慢性肝衰竭和失代偿期肝硬化患者血气分析的变化

目的探讨慢性肝衰竭和失代偿期肝硬化患者血气分析变化的临床意义。方法回顾性分析我科收治的37例慢性肝衰竭和失代偿期肝硬化患者的血气分析资料。结果2例患者出现明显的缺氧表现,4例患者出现立位性缺氧表现,11例患者感轻度胸闷;在36例存在酸碱失衡的患者,慢性肝衰竭组存在单纯酸碱失衡9例,两重酸碱失衡10例,三重酸碱失衡2例,失代偿期肝硬化组存在单纯酸碱失衡8例,两重酸碱失衡7例。两组患者在酸碱失衡的类型方面无统计学差异;两组均以碱中毒为主。慢性肝衰竭组中比例较高的三种类型依次为呼吸性碱中毒合并代谢性酸中毒（38．1％）、呼吸性碱中毒（23．8％）和代谢性碱中毒（14．3％）,单纯性代谢性酸中毒比例最低（4．8％）。失代偿期肝硬化组中比例较高的三种类型依次为呼吸陛碱中毒（46．7％）、呼吸性碱中毒合并代谢性碱中毒（26．7％）和呼吸性碱中毒合并代谢性酸中毒（20．0％）,代谢性碱中毒比例最低（6．7％）。结论慢性肝衰竭和失代偿期肝硬化患者存在酸碱失衡和低氧血症,动态监测血气分析并及时对症治疗对此类患眷具有重要的临床意义。     

Acid-base disturbance in patients with fulminant hepatic failure.

Forty-two arterial blood pH and gas determinations were carried out on 11 patients with fulminant hepatic failure. The most common type of acid-base disturbance was that of respiratory alkalosis in 22 cases (52.4%). This was partially compensated in 13 subjects (31.0%) while an accompanying metabolic alkalosis was present in 9 (21.5%). Partially compensated metabolic acidosis was observed on 15 occasions (35.7%), all of which were in patients with laboratory evidence of impaired renal failure. The mental status of the patients was evaluated in each of the categories of acid-base disturbances. Some degree of correlation was evident between the PCO2 and the magnitude of base excess and that of the severity of the encephalopathy. The lower PCO2 and greater negative base excess values tended to be nearly always present in totally comatose subjects. By contrast, there was no clear cut relationship between pH and mental state.     

Effect of hypocapnia on intracellular pH during metabolic acidosis.

Separate and combined effects of acute metabolic acidosis and hypocapnia were determined in skeletal and cardiac muscles of intact rats. Normocapnic metabolic acidosis, imposed by intraperitoneal injection of hydrochloric acid (6 mEq/kg), did not change skeletal muscle intracellular acid--base parameters. Hypocapnia, induced by mechanical hyperventilation, resulted in intracellular alkalosis within skeletal muscle during both respiratory alkalosis and compensated metabolic acidosis; changes of skeletal muscle intracellular bicarbonate concentration per unit change in carbon dioxide tension were identical during these two experimental procedures. These data suggest that processes other than physicochemical buffering neutralize protons taken into skeletal muscle cells during acute metabolic acidosis. The acid--base state of the heart was quite stable during these experimental manipulations; thus, it appears that cardiac muscle has an extraordinary buffering ability. Moreover, our data suggest that processes other than physicochemical buffering maintain cardiac intracellular pH normal during hypocapnia.     

