Effect of early versus delayed activation of thoracic epidural anesthesia on plasma pro-atrial natriuretic peptide to indicate deviations in central blood volume during esophagectomy

2019 ◽  
Vol 44 (8) ◽  
pp. 787-792
Author(s):  
Rune B Strandby ◽  
Rikard Ambrus ◽  
Michael P Achiam ◽  
Jens P Goetze ◽  
Niels H Secher ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Blood Volume ◽  
Epidural Anesthesia ◽  
Fluid Balance ◽  
Thoracic Epidural Anesthesia ◽  
Central Blood Volume ◽  
Search Query ◽  
Open Esophagectomy ◽  
Thoracic Epidural

Background and ObjectivesA side effect to thoracic epidural anesthesia (TEA) is hypotension induced by central hypovolemia. This study addressed whether early activation (EA) versus late activation (LA) of TEA affects plasma pro-atrial natriuretic peptide (proANP) reflecting deviations in the central blood volume (CBV). We hypothesized that EA TEA would reduce plasma proANP, thus reflecting a decrease in CBV.MethodsA randomized, controlled, single-blinded trial was conducted. Patients undergoing open esophagectomy were randomized to EA (n=25, after induction of general anesthesia) or LA TEA (n=25, after re-established gastric continuity) with the epidural catheter placed at the interspaces Th7-8 or Th8-9. Plasma proANP was determined repetitively along with hemodynamic variables and administration of fluid/vasopressors as postoperative complications were noted.ResultsWith EA TEA, plasma proANP decreased following induction of anesthesia to the end of surgery (13%; 113±68 to 99±49 pmol/L; p=0.026), but that was not the case in the LA group (3%; 97±44 to 94±49 pmol/L; p=0.565) despite equal fluid balance (+1584±582 vs +1560±563 mL; p=0.888). Accordingly, the EA group required excessive treatment with vasopressors to maintain MAP >60 mm Hg during surgery (2.7±2 vs 1.6±1.4 ephedrine boluses; p=0.033 and infusion of phenylephrine for 216±86 vs 58±91 min; p<0.001). Plasma proANP and fluid balance were correlated only for EA patients (r=0.44; 95% CI 0.04 to 0.91; p=0.033).ConclusionsEA TEA reduces plasma proANP indicating that CBV becomes affected. Based on a correlation between plasma proANP and fluid balance, a 2000 mL volume surplus of lactated Ringer’s solution is required to maintain plasma proANP stable during open esophagectomy.Trial registration number2014-002036-14 (https://www.clinicaltrialsregister.eu/ctr-search/search?query=2014-002036-14).

Atrial natriuretic peptide reverses angiotensin-induced venoconstriction in dogs

1989 ◽  
Vol 257 (4) ◽  
pp. H1062-H1067 ◽  
Author(s):  
R. W. Lee ◽  
R. G. Gay ◽  
S. Goldman
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Blood Volume ◽  
Left Ventricular ◽  
Ang Ii ◽  
Central Blood Volume ◽  
Venous Compliance ◽  
Induced Hypertension

To determine whether atrial natriuretic peptide (ANP) can reverse angiotensin (ANG II)-induced venoconstriction, ANP was infused (0.3 micrograms.kg-1.min-1) in the presence of ANG II-induced hypertension in six ganglion-blocked dogs. ANG II was initially administered to increase mean arterial blood pressure (MAP) 50% above control. ANG II did not change heart rate or left ventricular rate of pressure development (LV dP/dt) but increased total peripheral vascular resistance (TPVR) and left ventricular end-diastolic pressure (LVEDP). Mean circulatory filling pressure (MCFP) increased, whereas cardiac output and venous compliance decreased. Unstressed vascular volume did not change, but central blood volume increased. ANP infusion during ANG II-induced hypertension resulted in a decrease in MAP, but TPVR did not change. There were no changes in heart rate or LV dP/dt. ANP decreased cardiac output further. LVEDP returned to base line with ANP. ANP also decreased MCFP and normalized venous compliance. There was no significant change in total blood volume, but central blood volume decreased. In summary, ANP can reverse the venoconstriction but not the arterial vasoconstriction produced by ANG II. The decrease in MAP was due to a decrease in cardiac output that resulted from venodilatation and aggravation of the preload-afterload mismatch produced by ANG II alone. Because TPVR did not change when MAP fell, we conclude that the interaction between ANG II and ANP occurs primarily in the venous circulation.

Circulating atrial natriuretic peptide (ANP) and central blood volume (CBV) in cirrhosis

2008 ◽  
Vol 6 (6) ◽  
pp. 361-368 ◽  
Author(s):  
Jens H. Henriksen ◽  
Hans Jørgen Schütten ◽  
Flemming Bendtsen ◽  
Jørgen Warberg
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Blood Volume ◽  
Central Blood Volume ◽  
Atrial Natriuretic

Fluid-regulating hormones during exercise when central blood volume is increased by water immersion

1992 ◽  
Vol 262 (5) ◽  
pp. R779-R785 ◽  
Author(s):  
L. M. Sheldahl ◽  
F. E. Tristani ◽  
T. P. Connelly ◽  
S. G. Levandoski ◽  
M. M. Skelton ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Plasma Renin Activity ◽  
Natriuretic Peptide ◽  
Blood Volume ◽  
Arginine Vasopressin ◽  
Water Immersion ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Central Blood Volume

To examine the influence of an increase in central blood volume with head-out water immersion (WI) on fluid-regulating hormones during exercise, 10 healthy men underwent upright leg cycle exercise on land and with WI. Venous plasma renin activity and plasma venous concentrations of atrial natriuretic peptide, plasma aldosterone, and arginine vasopressin were determined at exercise intensities corresponding to approximately 40, 60, 80, and 100% peak oxygen consumption (VO2) and at minutes 1 and 5 of seated rest recovery within each environment. Peak VO2 did not differ on land and with WI. Atrial natriuretic peptide concentration was higher (P less than 0.05) and plasma renin activity was lower (P less than 0.05) in water than on land at 40% peak VO2 through minute 5 of recovery. Plasma aldosterone and arginine vasopressin concentrations were lower (P less than 0.05) in water at peak exercise and at minutes 1 and 5 of recovery. Osmolality and plasma sodium and potassium concentrations during exercise were similar in water and on land. The results indicate that WI alters the circulating levels of several hormones involved in fluid and electrolyte regulation during exercise. These hormonal alterations can best be explained by stimulation of low-pressure baroreceptors and atrial stretch due to increased central blood volume with head-out WI.

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