hypotension after the release of aortic cross clamp in patients undergoing open heart surgery

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1993;9(2):100-102 i{iii i{ iiiiiiiii ORIGINAL ARTICLt Hypotension After the Release of Aortic Cross Clamp in Patients Undergoing Open Heart Surgery Andrea Cooper, Deepak Tempe, S. K. Sinha, A. S. Tomar, M. Akhter, B. K. Gupta, S. K. Khanna One hundred consecutive adult patients under- going various elective open heart surgicalproce- dures were included in this prospective study. An indwelling radial arterial cannula was used to measure mean arterial pressure (MAP). Sys- temic vascular resistance (SVR) during bypass was calculated using the formula SVR - MAP x 80/ pump flow dynes-sec-cm 5. Patients in whom va- sodilators were used during cardiopulmonary bypass were excluded. Measurements were made just before the release of aortic cross clamp when the pumpftows were norma~" and 1,3,5 and 10 minutes following the cross clamp release. There were 60 males and 40females with a mean age of 29.4 • 13.gyears and mean weight of 46• Kg. The MAP fell from 65• to 47• (p<0.O0001) and the SVR fell from 1699• to 1163• dynes-sec-cm 5 (p<O.O0001) one minute after the release of aortic cross clamp. There was some recovery during the subsequent period, but the change continued to remain statistically sig- nificant upto 10 minutes after the release of aortic cross clamp. MAP and SVR decreased in all except 9 and 3 patients respectively at 1 minute. The mean temperature at the time of release of aortic cross clamp was 33.7+-2.7~ There was a poor correlation between the temperature and duration of bypass and extent of decrease in MAP and/or SVR. We conclude that there is a significant decrease in MAP (2796) andSVR (3196) after the release of aortic cross clamp and it persists for 10 minutes. From the Departments of Anaesthesiology and Cardiothoracic Surgery, G B Pant Hospital, New Delhi, India Address for correspondence : Dr Deepak Tempe, D-6, Mirdard Lane, Maulana Azad Medical College Campus, New Delhi 110 002, INDIA. A decrease in mean arterial pressure (MAP) often accompanies release of the aortic cross clamp during open heart surgery. The reasons ascribed to this phenomenon are reactive myoacardial hyperaemia and vasodilator effect of myocardial stretch receptors 1 and the addition of a fully dilated myocardial vascular bed to the circulation. 2 To the best of our knowledge, the magnitude of the decrease in MAP has not been reported. We, therefore, investigated the extent of the decrease in MAP and systemic vascular resistance (SVR) following the release of the aortic cross clamp in patients undergoing open heart surgery. Material and Methods One hundred consecutive adult patients (60 males) who underwent elective open heart sur- gery were included. The mean age was 29.4+13.9 years and mean weight was 46+13 Kg. Patients were premedicated with morphine 0.2 mg Kg -1 and promethazine hydrochloride 25 mg intramus- cularly, 1-2 hours before operation. Anaesthesia was provided with morphine (approximately lmg Kg q) with pancuronium bromide used as a muscle relaxant. Anaesthesia was maintained before by- pass with nitrous oxide and oxygen using a fractional concentration of oxygen (FIO2) of 0.33, and supplemented with halothane. Standard by- pass techniques with Ringer lactate prime was used. Cold potassium cardioplegia (either blood or crystalloid) with moderate hypothermia (28~ 100

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1993;9(2): 100-102

i{iii i{ iiiiiiiii

ORIGINAL ARTICLt

Hypotension After the Release of Aortic Cross Clamp in Patients Undergoing Open Heart Surgery Andrea Cooper, Deepak Tempe, S. K. Sinha, A. S. Tomar, M. Akhter, B. K. Gupta, S. K. Khanna

One h u n d r e d consecut ive adul t pa t i en t s under- go ing var ious elective open hear t surgicalproce- dures w e r e included in this p rospec t i ve s tudy. A n indwel l ing radia l ar ter ia l cannula was used t o m e a s u r e m e an ar ter ia l p r e s s u r e (MAP). Sys- temic vascu lar res is tance (SVR) dur ing bypass was ca lcula ted us ing the f o r m u l a SVR - MAP x 8 0 / p u m p f l o w dynes-sec-cm 5. Pat ien ts in w h o m va- sod i la tors were u s ed dur ing card iopu lmonary bypass were excluded. Measuremen t s were made j u s t be fore the release o f aor t ic cross c lamp w h e n the p u m p f t o w s were norma~" and 1,3,5 and 10 m inu t e s f o l l ow ing the cross c lamp release. There we r e 60 males and 40 females wi th a mean age o f 29.4 • 13 .gyears a n d mean we igh t o f 46• Kg. The MAP f e l l f r o m 65• t o 47• (p<0.O0001) and the SVR f e l l f r o m 1699• to 1163• dynes-sec-cm 5 (p<O.O0001) one minu te a f ter the release o f aort ic cross clamp. There was some recovery dur ing the subsequen t period, but the change cont inued to remain statistically sig- n i f icant up to 10 minutes a f ter the release o f aor t ic cross clamp. MAP a n d SVR decreased in all e x c e p t 9 a n d 3 pa t ien t s respect ively at 1 minute . The m e a n t empera ture at the t ime o f release o f aor t ic cross c lamp was 33.7+-2.7~ There was a p o o r corre la t ion be tween the t empera ture and dura t ion o f bypass and ex t en t o f decrease in MAP a n d / o r SVR. We conclude tha t there is a s igni f icant decrease in MAP (2796) andSVR (3196) a f ter the release o f aort ic cross clamp and it p e r s i s t s f o r 10 minutes .