肝硬变腹水患者钾钠氯及酸碱失衡

目的研究肝硬变腹水患者的钾、钠、氯及酸碱失衡。方法肝硬变腹水患者１５４例，血Ｋ＋、Ｎａ＋、Ｃｌ－测定采用ＥＥＬ公司自动分析仪及火焰光度计。血气及酸碱度测定采用ＩＬ１３０２型自动微机分析仪。结果低血钾者５７例，高血钾者６例，低血钠者８１例，高血钠者１２例，低血氯者３４例，高血氯者８例。２４例血气及酸碱度测定结果显示，以碱中毒者为主。依次为呼碱、呼碱＋代酸、代酸、代碱、呼酸。本组高血钾、低血钠与Ｃｈｉｌｄ分级、ＢＵＮ、Ｃｒ值相关。从本组资料表明，重症肝硬变腹水患者水盐代谢失衡多为医源性所致，且加重原有失衡。高钾血症、急性低钠血症及高钠血症大多如此，多为住院后发生，常可危及生命。结论肝硬变腹水患者的高钾血症、低钠血症和高钠血症大多在肝肾功能低下，不适当的治疗所致，是影响预后的重要因素     

Oxygen-transport function of the blood and endothelial dysfunction in patients with angina pectoris and arterial hypertension

Parameters of oxygen-transport function of the blood and function of the endothelium were studied in 49 patients with stable angina pectoris of I and II functional class with or without concomitant 2nd degree arterial hypertension. All patients received pathogenetic therapy. Signs of endothelial dysfunction were found in group III in which endothelium dependent vasodilation (8.22 +/- 1.71%) was 73.4% (p1 < 0.001) lower than in control group and 47.2% (p3 < 0.05) lower than in patients with class I angina. In all groups baseline content of nitrates/nitrites was lower. Main parameters of acid-base balance were lowered in patients of group III evidencing for emergence of signs of metabolic acidosis and hypoxia. Lowering of hemoglobin affinity to oxygen and its rise after therapy was also revealed. Maximal lowering of this parameter (-10.2%, p2 < 0.05) reflecting shift of oxyhemoglobin dissociation curve to the right was noted in group II. Endothelium can participate in formation of these disturbances because its dysfunction is associated with deranged release of NO in various parts of vascular tree. This affects formation of various NO-derivatives of hemoglobin and oxygen transport system of the blood.     

Plasma lipoprotein and apolipoprotein profile in alcoholic patients with and without liver disease: on the relative roles of alcohol and liver injury

In the present study, we report on alterations in plasma lipid, lipoprotein and apolipoprotein patterns in three separate populations of alcoholic patients, one without liver damage (Group I), a second presenting steatosis or mild alcoholic hepatitis or both (Group II) and a third with alcoholic cirrhosis (Group III), using a healthy, normolipidemic, nonalcoholic group as controls (Group C). Total plasma cholesterol levels were elevated in Groups II and III when compared with Groups I and C, while the ratio of esterified to free cholesterol was considerably lower in Group III than in the other groups. Plasma apo-AI levels were higher in Groups I and II than in Group C, but varied over a wide range in Group III. Apo-AII was present at higher concentrations in Groups I and II than in both Groups III and C. In contrast, no significant differences were detected in total apo-B levels, irrespective of the group. Modifications in the chemical composition of plasma lipoproteins primarily concerned a reduction in the cholesteryl ester content of low-density lipoproteins (LDL) and high-density lipoprotein (HDL) in Group III, this being compensated by a reciprocal increase in triglyceride. In addition, Group III lipoproteins, with the exception of HDL3 (density 1.100 to 1.140 gm per ml), exhibited a greater content of phospholipids than those of corresponding density from patients in Groups I and II. No significant differences were found in very low-density lipoprotein concentrations, while LDL levels increased in parallel with the severity of liver injury. In Groups I and II, HDL2 concentrations were elevated relative to Group C, while HDL3 decreased in parallel with the degree of impairment of liver function and thus from Group C to Group III.(ABSTRACT TRUNCATED AT 250 WORDS)     

Metabolic alkalosis contributes to acute hypercapnic respiratory failure in adult cystic fibrosis

