Doctoral Degrees (Anaesthesiology and Critical Care)

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Global and regional myocardial and circulatory function during anaesthesia in the normal heart and in the presence of threatening or overt myocardial ischemia
(Stellenbosch : Stellenbosch University, 2013-12) Coetzee, Andreas Retief; Coetzee, J. F.; Stellenbosch University. Faculty of Medicine and Health Sciences. Dept. of Anaesthesiology and Critical Care.
AFRIKAANSE OPSOMMING: Hierdie DSc is fundeer op ‘n aantal aspekte rondom ‘n sentrale tema naamlik die algemene en streeksfunksie van die normale hart of die hart blootgestel aan die risiko van miokardiale isgemie. Die werk is oor ‘n bestek van 25 jaar gedoen en sluit in eksperimentele werk in groot en kleindiere sowel as data verkry in pasiënte. Hoofstuk 1 handel met globale en streeksfunksie in die normale hart met die klem op die meer moderne benadering tot die koppeling van die hart met die sirkulasie en effek van middels op die twee komponente. Hierdie hoofstuk het waardevolle inligting gegee t.o.v. fisiologie maar ook gehelp om die middels te kies vir daaropvolgende studies. Hoofstuk 2 bevat navorsing wat verwys na die hart met kroonaarstenose. Onder andere word gesteun op ‘n dieremodel van kroonaarstenose. Die hoofstuk sluit data in wat , as eerste en unieke bydrae, gewys het dat inhalasie narkose middels die reperfusie besering van die hart kan verminder. Hierdie data het spesifiek bygedra om die kliniese praktyk van narkose vir hierdie pasiënte te verander. Hoofstuk 3 verwys na werk gedoen om die hart gedurende elektiewe chirurgiese arres te oksigeneer. Die effektiwiteit van verskillende kardioplegiese vloeistofsamestellings is ook krities ontleed. Die vierde hoofstuk handel met ‘n ernstige kliniese probleem naamlik akute pulmonêre hipertensie. By pasiënte met akute long besering is hierdie verskynsel baiemaal die oorsaak van dood en of moeitevolle oksigenasie. Die werk het gelei tot beter insigte t.o.v. pasiënt hantering tot die punt dat baie van die pasiënte vandag gered kan word.
Renal dysfunction associated with infrarenal cross clamping of the aorta during major vascular surgery
(Stellenbosch : Stellenbosch University, 2000-03) Van der Merwe, Wynand Louw; Coetzee, Andre; Stellenbosch University. Faculty of Medicine & Health Sciences. Dept. of Anaesthesiology & Critical Care.
ENGLISH ABSTRACT: Acute renal failure still is, with the exception of cardiac deaths, the most important pathological process associated with perioperative mortality in patients operated for abdominal aortic aneurysms. The intraoperative change in renal blood flow (RBF) and glomerular function have been investigated in human and animal models, particularly over the past 15 years. Despite large variation in study populations, measurement techniques and study designs in general, a significant body of evidence has developed which suggests infrarenal aortic clamp-induced renal ischemia to be the cause of postoperative acute renal failure when this complication does occur. It is rather surprizing then that, despite some recent studies which have reported on various pharmacological interventions to prevent intraoperative renal ischemia (with variable success), very little has apparently been done to unravel the pathogenesis and exact pathophysiology of this potentially lethal complication. Although a number of investigators suggest the possibility of hormonal involvement (particularly reninangiotensin, antidiuretic hormone (ADH) and catecholamines) in the process, the exact role of these mediators have not been explored (or reported) in a structured fashion. In an initial human study, renal hemodynamics and function were measured from the preoperative period, during the intraoperative phase and at least until 4 hours after aortic unclamping. To investigate the possibility of a temporal relationship between renal changes and fluctuations in hormonal concentrations, plasma concentrations of relevant hormones were determined at every sampling period where renal parameters were measured. The decrease in RBF and glomerular filtration rate (GFR) which we demonstrated to coincide with infrarenal aortic cross clamping, is consistent with results previously published. We demonstrated persistence of the impairment of these parameters as long as 4 hours into the postoperative phase; which has previously only been reported for the period until immediately after aortic unclamping with the abdomen still open. The persistence of a depressed GFR until the time of discharge of patients is cause for concern, particularly in patients with compromised renal function prior to surgery. Of the measured hormones with a potential influence on RBF and nephron function, renin was the only mediator where changes in plasma concentrations coincided with the depression of RBF and GFR after aortic cross clamping. The design of our study did not allow us to conclude whether the concomitant increase in angiotensin II was primarily responsible for the change in