From the Departments of Anaesthesiology and Cardiothoracic Surgery, G B Pant Hospital, New Delhi, India

Address for correspondence : Dr Deepak Tempe, D-6, Mirdard Lane, Maulana Azad Medical College Campus, New Delhi 110 002, INDIA.

A decrease in mean arterial pressure (MAP) often accompanies release of the aortic cross clamp during open heart surgery. The reasons a sc r ibed to this p h e n o m e n o n are reac t ive myoacardial hyperaemia and vasodi la tor effect of myocardial stretch receptors 1 and the addit ion of a fully dilated myocardial vascular bed to the circulation. 2 To the best of our knowledge , the magnitude of the decrease in MAP has not been reported. We, therefore , invest igated the extent of the decrease in MAP and systemic vascular resistance (SVR) fol lowing the release of the aortic cross clamp in patients unde rgo ing open heart surgery.

Ma te r i a l a n d M e t h o d s

One hundred consecut ive adult patients (60 males) who u n d e r w e n t elective open heart sur- gery were included. The mean age was 29.4+13.9 years and mean weight was 46+13 Kg. Patients were premedica ted with morphine 0.2 mg Kg -1 and promethazine hydroch lor ide 25 mg intramus- cularly, 1-2 hours be fore operat ion. Anaesthesia was provided with morphine (approximate ly lmg Kg q) with pancuron ium bromide used as a muscle relaxant. Anaesthesia was maintained before by- pass with nitrous oxide and oxygen using a fractional concent ra t ion of oxygen (FIO2) of 0.33, and supp lemented with halothane. Standard by- pass techniques with Ringer lactate prime was used. Cold potass ium cardioplegia (e i ther b lood or crystalloid) with modera te hypothermia (28~

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COOPER et al Hypotension after the release of aortic cross clamp

was u s e d for m y o c a r d i a l p ro tec t ion . An indwel l ing radial arterial c a n n u l a was u s e d to m e a s u r e MAP. SVR was c a l c u l a t e d u s ing the f o r m u l a SVR = M A P x 8 0 / p u m p f l o w d y n e s - s e c - c m -s. Cent ra l ve- n o u s p r e s s u r e w a s m a i n t a i n e d at ze ro a n d no a t t e m p t was m a d e to fill the hear t d u r i n g the s t u d y pe r i od . Pa t i en t s in w h o m v a s o d i l a t o r s w e r e u s e d du r ing c a r d i o p u l m o n a r y b y p a s s (CPB) w e r e e x c l u d e d . M e a s u r e m e n t s w e r e m a d e just b e f o r e the r e l ease o f the aor t i c c ross c l amp (con t ro l ) , just a f te r the r e l ease o f the aor t i c c ross c l a m p w h e n the p u m p f l ows w e r e no rm a l 2.4 l i t r e s / m V m i n this was t a k e n as ze ro m i n u t e ) a n d one , th ree , five and ten m i n u t e s f o l l o w i n g cross c l a m p re- lease . Dur ing this p e r i o d , the pa t i en t s w e r e awai t - ing r e w a r m i n g a n d the final s tage of the o p e r a t i v e p r o c e d u r e w a s b e i n g c o m p l e t e d . B e t w e e n 5-10 m i n u t e s f o l l o w i n g r e l ea se of c ross c l amp, 32 pa t i en t s w e r e c o m p l e t e l y s e p a r a t e d f rom CPB; h e n c e at ten m i n u t e s da ta is p r e s e n t e d f r o m on ly 68 pa t ien t s .

