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      Clinical review: Guyton - the role of mean circulatory filling pressure and right atrial pressure in controlling cardiac output

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          Abstract

          Arthur Guyton's concepts of the determinative role of right heart filling in cardiac output continue to be controversial. This paper reviews his seminal experiments in detail and clarifies the often confusing concepts underpinning his model. One primary criticism of Guyton's model is that the parameters describing venous return had not been measured in a functioning cardiovascular system in humans. Thus, concerns have been expressed in regard to the ability of Guyton's simplistic model, with few parameters, to model the complex human circulation. Further concerns have been raised in regard to the artificial experimental preparations that Guyton used. Recently reported measurements in humans support Guyton's theoretical and animal work.

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          Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: 2008

          R Phillip Dellinger, Mitchell Levy, Jean M. Carlet … (2007)
          Objective To provide an update to the original Surviving Sepsis Campaign clinical management guidelines, “Surviving Sepsis Campaign guidelines for management of severe sepsis and septic shock,” published in 2004. Design Modified Delphi method with a consensus conference of 55 international experts, several subsequent meetings of subgroups and key individuals, teleconferences, and electronic-based discussion among subgroups and among the entire committee. This process was conducted independently of any industry funding. Methods We used the GRADE system to guide assessment of quality of evidence from high (A) to very low (D) and to determine the strength of recommendations. A strong recommendation [1] indicates that an intervention's desirable effects clearly outweigh its undesirable effects (risk, burden, cost), or clearly do not. Weak recommendations [2] indicate that the tradeoff between desirable and undesirable effects is less clear. The grade of strong or weak is considered of greater clinical importance than a difference in letter level of quality of evidence. In areas without complete agreement, a formal process of resolution was developed and applied. Recommendations are grouped into those directly targeting severe sepsis, recommendations targeting general care of the critically ill patient that are considered high priority in severe sepsis, and pediatric considerations. Results Key recommendations, listed by category, include: early goal-directed resuscitation of the septic patient during the first 6 hrs after recognition (1C); blood cultures prior to antibiotic therapy (1C); imaging studies performed promptly to confirm potential source of infection (1C); administration of broad-spectrum antibiotic therapy within 1 hr of diagnosis of septic shock (1B) and severe sepsis without septic shock (1D); reassessment of antibiotic therapy with microbiology and clinical data to narrow coverage, when appropriate (1C); a usual 7–10 days of antibiotic therapy guided by clinical response (1D); source control with attention to the balance of risks and benefits of the chosen method (1C); administration of either crystalloid or colloid fluid resuscitation (1B); fluid challenge to restore mean circulating filling pressure (1C); reduction in rate of fluid administration with rising filing pressures and no improvement in tissue perfusion (1D); vasopressor preference for norepinephrine or dopamine to maintain an initial target of mean arterial pressure ≥ 65 mm Hg (1C); dobutamine inotropic therapy when cardiac output remains low despite fluid resuscitation and combined inotropic/vasopressor therapy (1C); stress-dose steroid therapy given only in septic shock after blood pressure is identified to be poorly responsive to fluid and vasopressor therapy (2C); recombinant activated protein C in patients with severe sepsis and clinical assessment of high risk for death (2B except 2C for post-operative patients). In the absence of tissue hypoperfusion, coronary artery disease, or acute hemorrhage, target a hemoglobin of 7–9 g/dL (1B); a low tidal volume (1B) and limitation of inspiratory plateau pressure strategy (1C) for acute lung injury (ALI)/acute respiratory distress syndrome (ARDS); application of at least a minimal amount of positive end-expiratory pressure in acute lung injury (1C); head of bed elevation in mechanically ventilated patients unless contraindicated (1B); avoiding routine use of pulmonary artery catheters in ALI/ARDS (1A); to decrease days of mechanical ventilation and ICU length of stay, a conservative fluid strategy for patients with established ALI/ARDS who are not in shock (1C); protocols for weaning and sedation/analgesia (1B); using either intermittent bolus sedation or continuous infusion sedation with daily interruptions or lightening (1B); avoidance of neuromuscular blockers, if at all possible (1B); institution of glycemic control (1B) targeting a blood glucose < 150 mg/dL after initial stabilization ( 2C ); equivalency of continuous veno-veno hemofiltration or intermittent hemodialysis (2B); prophylaxis for deep vein thrombosis (1A); use of stress ulcer prophylaxis to prevent upper GI bleeding using H2 blockers (1A) or proton pump inhibitors (1B); and consideration of limitation of support where appropriate (1D). Recommendations specific to pediatric severe sepsis include: greater use of physical examination therapeutic end points (2C); dopamine as the first drug of choice for hypotension (2C); steroids only in children with suspected or proven adrenal insufficiency (2C); a recommendation against the use of recombinant activated protein C in children (1B). Conclusion There was strong agreement among a large cohort of international experts regarding many level 1 recommendations for the best current care of patients with severe sepsis. Evidenced-based recommendations regarding the acute management of sepsis and septic shock are the first step toward improved outcomes for this important group of critically ill patients.
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            Does central venous pressure predict fluid responsiveness? A systematic review of the literature and the tale of seven mares.

