The P terminal vector in lead V1 of the electrocardiogram in cor pulmonale

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J. ELECTROCARDIOLOGY 15 (3), 1982, 205-208 Original Communications: The P Terminal Vector in Lead Vl of the Electrocardiogram in Cor Pulmonale BY PETER LYNCH, M.R.C.P. AND M.M. WEBB-PEPLOE, F.R.C.P. SUMMARY The P wave terminal victor in lead V~ Qf the ECG (VIPTV) was abnormal in 55 (80%) of 69 cases of cor pulmonale, but in none of 11 cases of isolated pulmonary valve stenosis. V,PTV is commonly abnormal in cor pulmonale and this is not likely to be due to pressure overload of the right heart. The commonly held association of an abnormal VIPTV with left atrial enlarge- ment may also be spurious in these cases. The terminal (negative) vector of the P wave in lead V~ of the ECG (V~PTV) is frequently abnor- mal in diseases causing pressure or volume overload of the left atrium. I"~ Chandraratna 6 sug- gests that it may also rarely be abnormal in disease Of the right heart. We assessed the fre- quency of an abnormal V~PTV in cor pulmonale and in isolated pulmonary valve stenosis. MATERIALS AND METHODS V~PTV was examined in 69 cases of cor pulmonale and in 11 cases of isolated pulmonary valve stenosis. Cot pulmonale was diagnosed if the patient fulfilled all of the following criteria: 1) diagnosis of cor pulmonale on hospital discharge; 2) clinical, radiological and spirometric evidence of chronic obstructive airways disease; 3) right axis deviation on the ECG of not less than +90 o and 4) partial or complete right bundle branch block. Patients with clinical or electrocardio- graphic evidence of ischemic, hypertensive or left sided valvular heart disease were excluded, but no attempt was made to estimate right or left heart volume or pressure overload in the remainder. Twenty-five of the 69 cases were female and the mean age overall was 62(SD 7) years. Pulmonary valve stenosis was diag- nosed at cardiac catheterisation and the degree of severity of the condition measured by the parameters shown in Table I. The ECGs used were those taken dur- ing the latest admission to hospital or immediately prior to cardiac catheterisation in the cases of From the Department of Cardiology, St. Thomas' ttospital, London SE1 England. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. w 1734 solely to indicate this fact. Reprint requests to: Major P. Lynch, R.A.M.C., British Military tlospital, Rinteln, BFPO 29, c/o London, England. pulmonary valve stenosis. They were recorded on Siemens Mingograph equipment {frequency response 0.05-550 herz) at a standard paper speed of 25 millimeters/second and calibrated at 10 millimeters = 1 millivolt. VIPTV was measured (in microvolt seconds) by the product of the amplitude of the wave in mierovolts and its duration in seconds, measure- ments being taken vertically and horizontally respec- tively from the point of junction of the wave with the subsequent isoelectrie line, as described by Morris. ~ The vector was regarded as abnormal when its magnitude was equal to or more than 3 microvolt seconds. Its direction was always negative. RESULTS V~PTV was equal to or greater than 3 microvolt seconds in 55 (80%) of 69 cases of cor pulmonale (Fig. 1) and in none of the 11 cases of isolated pulmonary valve stenosis (Table I). The mean ab- normal value in cot pulmonale was 9.75(SD7.5) microvolt seconds. DISCUSSION Though Morris took VIPTV to be abnormal when it was 4 microvolt seconds (-0.04 milli- meter seconds) or greater, many subsequently ac- cept 3 microvolt seconds or greater as abnor- mal. *s The high prevalence of abnormal V~PTV in cot pulmonale (80%) accords with its prevalence in diseases affecting the left heart, such as mitral stenosis (93%), ~ coronary artery disease (69%)2 and acute pulmonary oedema (100%). I~ Its mean value is equivalent to that found in severe left atrial enlargement such as that found in tight mitral stenosis2 Few studies of left ventricular function in cor pulmonale have been reported, however, and measurement of both pulmonary capillary wedge pressure and the echocardio- graphic left atrial dimension are notoriously dif- 205

Transcript of The P terminal vector in lead V1 of the electrocardiogram in cor pulmonale

J. ELECTROCARDIOLOGY 15 (3), 1982, 205-208

Original Communications:

The P Terminal Vector in Lead Vl of the Electrocardiogram in Cor Pulmonale

BY PETER LYNCH, M . R . C . P . AND M . M . WEBB-PEPLOE, F . R . C . P .

