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İshalli bir buzağıda ventriküler flatter ve fibrilasyon olgusu

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A CASE OF VENT'RICULAR ·FLUTT!E.R AND Fl!B:RILLATION IN A OALF SUFFıERING FROM DLAJRRHtEA

İshalli bir buzağıda ventriküler flatter ve fibrilasyon olgusu

hbdullah BAŞOGLU1 Küırşat TURGUT~ Özet : Üç gündür isihal şi kayeti olan bir buzağının çekilen elektro-kardiyografisinde ventriküler fiatter ve filbrilasyon teşhis edildi. Buza-ğıda dehidrasyonla birlikte aşırı zayıflama vardı ve klinik tablo çok ağır­ dı. Heınatolojik mua:yenede; hiperkalemi (il.2.5 mEq/L) ve hiperMoremi

(1:59' n1Eq./L) tesbit edildi. Serum Na+ (156 ınEq/L) ve Ca++ (~10.4:3 mg/dl) kons!.intrasyonlaii'l noırmal sınırlar i·çindeydi. Buzağı kliniğe ge-tirildikten otuz dakika s01nra öldü. Otopside, kalpte herhangi bir or;ganik bozukluğa rast·lanmadı.

Summary : Ventricular flutter and fihrilation was diagnosed by means of ECG in a calf ısuffe.ring from diCllrrheıa for tihree days. The caH ıwas dehydrated, eımaciated and in morilbund status. Evaluation of blood sel!mple Tevealed hyperkalemia (1ı2.5 m'Eq/L) and hyperchloremia (15'9 ·niEq/L). Serum Na+ (156 mEq/L) and oa++ (10.34 mg./dl) levelıs were Wlithin normal range. She died at tlhirty minutes after arriıval. At ne-·cropsy, there ·was

no

any .organic disorder in the heart.

Introduction

VentT:i"cular flutter and filbriU:ation are rapid, irreıgular car.diac rhythm. ·The diıagnosis must be made electrocardiographically s"ince the periphera1 pulses are not palpaıble and heart beat is inaudilble (7).

-It has been reported that ventrıicular flutter is a progresnive stuation. In most eases, it is followed by ventricular fibrillation (ıl, 9). Bot:h ven-tricular flutteır and fibrHlaıtion occur in the tlherm1naıl stages of most sud-denly fatal disease including lightninıg stroke, plant poisonings suc'lı as

Cl) Öğr. Gör. Dr., S. ü. Veteriner Fakültesi, İç Hast. Bilim Dalı, Konya.

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260 Abdullah Başoğlu - Kürşat Turgut

acute phal::ı..ris tox.ieity, overdose with anel.3thetics, se\Vere toxemia and in tıhe therminal phases of most acquired cardiac disease (2).

Dbrrhea in new':Jorn calves under 10 days of age is one of the ınost co.mmoj_ı_ diseases. It is characterised clinkally by acute profuse watery diarrhea, progressive delhydration and acidosis and death iri a fe'w days or earlier (.2). It causes severe ac~d-lbase and electrolyte disturıbance. Hyperkalemic, hyperc'hloremic, nor:mal anion gap, meta'bolic acidosis

develop with 1Jhe severity of the disease (4).

Reports of electrocardiogra phic diagnosis of arr•hythmias in cattle arre few. Cases of atrial f~brillation in cattle have been reported most com-ınonly (3, '8). Ho'wever, we coulıd not find a report deal wıftJh ventric~Iar flutter and filbrillation in calvel3. That's why, we wanlted to represent t\his case detected for the first time in our clinics.

Case

A one week O'ld crosG ibreed Holstein Fresian calf wıas admitted with ~t history of diarrhea for tıh:ree days to the clinics of Internal Medinidne, Faculty of Veterinary Medinicine, Konya.

'I'he calf ·was dehydrated, emaciate.d and in mnr1bund status. Rectal tem-pe.ratuı-e and respiration rıate 40

oc

and 60/min respectively. Peripheral pulse cou1d not be palpeted and heart soundl3 could not be auscultated clearly. Electrocardiogra·m was recorded on a 3-channal portalble electro-cardiograpih (*). Recordings were made w:ith calf in right lıateral recum-ibency. Electrodes were ·placed according to the teclhnique descri1bed by Deroth (ı5). Recordings we.re made at a paper speed of ,2'5 mm/see and sensitivty of 1 (1 cm, lınV). Ventricular flutter and fibrilation were evident on the ECG (Fig. 1).

Evaluation of blood samp•le obteined froın the calf revea.ıed hyper-kalemia (\12.5 mEq/L) and hyperchloremia (159 m'Eq/L). Serum Na+

(1'5'6 m.Eq/L) and Ca++ (ıl0:.3ı4 mg/dl) levels were within riormal range.

' ' '

Immediately, Adrenaline was injected intravenously. But, the calf conditifJn deteriorated rapidly and she died at thirty minutes after arriv-al. At necropsy, there was subı3erous and submucosa.l petechiıal hemo-r-rhages. There was no any organic disorder in the hearth. At the bacteri.;. ological examina1ion, Escherichia coli enteritis was dia.gnosed.

