Transcript Buffer Solutions May Compromise Cardiac Resuscitation by Reducing Coronary Perfusion Pressure

Buffer Solutions May Compromise
Cardiac Resuscitation by Reducing
Coronary Perfusion Pressure
• JAMA. 1991;226:2121-2126 Kette, Weil, Gazmuri
Chicago, IL
• Objective: to investigate effects of hypertonic
buffer solutions on coronary perfusion pressure
and resuscibility during experimental closed-chest
cardiac resuscitation
• Design: Randomized, placebo controlled
• Setting:Mammailian research lab, 44 domestic pigs
Buffer Solutions May Compromise
Cardiac Resuscitation by Reducing
Coronary Perfusion Pressure
• Interventions: Cardiac arrest was induced by ventricular
fibrillation in mechanically ventilated pigs anesthetized with
pentobarbital sodium. Precordial compression was started
at third minute of untreated VF and maintained for an
interval of 8 minutes. A hypertonic solution of sodium
bicarbonate, Carbicarb, or sodium chloride or an isotonic
solution of sodium chloride was infused into the right
atrium over a 1-minute interval starting at the sixth minute
of VF. Restoration of spontaneous circulation was
attempted by DC transthoracic countershock after 11
minutes of VF
• Main Outcomes Measures: Plasma osmolality, CPP and
cardiac resuscibility
• Results: Infusion of hypertonic buffer and sodium chloride
solutions increased plasma osmolality from an average of
280 to 330 mOsm/kg. This was accompanied by a
significant decrease in the aortic pressures and CPPs
generated during precordial compression. No such changes
occurred after infusion of isotonic sodium chloride.
Restoration of spontaneous circulation, as in earlier studies,
was contigent on the levels of CPP proir to attempted
defibrillation. Accordingly, none of the 13 animals in which
CPP declined to less than 10 mm Hg after infusion of
hypertonic solutions were successfully resuscitated. This
contrasted with nine animals that received isotonic sodium
chloride and served as controls. Coronary perfusion
pressure consistently exceeded 10 mm Hg in these control
animals, and spontaneous circulation was restored in each
instance.
Buffer Solutions May Compromise
Cardiac Resuscitation by Reducing
Coronary Perfusion Pressure
• Conclusion: Hypertonic solutions and specifically
buffer solutions administered in the absence of
vasopressor agents may adversely affect cardiac
resuscitation efforts by reducing CPP below critical
thresholds.
Bicarbonate Does Not Improve
Hemodynamics in Critically Ill
Patients Who Have Lactic Acidosis
• Annals of Internal Medicine. 1990;112:492-498.
Cooper,Walley British Columbia, Canada
• Objective: To determine whether correction of
acidemia using bicarbonate improves
hemodynamics in patients who have lactic acidosis
• Design: Prospective, randomized, crossover, blinded
• Setting: ICU tertiary hospital
• Patients: 14 with metabolic acidosis, all with PA
catheters, 13 on catecholamines
Bicarbonate Does Not Improve
Hemodynamics in Critically Ill
Patients Who Have Lactic Acidosis
• Measurements and Main Results:
– Sodium bicarbonate increased arterial pH, HCO3-,
PaCO2 and decreased plasma ionized calcium.
– NaHCO3 and NaCl both transiently increased PCWP
and CO.
– MAP was unchanged.
– Hemodynamic responses to NaCO3 and NaCl were the
same
Bicarbonate Does Not Improve
Hemodynamics in Critically Ill
Patients Who Have Lactic Acidosis
• Conclusions: Correction of acidemia using sodium
bicarbonate does not improve hemodynamics in
critically ill patients who have metabolic acidosis
and increased blood lactate or the cardiovascular
response to infused catecholamines in these
patients. Sodium bicarbonate decreases plasma
ionized calcium and increases PaCO2.
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Effects of Bicarbonate Therapy on
hemodynamics and tissue oxygenation in
patients with lactic acidosis
Critical Care Medicine 1991;19:1352-1356
Mathieu, Neviere Lille, France
Objective: To determine whether correction of
acidemia using bicarbonate improves
hemodynamics variables and tissue oxygenation in
patients with lactic acidosis
Design: Prospective, randomized, blinded, crossover
Patients: 10 with metabolic acidosis, increased
lactate, no severe renal failure
Effects of Bicarbonate Therapy on
hemodynamics and tissue oxygenation in
patients with lactic acidosis
Method: NaHCO3 (1 mmol/kg) or equal volume of
NaCl was injected IV at the beginning of two
successive 1-hr study periods. Arterial and venous
blood gas measurements, plasma electrolytes,
osmolality, lactate, 2,3-DPG, oxygen hemoglobin
affinity, hemodynamics, oxygen delivery and
oxygen consumption measurements were obtained
before and repeatedly during the study period after
injection of NaHCO3 and NaCl.
Effects of Bicarbonate Therapy on
hemodynamics and tissue oxygenation in
patients with lactic acidosis
• Measurements and Main Results:
– NaHCO3 increased arterial and venous pH, serum
bicarbonate, PaCO2, PvCO2
– Hemodynamic responses were similar
– Tissue oxygenation was not modified
– No changes in serum Na, osmolality, arterial and venous
lactate, red cell 2,3-DPG, hemoglobin affinity for O2
observed
Effects of Bicarbonate Therapy on
hemodynamics and Tissue Oxygenation
in Patients With Lactic Acidosis
• Conclusion: Administration of sodium bicarbonate
did not improve hemodynamic variables in
patients with lactic acidosis, but did not worsen
tissue oxygenation.