org/heartweb/0199/p0001.htm

WIDE QRS COMPLEX TACHYCARDIA: A NEWLY SIMPLIFIED DIAGNOSTIC CRITERIA Hassan Khaled Nagi, Khaled Farouk, Ahmed Abd El-Aziz, Sherif Hamed, Mohamed Hammouda, and Sherif Mokhtar Critical Care Medicine, Cairo University, Egypt

ABSTRACT

Diagnosis of ventricular tachycardia (VT) has been always a diagnostic challenge. Physicians under training frequently misdiagnose wide complex tachycardia and are more tempted to think of aberrant SVT thus justifying the use of iv calcium blockers, or lanoxin with adverse hemodynamic consequences. All published criteria to diagnose wide complex tachycardia were based on complicated analysis of QRS morphology, duration and relative ratios of r/s in different leads, a rather non practical way in the critical care setting. We are hereby reporting a newly tested simplified scheme based on analysis of QRS morphology in 4 leads only rather than a complete twelve lead ECG analysis. Our data were obtained from 815 pts (61 male, 20 female, mean age 47.8+13.9 years) admitted with a diagnosis of wide complex tachycardia (QRS > 120 ms). Clinical diagnoses included ischemic HD in 28 pts, dilated CM in 13, congenital HD in 3, HTN in 7 and rheumatic HD in 6 pts. All had an electrophysiological study (EPS) which confirmed the tachycardia origin. ECG tracings during the tachycardia were analyzed for the polarity of QRS in leads I, II, V1 and V6. The presence of predominantly negative QRS in at least two out of those four leads (lead I or V6 to be included) was looked for.

Of the 81 pt. studied, 56 had EPS diagnosis of VT. Of the latter, 51 (89.2%) were correctly diagnosed by our newly suggested criteria. Absence of these criteria correctly diagnosed SVT with aberration in all the 25 pts with SVT. Sensitivity, specificity, positive predictive and negative predictive values were 89.2%, 100%, 100% and 80.6% respectively.

Predominantly negative QRS in at least two out of four leads (I, II, V1 and V6, with either Lead I or V6 included) diagnosed VT in 89.2% of cases, SVT in 100% of cases. Thus 94.5% of all cases were correctly diagnosed. Presented for the first time, they can be used as a simple approximate tool to differentiate wide complex tachycardia in critical care settings and may help avoid misdiagnosis with its therapeutic risks.

7.1INTRODUCTION

A plethora of ECG criteria have been developed over the last few years to distinguish between VT and aberrantly conducted SVT (1-10). Most of these criteria are full of details such as precise measurement of waveform intervals in milliseconds recorded from specific leads. Therefore it is not surprising that recently advanced cardiac life support do not recommend using these criteria to distinguish between VT and aberrantly conducted SVT because this distinction is too difficult and time consuming in the immediate care setting. In these guidelines, clinicians are urged to treat patients and not the cardiac monitor (11).

Unfortunately, clinical findings such as patients blood pressure or level of consciousness, have not proven reliable in distinguishing SVT from VT. In fact recent reports (12-14) confirm that when patients signs and symptoms are used to make the diagnosis, wide QRS tachycardia are frequently misdiagnosed and patients suffer disastrous outcome. For example, in two recent reports (12-14) when patients with haemodynamically stable VT were misdiagnosed as having SVT with aberration and treated with IV verapamil, outcome included acute severe hypotension requiring vasopressor, acceleration of the tachycardia, degeneration of VT into VF requiring defibrillation, and a systole following cardioversion. More recently, the danger of administrating verapamil in these patients have been appreciated and adenosine has been recommended (11). Adenosine can provide important diagnostic information regarding the tachycardia mechanism, however it may not be as safe as originally thought in the immediate care setting. For example, adenosine has triggered torsades de points in the presence of long Q-T syndrome (15), has caused atrial fibrillation and dangerous acceleration of ventricular rate in patients with atrial fibrillation or flutter (16-20).

In 1978 Wellens published his morphologic criteria to diagnose wide complex tachycardia based on retrospective analysis of hundreds of ECG tracings, other published criteria were all based on complicated analysis of QRS morphology, duration and relative relation of r/s in different leads which was rather non practical in the critical care setting. We are hereby presenting a new simplified approach for wide QRS complex tachycardia especially in the critical care settings based on the polarity of QRS in both limb leads (I, II) and chest leads (V1, V6). These leads were chosen in particular because they represent the principal deflection in bundle branch block (BBB).