            Paul E Marik, Michael Baram, Bobbak Vahid (2008)
            Central venous pressure (CVP) is used almost universally to guide fluid therapy in hospitalized patients. Both historical and recent data suggest that this approach may be flawed. A systematic review of the literature to determine the following: (1) the relationship between CVP and blood volume, (2) the ability of CVP to predict fluid responsiveness, and (3) the ability of the change in CVP (DeltaCVP) to predict fluid responsiveness. MEDLINE, Embase, Cochrane Register of Controlled Trials, and citation review of relevant primary and review articles. Reported clinical trials that evaluated either the relationship between CVP and blood volume or reported the associated between CVP/DeltaCVP and the change in stroke volume/cardiac index following a fluid challenge. From 213 articles screened, 24 studies met our inclusion criteria and were included for data extraction. The studies included human adult subjects, healthy control subjects, and ICU and operating room patients. Data were abstracted on study design, study size, study setting, patient population, correlation coefficient between CVP and blood volume, correlation coefficient (or receive operator characteristic [ROC]) between CVP/DeltaCVP and change in stroke index/cardiac index, percentage of patients who responded to a fluid challenge, and baseline CVP of the fluid responders and nonresponders. Metaanalytic techniques were used to pool data. The 24 studies included 803 patients; 5 studies compared CVP with measured circulating blood volume, while 19 studies determined the relationship between CVP/DeltaCVP and change in cardiac performance following a fluid challenge. The pooled correlation coefficient between CVP and measured blood volume was 0.16 (95% confidence interval [CI], 0.03 to 0.28). Overall, 56+/-16% of the patients included in this review responded to a fluid challenge. The pooled correlation coefficient between baseline CVP and change in stroke index/cardiac index was 0.18 (95% CI, 0.08 to 0.28). The pooled area under the ROC curve was 0.56 (95% CI, 0.51 to 0.61). The pooled correlation between DeltaCVP and change in stroke index/cardiac index was 0.11 (95% CI, 0.015 to 0.21). Baseline CVP was 8.7+/-2.32 mm Hg [mean+/-SD] in the responders as compared to 9.7+/-2.2 mm Hg in nonresponders (not significant). This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVP/DeltaCVP to predict the hemodynamic response to a fluid challenge. CVP should not be used to make clinical decisions regarding fluid management.
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              Determination of cardiac output by equating venous return curves with cardiac response curves.

              Robert A Guyton (1954)
              Article 0 comments Cited 55 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Crit Care
                Title: Critical Care
                Publisher: BioMed Central
                ISSN (Print): 1364-8535
                ISSN (Electronic): 1466-609X
                Publication date (Print): 2010
                Publication date (Electronic): 1 December 2010
                Publication date PMC-release: 01 December 2011
                Volume: 14
                Issue: 6
                Page: 243
                Affiliations
                [1 ]Critical Care Medicine, Vancouver General Hospital, ICU, JPPN, 2nd Floor, Room 2438, 899 West 12th Avenue, Vancouver, BC, V5Z 1M9, Canada
                [2 ]Heart + Lung Institute, St. Paul's Hospital, Room 166, 1081 Burrard Street, Vancouver, BC, V6Z 1Y6, Canada
                [3 ]Health and Integrative Physiology Lab, Osborne Ctr Unit II - Room 208, School of Human Kinetics, 210 - 6081 University Boulevard, Vancouver, BC, V6T 1Z1, Canada
                Article
                Publisher ID: cc9247
                DOI: 10.1186/cc9247
                PMC ID: 3220048
                PubMed ID: 21144008
                SO-VID: 0e278776-64f2-4e64-a725-c6a3be3a72b7
                Copyright © Copyright ©2010 BioMed Central Ltd
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                Subject: Review

                ScienceOpen disciplines: Emergency medicine & Trauma
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                ScienceOpen disciplines: Emergency medicine & Trauma

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