«LUCAS - Lund University Cardiopulmonary Assist System Liao, Qiuming Published: 01/01/2011 Link to publication Citation for published version (APA): ...»
8. Left carotid artery with an ultrasonic blood flow probe Fig 9. Schematic drawing of the porcine vascular system of importance for the present thesis. The pig anatomy is slightly different from human anatomy, having 2 brachiocephalic trunks.
Fig 10. The pressure- and carotid flow curves. There was no ROSC in the manual group, whereas 5 of 6 animals obtained ROSC with LUCAS-CPR. Data shown as mean ± SEM, n = 6. CAF = carotid arterial blood flow, SAP, MAP, DAP = systolic, mean and diastolic intrathoracic aortic pressure. VF = induction of ventricular fibrillation. Def = defibrillation.
Fig 11. Typical pressure curves obtained in a 20-25 kg pig during manual CPR and LUCAS-CPR (left two panels). The area between the curves for intrathoracic aortic pressure and right atrial pressure gives a picture of the coronary perfusion pressure. ote the biphasic positive curves and greater area between the curves during LUCAS-CPR. In the right panel is shown the mean coronary perfusion pressure with SEM on one side of the mean.
28-33 kg pigs (III) Sixteen 28-33 kg pigs were stratified into 2 groups of 8 animals. After 5 minutes of ventricular fibrillation, CPR was run for 20 minutes before the first defibrillation was given (simulating prolonged CPR for VF resistant to defibrillation) (Fig 12).
All animals in the LUCAS group achieved ROSC, compared to 3 of 8 animals in the manual group (p0.03, Fischer’s Exact Test). The coronary perfusion pressure in the LUCAS group varied between 18 and 25 mmHg, whereas in the manual group it varied between 5 and 10 mmHg (Fig 13). The compression pressure in the ascending aorta and the ETCO2 were significantly higher in the LUCAS group.
Intrathoracic aortic pressure (mmHg) Fig 12. The design of the study (upper panel). The number of pigs with return of
spontaneous circulation (ROSC) is indicated within the ROSC rectangle. VF:
ventricular fibrillation; CPR: cardiopulmonary resuscitation; D1-D6:
defibrillations; A: adrenaline 0.01 mg/kg given intravenously. The lower panel shows the mean systolic pressure and during CPR the compression pressure, in the intrathoracic aorta during the experiment. The CPR period is marked. The break in the manual CPR curve marks where n is changed from 8 to 3 individuals.
Mean±SEM is included in 2 places in each curve; n=8, except for the ROSC period for manual CPR, where n=3.
Fig 13. The coronary perfusion pressure during LUCAS-CPR and manual CPR.
ormothermic versus hypothermic CPR (I) Three of the 8 pigs achieved ROSC in the normothermic group and 6 of the 8 in the hypothermic group (Fig 14). The surface cooling was done with ice placed directly on the skin during the first 30 minutes of the 1-hour LUCAS-CPR period.
In the normothermic group, the coronary perfusion pressure, which was between 15 and 18 mmHg during the first 20 minutes, then began to decrease and at the
Fig 14. LUCAS-CPR during 1 hour of ventricular fibrillation (VF) with normothermia (left panel) and surface cooling (right panel) during the first half hour. Temperature, systolic, mean and diastolic (SAP, MAP, DAP) intrathoracic aortic pressure, coronary perfusion pressure, and right carotid arterial blood flow are shown as mean ± SEM. n=8.
end of the 60-minute period it was between 0 and 5 mmHg. In the surface cooling group, the coronary perfusion pressure increased from 15 to 20 mmHg within 5 minutes of cooling, and continued to increase to 25 mmHg over the next 55 minutes. The esophagus temperature was 34°C after 30 minutes, the ice was then removed, but an afterdrop of 2°C occurred, so that after 1 hour of LUCAS-CPR the esophagus temperature was 32°C. The reactive hyperaemia after ROSC was higher in the normothermic group (Fig 14).