BACKGROUND: and study objectives: Patients with end-stage cystic fibrosis (CF) develop respiratory failure and hypercapnia. In contrast to COPD patients, altered electrolyte transport and malnutrition in CF patients may predispose them to metabolic alkalosis and, therefore, may contribute to hypercapnia. The aim of this study was to determine the prevalence of metabolic alkalosis in adults with hypercapnic respiratory failure in the setting of acute exacerbations of CF compared with COPD. DESIGN: Levels of arterial blood gases, plasma electrolytes, and serum albumin from 14 consecutive hypercapnic CF patients who had been admitted to the hospital with a respiratory exacerbation were compared with 49 consecutive hypercapnic patients with exacerbations of COPD. Hypercapnia was defined as a PaCO(2) of > or = 45 mm Hg. RESULTS: Despite similar PaCO(2) values, patients in the CF group were significantly more alkalotic than were those in the COPD group (mean [+/- SD] pH, 7.43 +/- 0.03 vs 7.37 +/- 0.05, respectively; p < 0.01). A mixed respiratory acidosis and metabolic alkalosis was evident in 71% of CF patients and 22% of COPD patients (p < 0.01). The mean concentrations of plasma chloride (95.1 +/- 4.9 vs 99.8 +/- 5.2 mmol/L, respectively; p < 0.01) and sodium (136.5 +/- 2.8 vs 140.4 +/- 4.5 mmol/L, respectively; p < 0.01) were significantly lower in the CF group, and the levels of serum albumin were significantly reduced (27.4 +/- 5.8 vs 33.7 +/- 4.8 mmol/L, respectively; p < 0.01). CONCLUSION: Metabolic alkalosis contributes to hypercapnic respiratory failure in adults with acute exacerbations of CF. This acid-base disturbance occurs in conjunction with reduced total body salt levels and hypoalbuminemia.     

Acid-base disorders in hyperglycemia of insulin-dependent diabetic patients on chronic dialysis

The authors studied hyperglycemia occurring in insulin-dependent diabetic patients on chronic dialysis to determine the types of associated acid-base disorders, their treatment, and any differences from hyperglycemia in diabetic patients with intact renal function. Eighty-eight episodes of serum glucose greater than 25 mmol/L were observed, 23 in hemodialysis patients and 65 in patients on continuous peritoneal dialysis. Treatment consisted of low-dose insulin in 77 episodes and low-dose insulin plus saline in 11; no base was administered. Seventeen episodes (19%) presented with ketoacidosis. Arterial blood gas determinations were carried out at presentation in 37 of the episodes without ketoacidosis. Of these, 12 had respiratory alkalosis, six had respiratory acidosis and severe pulmonary edema, 14 had other single or mixed acid-base disorders, and only five had normal acid-base status. Insulin corrected the ketoacidosis in all instances and both pulmonary edema and respiratory acidosis in five of six instances. In eight cases metabolic alkalosis developed during treatment, without external acid loss. At the completion of treatment respiratory alkalosis was present in half the cases. No difference was noted between patients treated with hemodialysis or peritoneal dialysis. Insulin alone is sufficient for the management of hyperglycemia in dialysis patients. Certain acid-base disorders persist, but do not need further treatment. Hyperglycemia in patients on dialysis is characterized by infrequent development of metabolic acidosis and frequent presentation with respiratory alkalosis, by respiratory acidosis that is corrected by insulin, and by metabolic alkalosis developing during treatment without external cause.     

Role of atrial natriuretic factor in sodium and water retention in patients with schistosomal hepatic fibrosis.

Fifty subjects divided into three groups were studied: Group I: 10 normal adult subjects as controls. Group II: 20 patients with schistosomal hepatic fibrosis (SHF) without ascites (compensated stage). Group III: 20 patients with SHF with ascites. In all these patients plasma atrial natriuretic factor (ANF), serum aldosterone and serum osmolality were determined. There was a significant decrease in the plasma ANF in groups II and III compared to group I. There was a significant increase in the serum aldosterone level in group III compared to groups I and II. No significant difference was noted in serum sodium and potassium levels among the three groups. There was a significant decrease in serum osmolality in groups II and III compared to group I.     

