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Genuine effects of ventricular fibrillation upon myocardial blood flow, metabolism and catecholamines in patients with aortic stenosis

Sandstedt, B ; Ponten, J ; Olsson, Bertil LU and Edvardsson, N (2004) In Scandinavian Cardiovascular Journal 38(2). p.113-120
Abstract
Objective-Ventricular fibrillation (VF) is life-threatening because of its haemodynamic and metabolic effects. The purpose was to examine if VF also has primary effects per se. We therefore investigated the early effects of VF on myocardial blood flow, metabolic characteristics and catecholamine concentrations in patients undergoing surgery for aortic stenosis. Design-The immediate effects of up to 5 min of VF were studied in 21 patients during cardiopulmonary bypass (CPB) before valve replacement. Results-During VF the global myocardial oxygen consumption, coronary blood flow and vascular resistance were unchanged, and the mean arterial pressure (on CPB) decreased from 70 to 51 mmHg (p<0.02). Fibrillation induced a high myocardial tone... (More)
Objective-Ventricular fibrillation (VF) is life-threatening because of its haemodynamic and metabolic effects. The purpose was to examine if VF also has primary effects per se. We therefore investigated the early effects of VF on myocardial blood flow, metabolic characteristics and catecholamine concentrations in patients undergoing surgery for aortic stenosis. Design-The immediate effects of up to 5 min of VF were studied in 21 patients during cardiopulmonary bypass (CPB) before valve replacement. Results-During VF the global myocardial oxygen consumption, coronary blood flow and vascular resistance were unchanged, and the mean arterial pressure (on CPB) decreased from 70 to 51 mmHg (p<0.02). Fibrillation induced a high myocardial tone and a probable functional aortic insufficiency, which instantly equilibrated left ventricular and aortic pressures. Signs of myocardial ischaemia and acidosis developed after 4 min: a decrease in the pH of coronary sinus blood from 7.38 to 7.32 (p<0.001), an increased release of lactate from 32 to 137 mumol/min (p<0.001) and potassium from 29 to 73 μmol/min (p<0.05). The noradrenaline net release increased from 0.021 to 0.58 nmol/min (p<0.02) after 1.5 min of VF and then decreased. The adrenaline net uptake remained low and unchanged (17-28%). Conclusion-VF in patients with aortic stenosis was rapidly followed by myocardial ischaemia, acidosis and a transient increase in the myocardial noradrenaline net release despite sufficient coronary perfusion and unchanged global myocardial oxygen consumption. The VF instantly induced equilibration of left ventricular and aortic pressure and probably caused a relative underperfusion of the subendocardium. These factors all support persistence of VF. (Less)
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author
; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
ventricular fibrillation, noradrenaline, metabolism, cardiopulmonary bypass, adrenaline, aortic valve stenosis, ventricular hypertrophy
in
Scandinavian Cardiovascular Journal
volume
38
issue
2
pages
113 - 120
publisher
Taylor & Francis
external identifiers
  • wos:000221110600009
  • pmid:15204237
  • scopus:2442666451
ISSN
1651-2006
DOI
10.1080/14017430410028591
language
English
LU publication?
yes
id
a7613a3f-4dca-4299-aa96-e2e9838aec6b (old id 280083)
date added to LUP
2016-04-01 15:28:52
date last changed
2022-01-28 05:32:39
@article{a7613a3f-4dca-4299-aa96-e2e9838aec6b,
  abstract     = {{Objective-Ventricular fibrillation (VF) is life-threatening because of its haemodynamic and metabolic effects. The purpose was to examine if VF also has primary effects per se. We therefore investigated the early effects of VF on myocardial blood flow, metabolic characteristics and catecholamine concentrations in patients undergoing surgery for aortic stenosis. Design-The immediate effects of up to 5 min of VF were studied in 21 patients during cardiopulmonary bypass (CPB) before valve replacement. Results-During VF the global myocardial oxygen consumption, coronary blood flow and vascular resistance were unchanged, and the mean arterial pressure (on CPB) decreased from 70 to 51 mmHg (p&lt;0.02). Fibrillation induced a high myocardial tone and a probable functional aortic insufficiency, which instantly equilibrated left ventricular and aortic pressures. Signs of myocardial ischaemia and acidosis developed after 4 min: a decrease in the pH of coronary sinus blood from 7.38 to 7.32 (p&lt;0.001), an increased release of lactate from 32 to 137 mumol/min (p&lt;0.001) and potassium from 29 to 73 μmol/min (p&lt;0.05). The noradrenaline net release increased from 0.021 to 0.58 nmol/min (p&lt;0.02) after 1.5 min of VF and then decreased. The adrenaline net uptake remained low and unchanged (17-28%). Conclusion-VF in patients with aortic stenosis was rapidly followed by myocardial ischaemia, acidosis and a transient increase in the myocardial noradrenaline net release despite sufficient coronary perfusion and unchanged global myocardial oxygen consumption. The VF instantly induced equilibration of left ventricular and aortic pressure and probably caused a relative underperfusion of the subendocardium. These factors all support persistence of VF.}},
  author       = {{Sandstedt, B and Ponten, J and Olsson, Bertil and Edvardsson, N}},
  issn         = {{1651-2006}},
  keywords     = {{ventricular fibrillation; noradrenaline; metabolism; cardiopulmonary bypass; adrenaline; aortic valve stenosis; ventricular hypertrophy}},
  language     = {{eng}},
  number       = {{2}},
  pages        = {{113--120}},
  publisher    = {{Taylor & Francis}},
  series       = {{Scandinavian Cardiovascular Journal}},
  title        = {{Genuine effects of ventricular fibrillation upon myocardial blood flow, metabolism and catecholamines in patients with aortic stenosis}},
  url          = {{http://dx.doi.org/10.1080/14017430410028591}},
  doi          = {{10.1080/14017430410028591}},
  volume       = {{38}},
  year         = {{2004}},
}