Hemodynamics of ventricular fibrillation (II) Figure 15 shows frozen pictures from a video uptake after induction of ventricular fibrillation and figures 16-18 shows the blood pressure, blood flow and intrapleural pressure curves. Blood circulation continues for 5 minutes after ventricular fibrillation, i.e., it continues as long as the aortic pressure is higher than the pressure in the right atrium. The right ventricle increases gradually in size, as the right atrial pressure increases, and this causes a form of tamponade since the pericardial pressure increases in parallel with the right atrial pressure. After 5 minutes, the right ventricle is distended, and there is no coronary perfusion pressure. Defibrillation of such a heart, even if sinus rhythm is obtained, will give no return of spontaneous circulation due to the distended right ventricle without coronary perfusion. It takes a minimum of 90 seconds of chest compressions to build up an adequate coronary pressure. As seen in figure 16, during the first minute of chest compressions the coronary perfusion pressure is negative, i.e., the pressure in the right atrium during the decompression phase is higher than the pressure in the descending aorta.
Fig 15. Frozen pictures from the video uptake after induction of ventricular fibrillation. The anterior part of the right and the left ventricle on each side of LAD is seen. The right ventricle grows in size and is severely distended after 5 minutes.
Fig 16. Intrathoracic aortic pressure (red curves), pressure in the right atrium (blue curves) and computed coronary perfusion pressure (black curve) are shown during 6.5 min of ventricular fibrillation followed by 3.5 min of mechanical chest compressions. Systolic, diastolic and mean pressure are shown to the left (Base), and compression, decompression and mean pressure to the right (during CPR).
The curves represent the mean values from 12 pigs. For the sake of clarity, the standard error of the mean is not shown.
Fig 17. The blood flow in the left internal carotid artery during 6.5 min of ventricular fibrillation followed by 3.5 min of mechanical chest compressions. The mean value ± SEM is shown from 12 pigs.
Fig 18. Pressure recordings of the first 10 min of ventricular fibrillation in one pig in which intrapericardial pressure was also registered. AP=intrathoracic aortic pressure, RAP=right atrial pressure.
Fig 19. The design of the experiments. The number of pigs with ROSC (return of spontaneous circulation) is indicated within the ROSC rectangle.
D=Defibrillation. VF=Ventricular Fibrillation. CPR=CardioPulmonary Resuscitation.
Group I: defibrillation was done after 6.5 minutes of ventricular fibrillation without chest compressions before or after. Four of six animals were successfully defibrillated on the first attempt and sinus rhythm with bundle branch block was recorded. However, this was pulseless electrical activity without arterial pressure or blood flow.
Group II: Delayed defibrillation after chest compressions. After 2 minutes of chest compressions, an adequate coronary perfusion pressure was obtained, but when the chest compressions were interrupted, to obtain readable ECG, the adequate coronary perfusion pressure was lost within seconds, and when defibrillation was done, ROSC was obtained in only one pig (Fig 20). The 30-second LUCAS-CPR periods between the defibrillations were too short to obtain a coronary perfusion pressure as seen in the figure: during LUCAS-CPR it was negative, i.e., the right atrial pressure was higher than the ascending aortic pressure during the decompression phase with no flow in the coronary arteries as a consequence.
Fig 20. Coronary perfusion pressure during 3.5 min of mechanical compressions and during defibrillation attempts with (II) and without (III) interrupting the chest compressions. Mean value ± SEM, n=5 in each group.
Injuries after manual CPR versus LUCAS-CPR (III) There were significantly (p0.01) more rib fractures in the manual group: 33 on the left side and 21 on the right side, as compared to 30 on the left side and 2 on the right side in the LUCAS group. Two serious injuries occurred in the manual group, one right sided pressure pneumothorax and one vertical deep liver rupture with 500 ml blood in the abdomen, which is about 20% of the blood volume of a pig this size.
COMME TS The results from the three studies have been discussed in detail in each article. The comments below deal with issues that must be considered for a better understanding of the results.
Porcine versus human thorax The human thorax in the supine position is like an egg lying on its side, whereas in the same position the porcine thorax is like an egg standing on its end, see figure 21.
Fig 21. Schematic drawings of a human (left) and porcine (right) thorax.