Is the hypotension of cirrhosis a GABA-mediated process?

Systolic and diastolic blood pressures were recorded in 176 ambulant patients with chronic liver disease, including 36 patients with compensated cirrhosis (Group I), 119 patients with noncirrhotic chronic liver disease (Group II) and 21 patients with benign structural or functional liver disease (Group III). Group I patients had significantly lower systolic (113.0 +/- 2.2 mm Hg, mean +/- S.E.) and diastolic (65.3 +/- 1.7 mm Hg) pressures than Group II patients (125.8 +/- 3.5 and 76.6 +/- 1.5 mm Hg, respectively (p less than 0.0001) or Group III patients (125.1 +/- 3.4 and 77.5 +/- 2.4 mm Hg, respectively) (p less than 0.0001). Serum levels of GABA, a potent amino acid neurotransmitter with known vasodilatory effects in vitro, were higher in Group I patients (1.12 +/- 0.26 microM, mean +/- S.E.) than in Group II patients (0.41 +/- 0.05 microM) (p less than 0.005) or Group III patients (0.34 +/- 0.03 mM) (p less than 0.05). A constant infusion of GABA into the systemic circulation of six adult dogs, at rates required to achieve serum GABA levels within one order of magnitude of those observed in humans with cirrhosis, resulted in a 17.0 +/- 4.3 mm Hg decrease in systolic pressure (p less than 0.05) and a 10.8 +/- 3.7 mm Hg decrease in diastolic pressure (p less than 0.05). Control amino acids were not vasoactive. The results of this study suggest that, in addition to other vasoactive compounds, a GABA-mediated process might contribute to the hypotension observed in patients with compensated cirrhosis.     

急性心肌梗死患者血气变化及酸碱失衡分析

目的：探讨急性心肌梗死（AMI）患者的酸碱失衡类型及临床意义。方法：回顾性分析134例AMI患者动脉血气参数（pH、PaO2、PaCO2、HCO3^-）、酸碱失衡类型和电解质资料。结果：134例患者动脉血氧分压（PaO2）〈80mmHg者72例（53％）;发生不同类型酸碱失衡113例（84％）,最常见是呼吸性碱中毒并代谢性酸中毒（呼碱代酸）,有24例（18％）,其次为呼吸性酸中毒并代谢性酸中毒（呼酸代酸）、单纯性呼碱、单纯性代酸等,单纯性酸碱失衡43例（32％）,二重性酸碱失衡64例（48％）,三重性酸碱失衡（TABD）6例（4％）。结论：AMI患者常发生低氧血症和酸碱失衡,伴有心源性休克时容易伴有代酸;严重代谢性酸中毒合并呼酸是病情严重的标志。     

Octreotide inhibits hepatic fibrosis,bile duct proliferation and bacterial translocation in obstructive jaundice

BACKGROUND/AIMS: The protective effect of octreotide on bacterial translocation, bile duct epithelial proliferation and hepatic fibrosis was studied in an experimental obstructive jaundice model. METHODOLOGY: Forty-five healthy Wistar albino rats were randomly divided into three groups. Group I (n = 15): Median laparotomy and common bile duct manipulation performed (Sham group). Group II (n = 15): Laparotomy and common bile duct ligation performed. Group III (n = 15): After laparotomy and common bile duct ligation octreotide (Sandostatin, sandoz) was given. Simultaneously group I and II received 3 cc 0.9% NaCl and group III received 20 micrograms/kg/daily octreotide subcutaneously every 8 hours during 9 days. Two days after the procedure all rats were opened under ether anesthesia and sterile conditions. Group I had simple laparotomy but group II and III also had common bile duct ligation by 5/0 prolene. Seven days after the surgery (9th day after treatment) all rats underwent laparotomy and tests for bacterial translocation, liver biochemical tests and histopathologic analysis of liver and small bowel were carried out. RESULTS: In group II cecal population levels of bacteria were significantly higher than group I and group III (p < 0.05). In group II there was also statistically significant bacterial translocation to the mesenteric lymph nodes. Pathological changes were found in terminal ileum samples in group II which seemed to improve in group III. Hepatocyte function was preserved with octreotide treatment which also significantly decreased bile duct proliferation and periportal fibrosis in response to biliary obstruction. CONCLUSIONS: This experimental study showed that octreotide is effective in preventing bacterial translocation, bile duct proliferation and hepatic fibrosis in obstructive jaundice.     