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_y

A

~.43.1

B

Fi.gure 1. Eiectrocardiograms recorded from the calf. A: Ventricular fJutter. B: Ventricu1ar filbrilation. Paper speed 25 mm/see. ' ~ t ,.r'"--"'i,\

v·-\r" "

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~

rFr ct> Q ~ ::ı ~ '"t c;· ı:: ~ '"t ~ ı:;: ~ ~ '"t

~

A ~ ~ ~ ... ~ ~ c:;· ::ı

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=

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262 Abdullah Başoğlu -:- Kürşat-Turgut

- - - · - - --

-Discussion

It has been reported tlhat ventricular flutter is a very ra·re condition.

It is a pro.gresısive stuation and take a sudden tu~n to ventricular f~brila­ tion (1, 9, -13). QR;S coımplex:s and T waves are too laiige and in abnormal structure in the ventricular flutter_. But, they are in the saıme shape. When one of the cardiac cyclus finish, the following cyc1us start, so complexes are fallaw to each other continuous1y That's why, QRS com-plex, ST segment anicl T wav e can not be con!firmed separetly (.1, -1·3), In the ventricular f.ibrillation, since the ventri-cular contractions are-erratic, the EOG shoWI3 bizarre ventricular pattern of varying si~e and configura-tion (7). Ele.ctrocardiographic properties of botlh ventricular f1utter and ftbrillation were evident on the. ECG reeord of the ca1f (Fig. 1). Most ex-perimental evidence suggests that cardiac arrhy;tıhımias are due to afbnor-malities in eel'lular conduction or automatıcity. Oardiac' conduction can be altered .by electrolyte, acid~,b~se disturbane~s and or.ganic cardiac diseases ('10).

Potassium (K+), calcium (Ca++), sodium (Na-+) and maıgnesium

(Mg+~-) play a role in tıhe ge·r_ıesits of experimental arrhythmias. In the elinical settinıg, ihoweıver, altered K+ conceutration. is re-sponsiible for the wast majority of such arrlhythmias (6). ltı an expe.rimental study (i11),

it was found that there was_ ~ transient phase of acceleration of intra-ventricular conduction as K+ is eleıvated moderalety but, further rise of K+ intraventricular conduction was depressed. In an another study (:1'2), it ha13 be en -pointed out that in the fa ce of slow ly risinıg plascrna K+, the mechanism of death was caTdifiC standstill due to diffuse depıression of intraventricular conduction ~nd only occasionally due to ventricular fi-briHation. S?, _dertected high serum K+ concentration in this case may be responsible _for atrial fiatter aınd fihrillation.

It has been reported tihat the most comman cause of atrial fiibrilla-tion is aıcute ıinyocardial infaretion (7). · Howeve.r, ·the1re was no any or-ganic -disorder in the hearth at necropsy in thi!3 case.

In conclus~on, we found tihat EOG ·was an. essantia:ı procedure to deteıımine the cardiac arrhythmias in calves. High serum K+ cancentra-tion .mig1ht play a role in the development of ventricular flutter and fi-briHation.

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A C'ase Of Ventricular Fluttier And Fi'brillation in A Calf... 263

References

1 - Birand, A. (l97ı8). Elektrokardtyogra'fi. Be ta Yayınevi, 8dana.

2 - Blood, D. C., Radostits, O. M. and Henderson, J. A. ('1,91813·). Veterinary

Medicine, Sixth Editton. Bailliere Tindall, London.

3 - Brigıhtling, P. and Townsend, H. G. G. (198,3). .Aıtrial fıi!brillation in ten

cows. Can. Vet. J., 24, 3:31-3ı34.

4 - Broıbst, D. (1983.). PathophY'siological and ad.aptive chang·es in acidhase

disorders. J. A. V. M. A. 18:3, 7, 7713-780.

5 ---o Deroth, L. (,19.8'0). Electrocardiographic para.meters in the normal lactatinıg

Holstein cows. Can. Vet. J., 2,1, ı2'7:1-ı2·7'7.

·6 - Fi~ch, C. (!197'3). Relation of electrolyte disturbances to cardia.c

ar-rhrthmias. Circulaıtion, 157, .308-4'19.

7 - Q'öldman, M. J. (1197ı6). Princi.ples of elinical electrocardiography. 10 th.

Edition. Lange Medical Publications. Los Altos, California.

8 - Guirk, S. M., Muir, w. W., Sams, R. A. and Rings, D. M. (.1·983). Atrial

ftbrillatıion in cows : elinical findings and therapeutic cons1derations.

J.A.V.M.A . .1812, 112, 1~'80-1386.

9 - Herıve, D. (119187). Insuffisance circulatoire aigue. Pr.atique Medicale at

Chirurgicale de I' Animal de Compagnie, 5, 333·-345.

10 - HoHman, B. E. and Fosen, M. R. (1981). Cellular mechanisms for card1ac

.arrhythmias. Gircs. 'Res., 4·9, 1-15.

1!1 - Mendez, C., Erlij, K. and Moe, G. K. (,19ı6.4). lındir·ect action of epinephrıine

on intraventricular conduction time. Circ. Res., 1'4, 318·-3J2ıl.

12 -Nahum, L. H. and Hoff, H. E. ('196•9). Obser•vations on potassiurn f~brilla­

tion. J. Pharmacol., Exp. Ther., 6·5, 3:2·5-312:9.

13 -Oktay, S. Süleymanlar, G. (1984). Pratik elektrokardiyografi. Hacettepe

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