METHODS

We retrospectively and prospectively analyzed the 12-lead ECG of 81 monomorphic wide (>120 ms) QRS tachycardias records from 81 patients who underwent cardiac electrophysiological study (EPS) at the critical care department of Cairo University. (61 male, 20 female, mean age 47.8+13.9 years) clinical diagnosis included ischemic HD in 28 patients, dilated CM in 13 pts, congenital HD in 3 patients, HTN in 7 pts. and rheumatic HD in 6 pts. In all pts. the site of origin of the tachycardia was diagnosed by EPS (VT vs SVT).

Analysis: QRS morphology of the four chosen leads (I, II, V1 and V6) were introduced in computer guided software and analysis proceeded so as to find the commonest morphology (rS, QS, R … etc) among ECG tracings in each of these leads among different group (VT, SVT) and the commonest combination of predominantly negative complex using two leads at a time, and also these tracings were subjected to analysis using both Brugada algorithm 1991 (8) and A-John Camm criteria 1994 (21).

RESULTS

Among 81 pts studied EP studies confirmed the diagnosis of VT in 56 pt. Out of the 56 ECG of VT 51 (89.2%) showed at least two predominantly -negative QRS complex (rs, or QS) among the four chosen lead with inclusion of lead I or V6. In all the 25 pts with SVT (100%) there was no single ECG with predominantly -negative complex in 2 out of the 4 leads. The calculated sensitivity, specificity, positive predictive and negative predictive values using our new ECG lead criteria for diagnosis of VT were 89.2, 100%, 100%, 80.6% respectively. Table 1 shows the prevalence of negative QRS complex in each of the 4 chosen leads in the pt with VT vs pt with SVT.

Multiple logistic regression in a forward manner was conducted using lead I, II, V1 and V6 as independent predictors. Lead I, II proved to be the best predictor with overall predictive accuracy 87% (Table 2).

Comparison between the newly conducted criteria and the conventional criteria of Brugada 1991 and John Camm 1994:

We subjected the 81 ECGs to reanalysis using the criteria of A.John Camm 1993 (21) which diagnose VT by default diagnosis of SVT with aberration based on the typical morphology of BBB and the 4 steps algorithm conducted by Brugada et al., 1991 (8).

Table 3 shows the chi-square and P value of each criteria when applied separately compared to the final EPS diagnosis. Using the discriminative analysis the calculated sensitivity, specificity and predictive value were as follow (Table 4):

In the 12-lead ECG of wide QRS tachycardia shown in Fig. 1 it was correctly diagnosed as SVT by our new criteria (only V1 is negative) and also by Camm group criteria whereas it was misdiagnosed as VT by Brugada. Again in the example shown in Fig. 2 it was correctly diagnosed as VT by our new criteria whereas it was misinterpreted as SVT by both Brugada and Camm group criteria.

We studied the value of 1st and 2nd step in Brugada Algorithm which are absent RS and RS intervals > 100 ms and how much they contribute to diagnosis of VT results was as follow (Table 5):

Out of the 81 cases RS was absent in 28 cases, 24 cases (42.9%) were correctly diagnosed as VT and 4 cases were misdiagnosed with calculated sensitivity, specificity (42.8%, 84% respectively). Out of the 81 pts only 25 pts were having an RS intervals >100 ms, 20 cases (30.9%) were having VT and the remaining 5 were misdiagnosed with calculated sensitivity, and specificity as follow 44% and 74%.

DISCUSSION

This study demonstrated that analysis of only 4 leads out of the 12 lead ECG recorded during wide QRS complex tachycardia could predict the origin of these tachycardia with high specificity and sensitivity. The rationale beyond choosing morphology in these four leads is that divergence of diagnostic criteria of pure pattern of BBB in limb leads (I, II) and pericordial leads (V1, V6) would throw doubt in the diagnosis of pure BBB and would rather point to the possible existence of ventricular depolarization.