The va lue s o b t a i n e d at va r ious t ime in te rva l s w e r e c o m p a r e d u s ing o n e w a y ana lys i s o f var i - ance (Anova) a n d if f o u n d s igni f icant , s t u d e n t s ' t ' test ( two ta i led) w a s app l i ed . P e a r s o n ' s cor re la - t ion coe f f i c i en t w a s ca l cu l a t ed to f ind ou t the r e l a t i o n s h i p b e t w e e n the t e m p e r a t u r e a n d du ra -

t ion of b y p a s s a n d e x t e n t o f d e c r e a s e in MAP a n d / or SVR. A P va lue o f less than 0.05 w a s d e e m e d s igni f icant .

R e s u l t s

The va r i ous surg ica l p r o c e d u r e s p e r f o r m e d were , mitral va lve su r ge ry ( o p e n mitral v a l v o t o m y - OMV, mitral va lve r ep l acem en t -MVR ) -45, aor t ic va lve r e p l a c e m e n t (AVR) - 7, d o u b l e va lve p r o c e - d u r e s (OMV+AVR, MVR+AVR) -12, c o r o n a r y ar- tery b y p a s s g ra f t ing (CABG) - 14, a n d o t he r s (atrial s ep ta l de fec t , ven t r i cu l a r s ep ta l de fec t , atrial m y x o m a s e tc) -22. The m e a n d u r a t i o n of aor t ic c ross c l a m p i n g a n d CPB was 53_+27 min a n d 90+48 m i n u t e s r e s p e c t i v e l y . T h e r e s u l t s a re s u m m a r i s e d in T a b l e I. The MAP fell f r o m 65_+14 to 47_+15 m m H g (p<0 .00001) and the SVR fell f rom 1699_+511 to 1163_+365 d y n e s - s e c - c m "s (p<0.O0001) o n e m i n u t e a f t e r the r e l ease of aor t ic c ross c l amp. A l though the re w a s s o m e r e c o v e r y d u r i n g the s u b s e q u e n t p e r i o d , the c h a n g e c o n t i n u e d to re- ma in s ta t is t ical ly s ign i f ican t u p t o ten m i n u t e s

20-30 31-40 41-50 MEAN ARTERIAL PRESSURE ( mmHg )

28 26 24 22 20 18 16 14 12 10 08 06 04 02 0

51-60 61-70 71+

Fig 1. Distribution of mean arterial pressure at one minute after the release of aortic cross clamp.

af te r the r e l ea se of aor t i c c ross c l amp. MAP a n d

SVR d e c r e a s e d in all e x c e p t n i n e a n d th ree pa- t ients r e s p e c t i v e l y at o n e m i n u t e . Fig 1 s h o w s the d i s t r i bu t ion o f m e a n ar te r ia l p r e s s u r e at o n e m i n u t e a f te r the r e l ea se o f ao r t i c c ross c l amp . MAP w a s less than 50 m m H g in 64 p a t i e n t s at o n e minu t e . The m e a n t e m p e r a t u r e at the t ime o f

r e l ease o f the aor t ic c ross c l a m p w a s 33.7+2.7~ A p o o r co r r e l a t i on was f o u n d b e t w e e n the te.m- p e r a t u r e a n d the du ra t i on of b y p a s s a n d ex t en t o f d e c r e a s e in MAP a n d / o r SVR wi th an ' r ' v a lue r ang ing b e t w e e n 0.08 a n d 0.16. T h e r e w a s a lso no

T a b l e I . H a e m o d y n a m i c da ta o v e r the s t u d y )er iod

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Indian Journal of Thoracic and Cardiovascular Surgery Volume 9; Number 2: December 1993

d i f f e r e n c e in the ex t en t o f d e c r e a s e in MAP an d SVR in the va r ious types of surgical p r o c e d u r e s e x c e p t tha t in the 'o thers ' g r o u p the dec rease in MAP was less as c o m p a r e d wi th var ious valve p r o c e d u r e s (P<0.01).

D i s c u s s i o n

T h e r e are wide d i f f e r e n c e s in o p i n i o n con- c e rn i ng the f low rate and b l o o d pressure u s e d d u r i n g CPB. The re are s o m e ~,3 w h o be l i eve that MAP is impor tan t , whi le o the r s 4-7 feel that MAP is not . H e c k e r e t a l 3 in 1991 r e c o m m e n d e d that MAP s h o u l d be m a i n t a i n e d at or a b o v e 50mmHg to d e c r e a s e the i nc ide nce o f pos t CPB centra l ner- vous dys func t ion . They c o n s i d e r e d cerebral b l o o d f low to be d e p e n d e n t on pe r fu s ion p res su re r ega rd l e s s of p u m p f low rate. The impor t ance o f ma in t a in ing MAP a b o v e 60 -70mmHg for c o r o n a r y p e r f u s i o n in pa t ien t s u n d e r g o i n g CABG has also b e e n e m p h a s i s e d . 1 This is par t icular ly impor t an t a f te r the re lease of the aor t ic cross c lamp ( the fall b e i n g p r e d i c t e d ) w h e n the p rox imal ana s tomos i s is ye t to be c o m p l e t e d and the c o r o n a r y pe r fu s ion is still t h r o u g h the d i s e a s e d c o r o n a r y vessels .

