Hemodynamics of experimental acute gastric dilatation

Engler, Harold S.; Kennedy, T.; Ellison, Lois T.; Purvis, Jerry G.; Moretz, William H.

doi:10.1016/0002-9610(67)90221-8

Cited by 15 publications

(4 citation statements)

References 2 publications

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“…There have been multiple previous studies evaluating cardiac function in experimental and naturally acquired GDV which have produced largely conflicting results 1–5,7,10–16 . Several early studies documented decreases in cardiac output, myocardial oxygen consumption, and coronary sinus blood flow in dogs with experimentally induced and naturally acquired GDV 7,14–15 .…”

Section: Introductionmentioning

confidence: 99%

Evaluation of cardiac performance of the dog after induction of portal hypertension and gastric ischemia

MacPhail¹,

Monnet²,

Pelsue³

et al. 2006

J Vet Emergen Crit Care

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Objective: To determine changes in hemodynamic and cardiac energetic parameters in dogs after induction of portal hypertension and gastric ischemia. These blood flow alterations are similar to changes seen in splanchnic blood flow in dogs with gastric dilatation volvulus syndrome (GDV). Design: Original experimental study. Setting: Veterinary teaching hospital. Animals: Seven purpose-bred, intact male dogs. Interventions: Standard midline laparotomy and median sternotomy were performed under general anesthesia. Dogs were instrumented to obtain arterial blood pressure, aortic flow, cardiac chamber pressures, central venous pressure, portal flow, and portal pressure. Colored microsphere technology was used for the determination of myocardial blood flow. Measurements and samples were obtained at baseline, following induction of portal hypertension, and after induction of portal hypertension and gastric ischemia. Measurements and main results: Left ventricular myocardial blood flow was increased from 81.8 AE 20.1 mL/ 100 g/min at baseline to 127.7 AE 57.2 mL/100 g/min (P 5 0.02) after induction of portal hypertension and gastric ischemia. Myocardial oxygen consumption increased from 142.2 AE 27.4 J/min/100 g at baseline to 219.1 AE 33.4 J/min/100 g (P 5 0.003) after induction of portal hypertension and gastric ischemia, but cardiac external work remained unchanged (13.67 AE 6.2 to 13.27 AE 9.6 J/min; P 5 0.78; power 5 0.79). Cardiac efficiency decreased from 11.6 AE 6.1% at baseline to 7.6 AE 5.1% (P 5 0.017) after induction of portal hypertension and gastric ischemia. Conclusions: Transfer of energy within the myocardium was less efficient after induction of portal hypertension and ischemia of the stomach wall. On the basis of these results, alterations in cardiac function associated with GDV may result from deterioration of cardiac efficiency.

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Section: Introductionmentioning

confidence: 99%

Evaluation of cardiac performance of the dog after induction of portal hypertension and gastric ischemia

MacPhail¹,

Monnet²,

Pelsue³

et al. 2006

J Vet Emergen Crit Care

View full text Add to dashboard Cite

show abstract

“…The method described in the present paper seems to be relatively safe. This is proved in part by the measurement of venous pressure, which did not produce any evidence of shock in the dogs studied, although shock might be expected after transient occlusion of blood flow in the caudal vena cava (1,6). The increase of the venous blood pressure in the caudal vena cava observed after the removal of the blockade can be regarded as an effect of the administration of the contrast medium, which as with other media used for angiography, produces a decrease of the arterial blood pressure and an increase of the venous blood pressure (2).…”

Section: Discussionmentioning

confidence: 85%

Visualization of the Vertebral Canal Veins in the Dog: A Radiological Method

Koper¹,

M²

1977

Veterinary Radiology

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“…In addition, GI can result in an increase in intra-abdominal pressure, which can reduce venous return and increase afterload, resulting in an increase in systemic vascular resistance. GI can also lead to a decrease in functional residual capacity, which may have further implications on ventilation [ 19 , 20 ]. Therefore, it is necessary to remain vigilant concerning the risk of GI during and after resuscitation to reduce avoidable complications.…”

Section: Discussionmentioning

confidence: 99%

Gastric Inflation in Prehospital Cardiopulmonary Resuscitation: Aspiration Pneumonia and Resuscitation Outcomes

Kim¹,

Kim²,

Han³

et al. 2023

Rev. Cardiovasc. Med.

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Background: Gastric inflation (GI) can induce gastric regurgitation and subsequent aspiration pneumonia, which can prolong intensive care unit stay. However, it has not been verified in patients with out-of-hospital cardiac arrest (OHCA). This study aimed to investigate the incidence of GI during prehospital resuscitation and its effect on aspiration pneumonia and resuscitation outcomes in patients with out-of-hospital cardiac arrest. Methods: This was a multicenter, retrospective, observational study. Patients with non-traumatic OHCA aged 19 years who had been admitted to the emergency department were enrolled. Patients who received mouth-to-mouth ventilation during bystander cardiopulmonary resuscitation (CPR) were excluded from the evaluation owing to the possibility of GI following bystander CPR. Patients who experienced cardiac arrest during transportation to the hospital who were treated by the emergency medical service (EMS) personnel, and those with a nasogastric tube at the time of chest or abdominal radiography were also excluded. Radiologists independently reviewed plain chest or abdominal radiographs immediately after resuscitation to identify GI. Chest computed tomography performed within 24 h after return of spontaneous circulation was also reviewed to identify aspiration pneumonia. Results: Of 499 patients included in our analysis, GI occurred in approximately 57% during the prehospital resuscitation process, and its frequency was higher in a bag-valve mask ventilation group (n = 70, 69.3%) than in the chest compression-only cardiopulmonary resuscitation (n = 31, 55.4%), supraglottic airway (n = 180, 53.9%), and endotracheal intubation groups (n = 3, 37.5%) ( p = 0.031). GI was inversely associated with initial shockable rhythm (adjusted odds ratio [OR] 0.53; 95% confidence interval [CI]: 0.30–0.94). Aspiration pneumonia was not associated with GI. Survival to hospital discharge and favorable neurologic outcomes were not associated with GI during prehospital resuscitation. Conclusions: GI in patients with OHCA was not associated with the use of different airway management techniques.

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Hemodynamics of experimental acute gastric dilatation

Cited by 15 publications

References 2 publications

Evaluation of cardiac performance of the dog after induction of portal hypertension and gastric ischemia

Evaluation of cardiac performance of the dog after induction of portal hypertension and gastric ischemia

Visualization of the Vertebral Canal Veins in the Dog: A Radiological Method

Gastric Inflation in Prehospital Cardiopulmonary Resuscitation: Aspiration Pneumonia and Resuscitation Outcomes

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