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PubMed1980

Thiopeptin for the prevention of ovine lactic acidosis induced by diet change.

Inclusion of thiopeptin, a sulfur-containing peptide antibiotic, at 0, 2.75, 5.5, 8.25, 11 and 22 ppm in the feed was evaluated in 8-week growth trials with 252 lambs. An abrupt diet shift to micronized milo at the start of the trials was used to provide a lactic acidosis challenge. Five of 78 control lambs died within 48 hr after the challenge. In lambs fed diets containing thiopeptin at levels of 11 ppm or more, there was no evidence of lactic acidosis. Lambs given thiopeptin at 11 ppm or more ate 11% more (P less than .05) and gained 20% more (P less than .05) than controls during the 8-week trial. Most of the improvement occurred during the first 2 weeks. Incidence of death was lower among lambs given thiopeptin at 2.75 to 8.25 ppm, but these animals showed no improvement in performance. In another study, abruptly shifting lambs to the micronized milo diet was found to provide an acute lactic acidosis challenge. After the shift, four of eight lambs developed ruminal lactic acidosis, with one dying of systemic lactic acidosis, with one dying of systemic lactic acidosis when plasma lactate exceeded 20 mumoles/ml. In affected lambs, ruminal lactate increased rapidly from an initial level of .2 mumoles/ml to over 130 mumoles/ml within 12 hr of consumption of the milo. Ruminal lactate returned to normal levels of less than 1 mumole/ml by 30 hr in lambs that recovered. High ruminal concentrations of lactate reduced total volatile fatty acids (VFA), and ruminal pH reflected total ruminal acids. Lactic acidosis did not occur in eight lambs after the switch to micronized milo when thiopeptin was included in the feed at 22 ppm. Ruminal lactate was reduced by 68% (P less than .01) and total ruminal VFA increased by 33% (P less than .05) in lambs fed thiopeptin in comparison with average levels in all controls.

Acidosis↗
PubMed1981

Prevention of lactic acidosis in cattle by lasalocid or monensin.

Intraruminal administration of lasalocid or monensin (1.3 mg/kg body weight) effectively prevented in glucose- or corn-induced lactic acidosis in cattle. Administering the antibiotics for 7 days before experimentally inducing acidosis with corn (27.5 g/kg body weight), effectively prevented acidosis, while 2 days' were sufficient to prevent glucose-induced acidosis (12.5 g/kg body weight). The different responses observed in the two trials probably stemmed from the difference in amounts of carbohydrate used to induce acidosis. Antibiotic-treated cattle had higher rumen pH values and lower L(+) and D(-) lactate concentrations that control cattle that received no antibiotics. Ruminal VFA in control cattle decreased, while total VFA and the molar proportion of propionate increased in antibiotic-treated cattle after grain engorgement. Control cattle exhibited classic signs of acidosis, such as lowered blood pH; increased blood lactate, particularly D(-) isomer; hemoconcentration, and depleted alkali reserve with a pronounced based deficit. Antibiotic-treated cattle exhibited no signs of systemic acidosis.

Acidosis↗
PubMed1990

Effect of diseases, production, and season on traumatic reticuloperitonitis and ruminal acidosis in dairy cattle.

Logistic regression was used to investigate the effects of host characteristics, production, and 23 veterinary diagnoses on the risks of two reticuloruminal disorders, ruminal acidosis and traumatic reticuloperitonitis among 61,124 Finnish Ayrshire cows. Lactational incidence risks were .3% for ruminal acidosis and .6% for traumatic reticuloperitonitis. The relative risk of ruminal acidosis was not related to parity, whereas the risk of traumatic reticuloperitonitis decreased with increasing parity. The risk of traumatic reticuloperitonitis was not related to milk yield of individual affected cows in their current or previous lactation (305-d, 4% FCM), whereas the risk of ruminal acidosis increased with current milk yield. Ketosis, early metritis, nonparturient paresis, and acute and chronic mastitis were risk factors for both reticuloruminal disorders. Parturient paresis was a risk factor for ruminal acidosis. Foot and leg problems were risk factors for traumatic reticuloperitonitis. Herd milk yield in the current or previous lactations was not a risk factor for either disorder nor were the two disorders risk factors for each other. Ruminal acidosis, but not traumatic reticuloperitonitis, had significant seasonal variation with the risk being least in summer. The low risk of ruminal acidosis in summer was not due to seasonality of calving.