老年肺心病并发多器官功能不全综合征71例临床分析

目的探讨老年多器官功能不全综合征(MODSE)与电解质、血气分析及病死率的关系。方法分析71例老年肺心病合并MODSE的临床资料,将其分成衰竭前期组与衰竭期组,对其肺、心、肾、脑、肝等多器官功能进行评价,对其电解质、血气分析进行统计,并分析诱因构成。结果感染是MODSE的主要诱因,衰竭期组低钠血症、呼吸性酸中毒合并代谢性酸中毒、呼吸性酸中毒合并代谢性碱中毒的发生率以及2个器官功能不全病死率显著高于衰竭前期组;MODSE病死率随器官功能不全数目增多而增加。结论重视MODSE的早期预警和干预,重视MODSE的肺启动作用,可防止MODSE的发生;重视MODSE衰竭前期救治,减少功能不全器官数,才能降低病死率、改善预后。     

Acid-base disturbances in acute asthma

The clinical features, arterial blood gases, and acid-base profile were examined in 229 consecutive episodes of acute asthma in 170 patients who required hospitalization. A simple respiratory alkalosis was the most common acid-base disturbance, occurring in 48 percent of the episodes. Metabolic acidosis, either alone or as part of a mixed disturbance, was noted in 28 percent. Of 60 episodes presenting with respiratory acidosis, 37 (62 percent) had a coexistent metabolic acidosis. Metabolic acidosis was more likely to occur in male subjects and in patients with evidence of more severe airflow obstruction. Patients with metabolic acidosis had an average anion gap of 15.8 mEq/L; these patients were more hypoxemic than those without metabolic acidosis and there was a significant inverse correlation between the anion gap and the degree of hypoxemia. We conclude that metabolic acidosis is a common finding in acute, severe asthma and suggest that the pathogenesis of lactic acidosis is multifactorial and includes contributions from lactate production by respiratory muscles, tissue hypoxia, and intracellular alkalosis.     

A prospective randomized trial comparing somatostatin, balloon tamponade and the combination of both methods in the management of acute variceal haemorrhage.

The aim of this study was to compare the efficacy of: (i) somatostatin infusion, (ii) balloon tamponade with the Sengstaken-Blakemore tube and (iii) the combination of both methods, in the management of acute variceal haemorrhage. Ninety-two consecutive patients with liver cirrhosis who proved to have active variceal bleeding on emergency endoscopy were studied. Thirty-one patients were randomly assigned to an intravenous infusion of 250 micrograms/h of somatostatin (Group I), 30 to the Sengstaken-Blakemore tube (Group II) and 31 to the combination of both methods (Group III). Somatostatin was administered for 24 h, while the gastric and esophageal balloons remained inflated for 48 and 24 h, respectively, then deflated. Patients were under observation for a further 24-h period after withdrawal of treatment. If bleeding recurred, the same treatment was repeated in each group. Following treatment the bleeding was controlled initially in 22 patients (71%) in Group I, in 24 (80%) in Group II and in 25 (80.6%) in Group III. In Group II a significantly (p less than 0.05) higher proportion of patients (14/24) rebled as compared to Groups I (5/22) and III (6/25). Bleeding was controlled following retreatment in four, ten and five patients of the three respective groups. There were marked differences, in the number of complications noticed with each form of therapy. Only three patients (9.7%) in Group I developed complications (p less than 0.05) as compared to ten (33%) in Group II and ten (32%) in Group III. Hospital mortality in all three treatment groups was not significantly different.(ABSTRACT TRUNCATED AT 250 WORDS)     

Equilibrium of acidifying and alkalinizing metabolic acid-base disorders in cirrhosis.

