title: Effects of clinically relevant acute hypercapnic and metabolic acidosis on the cardiovascular system: an experimental porcine study.
abstract: BACKGROUND
  Hypercapnic acidosis (HCA) that accompanies lung-protective ventilation may be considered permissive (a tolerable side effect), or it may be therapeutic by itself. Cardiovascular effects may contribute to, or limit, the potential therapeutic impact of HCA; therefore, a complex physiological study was performed in healthy pigs to evaluate the systemic and organ-specific circulatory effects of HCA, and to compare them with those of metabolic (eucapnic) acidosis (MAC).
  
  
  METHODS
  In anesthetized, mechanically ventilated and instrumented pigs, HCA was induced by increasing the inspired fraction of CO2 (n = 8) and MAC (n = 8) by the infusion of HCl, to reach an arterial plasma pH of 7.1. In the control group (n = 8), the normal plasma pH was maintained throughout the experiment. Hemodynamic parameters, including regional organ hemodynamics, blood gases, and electrocardiograms, were measured in vivo. Subsequently, isometric contractions and membrane potentials were recorded in vitro in the right ventricular trabeculae.
  
  
  RESULTS
  HCA affected both the pulmonary (increase in mean pulmonary arterial pressure (MPAP) and pulmonary vascular resistance (PVR)) and systemic (increase in mean arterial pressure (MAP), decrease in systemic vascular resistance (SVR)) circulations. Although the renal perfusion remained unaffected by any type of acidosis, HCA increased carotid, portal, and, hence, total liver blood flow. MAC influenced the pulmonary circulation only (increase in MPAP and PVR). Both MAC and HCA reduced the stroke volume, which was compensated for by an increase in heart rate to maintain (MAC), or even increase (HCA), the cardiac output. The right ventricular stroke work per minute was increased by both MAC and HCA; however, the left ventricular stroke work was increased by HCA only. In vitro, the trabeculae from the control pigs and pigs with acidosis showed similar contraction force and action-potential duration (APD). Perfusion with an acidic solution decreased the contraction force, whereas APD was not influenced.
  
  
  CONCLUSIONS
  MAC preferentially affects the pulmonary circulation, whereas HCA affects the pulmonary, systemic, and regional circulations. The cardiac contractile function was reduced, but the cardiac output was maintained (MAC), or even increased (HCA). The increased ventricular stroke work per minute revealed an increased work demand placed by acidosis on the heart.
authors.forename: Milan
authors.initials: M
authors.lastname: Stengl
authors.forename: Lenka
authors.initials: L
authors.lastname: Ledvinova
authors.forename: Jiri
authors.initials: J
authors.lastname: Chvojka
authors.forename: Jan
authors.initials: J
authors.lastname: Benes
authors.forename: Dagmar
authors.initials: D
authors.lastname: Jarkovska
authors.forename: Jaromir
authors.initials: J
authors.lastname: Holas
authors.forename: Patrik
authors.initials: P
authors.lastname: Soukup
authors.forename: Jitka
authors.initials: J
authors.lastname: Sviglerová
authors.forename: Martin
authors.initials: M
authors.lastname: Matejovic
mesh_terms: D000142:Acidosis, Respiratory / Q000503:physiopathology*; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D002302:Cardiac Output / Q000502:physiology; D004562:Electrocardiography; D005260:Female; D006439:Hemodynamics; D006935:Hypercapnia; D008297:Male; D009200:Myocardial Contraction / Q000502:physiology; D013552:Swine; D014655:Vascular Resistance / Q000502:physiology