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During cardiopulmonary resuscitation (CPR), the electrocardiogram (ECG) is often obscured by noise. This noise is in the form of baseline variations in the ECG, which often necessitate stopping chest compressions to adequately assess the ECG. Because survival from cardiac arrest has been shown to be related to blood flow generated during CPR, and because interruption of chest compressions will reduce blood flow, survival may be compromised by these interruptions. Three possible sources for the noise were considered: the heart, which is deformed during CPR, which may introduce a mechanical-electrical interaction and alter the normal electrical pattern of the heart; the thoracic cavity, which may have large impedance variations because of CPR and thereby modulate the ECG; and the skin-electrode interface, which may be mechanically disturbed during CPR and thus produce polarization potentials that cause additional noise. CPR studies were performed on five dogs by using four different test conditions and six different types of electrodes. The test conditions were: electrode motion, which allowed mechanical disturbances of the skin-electrode interface without altering the thoracic impedance or deforming the heart; vest CPR; manual CPR; and respiration. The myocardial ECG, the bipolar and unipolar surface ECGs, and the thoracic impedance were monitored. Different types of surface ECG electrodes were used to determine whether the noise was dependent on electrode type or size. There were no baseline variations in the myocardial ECG during any of the test conditions. The thoracic impedance did vary during CPR, but the variations were temporally uncorrelated to the baseline variations in the ECG, and the variations were of similar magnitude as the variations caused by respiration, which produced no baseline changes in the ECG. Finally, the magnitude of the baseline variations in the ECG was substantially different for electrodes of different sizes and shapes, and electrode motion produced baseline variations that were identical to those produced during CPR. Therefore, it was concluded that the source of the noise in the ECG during CPR is the skin-electrode interface and, specifically, that the noise is related to the electrical properties of the electrode.

Pressures were measured in the right atrium, thoracic aorta, and pleural space during conventional cardiopulmonary resuscitation (CPR) and simultaneous ventilation compression cardiopulmonary resuscitation (SVC-CPR) in dogs, pigs, and a baboon. During both forms of closed chest resuscitation, the changes in atrial and aortic pressures were virtually identical over a range of 0-90 mm Hg and essentially equaled the change in pleural pressure measured at the most lateral portion of the chest cavity. During internal cardiac massage, there was no consistent relationship between right atrial and aortic pressures. However, even after the chest had been opened, the hemodynamics of external chest compression could be restored by the creation of a closed, air filled cavity surrounding the heart and great vessels. Thus, elevation of intrathoracic pressure, not direct cardiac compression, is essential to and determine circulation of blood during CPR.

Sternal displacement during CPR was measured in 11 adults and 2 manikins (Recording Resusci Anne) while the chest was compressed with variable maximum pulse compression force at a rate of 60/min with compression duration of 0.5-0.6 sec. In 10 patients, the pulsatile sternal elastic characteristic can be satisfactorily described with a 2nd degree polynomial F = beta Ds + gamma D2s, where beta = 54.9 +/- 29.4 (mean +/- SD) N/cm is the pulsatile initial elasticity and gamma = 10.8 +/- 4.1 N/cm2 is the posterior resiliency. The sternal characteristics of manikins were linear F = kDs with high elasticity constants, k = 131 and 142 N/cm. Therefore, the manikins tested differ significantly in elasticity characteristics from the human chest during resuscitation. In general, the manikin: (1) has markedly greater stiffness at the onset of compression, and (2) maintains a linear stiffness throughout the usual range of displacement, rather than becoming stiffer with greater chest displacement.