BACKGROUND AND AIMS: Conflicting results exist with regard to metabolic acid-base status in liver cirrhosis, when the classic concept of acid-base analysis is applied. The influence of the common disturbances of water, electrolytes and albumin on acid-base status in cirrhosis has not been studied. The aim of this study was to clarify acid-base status in cirrhotic patients by analyzing all parameters with possible impact on acid-base equilibrium. PATIENTS AND METHODS: Fifty stable cirrhotic patients admitted to a university hospital. Arterial acid-base status was analyzed using the principles of physical chemistry and compared with 10 healthy controls. RESULTS: Apart from mild hypoalbuminemic alkalosis, acid-base state was normal in Child-Pugh A cirrhosis. Respiratory alkalosis was the net acid-base disorder in Child-Pugh B and C cirrhosis with a normal overall metabolic acid-base state (Base excess-1.0 (-3.6 to 1.6) vs 1.1 (-0.2 to 1.1) mmol/l, P = 0.136, compared with healthy controls, median (interquartile range)). Absence of an apparent metabolic acid-base disorder was based on an equilibrium of hypoalbuminemic alkalosis and of dilutional acidosis and hyperchloremic acidosis. CONCLUSION: A balance of offsetting acidifying and alkalinizing metabolic acid-base disorders leaves the net metabolic acid-base status unchanged in cirrhosis.     

Blood gas analysis and acid-base balance in acute myocardial infarction. Personal observations (author's transl)].

Arterial pH, pO2 and pCO2 were analysed with Astup's micromethod on one hundred and three acute myocardial infarctions (A.M.I.) without metabolic, pulmonary and renal diseases. Following the clinical picute, the patients were divided into five groups and results were clinically and statistically evaluated (mean, standard deviation, Student's test "t", correlation coefficient "r" between pO2 and pulmonary arterial diastolic pressure): --Ist group (A.M.I. without complications): only mild hypoxemia; --IInd group (A.M.I. with slight left ventricular failure): more remarkable hypoxemia and hypocapnia, often with respiratory alkalosis; --IIIrd group (A.M.I. complicated by acute pulmonary oedema): mixed acidosis and severe hypoxemia; --IVth group (A.M.I. complicated by shock): prevailing metabolic acidosis and severe hypoxemia. Acidosis shows good correlations with the clinical picture; --Vth group (A.M.I. with serious arrhythmias): mixed and profound acidosis and important hypoxemia during ventricular fibrillation and cardiac arrest. In twenty patients hypoxemia and arterial pulmonary diastolic pressure showed a significant correlation.     

Prolonged and fractionated right atrial electrograms during sinus rhythm in patients with paroxysmal atrial fibrillation and sick sinus node syndrome

Intraatrial catheter mapping of the right atrium was performed during sinus rhythm in 92 patients: Group I = 43 control patients without paroxysmal atrial fibrillation or sick sinus node syndrome; Group II = 31 patients with paroxysmal atrial fibrillation but without sick sinus node syndrome; and Group III = 18 patients with both paroxysmal atrial fibrillation and sick sinus node syndrome. Atrial electrograms were recorded at 12 sites in the right atrium. The duration and number of fragmented deflections of the atrial electrograms were quantitatively measured. The mean duration and number of fragmented deflections of the 516 atrial electrograms in Group I were 74 +/- 11 ms and 3.9 +/- 1.3, respectively. The criteria for an abnormal atrial electrogram were defined as a duration of greater than or equal to 100 ms or eight or more fragmented deflections, or both. Abnormal atrial electrograms were observed in 10 patients (23.3%) in Group I, 21 patients (67.7%) in Group II and 15 patients (83.3%) in Group III (Group II versus Group I, p less than 0.001; Group III versus Group I, p less than 0.001). The mean number of abnormal electrograms per patient with an abnormal electrogram was 1.3 +/- 0.7 in Group I, 2.5 +/- 1.9 in Group II and 3.5 +/- 2.5 in Group III (Group I versus Group II, p less than 0.01; Group II versus Group III, p less than 0.05). A prolonged and fractionated atrial electrogram characteristic of paroxysmal atrial fibrillation can be closely related to the vulnerability of the atrial muscle.(ABSTRACT TRUNCATED AT 250 WORDS)     