Acidosis↗
PubMed1986

Lactic acidosis in pheochromocytoma.

Lactic acidosis is not generally recognized as a complication of pheochromocytoma. We review three prior case reports of lactic acidosis in patients with pheochromocytoma and one report of lactic acidosis following epinephrine poisoning and describe an additional case report of a patient with lactic acidosis in whom an unsuspected pheochromocytoma was discovered at autopsy. The pathophysiology of lactic acidosis in pheochromocytoma is related to the effect of catecholamines on intermediary metabolism and the peripheral circulation. Although the possible development of lactic acidosis in persons with pheochromocytoma is underappreciated, the differential diagnosis of lactic acidosis should include this tumor.

Acidosis, Lactic↗
PubMed2003

[Nephrogenic metabolic acidosis].

Metabolic acidosis is a major risk factor of kidney disease progression as a consequence of impaired H+ urinary excretion by the decreased kidney NH3 synthesis. Two key enzymes participate: a) Phosphate-dependent glutaminase under the genomic control of metabolic acidosis and b) Phosphate independent glutaminase localized on proximal tubule microvili under the nongenomic control. Two types of kidney disease metabolic acidoses are dominant: a) Hyperchloremic metabolic acidosis usually on the basis of hereditary or toxic alterations, isolated or as a part of Fanconi syndrome. b) Hyperphosphatemic metabolic acidosis of renal insufficiency. Metabolic acidosis shares serious consequences: metabolic acidosis increases protein catabolism of amino acids, inhibits proteosynthesis (albumin!), accelerates renal osteodystrophy development, modulates calcidiol and parathormone plasma levels and evokes insulin resistance. The present therapy requires full correction of metabolic acidosis!

Acidosis, Renal Tubular↗
PubMed1992

Metabolic acidosis accelerates whole body protein degradation and leucine oxidation by a glucocorticoid-dependent mechanism.

Previous work documented an acceleration of proteolysis and branched-chain amino acid oxidation when muscles from rats with chronic metabolic acidosis were incubated in vitro. The present study examines the impact of chronic metabolic acidosis on whole body amino acid turnover and oxidation in chronically catheterized, awake, male Sprague-Dawley rats using stochastic modeling and a primed continuous infusion of L[1-14C] leucine. Whole body protein turnover was accelerated by acidosis as reflected in a 70% increase in proteolysis and a 55% increase in protein synthesis. Amino acid oxidation was increased by 145% in rats with acidosis relative to control rats receiving diets identical in protein and calories based on a reciprocal pool model and plasma alpha-ketoisocaproate specific radioactivity. These changes were accompanied by a 104% increase in liver branched-chain ketoacid dehydrogenase (BCKAD) activity in rats with acidosis, similar to previously documented increases in skeletal muscle BCKAD activity caused by acidosis. In contrast, kidney BCKAD activity was decreased by 38%, illustrating the tissue specificity of the changes that were present. We conclude that chronic metabolic acidosis accelerates whole body protein turnover and reduces the efficiency of protein utilization by accelerating amino acid oxidation. These changes may require an intact glucocorticoid axis.

Acidosis↗
PubMed1991

[Distal tubular acidosis. Recent data].

