Pulmonary artery catheterization and thermodilution cardiac output determination in the management of critically burned patients

Aikawa, Naoki; Martyn, J. A. J.; Burke, John F.

doi:10.1016/0002-9610(78)90172-1

Cited by 65 publications

(15 citation statements)

References 22 publications

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“…The progressive fall in cardiac output which occurs after both experimental and clinical burn trauma has suggested the presence of myocardial depressant factors which contribute to cardiac contraction and relaxation deficits [1][2][3]. However, assessment of cardiac performance in the intact subject has remained difficult due to burn-mediated changes in preload and afterload, neurohumoral responses, and the release of a host of cytotoxic mediators [4 -9].…”

Section: Discussionmentioning

confidence: 99%

“…Altered vascular tone, cardiac contractile depression, and impaired diastolic relaxation have been described after burn trauma in animal models and in humans [1][2][3][4]. Decreased cardiac output was initially attributed by numerous investigators to fluid shifts, hypovolemia, and a fall in cardiac preload; however, other investigators have attributed postburn cardiac dysfunction to myocardial depressant factors in the serum and lymph [5][6][7].…”

Section: Introductionmentioning

confidence: 99%

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Calcium Antagonists Improve Cardiac Mechanical Performance after Thermal Trauma

Horton

White

Maass

et al. 1999

Journal of Surgical Research

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Calcium Antagonists Improve Cardiac Mechanical Performance after Thermal Trauma

Horton

White

Maass

et al. 1999

Journal of Surgical Research

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“…This disparate response between atrial and ventricular muscle with respect to protein and cyclic AMP concentrations is difficult to explain. Although no functional studies were performed, it is tempting to conclude that burn-induced ventricular dysfunction documented previously (Baxter et al, 1966;Aikawa et al, 1978;Martyn et al, 1980; may be related to the inability of the ventricle to hypertrophy (to increase in protein concentration) and increase contractility (via increased cyclic AMP levels) in response to chronic hypermetabolic demands. The lack of increase in cyclic AMP levels in ventricular muscle is surprising since catecholamines (Wilmore et al, 1974), which increase cyclic AMP levels via 8-adrenoceptors, are increased in burn trauma.…”

Section: Discussionmentioning

confidence: 99%

“…Thermal injury to man and animals evokes myocardial dysfunction (Baxter et al, 1966;Aikawa et al, 1978;Martyn et al, 1980). This dysfunction is apparent not only in the acute resuscitation phase but also in the hypermetabolic (recovery) phase of thermal injury (Martyn et al, 1980;.…”

Section: Introductionmentioning

confidence: 99%

Thermal trauma alters myocardial cyclic nucleotides and protein content in mice

Tomera

Martyn

1990

British J Pharmacology

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1 This study tested the hypothesis that the systemic effects of burn include altered metabolic activity in the heart. Metabolic activity was studied by measuring alterations in cyclic nucleotide levels and protein concentrations in atrial and ventricular muscle in mice at 14 and 22 days after a 20% body surface area (BSA) burn. Thermal injury was produced on the dorsal surface of anesthetized male CD mice by immersion in water at 95°C for 8s. This resulted in a full-thickness, 3°scald burn. In atrial and ventricular tissues, levels of adenosine 3': 5'-cyclic monophosphate (cyclic AMP) and guanosine 3': 5'-cyclic monophosphate (cyclic GMP) were analyzed by 125I-radioimmunoassay. 2 The protein content (mg prot g-dry wt) increased in the atria. The cyclic AMP content (nmol g-dry wt) was significantly increased fourfold and ninefold at 14 and 22 days, respectively, in atria from burned animals compared to controls. The cyclic AMP/cyclic GMP ratios were similarly increased.3 In the ventricle, the protein content and cyclic AMP levels were not altered, but the cyclic AMP/cyclic GMP ratios (nmol g ' dry wt) were increased at both 14 and 22 days. These changes both in atria and ventricles were less prominent when cyclic nucleotide concentrations or ratios were expressed as pmol mg-1 protein.4 The data confirm the hypothesis that a 20% BSA thermal injury evokes effects in sites remote from burn injury such as in the atria and ventricles. These effects include total body weight loss, elevated cyclic AMP, cyclic AMP/cyclic GMP ratios, and protein levels in the atria, and elevated cyclic AMP/cyclic GMP ratios in both atrial and ventricular tissues at 2 and 3 weeks after thermal injury. To prevent underestimation of cyclic nucleotide levels such changes should preferably be expressed on a prot g-dry weight basis.

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“…Although traditional clinical variables such as hourly urinary output, vital signs, and laboratory examination are often used as the clinical guideline for burn shock resuscitation, hemodynamic monitoring is thought to be more effective to guide fluid therapy in many literatures. [1][2][3][4][5][6][7][8] Pulmonary artery catheterization (PAC) is a traditional method in providing direct hemodynamic data. It may cause complications due to its invasive measures, 1,9 especially when the site of catheterization is located on burn wound.…”

mentioning

confidence: 99%