SUMMARY The P wave terminal victor in lead V~ Qf the ECG (VIPTV) was abnormal in 55 (80%) of 69

cases of cor pulmonale, but in none of 11 cases of isolated pulmonary valve stenosis. V,PTV is commonly abnormal in cor pulmonale and this is not likely to be due to pressure overload of the right heart. The commonly held association of an abnormal VIPTV with left atrial enlarge- ment may also be spurious in these cases.

The te rminal (negative) vec to r of the P wave in lead V~ of the ECG (V~PTV) is f requen t ly abnor- mal in diseases caus ing pressure or vo lume over load of the lef t a t r ium. I"~ Chand ra r a tna 6 sug- ges t s t ha t i t m a y also ra re ly be abnorma l in disease Of the r igh t hear t . We assessed the fre- quency of an abnormal V~PTV in cor pu lmonale and in isola ted p u l m o n a r y va lve stenosis .

MATERIALS AND METHODS V~PTV was examined in 69 cases of cor pulmonale

and in 11 cases of isolated pulmonary valve stenosis. Cot pulmonale was diagnosed if the patient fulfilled all of the following criteria: 1) diagnosis of cor pulmonale on hospital discharge; 2) clinical, radiological and spirometric evidence of chronic obstructive airways disease; 3) right axis deviation on the ECG of not less than +90 o and 4) partial or complete right bundle branch block. Patients with clinical or electrocardio- graphic evidence of ischemic, hypertensive or left sided valvular heart disease were excluded, but no at tempt was made to estimate right or left heart volume or pressure overload in the remainder. Twenty-five of the 69 cases were female and the mean age overall was 62(SD 7) years. Pulmonary valve stenosis was diag- nosed at cardiac catheterisation and the degree of severity of the condition measured by the parameters shown in Table I. The ECGs used were those taken dur- ing the latest admission to hospital or immediately prior to cardiac catheterisation in the cases of

From the Department of Cardiology, St. Thomas' ttospital, London SE1 England.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. w 1734 solely to indicate this fact. Reprint requests to: Major P. Lynch, R.A.M.C., British Military tlospital, Rinteln, BFPO 29, c/o London, England.

pulmonary valve stenosis. They were recorded on Siemens Mingograph equipment {frequency response 0.05-550 herz) at a standard paper speed of 25 millimeters/second and calibrated at 10 millimeters = 1 millivolt. VIPTV was measured (in microvolt seconds) by the product of the amplitude of the wave in mierovolts and its duration in seconds, measure- ments being taken vertically and horizontally respec- tively from the point of junction of the wave with the subsequent isoelectrie line, as described by Morris. ~ The vector was regarded as abnormal when its magnitude was equal to or more than 3 microvolt seconds. Its direction was always negative.

RESULTS V~PTV was equal to or g rea te r than 3 microvo l t

seconds in 55 (80%) of 69 cases of cor pu lmonale (Fig. 1) and in none of the 11 cases of i sola ted p u l m o n a r y va lve s tenosis (Table I). The mean ab- normal value in cot pu lmonale was 9.75(SD7.5) microvol t seconds.