Tubular acidosis is diagnosed when hyperchloremic acidosis is associated with inappropriate NH4 excretion (less than or equal to 40 mmol/24 hours). Urinary pH is variable because it depends on the secretion of H+ into the collecting duct and is inversely correlated with the amount of ammonia available in the urine. Administration of NaHCO3 for diagnostic purpose allows to eliminate proximal tubular acidosis and to measure the elevation of urinary PCO2 reflecting the secretion of H+ in the collecting duct. Hypokalemia points towards distal tubular acidosis, either by defect of H(+)-ATPases pumps, or by the incapacity to create a normal gradient of H+. In contrast hyperkalemia suggests distal tubular acidosis associated either with hypoaldosteronism or with diminution of trans-epithelial voltage or with pseudohypoaldosteronism. The incidence of distal tubular acidosis with hyperkalemia is increasing whereas distal tubular acidosis with hypokalemia remain rare.

Acidosis, Renal Tubular↗
PubMed1987

Hyperlactataemia and metabolic acidosis following paracetamol overdose.

Plasma lactate concentrations and acid-base status were determined in 53 patients poisoned with paracetamol. Eleven patients (Group 1) had plasma paracetamol concentrations below the standard treatment decision line; 19 cases (Group 2) presenting within 15 h of overdose had plasma paracetamol concentrations above the treatment line and received N-acetylcysteine. The remaining 23 patients (Group 3) arrived at hospital too late (more than 15 h after overdose) for treatment with N-acetylcysteine to be completely effective. Compensated metabolic acidosis was present on admission in 55 per cent of Group 1 and 42 per cent of Group 2 patients, and a further 21 per cent of cases in Group 2 had an uncompensated metabolic acidosis. Half the patients in Group 3 were acidotic: 22 per cent had a compensated and 26 per cent an uncompensated metabolic acidosis. On admission, the mean plasma lactate concentration was elevated in both Group 2 and Group 3 patients though not in Group 1 cases. Plasma lactate concentration then fell to normal in patients in Group 2 but became mildly elevated again in some cases at a time which coincided closely with the peak in serum aspartate aminotransferase activity. In patients presenting within 15 h of overdose there was a significant correlation between the elevation in plasma concentrations of lactate and paracetamol at admission. In patients presenting late (Group 3), plasma lactate remained elevated for longer than in Group 2 and acidosis and hyperlactataemia were prominent features in the four patients who died. This study demonstrates first that hyperlactataemia, with or without significant acid-base disturbance, is common following paracetamol overdose particularly in those who are severely poisoned. As uncompensated metabolic acidosis is found in 20 per cent of patients who present early and require protective therapy, it should be sought and corrected if it does not remit spontaneously. Second, half the patients presenting too late for effective treatment are acidotic and those with an uncompensated metabolic acidosis resistant to correction have a poor prognosis. Paracetamol poisoning should be considered in the differential diagnosis of metabolic acidosis of unknown aetiology.

Acetaminophen↗
PubMed1985

Effects of dopamine and dobutamine on hemodynamics and plasma catecholamine levels during severe lactic acid acidosis.

This study was designed to evaluate the effects of dopamine and dobutamine on hemodynamics and plasma catecholamine levels during experimental lactic acid acidosis in dogs. During the normal acid-base state (pH 7.4, PCO2 40 mm Hg), cardiac output and stroke volume were significantly increased and systemic vascular resistance was decreased by the infusion of dopamine or dobutamine 20 mcg/kg/min. Dobutamine produced identical changes in cardiac output, stroke volume, and systemic vascular resistance even during severe lactic acid acidosis (pH 7.0, PCO2 40 mm Hg). Dopamine, however, failed to increase cardiac output and stroke volume and to decrease systemic vascular resistance during lactic acidosis. The plasma norepinephrine level was elevated from 0.49 to 3.01 ng/ml during normal acid-based state and from 1.76 to 9.53 ng/ml during severe lactic acid acidosis by the infusion of dopamine. Dobutamine infusion did not affect the plasma norepinephrine level during normal acid-base state but reduced the level during lactic acid acidosis. The marked increase in plasma norepinephrine following dopamine infusion may explain both the decrease in cardiac output and the increase in systemic vascular resistance in response to dopamine infusion during severe lactic acid acidosis. These results indicate that dobutamine may be more useful than dopamine in improving cardiac output during severe acidosis.