The criteria was then made after the observation that VT usually has predominantly -negative QRS in at least 2 out of the four chosen leads including either lead I or V6. This was strongly supported by the morphology criteria described by Wellens et al., (3) that QS morphology in V6 strongly support diagnosis of VT. Moreover, typical BBB morphology described by Marriott’s (23) usually include lead I with V1, and V6 and it is well recognized that lead I and V6 are usually similarly upright. We studied the overall predictive value of the 4 leads when negative (78%) then we study the predictive values of each two leads with negative QRS we found that the combination of lead I, II has a highest predictive value (86.4%) when applying criteria of predominantly negative QRS at least 2 of 4 lead (I, II, V1, V6) provided that lead I or V6 included the overall predictive value increased to 90%. Thus the 4 leads new criteria is easy to interpret particularly in the critical care setting requiring no prices measurement not time consuming and there is no personal variability in application, as we selected 2 electrophysiologists and 2 residents to apply these criteria on all the 81 ECGs included, all of them came to the same result with an average time 10-15 minutes for the 81 ECG together.

Part of our study was to review the current criteria particularly Brugada 1991 (8) and John Camm 1994 (21). We found that the overall sensitivity, specificity positive predictive and negative predictive value of each were as follow:

Regarding Brugada algorithm with more meticulous analysis we found that the sensitivity of the 1st step which is absent RS is 42.8% and specificity is 84% and did not reach 100% as previously reported by Brugada et al., 1991.

In 2nd step (RS interval) 100 ms sensitivity (44%) specificity (74%). A finding comparable with data reported by Drew et al., 1995 (22) and the explanation for the increased overall sensitivity & specificity is step 4 where most of the cases were diagnosed by the morphology criteria described by Wellens et al.

Step 3. (The presence of AV dissociation) is highly specific as reported by Wellens et al., and Akhtar et al., yet it was visible on the standard 12 lead ECG in less than one tenth of patients with VT and was demonstrated only by electrophysiologists and not by residents. We agree with John Camm et al., (21) that the typical morphology of BBB was highly specific and sensitive in diagnosing VT by exclusion of SVT with aberration. Finally, despite the fact that both Brugada algorithm and John Camm criteria are very helpful in diagnosis of wide QRs complex tachycardia yet they take much time to interpret, require meticulous measurement and well trained doctors to apply. On the contrary we present new simple approach, easy to interpret with higher specificity 100% and positive predictive value 100%.

Conclusion:

We recommend using this new criteria of predominantly negative QRS complex in at least two out of four leads I, II, V1, V6 (L1 or V6 to be included) in diagnosis of wide complex tachycardia because it was both highly sensitive and specific in segregating VT from aberrantly concluded SVT, our new criteria presented for the 1st time can be used as a simple approximate tool to differentiate wide complex tachycardia in the critical care setting and may help avoid misdiagnosis with its attendant therapeutic risks.

REFERENCES

1. Sandler A, Marriott HJL. The differential morphology of anomalous ventricular complexes of RBBB-type in lead V1. Circulation 1965; 31:551-556.

2. Swanick EJ, LaCamera F, Marriott JHL. Morphologyical features of right ventricular ectopic beats. Am J Cardiol 1972; 30:888-891.

3. Wellens HJJ, Bar FW, Lie KI. The value of the electrocardiogram in the differential diagnosis of a tachycardia with a widened QRS complex. Am J Med 1978; 64:27-33.

4. Dongas J, Lehmann MH, Mahmud R, et al. Value of preexisting bundle branch block in the electrocardiographic differentiation of supraventricular from ventricular origin of wide QRS tachycardia. Am J Cardiol 1985; 55:717-721.

5. Caceres J, Bajwa T, Kadri N, et al. Significance of QRS axis In the differential differential diagnosis of wide QRS tachycardia. Circulation 1987; 76:IV-83.

6. Kindwall KE, Brown J. Josephson ME. Electrocardiographic criteria for ventricular tachycarida in wide complex left bundle branch block morphology tachycardias. Am J Cardiol 1988; 61:1279-1283.

7. Akhtar M, Shenasa M, Jazayeri M, et al. Wide QRS complex tachycardia: Reapraisal of a common clinical problem. Ann Intern Med 1988; 109:905-912.

8. Brugada P, Brugada J, Mont L, et al. A new approach to the differnetial diagnosis of a regular tachycardia with a wide QRS complex. Circulation 1991; 83:1646-1659.