DISCUSSION T h o u g h Morr is took VIPTV to be abnormal

when it was 4 mic rovo l t seconds ( - 0 . 0 4 milli- m e t e r seconds) or grea ter , m a n y subsequen t ly ac- cept 3 mic rovo l t seconds or g rea te r as abnor- mal. *s The high preva lence of abnormal V~PTV in cot pu lmona le (80%) accords wi th i ts p reva lence in diseases af fec t ing the left heart , such as mi t ra l s tenosis (93%), ~ co ro n a ry a r t e ry disease (69%)2 and acu te p u l m o n a r y oedema (100%). I~ I t s mean value is equiva len t to t h a t found in severe left a t r ia l en la rgemen t such as tha t found in t i gh t mi t ra l s tenosis2 Few s tudies of left ven t r i cu la r funct ion in cor pu lmona le have been repor ted , however, and m e a s u r e m e n t of bo th p u l m o n a r y capi l la ry wedge p r e s su re and the echocardio- graphic lef t a t r ia l d imens ion are no tor ious ly dif-

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TABLE I

Vl PTV in isolated pulmonary valve stenosis.

No

PV R V M W l LA V1PTV Age gradient RVEDP RVEP L /min /mm pressure uV

Years mm Hg mm Hg mm Hg H g / M 2 mm Hg secs

1 2 15 3 14 12.7 6 < 3 2 4 12 - 3 14 7.8 0 < 3 3 37 162 7 119 82 .0 " 10 < 3 4 48 97 4 57 18.7 5 < 3 5 15 126 4 76 24 .9 3 < 3 6 14 12 6 15 8 .4 7 < 3 7 4 11 8 14 3.6 10 < 3 8 8 34 4 18 9.7 7 < 3 9 17 14 0 22 12.0 4 < 3 0 13 67 6 41 13.2 7 < 3 1 6 10 1 18 14.7 3 < 3

LA -- left atrium PV -- pulmonary valve RVEP -- mean right ventricular ejection pressure RVEDP - - right ventricular end-diastolic pressure RVMWl -- right ventricular minute work index

ficult. Pos t mortem studies have purported to show left ventricular hypertrophy, '3,'' bu t left heart catheterisation has shown no rise in left ventricular end-diastolic pressure,'S, ~8 and critical reviews have reported left ventricular function in cor pulmonale as normal, or appropriate to the ad- vanced age of the patients.'7, '~

Right to left shunting through a stretched foramen ovale might result in left atrial enlarge- ment but this has not been shown to occur in more than 30% of cases29 While coronary artery

disease and cor pulmonale share a common aetiological factor in cigarette smoking, myocar- dial ischemia is unlikely to be the cause of the ab- normal vector since, on present criteria, that cor- relation only holds good in symptomatic cases s with left ventricular contraction abnormalities2 and even then the mean abnormal value is less than 4 microvolt seconds. V~PTV has rarely been described as abnormal in right heart disease per se, and the mechanism postulated is the posterior rotation of a very large right atr ium2 Interatrial

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FIGURE 1. V I P T V IN COR P U L M O N A L E

I I

I0

9

8

~ s

E 3

1

<3

Mean of SS a b n o r m a l values = 9 '7S|$D: l :7 -w seconds

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3 4 S w 7 8 9 I0 I! 12 1:3 14 IS 16 17 |8 19 2021 22 2124 2S 26 2~7 28 2~

V 1 P T V in m i c r o v o l t seconds Fig. 1. V,PTV in cor pulmonale.

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V 1 PTV IN COR PULMONALE 207

block has also been suggested as the cause of the abnormal vec tor" though others have failed to find the inferred prolongation of the time of its in- scription. '~ Nelson '* showed tha t the intracardiac blood has an effect on both P and QRS wave in- scription in dogs, and tha t a high hematocri t resulted in an increase in the magnitude of the P vector. RosenthaF ~ made similar observations during acute changes of hematocri t in humans. The high hematocri t of cor pulmonale may, at least in part, explain the abnormal vector, especially since abnormal ventricular conduction was a criterion for selection. The cases of pul- monary stenosis were much younger than those with cor pulmonale. As ye t there is no data on the effect on V~PTV of age or chronicity.