Acid-Base Equilibrium↗
PubMed1984

Amelioration of metabolic acidosis by dietary potassium restriction in hyperkalemic patients with chronic renal insufficiency.

Hyperkalemia has been implicated in the pathogenesis of metabolic acidosis in chronic renal insufficiency because acidosis is ameliorated after administration of medications that correct hyperkalemia: mineralocorticoids, diuretics, intestinal K+-binding agents. However, the acidosis-ameliorating effect of these medications may be a consequence not of their ability to correct hyperkalemia, but of their ability to directly stimulate renal or intestinal excretion of acid. To investigate the specific effect of correcting hyperkalemia, balance studies were performed wherein hyperkalemia was corrected solely by restriction of dietary K+ in three patients with moderate chronic renal insufficiency (Ccreat 36, 44, and 58 ml/min/1.73 m2, respectively). Reduction of K+ intake was effected by substitution of Na+ for K+ in the electrolyte supplement to a whole-food diet of low K+ content. This maneuver resulted in correction of hyperkalemia and sustained amelioration of metabolic acidosis in each patient. Net acid excretion increased only transiently, and not enough to fully account for the magnitude of the increment in plasma [HCO3-], suggesting that an extrarenal mechanism of HCO3- input to the systemic circulation was the major factor that ameliorated the systemic acidosis. Evidence of an extrarenal mechanism was obtained only during the phase of decreasing plasma [K+]. Subsequently, during sustained normokalemia, the increased plasma [HCO3-] was maintained as a consequence of a sustained increase in total renal H+ secretion, evidenced by complete reabsorption of the increased filtered load of HCO3- and no reduction in net acid excretion from control values. These results indicate that in some patients with moderate chronic renal insufficiency, metabolic acidosis is ameliorated when hyperkalemia is corrected by restriction of dietary K+ (Na+ substitution) without otherwise changing diet composition and without administration of medication. Amelioration of the acidosis is predominantly effected by extrarenal mechanisms, and is sustained by an increase in the set point at which plasma [HCO3-] is regulated by the kidney.

Acidosis, Renal Tubular↗
PubMed1984

Hypochloremia as a consequence of anion gap metabolic acidosis.

Anion gap acidosis is generally regarded as featuring a rather precise balance between the decrement in plasma HCO-3 and the increment in anion gap plasma Cl- remaining normal. In theory, therefore, the finding of hypochloremia in conjunction with an anion gap acidosis should evidence a coexisting metabolic alkalosis. In the clinical setting, however, hypochloremia is occasionally found in patients with anion gap acidosis but without exposure to a recognized alkalosis-inducing process. To examine the possibility that an element of hypochloremia might, under certain circumstances, be an integral part of the underlying acidosis, we studied three forms of anion gap acidosis in unanesthetized, nephrectomized rats. In protocol I, 7 mEq/kg H+ as H2SO4 was infused over 1 hour. In protocol II, 24 mEq/kg H+ as D,L-lactic acid was infused over 3 hours. In protocol III, rats were maintained in the anephric state for approximately 28 hours to permit uremic acidosis to develop. In each protocol, plasma C1- fell significantly (-8.0, -12.0, and -7.0 mEq/L in protocols I, II, and III, respectively) and contributed substantially to the observed increment in anion gap. A possible explanation for this acidosis-induced hypochloremia is expansion of the extracellular compartment secondary to the extrusion of cellular cation that occurs in the process of buffering.

Acidosis↗
PubMed1984

Effect of furosemide on urinary acidification in distal renal tubular acidosis.