On the cont rary Kolka and Hi lberman s s h o w e d that l ow p re s su re du r ing CPB did not cor re la te wi th ce rebra l injury, The ave rage MAP in the i r s t udy was 49mrnHg. Aren and c o w o r k e r s <7 dem- o n s t r a t e d t h a t h y p o t e n s i o n p r o d u c e d b y p ro s t acyc l i n du r ing CPB did no t have an in- c r e a s e d risk of p o s t o p e r a t i v e cerebra l damage . G o v i e r e t a l s h a v e s h o w n t h a t c e r e b r a l a u t o r e g u l a t i o n is p r e s e r v e d du r ing h y p o t h e r m i c CPB d o w n to p ressu res o f 30mmHg. The pha rma- co log ica l t r ea tmen t of ar ter ial p ressure b e t w e e n 30 a n d l l 0 m m H g is no t n e c e s s a r y dur ing h y p o - t he rmic CPB in pa t ien t s wi th normal ce rebra l c i r cu la t ion a nd fur ther , the use of va sop re s so r s is o b j e c t i o n a b l e on the g r o u n d that it may in te r fe re wi th renal pe r f u s ion to a g rea te r d e g r e e than l o w e r p e r f u s i o n p res su re . ~ It must, h o w e v e r , be r e m e m b e r e d that at the t ime of re lease of the aor t ic c ross clamp, the pa t i en t s are usua l ly w a r m and also the MAP is i m p o r t a n t at this s tage in pa t i en t s u n d e r g o i n g CABG. It is pe rhaps , due to

this reason , that m an y a n a e s t h e s i o l o g i s t s still p re fe r to ad m in i s t e r an a lpha agon is t at this s tage to increase the MAP to 60 -70mmHg in pa t ien ts u n d e r g o i n g CABG a l t h o u g h the n e e d to do so may be less wel l felt in pa t ien t s in w h o m the p rox imal a n a s t o m o s i s is p e r f o r m e d b e f o r e go ing on bypass .

We c o n c l u d e that there is a s ign i f ican t de- crease in MAP (27~ and SVR (310/6) af ter the re lease of the aor t ic cross c lamp an d it pers is ts for a b o u t ten minu tes . W h e t h e r to t rea t this or not will d e p e n d u p o n the prac t ice and p r e f e r e n c e s of i n d i v i d u a l c a r d i o v a s c u l a r s u r g i c a l a n d a n a e s t h e s i o l o g y teams r ega rd ing the ideal pres- sures dur ing CPB.

R e f e r e n c e s

1. Tinker JH, Roberts SL. Management of cardiopul- monary bypass. In KaplanJ, ed. CardiacAnestbesia, 2nd ed, Philadelphia, WB Saunders Company 1987: 907.

2. Tinker. JH Cardiopulmonary bypass - technical aspects. In Thomas SJ, ed. Manual of Cardiac Anesthesia New York, Churchill Livingstone 1984: 383.

3. Hecker BR, Knopes KD. Optimal pressures and flows during cardiopulmonary bypass. Pro and Con. J Cardiotborac Vasc Anesth 1991; 5:402-4.

4. Garman JK. Optimal pressures and flows during cardiopulmonary bypass. Pro and Con. J Cardiotborac Vasc Anestb 1991; 5:399-401.

5. Kolkka R,.Hilberman M. Neurologic dysfunction following cardiac operation with low flow, low pressure cardiopulmonary bypass. J Thorac Cardiovasc Surg 1980; 79:432-7.

6. Aren C, Blomstrand C,m Wikkelso C, Radegram K. Hypotension induced by PGI 2 treatment during CPB does not increase the risk of crebral complications. J Thorac Cardiovasc Surg 1984; 88:748-53.

7. Aren C, Badr G, Fedderson K, Radegram K. Somatosensory evoked potentials and cerebral metabolism during cardiopulmonary bypass with special reference to hypotension induced by prostacyclin infusion. J Thorac Cardiovasc Surg 1985; 90:73-9.

8. Gorier AV, Reves JG, McKay RD, et al. Factors and their influence on regional cerebral blood flow during nonpulsatile cardiopulmonary bypass. Ann Thorac Surg 1984; 38:592-600.

9. Gorier AV. Low perfusion pressure with the onset of cardiopuhnonary bypass. In Reeves JG, Kenneth DH, eds. Common Problems in Cardiac Anesthesia. Chicago, Year- book Medical Publishers, 1987: 40.

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