The anterior-posterior diameter of 20-25 kg pigs is around 20 cm, which is the same as for adult humans of mean size (I).
The Utstein-style guidelines for uniform reporting of laboratory CPR-research (23) advocate the use of 20-25 kg pigs, because a compression depth of 5 cm will give a 25% reduction of the anterio-posterior diameter, and that is what the international guidelines recommend (19-22).
There are important differences between human and pig thorax anatomy that have implications in CPR studies. In pigs, the heart is positioned more centrally in the thorax cavity surrounded by lung tissue on all sides (I). In humans the right ventricle is positioned just under the sternum. This difference makes it more difficult to get a compression effect on the heart in pigs where the compressions affect the heart only by `the thoracic pump mechanism´, i.e., a chest compression increases the intrathoracic pressure which in turn affects the heart. In humans not only `the thoracic pump mechanism´ but also a `heart pump mechanism´ works, i.e. direct compression of the heart by chest compressions. Patients with chronic obstructive pulmonary disease (COPD) have a thorax that is more like the porcine thorax with lungs surrounding the heart on all sides. Due to these differences it is more difficult to obtain high arterial compression pressures in pigs than in humans.
0.0 0.2 0.4 0.6 0.8 1.0 0.0 0.2 0.4 0.6 0.8 1.0
Fig 22. The coronary perfusion pressure curves in the intrathoracic aorta (triangles) and the right atrium (circles) during two cycles of CPR in the manual CPR (left) and LUCAS-CPR (right) groups just after a ventilation. A bar is inserted before one compression in both panels. The 0.05-second long bar shows where in the cycle CPP is calculated (as the difference between the pressure in aorta and right atrium). The level of the bar shows the CPP in this registration; 7 mmHg in the manual group and 22 mmHg in the LUCAS group.
During the decompression phase, both the ascending aortic pressure and right atrial pressure diminish, and right atrial pressure most. The difference between these 2 pressures during the decompression phase is the coronary pressure resulting in a coronary blood flow. It can be measured as the lowest registered intraaortic pressure minus the lowest registered right atrial pressure during the decompression phase, or it can be measured as the difference at the end of the decompression phase (III). A coronary perfusion pressure higher than 15 mmHg is one indication that the coronary flow is at the minimum for ROSC to be obtained, both in humans (24-26) and in pigs (I).
ETCO2 as an indication of cardiac output during CPR If the ventilation during CPR is standardized, ETCO2 is an indication of cardiac output during CPR, the higher the ETCO2, the higher the cardiac output. It is easy to hyperventilate during CPR if the ventilation is done manually, and then ETCO2 is not to be trusted. But for experimental use, with standardized ventilation in all groups to be compared, it is a valuable tool to judge the cardiac output obtained during CPR.
Carotid artery blood flow in pigs In pigs the carotid artery supplies mainly extracranial muscles, and cannot be used as an indication of cerebral flow (27).
Hypothermia induced during on-going CPR In cardiac surgery hypothermia has been used routinely since the 1950-ties. For routine cardiac surgery with extracorporeal circulation, the patient is cooled to 32°-28°C, and when major surgery is needed, e.g., for dissection of the ascending aorta, target temperatures between 22°-16°C are often used.
There is no consistent definition of hypothermia, but for doctors treating hypothermic patients without extracorporeal circulation, mild hypothermia is defined as temperatures down to 32°C and moderate hypothermia down to 28°C.
A patient with a body temperature below 28°C would by most doctors be characterized as being in deep hypothermia.
In study I we wanted to study the effect of mild hypothermia. In pigs the metabolism will be reduced by about 6-7% per degree Celsius that the body temperature is lowered (28-29). A reduction of body temperature from 38°C (normal in pigs) to 32°C will reduce the metabolism by 35-45%, with the consequence that less circulation will be needed to ensure an adequate organ perfusion. The pigs treated with hypothermia and LUCAS-CPR for 1 hour developed a metabolic acidosis over time, indicating that the organ perfusion was not adequate, although it was better than for the normothermic pigs.