Furosemide stimulates urinary acidification in normal humans probably by increasing distal Na delivery and transport, thus creating a favorable electric gradient for H+ and K secretion. Therefore, furosemide should stimulate urinary acidification in patients with distal renal tubular acidosis, provided the distal nephron is capable of transporting Na and the H+ pumps can respond to the favorable electric gradient. We examined the effect of short-term furosemide administration on urinary acidification in five normal participants and 12 patients with normokalemic, hypokalemic, or hyperkalemic distal renal tubular acidosis. In controls, furosemide decreased urine pH and increased net acid and K excretion. In six of eight patients with normokalemic or hypokalemic renal tubular acidosis, furosemide decreased urine pH and increased net acid and K excretion to levels not significantly different from control values. The patients that had normal responses were interpreted as having a rate-dependent or gradient distal renal tubular acidosis, and thus increased distal Na delivery created a favorable electric gradient for H+ and K secretion. The normokalemic patients who did not have a response were considered to have a defect in the pumps (secretory defect). Of the four hyperkalemic patients, two had a voltage-dependent defect and the other two had aldosterone deficiency. The patients with selective aldosterone deficiency had low baseline urine pH values that did not change with furosemide administration, but net acid and K excretion did increase significantly. The patients with voltage-dependent defect did not lower urine pH or increase net acid and K excretion. Our data demonstrate that administration of furosemide enhances urinary acidification in certain patients with distal renal tubular acidosis. We suggest that furosemide administration may be useful in the characterization of the mechanism responsible for distal renal tubular acidosis and in the treatment of distal renal tubular acidosis in selected patients.

Acidosis, Renal Tubular↗
PubMed1980

Pathophysiology of chronic renal tubular acidosis induced by administration of amiloride.

Amiloride is a "potassium-sparing" diuretic agent of moderate natriuretic potency with site of action in postmacula densa segments of the distal nephron. In isolated segments of mammalian cortical distal nephron, amiloride diminishes sodium reabsorption and transtubular electrical PD and inhibits potassium secretion. We investigated the effects of long-term administration of a demonstrably maximal dose of amiloride (1.0 mg/kg b.i.d.) on plasma and urine acid-base and electrolyte composition in fixed steroid-replaced ADX dogs. Amiloride administration resulted in potassium retention and hyperkalemia and reduced net acid excretion and caused chronic hyperchloremic metabolic acidosis. The cumulative reduction in net acid excretion and severity of systemic acidosis were not significantly different in additional groups in which potassium retention was prevented by restriction of dietary potassium during amiloride administration or in which amiloride was administered to animals with pre-existing dietary potassium depletion. The response of urine pH and ammonium excretion, however, differed among groups. In the steady state of chronic acidosis, urine pH and ammonium concentration were lowest in the hyperkalemic group and highest in the hypokalemic group, and among the three groups pH and ammonium were positively correlated (r = 0.67, p less than 0.001). Ammonium concentration varied inversely with plasma potassium concentration. Net acid excretion rates returned to control levels during the steady state of chronic amiloride-induced acidosis in the three groups. During continued amiloride administration, sustained correction of acidosis by long-term oral administration of sodium bicarbonate did not result in negative values of net acid excretion; that is, amiloride did not cause net wasting of base at normal plasma bicarbonate concentration. The results of these studies suggest that chronic amiloride administration results in a sustained impairment of renal hydrogen ion secretion restricted to the distal nephron and not dependent on alterations in potassium balance. Differences in potassium balance (positive or negative) appeared to influence only the availability of ammonia for diffusion into urine and steady-state urine pH, but not the steady-state net rate of renal hydrogen ion secretion during amiloride. These studies identify an experimental model of chronic distal renal tubular acidosis in which external hydrogen ion balance is re-established during chronic acidosis even when the availability of ammonia for excretion is decreased.

Acidosis, Renal Tubular↗
PubMed1996

Necessary but not sufficient: the role of glucocorticoids in the acidosis-induced increase in levels of mRNAs encoding proteins of the ATP-dependent proteolytic pathway in rat muscle.