Metabolic acidosis in severe acute asthma. Effect of alkaline therapy]

Respiratory acidosis of severe acute asthma is a severity factor. In this paper the treatment of associated metabolic acidosis is discussed. Among 34 consecutive episodes of severe acute asthma with acidosis (pH < 7.35) treated with continuous adrenaline perfusion, theophylline and hydrocortisone hemisuccinate, respiratory acidosis was observed in 12, metabolic acidosis in 2 and mixed respiratory and metabolic acidosis in 20. The association of hypercapnic acidosis with hypochloraemic acidosis reflected a time of installation longer than when respiratory acidosis only was present (p < 0.05). Among the 22 patients who had metabolic acidosis on admission, 14 were treated with 168 +/- 82 mmol of sodium bicarbonate, the remaining 8 patients being untreated and acting as controls. The rapidity with which pH was corrected was the same in the treated and untreated groups (9.1 +/- 5.5 hours vs 6.7 +/- 3.7 hours), whereas dyspnoea (respiratory rate < 18/min) was more rapidly corrected in the treated group that in controls (11.6 +/- 5.7 hours vs 5.9 +/- 5.9 hours; p < 0.05). It is concluded that in more than 50% of the cases respiratory acidosis of severe acute asthma is associated with a metabolic acidosis. Correcting this metabolic acidosis with sodium bicarbonate results in improvement of respiration, perhaps by facilitating the action of bronchodilator catecholamines.     

Angiographic correlates of anterior ST segment depression in acute inferior wall myocardial infarction.

This study was conducted prospectively to assess the correlation between the pattern of anterior ST segment depression on the admission electrocardiogram and the in-hospital morbidity and mortality in patients with acute inferior wall myocardial infarction. Coronary angiography was also done to assess its correlation, if any, with pattern of anterior ST segment depression. Our study cohort comprised of 165 consecutive patients with acute inferior wall myocardial infarction divided into four groups based on admission electrocardiogram. Group I (n = 33): patients with no anterior ST segment depression; group II (n = 16): patients with ST segment depression in leads V1-V3; group III (n = 71): patients with ST segment depression in leads V4-V6, I and aVF, and; group IV (n = 45): patients with ST segment depression in all anterior leads (V1-V6, I, aVL). The outcomes were analysed in terms of high grade atrioventricular block, Killip class II or higher failure, and in-hospital mortality. Coronary angiography was performed to analyse coronary anatomy. Group IV patients had increased incidence of complete heart block (37.8% vs 15.2% in the total group) (p < 0.001) and increased mortality (11.1% vs 4.2% in the total group) (p < 0.05). This group also had greater incidence of triple vessel disease (76.7%) (p < 0.001). Group II patients had greater incidence of double vessel disease (88.9%) (p < 0.05) and had no triple vessel disease. Group III patients had double vessel disease (76.5%) (p < 0.05) or triple vessel disease (23.5%) (p = NS) and no single vessel disease. Coronary angiography in group II showed greater incidence of involvement of left circumflex artery and right coronary artery while in group III there was left anterior descending artery and right coronary artery disease. We conclude that patients with anterior ST segment depression in group III and group IV categories are in high risk subset with acute inferior wall myocardial infarction.