Sodium bicarbonate in cardiac arrest: A reappraisal

Vukmir, Rade B.; Bircher, Nicholas G.; Šafář, Peter

doi:10.1016/s0735-6757(96)90133-3

Cited by 38 publications

(20 citation statements)

References 144 publications

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“…Second, buffering of HCA toward arbitrary pH goals is a controversial but common practice (17,18). Aside from the controversy surrounding the systemic effects of this practice (19,20), the pulmonary effects, in terms of ALI, have not been defined.…”

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confidence: 99%

Buffering Hypercapnic Acidosis Worsens Acute Lung Injury

Laffey

Engelberts

Kavanagh

2000

Am J Respir Crit Care Med

196

115

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Hypoventilation, associated with hypercapnic acidosis (HCA), may improve outcome in acute lung injury (ALI). We have recently reported that HCA per se protects against ALI. The current study explored whether the mechanisms of protection with HCA were related to acidosis versus hypercapnia. Because CO(2) equilibrates rapidly across cell membranes, we hypothesized that (1) HCA would afford greater protection than metabolic acidosis. We further hypothesized that (2) buffering HCA would attenuate its protection. Forty isolated perfused rabbit lung preparations were randomized to: control (normal pH, PCO(2)); HCA; metabolic acidosis; or buffered hypercapnia. After ischemia-reperfusion (IR) injury wet:dry ratio was greatest with control and buffered hypercapnia, and rank order of capillary filtration coefficient was: control approximately buffered hypercapnia > metabolic acidosis > HCA. Isogravimetric pressure reduction was greatest with buffered hypercapnia. Despite comparable injury, pulmonary artery pressure elevation was less with buffered hypercapnia versus control. In vitro xanthine oxidase (XO) activity depended on pH, not PCO(2). We conclude that: (1) HCA and metabolic acidosis are protective, but HCA is the most protective; (2) buffering HCA attenuates its protection; (3) buffering HCA causes pulmonary vasodilation; (4) because metabolic acidosis and HCA similarly inhibit in vitro XO activity, the differential effects cannot be explained solely on the basis of extracellular XO activity.

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mentioning

confidence: 99%

Buffering Hypercapnic Acidosis Worsens Acute Lung Injury

Laffey

Engelberts

Kavanagh

2000

Am J Respir Crit Care Med

196

115

View full text Add to dashboard Cite

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“…The present dose of atropine (1 mg/kg) may not completely intercept the vagal activation, but mechanisms other than baroreflex activation during hypercapnia might also contribute to a reduction in HR. Hypercapnia or acidosis may directly decrease HR (19,34).…”

Section: Discussionmentioning

confidence: 99%

Transient hypercapnic stress causes exaggerated and prolonged elevation of cardiac and renal interstitial norepinephrine levels in conscious hypertensive rats

Sobajima

Nozawa

Nakadate

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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The responses of sympathetic nerve activity to transient stress can be exaggerated in salt-sensitive (SS), hypertensive subjects. Cardiac and renal interstitial norepinephrine (iNE) levels during and after transient hypercapnia were investigated in conscious SS rats. Dahl SS and salt-resistant (SR) 6-wk-old rats were fed a high-salt diet, and at 12 wk iNE levels in the heart and kidney were determined using microdialysis with probes inserted in the left ventricular (LV) wall and kidney. A telemetry system determined blood pressure and heart rate (HR) in separate animals. After recovery from the operation, data were collected before, during, and after exposure to normoxic 10% CO 2 for 25 min under unanesthetized conditions. The plasma NE concentrations at baseline did not differ between the two strains. Both cardiac and renal iNE levels were much higher in SS rats than in SR rats at baseline as well as during hypercapnic stress. After stress, the markedly increased iNE levels of SS rats were prolonged in the LV as well as in the kidney. During hypercapnic stress, HR decreased in both SS and SR rats, while sudden increases in HR immediately after the withdrawal from stress were followed by its slower reduction in SS rats compared with SR rats. In conclusion, transient hypercapnic stress causes exaggerated and prolonged elevation of iNE levels in the heart as well as in kidneys of SS animals. salt-sensitive; interstitial norepinephrine; hypercapnia CENTRAL SYMPATHOEXCITATION and renal fluid retention may be involved in the development of salt-sensitive (SS) hypertension. Transient environmental or mental stress in SS animals and subjects causes a greater increase in blood pressure (BP) and renal sympathetic nerve (SN) activity and greater antinatriuresis compared with salt-resistant (SR) animals and subjects (2,3,9,16). Hypertension is also accompanied by increased chemoreflex sensitivity (29, 33) and, therefore, hypoxic and/or hypercapnic stress could augment SN activity in SS hypertensive subjects complicated by sleep apnea syndrome. Thus, the enhanced SN responsiveness to stress may play a role in the high morbidity or mortality of SS hypertensive subjects. However, it remains unclear whether the augmented response of renal SN activity to transient stress occurs in parallel to the response in other organs, especially in the heart, because it is difficult to directly determine cardiac SN activity in conscious animals. Kamiya et al. (11) reported that muscle SN activity parallels the renal and cardiac SN activity in response to baroreceptor pressure changes in anesthetized rabbits. In contrast, others have reported that central or peripheral stimuli cause selective and differential influences on the SN activity of each organ in anesthetized and conscious animals (13,36,37).Previous studies have shown that cardiovascular recovery from stress plays an important role in the pathogenesis of hypertension and is a predictor of overall mortality (1, 5). Sustained increases in SN activity after transient stress may accel...

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“…35 No high-quality evidence supports the efficacy of sodium bicarbonate or calcium chloride for patients with cardiac arrest, and bicarbonate therapy may have adverse effects on acid-base balance, electrolyte levels, cardiac function, and cellular metabolism. [37][38][39] Anecdotally, calcium and bicarbonate administration may transiently stabilize hemodynamics in refractory shock or prolonged cardiac arrest, but only as a temporizing measure. 37,57 Glover et al 58 did not show improved outcomes with any ACLS medication; increased use of epinephrine, atropine, and sodium bicarbonate was associated with a decreased likelihood of hospital survival.…”

Section: Interventionsmentioning

confidence: 99%