renal hemodynamics, or whether the raised renin (and angiotensin) levels were stimulated by the decrease in RBF induced by another mechanism. In another patient group, we demonstrated that the combination of mannitol and dopamine provided no protection against the deleterious effects of aortic cross clamping. In fact, the high urine volumes produced under the influence of these agents (which did not correlate with RBF at the corresponding periods), is likely to prompt a false sense of security. Given the lack of any objective benefit afforded by these agents, their use in these clinical circumstances should be discouraged. The animal studies were aimed at elucidation of the exact role of angiotensin in the pathogenesis and pathophysiology of the renal changes associated with infrarenal aortic clamping, as well as the interaction of angiotensin with other modulators for which an interactive relationship had been described previously under other experimental and/or clinical circumstances. The first study showed that, although renin (and thus angiotensin) concentrations were high after aortic unclamping, the hormone had no pathogenic or pathophysiological role of significance in the observed renal changes during this period (since blocking angiotensin II activation by the prevention of renin release, or by inhibiting the conversion enzyme, did not prevent a substantial decrease in RBF or GFR during that period). Preventing angiotensin II activation did, however, prevent renal changes during aortic clamping. This beneficial effect did not establish a primary role for angiotensin during that period, since the favourable influence could also (at least partially) be explained by prevention of the permissive influence of angiotensin on other vasoconstrictors and/or other vasodilatory influences of ACE inhibition and [1- blockade which are unrelated to angiotensin. This study did indicate that (at least partially) different mechanisms are responsible for the renal changes seen during aortic clamping, and after aortic unclamping. The second study explored the role of calcium in the renal pathophysiological changes during aortic clamping and after unclamping. The protective influence effected by the administration of a Ca2 + -blocker suggest the dependence of the renal vasoconstrictive and glomerular pathophysiological process( es) on the cellular influx of Ca2 + through voltage-gated channels. It unfortunately provides no definitive insight into the primary instigators of these processes. However, it does offer a clinically useful method of preventing these changes and protecting the kidney against ischemic injury during abdominal aortic surgery. The third component of the animal studies demonstrates the importance of the protective effect of renal prostaglandins during the specific experimental (and probably also the clinical) circumstances. Again, it does not provide definitive information on the mediators responsible for the renal changes, since the deleterious effects of numerous endogenous substances have previously been shown to be counterbalanced by intrarenal synthesis of prostaglandins under various experimental and clinical circumstances. The extent of the pathophysiological and ultrastructural changes which occurred under the influence of a NSAID does, however, suggest that these drugs should not be used under these clinical circumstances. The last component of the study provides evidence that angiotensin only plays a secondary/supplementary role in the renal pathophysiological process even during aortic clamping. This may explain the contradictory evidence regarding the potential beneficial effect of ACE inhibition (on renal hemodynamics and glomerular function) during abdominal aortic surgery (Licker et al. 1996, Colson et al. 1992a). Based on our studies, ACE inhibition can not be supported for this purpose.
A study of right ventricular function during one lung anesthesia
(Stellenbosch : University of Stellenbosch, 2004-04) Levin, Andrew Ian; Coetzee, Andre; University of Stellenbosch. Faculty of Health Sciences. Dept. of Anaesthesiology and Critical Care.
ENGLISH ABSTRACT: A significant decrease in lung volume is reported to occur in the dependent lung during OLA in the LDP. This decrease in lung volume can result in an acute increase in opposition to RV ejection. The potential problem is that the right ventricle is a thin walled structure that can generate considerably less work than the thicker walled LV. It possesses little reserve to deal with an acute rise in afterload as may occur during acute lung injury or after lung resection. Therefore, this increase in afterload during OLA may potentially impair RV-PA coupling. Albeit this potential problem exists, the changes in RV afterload and how the right ventricle performs during OLA have not been well studied. Arterial hypoxemia, due mainly to venous blood being shunted via the non-ventilated lung, may present a clinical problem during one lung ventilation.

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