Physiology of Circulation during Closed Chest Compressions
Two mechanisms of blood flow during closed chest compression have been described.15,31 In the cardiac pump mechanism, the heart is compressed between the sternum and spine, resulting in ejection of blood from the heart into the aorta with the atrioventricular valves preventing backward blood flow. In the thoracic pump mechanism, chest compression raises intrathoracic pressure, forcing blood out of the chest; the venous valves and dynamic venous compression prevent backward flow and the heart acts as a passive conduit. The 2 mechanisms are not mutually exclusive (Fig. 82-2). Fluctuations in intrathoracic pressure play a significant role in blood flow during most resuscitations and the cardiac pump mechanism contributes to blood flow under some circumstances. The predominant mechanism probably varies from victim to victim and even during the course of resuscitating a single victim.
Possible mechanisms for blood flow during CPR include direct cardiac compression and the thoracic pump. With direct cardiac compression, an increase in chest compression rate causes an increase in blood flow by squeezing the heart between the vertebral column and sternum. With the thoracic pump mechanism, factors that increase pleural pressure cause an increase in pressure within the heart chambers and, ultimately, an increase in blood flow.
Successful resuscitation in experimental models is associated with myocardial blood flows of 15 to 20 mL/min/100 g (Table 82-2).32 Obtaining such flows requires that closed chest compressions generate adequate cardiac output and coronary perfusion pressure. During CPR, coronary perfusion occurs primarily during the relaxation phase (diastole) of chest compression. In animal models the critical myocardial blood flow is associated with aortic "diastolic" pressure exceeding 40 mm Hg and coronary perfusion pressure (aortic diastolic minus right atrial diastolic pressure) exceeding 25 mm Hg.32-42 One report has confirmed similar findings in humans, noting that all patients with successful return of spontaneous circulation had coronary perfusion pressures higher than 15 mm Hg.42 Critical coronary perfusion pressure develops slowly when chest compressions are begun and is lost quickly when compressions are paused (Fig. 82-3). Again, for successful resuscitation, interruptions of chest compressions must be avoided whenever possible.
Table 82-2 Physiological Variables Associated with Successful Resuscitation ||Download (.pdf)
Table 82-2 Physiological Variables Associated with Successful Resuscitation
|Myocardial blood flow||15-20 mL/min/100 g|
|Arterial diastolic pressure||40 mm Hg|
|Coronary perfusion pressure||15-25 mm Hg|
|End-tidal carbon dioxide||>10 mm Hg|
Aortic (Ao) and right atrial (RA) pressure tracings during single rescuer CPR providing 15 compressions followed by 2 breaths. There is little difference in Ao and RA pressure during chest compression ("systole"). When chest compressions are begun, Ao pressure during relaxation ("diastole") increases slowly (yellow arrow), providing the pressure difference for coronary perfusion (blue arrows), but is lost quickly during the pause for ventilations.
During CPR, cardiac output is severely depressed, ranging from 10% to 33% of prearrest values in experimental animals. Nearly all of the cardiac output is directed to organs above the diaphragm. Brain blood flow is 50% to 90% of normal and myocardial blood flow 20% to 50% of normal, and lower extremity and abdominal visceral flow is reduced to less than 5% of normal. Total blood flow tends to decrease with time, but the relative distribution of flow does not change. Flow to the brain and heart are improved by the administration of vasopressors, and flow to organs below the diaphragm is unchanged or further reduced.
Physiology of Gas Transport during CPR
During CPR, measurement of blood gases reveals an arterial respiratory alkalosis and a venous respiratory acidosis because the arterial PCO2 is reduced and the venous PCO2 is elevated. The cause is not respiratory in origin. Rather, these changes result from reduced cardiac output. During the low-flow condition of CPR, excretion of CO2 (milliliters of CO2 per minute in exhaled gas) is decreased to approximately the same extent as is cardiac output. This reduced CO2 excretion is primarily a result of shunting of blood flow away from the lower half of the body. The exhaled CO2 reflects only the metabolism of the part of the body that is being perfused. In the nonperfused areas, CO2 accumulates during CPR. When normal circulation is restored, the accumulated CO2 is washed out and a temporary increase in CO2 excretion is seen.
Although CO2 excretion is reduced during CPR, the mixed venous partial pressure of CO2 (PvCO2) is usually increased.43 Two factors account for this elevation. Buffering acid causes a reduction in serum bicarbonate so that the same blood CO2 content results in a higher PvCO2. In addition, the mixed venous CO2 content is elevated. When flow to a tissue is reduced, not all the produced CO2 is removed, and CO2 accumulates, increasing the tissue partial pressure of CO2. This allows more CO2 to be carried in each aliquot of blood, and mixed venous CO2 content increases. If flow remains constant, a new equilibrium is established where all CO2 produced in the tissue is removed but at a higher venous CO2 content and partial pressure. In contrast to the venous blood, arterial CO2 content and partial pressure (PaCO2) are decreased during CPR. This accounts for most of the observed increase in the arterial–venous CO2 content difference. Although venous blood may have an increased CO2, the marked reduction in cardiac output with maintained ventilation results in very efficient CO2 removal.