Muscle protein degradation is accelerated by the acidosis associated with chronic renal failure. In isolated muscles from acidotic rats, a cytosolic, ATP-dependent proteolytic pathway is stimulated with a concurrent increase in the abundance of mRNAs encoding ubiquitin and subunits of the 26S proteasome complex associated with this degradative pathway. Adrenalectomy (ADX) prevents the acidosis-induced increase in muscle protein degradation unless high physiologic doses of glucocorticoids are administered to acidotic, adrenalectomized rats. We have examined the roles that acidosis and glucocorticoids have in the increase in mRNAs encoding proteins of the ATP-dependent-ubiquitin-proteasome proteolytic pathway in ADX rats. We found that ubiquitin and proteasome C2 and C9 subunit mRNA levels are increased in the white fiber, extensor digitorus longus (EDL) and mixed fiber, gastrocnemius muscles from acidotic ADX rats that received dexamethasone whereas acidosis alone or dexamethasone alone failed to increase these mRNAs. In contrast, acidosis plus dexamethasone decreased the total RNA content in both muscles. These data suggest that in muscle, the response to acidosis involves the specific activation of the ATP-ubiquitin-proteasome proteolytic pathway. Moreover, glucocorticoids are required but not directly responsible for the acidosis-induced increase in the mRNAs encoding proteins of this degradative pathway.

Acidosis↗
PubMed1996

Effects of Carbicarb and sodium bicarbonate on hypoxic lactic acidosis in newborn pigs.

BACKGROUND: Use of sodium bicarbonate (NaHCO3) may result in intracellular acidosis due to the generation of CO2. Carbicarb, has been reported to be superior to sodium bicarbonate (NaHCO3) because of lesser generation of CO2. The present study was designed to investigate whether Carbicarb or NaHCO3 is superior to normal saline in the treatment of hypoxic lactic acidosis. METHODS: Hypoxia was induced by ventilation with 8% O(2) in 30 piglets with fixed ventilation. When the pH fell to < 7.2, hypoxia was reversed by placing the animals in 21% O2 (experiment 1) or 100% O(2) (experiment 2) and either saline, Carbicarb or NaHCO3 were given. Data were collected for 120 minutes after therapy. RESULTS: In both experiment 1 (severe acidosis, pH < or = 7.1) and 2 (moderate acidosis, pH < or = 7.2) use of Carbicarb and NaHCO3 increased the arterial carbon dioxide tension (pCO2) significantly (p < 0.05). With moderate acidosis: 1) use of alkalinizing agents compared to saline resulted in an initial improvement in arterial pH at 1 minute, but thereafter, the differences were not statistically significant; and 2) there were no differences in hemodynamic variables and plasma lactic acid concentration between the three groups. CONCLUSIONS: The data demonstrate that 1) both Carbicarb and NaHCO3 significantly increase arterial pCO2; and 2) use of either alkalinizing agent in moderate acidosis does not alter the course of acidosis.

Acid-Base Equilibrium↗
PubMed1996

[The effect of subclinical and acute ante partum acidosis in cows on the course of pregnancy with regard to the steroid hormone profile].

Experiment 1: In a field experiment in 19 of 87 cows being in day 260-265 of pregnancy subclinical metabolic acidosis was found. The control group included 10 healthy cows in the same stage of pregnancy. Blood samples from cows of both groups were collected once daily until day 2 post partum for determination of oestrogens, progesterone and cortisol. Dystocia was found in four and retained placenta in three cows having acidosis. These cows had lower oestrogens and markedly higher cortisol and progesterone concentrations during parturition. Course of pregnancy and delivery in control cows an without any difficulties and hormonal profiles in these cows were typical. Experiment 2: On day 265 of pregnancy experimental acute acidosis was evoked in five cows and five other cows served as control. Sampling of blood was the same as in experiment 1. Acidosis caused on day 269 in two cows premature birth with retained placenta. Moreover concentrations of studied steroids were atypical. In three other cows with acidosis course of pregnancy and delivery was without any trouble. Only cortisol was increased while progesterone and oestrogen values were in agreement with concentrations of control cows. Data suggest that metabolic acidosis can cause dystocia, premature birth and retained placenta. Furthermore, acidosis clearly affects the profile of steroid hormones.