9. Drw BJ, Scheinman MM. Value of electrocardiographic leads MCL1, MCL6 and other selected leads in the diagnosis of wide QRS complex tachycardia. J Am Coll Cardiol 1991; 18:1025-1033.

10. Griffith MJ, deBelder MA, Linder NJ, et al. Difficulties in the use of electrocardiographic criteria for the differential diagnosis of left bundle branch pattern tachycardia in patient with a structurally normal heart. Eur Heart J 1992; 13:478-483.

11. Guidelines for cardiopulmonary resuscitation and emergency cardiac care. Emergency Cardiac Care Committee and Subcommittees, American Heart Association. Part III. Adult advanced cardiac life support. JAMA 1992; 268:2199-2241.

12. Stwart RB, Bardy GH, Greene HL. Wide complex tachycardia: Misdiagnosis and outcome after emergent therapy. Ann Intern Med 1986; 104:766-771.

13. McGovern B, Garan H, Ruskin JN. Precipitation of cardiac arrest by verapamil in patients with Wolff-Parkinson-White syndrome. Ann Intern Med 1986; 104:791-794.

14. Buxton AE, Marchlinski FE, Doherty JU, et al. Hazards of intravenous verapamil for sustained ventricular tachycardia. Am J Cardiol 1987; 59:1107-1110.

15. Wesley RC, Turnquest P. Torsades de points after intravenous adenosine in the presence of prolonged QT syndrome. Am Heart J 1992; 123:794-796.

16. Biaggioni I, Killian TJ, Mosqueda-Garcia R, et al. Adenosine increases sympathetic nerve traffic in humans. Circulation 1991; 83:1668-1675.

17. Rankin AC, Rae AP, Houston A. Acceleration of ventricular response to atrial flutter after intravenous adenosine. Br Heart J 1993; 69:263-265.

18. Brodsky MA, Allen BJ, Grimes JA, et al. Enhanced atrioventricular conduction during atrial flutter after intravenous adenosine. N Engl J Med 1994; 330:288-289.

19. Meurer MK. A21-year-old woman with rapid atrial fibrillation adenosine administration. J Emerg Nurs 1991; 17:135-136.

20. White RD, Acceleration of the ventricular response in paroxysmal lone atrial fibrillation following the injection of adenosine. Am J Emerg Med 1993; 11:245-246.

21. Michael J Griffith, Clifford J Garratt, Paul Mounsey, A John Camm. Ventricular tachycardia as default diagnosis in broad complex tachycardia. Vol 343, Feb. 12, 1994.

22. Barbara J. Drew and Melvin M. Scheinman. ECG criteria to distinguish between aberrantly conducted supraventicular tachycardia and ventricular tachycardia: practical aspects for the immediate care setting. Pacing and Clinical electrophysiology, Vol. 18, Dec. 1995.

23. Marriot’s practical electrocardiography, Galen S. Wagner, M.D., 1994.

Table 1 shows the prevalence of predominantly negative QRS complex in the 4 chosen leads in SVT vs VT.

	Lead I	Lead Ii	Lead V1	Lead V6
VT SVT	37 (66%) 0 (0%)	40 (71%) 6 (24%)	26 (46%) 16 (64.3%)	40 (71%) 0 (0%)

Table 2 shows a multiple logistic regression in a forward manner using lead I and II, as independent predictors

	B	R	Significance
Lead I Lead II	-2.568 -1.878	-0.358 -0.26	<0.0001 <0.0024

Table 3 shows the Chi-square and P-value of each set of criteria when applied separately and compared to the final EPS diagnosis

	Brugada (8)	Camm group (21)	The New criteria
X2	24	35	58
P value	0.0001	0.0001	0.0000

Table 4 shows the discriminative analysis of the three criteria

	Brugada (8)	Camm group (21)	The New Criteria
Sensitivity Specificity +ve predictive value -ve predictive value	89.2% 68.4% 84.7% 76.7%	82.1% 88% 93.8% 68.7%	89.2% 100% 100% 80.6%

Table 5 shows the sensitivity and specificity of the first two steps in Brugada algorithm

	Absent RS	RS intervals > 100 ms
Sensitivity	42.8%	44%
Specificity	84%	74%

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