In conr this s tudy shows tha t V~PTV is common!y abnormal in cor pulmonale and tha t this is not likely to be due to intrinsic r ight hear t disease. Nor is it clearly the result of associated left hear t pathology, the frequency and magni- tude of the abnormal vector being compatible only with severe left atrial enlargement which has not been demonstra ted in cor pulmonale. The assumption tha t an abnormal V~PTV implies left atrial enlargement should therefore be made with caution in pat ients with cor pulmonale.

R E F E R E N C E S 1. MORRIS, J J, ESTES, F H, WIIALEN, R E, TIIOMP"

SON, H K AND MCINToSII, H D: P wave analysis in valvular heart disease. Circulation 29:242, 1964

2. CIIIRIFE, R, FEITOSA, G S AND FRANKL, W S: Elec- trocardiographic detection of left atrial enlarge- ment; Correlation of P wave with left atrial dimen- sion by echocardiography. Br Heart J 37:1281, 1975

3. KOLBEL, F, ASCIIERMANN, M, BARCAKOVA, J AND VANCURA, J: Changes in the P wa~/e terminal seg- ment correlated with left ventricular end-diastolic pressure. Cor Vasa 19:100, 1977

4. FORFANG, K AND SIMONSEN, S: Correlation between P wave terminal force and hemodynamic parame- ters in aortic stenosis; Prediction of left ventricular end-diastolic pressure. Cardiology 59:222, 1974

5. WAGGONER, A D, ADYANTIIAYA, A V, QUINONES, M A AND ALEXANDER, J K: Left atrial enlargement; Echocardiographic assessment of electrocardio-

graphic criteria. Circulation 54:553, 1976 6. CtIANDRARATNA, P A N: On the significance of an

abnormal P terminal force in Lead V1. Am Heart J 95:267, 1978

7. BETIIELL, H J N AND NXXON, P G F: P wave of the electrocardiogram in early ischemic heart disease. Br Heart J 34:1170, 1972

8. FORFANG, K AND ERIKSSON, J: Significance of P wave terminal force in presumably healthy middle aged men. Am Heart J 96:739, 1978

9. StIETTIGAR, U R, BARRY, W H AND HULTGREN, H N: P wave analysis in ischemic heart disease; An echocardiographic, hemodynamic and angiocardio- graphic assessment. Br Heart J 39:894,1977

10. HEIKKLA, J, HUGENIIOLTZ, P G AND TABAKIN, B S: Prediction of left heart filling pressure and its se- quential change in acute myocardial infarction from the terminal force of the P wave. Br Heart J 35:142, 1973

11. JOSEPtISON, M E, KASTOR, J A AND MORGANROTII, J: Electrocardiographic left atrial enlargement; Electrophysiologic, echocardiographic and hemo- dynamic co r re l a t e s . Am J Cardiol 39:967, 1977

12. NELSON, C V, RAND, P W, ANGELAKOS, E T AND HDGENIIOLTZ, P G: Effect of intracardiac blood on the spatial vectorcardiogram. Circ Res 31:95, 1972

13. KOUNTZ, W B, ALEXANDER, H L AND PRINZMETAL M: The heart in emphysema. Am Heart J 11:163, 1936

14. SCOTT, R W AND GAnVIN, C F: Cor pulmonale; Observations in fifty autopsy cases. Am Heart J 22:56, 1941

15. DAVIES, H AND OVERY, H R: Left ventricular func- tion in cor pulmonale. Chest 58:8, 1970

16. KRAYENBUEIlL, H P, TURINA, J AND HESS, O: Left ventricular function in chronic pulmonary hyperten- sion. Am J Cardiol 41:1150, 1978

17. FRANK, M J, WEmSE, A B, Mosctms, C B AND LEVINSON, G E: Left ventricular function, metab- olism and blood flow in chronic cor pulmonale. Cir- culation 47:798, 1973

18. TIIOMAS, A J: Chronic pulmonary heart disease. Br Heart J 34:653, 1972

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Equipped with his five senses, man explores the universe around him and calls the adventure science.

- -Edwin Powell Hubble