- Poster presentation
- Open Access
Confounding hemodynamic effects of assisted ventilation in hemorrhagic states
© BioMed Central Ltd. 2004
- Published: 15 March 2004
- Metabolic Acidosis
- Hemodynamic Effect
- Positive Pressure Ventilation
- Assisted Ventilation
- Coronary Perfusion Pressure
The detrimental hemodynamic effects of positive pressure ventilation in hypovolemic states have been well described for more than 60 years. Nevertheless, typical paramedic training programs and applicable prehospital resuscitative trauma protocols in the United States and elsewhere often call for 'hyperventilation' therapy (e.g. rates > 15/min), particularly in moribund trauma patients. Typically, paramedics are trained to do so with the anecdotal rationale that they will 'pump in more oxygen' and better 'compensate for metabolic acidosis'. Therefore, considering that many of the patients receiving assisted ventilation are those with the most severe hemorrhage, there exists concern that such practices may be an under-recognized contributor to worse outcomes and that they may even over-ride or mask the potential positive effects of any resuscitative study interventions. To begin to address this issue, a study was performed to demonstrate that very slow respiratory rates (RRs) not only preserve adequate oxygenation and acid–base status in hemorrhagic states, but also that 'normal' or higher RRs worsen hemodynamics, even in cases of mild to moderate hemorrhage.
Eight pigs were ventilated with 12 ml/kg tidal volume (intubated, no positive end expiratory pressure, no lung disease);28% FiO2; and RR = 12/min. The pigs were then hemorrhaged to < 65 mmHg systolic arterial blood pressure (SABP). After reaching steady state, RRs were then sequentially changed every 10 min to 6, 20, 30, and 6/min, respectively.
With RRs at 6/min, the animals maintained pH >7.25/SaO2 > 99%, but increased mean SABP (65–84 mmHg; P < 0.05), time-averaged coronary perfusion pressure (CPP) (50 ± 2 to 60 ± 4 mmHg; P < 0.05) and cardiac output (Qt) (2.4–2.8 l/min; P < 0.05). With RRs = 20 and = 30, the SABP (73 and 66 mmHg), CPP (47 ± 3 and 42 ± 4 mmHg) and Qt (2.5 and 2.4 l/min) decreased, as did PaO2 and PaCO2 (< 30 mmHg) with P < 0.05 for each comparison, respectively. When RR returned to 6/min, SBP (95 mmHg), CPP (71 ± 6 mmHg), Qt (3.0 l/min) improved significantly (P < 0.05).
Following moderate hemorrhage, animals can maintain adequate oxygenation and ventilation with very slow RRs, while increasingly higher RRs progressively impair hemodynamics, directly resulting in diminished coronary perfusion and Qt. It is probable that these effects will be more pronounced in severe hemorrhagic states and may even contribute to worse outcomes and under-appreciated compromised study results. Current resuscitative protocols for trauma involving provision of positive pressure ventilation should be re-examined.