Acid-Base Equilibrium↗
PubMed1997

Effect of respiratory acidosis on body movements in the chronically instrumented fetal lamb.

BACKGROUND: In respiratory acidosis, it is reported that the fetal breathing movements as well as the fetal heart rate variability increase. As the increase of these two kinds of fetal activities is occasionally observed in normal conditions, it is difficult to distinguish respiratory acidosis and normal conditions by mere observation of these activities. As the third diagnostic variable, if a different fetal body movement response to respiratory acidosis is observed, it would be helpful for better diagnosis in combination with other activities. We investigated the effect of respiratory acidosis on body movements in the chronically instrumented fetal lamb. METHODS: A total of four experiments were performed on four ewes. Respiratory acidosis was induced in the fetus by maternal administration of a high carbon dioxide gas mixture for 1 hour. Fetal body movements were observed by real-time ultrasonography. The frequency of body movements was expressed as the number of each movement in a 30-minute period. RESULTS: The mean pCO2 increased from 42.9 +/- 4.9 mmHg to 62.9 +/- 14.8 mmHg, and the mean pH decreased from 7.368 +/- 0.04 to 7.209 +/- 0.04 during the experiments. The frequency of fetal body movements significantly decreased. The percentage reduction of these movements of the same fetus during the experiments as compared to the control periods were as follows; the high-frequency movements, 89.2 +/- 9.7%; the rolling movements, 55.6 +/- 13.5%; the simple movements, 78.3 +/- 18.4%. CONCLUSIONS: Normoxemic respiratory acidosis, which is reported to increase fetal breathing movements, caused a marked reduction in fetal body movements. These findings suggest that the ultrasonographic dissociation of fetal behaviors in respiratory acidosis would be potentially helpful in the diagnosis of impending fetal jeopardy.

Acidosis, Respiratory↗
PubMed1997

[Pre-pathologic-pathologic cardiotocographic pattern in second stage of labor. Analysis of the incidence of acidosis and recommendations for fetal blood gas analysis].

Fetal heart rate (FHR) patterns from 746 consecutive, documented vaginal deliveries within a 1 year period were reported on using the Hammacher Score. Characteristic FHR patterns were described and the frequency of acidosis calculated. FHR score, the single FHR parameters, baseline (BL), floatingline (FL) and oscillation type (OT) and the acid-base balance of the neonate were submitted to a correlation analysis according to Spearman. FHR patterns reported as ominous (FHR score > or = 5) were observed in 25.9% and were associated with a frequency of acidosis (pHUA < or = 7.20) of 38.1% Suspicious fetal heart rate patterns (FHR score 3-4) were seen in 60%, here the frequency of acidosis was 8.5%. With the inclusion of decelerations by the parameter FL an increased frequency of acidosis of 29% was registered only when 4 points were allocated. Total FHR score and the score parameter baseline (BL) correlated closest with the pH changes at the end of birth. Tachycardic FHR patterns showed the highest frequency of acidosis (55%) and ominous tracings (83%). The commonest FHR pattern, normocardia with decelerations (48%) exhibited only a low frequency of acidosis (8%) and ominous tracings (15%) with an average pH value of 7.27 +/- 0.08. To prevent an unnecessary operative delivery in the presence of an ominous FHR finding, whether in the late first stage or early second stage when birth is not imminent, a fetal blood analysis should be carried out. With a suspiciously assessed fetal heart rate pattern the fetal blood analysis will only rarely reveal a severe acidosis (pHUA < or = 7.10).

Acidosis, Respiratory↗