DOI: 10.1161/circ.148.suppl_1.218 ISSN: 0009-7322

Abstract 218: Effect of Airway Pressure and Localized Sternal Compression Upon Hemodynamics During Cardiopulmonary Resuscitation

Lyra Clark, Brian Harvey, Joshua W Lampe, George Beck, Karen L Moodie, Norman A Paradis
  • Physiology (medical)
  • Cardiology and Cardiovascular Medicine

Background: During cardiopulmonary resuscitation (CPR), chest compression (CC) and mechanical ventilation are cyclic in nature and each modulate the intrathoracic pressure (ITP). ITP is increased during the compression phase of CC, causing an increase in aortic pressure (AoP) and right atrial pressure (RAP) to drive forward blood flow. Similarly, positive pressure ventilation increases ITP during the inspiratory phase as pressure is transmitted through the lungs, which also has an impact on hemodynamics. The purpose of this analysis was to examine differences in hemodynamics during ventricular fibrillation (VF) arrest due to ventilation alone and during localized sternal CC of varying depths in a porcine model of cardiac arrest.

Methods: Domestic swine (n = 8) underwent electrically induced VF with ten-minute downtime, followed by resuscitation with mechanical ventilation and CC with active lift to neutral chest position. Mechanical ventilation was delivered using pressure-controlled synchronized intermittent mandatory ventilation (SIMV) mode (Vt 10 mL/kg, 10 bpm, trigger -6 cmH 2 O, PEEP 5 cmH 2 O, FiO 2 100). CPR was initiated with three minutes of ventilation only, followed by one minute of break-in CC at 1.0 in and 1.5 in prior to increase to depth of 2.0 in. AoP, RAP, esophageal pressure (Pes), and airway pressure (Paw) were examined over the ventilation cycle to determine the effect of each treatment upon parameters.

Results: Positive pressure ventilation caused similar changes to the Pes, RAP, and AoP values (3-5 mmHg). CC caused similar changes to Pes (3-5 mmHg), but much larger changes to the RAP and AoP (10-130 mmHg) depending on compression depth.

Conclusions: The ITP is not uniform during CC, creating only modest changes to Pes. This suggests that CC generate blood pressures, and presumably flows, through mechanisms other than ITP modulation. Understanding this interaction could improve our understanding of blood flow during CPR.

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