Decreased pulmonary blood flow during CPR causes lack of perfusion to many nondependent alveoli. The alveolar gas of these lung units has no CO2. Consequently, the level of mixed alveolar CO2 (ie, end-tidal CO2) will be very low and will correlate poorly with arterial CO2. However, end-tidal CO2 does correlate well with cardiac output during CPR. As flow increases, more alveoli become perfused, there is less alveolar dead space, and end-tidal CO2 measurements rise.
Technique of Closed Chest Compression
Cardiac arrest should be presumed in a patient unresponsive to vigorous stimulation with absent or gasping (agonal) respirations. Even experienced health care providers take too long and have difficulty detecting the presence or absence of a pulse in arrest victims. Therefore, if a pulse check is done before or during rescue efforts, it should not take more than 10 seconds and should not be relied upon to determine successful resuscitation. After that time, if the patient remains unresponsive and apneic, the emergency response system should be activated and CPR begun (Boxes 82-1 and 82-2).
Standard chest compression technique consists of the rhythmic application of pressure over the lower half of the sternum. For compressions to be effective in providing blood flow to the brain and heart, the patient must be on a firm surface with the head level with the heart. The rescuer should stand or kneel at the side of the patient so that the hips are level with the victim's chest. Using the weight of the entire upper body, the compression is delivered straight down with enough force to depress the sternum at least 2 in (5.0 cm) in adults and teens, and to one-third to one-half the depth of the chest in children and infants. Figure 82-4 illustrates the technique of chest compressions in infants. Following maximal compression, pressure is released completely from the chest. Chest compressions should be performed at a rate of 100 per minute. They are most effective if the compression and relaxation phases of the cycle are equal in length. This 50% compression time (compressions to relaxation) is easier to achieve at faster compression rates.
A. Two-finger method of external chest compression in infants. Rescuer places 2 fingers on the sternum and 1 fingerbreadth below the line intersecting the nipples and compresses 0.5 to 1 in at a rate of 100 compressions per minute. For the sake of clarity, ventilation is not shown. B. Encircling method of external chest compression in infants. Rescuer places thumbs over sternum 1 fingerbreadth below the line intersecting the nipples and clasps hands behind infant's back.
Alternative Techniques of Circulatory Support
In recent years, better understanding of circulatory physiology during CPR, especially involving the thoracic pump mechanism, has resulted in several proposals for alternative techniques or adjunct devices. Most are intended to provide better hemodynamics and extend the duration during which CPR can support viability. Unfortunately, none has proven reliably superior to the standard technique, and no improvement in survival from cardiac arrest has been demonstrated consistently. Initial studies suggested hemodynamic advantages for techniques that raised intrathoracic pressure (such as simultaneous ventilation/compression, abdominal binding with compression, pneumatic antishock garment). Further investigations found that these techniques raised right atrial pressure and intracranial pressure, often more than aortic pressure. Consequently, there was no improvement in cerebral or myocardial blood flow. Outcome studies found no improvement in resuscitation success compared to standard CPR. These techniques are currently not recommended for support of the cardiac arrest victim.
Interposed Abdominal Compression CPR
Interposed abdominal counterpulsation (IAC)-CPR consists of a dedicated rescuer providing manual abdominal compression between the xiphoid and umbilicus during the relaxation phase of conventional CPR.44 IAC-CPR increases venous return and compresses the abdominal aorta to produce retrograde aortic flow, closing the aortic valve and augmenting diastolic pressure. Although initial hemodynamic studies were encouraging, a large randomized study of out-of-hospital arrest found no improvement in survival compared to standard CPR.45 Two subsequent in-hospital studies using trained providers found improved return of spontaneous circulation (ROSC) and short-term survival with IAC-CPR compared to the standard technique.46,47 In general, there has not been improvement in long-term survival with the use of this technique. Reports of human studies demonstrate that the frequency of complications, including laceration of abdominal viscera or esophageal regurgitation, is not increased with IAC-CPR. During in-hospital resuscitation, IAC-CPR may be considered when there are sufficient personnel trained in its use. Its use for out-of-hospital arrest remains experimental.
Active Compression–Decompression CPR
Active compression–decompression (ACD)-CPR developed from the anecdotal report of CPR performed with a plumber's helper applied to the anterior chest wall.48 This suggested that active decompression of the chest wall might reduce intrathoracic pressure during the relaxation phase of chest compressions, leading to improved venous return, increased stroke volume with compression, and better blood flow. Devices that can be applied to the chest wall in order to enable active compression and decompression have been developed, but none is currently approved by the Food and Drug Administration for sale in the United States. Hemodynamic studies in animals and humans show that coronary and cerebral perfusion may be somewhat improved with this method compared to standard CPR, although when epinephrine is used, there is no difference between techniques.49,50 Clinical trials have found mixed results, with some showing short-term benefit but none showing long-term improvement in neurologically intact survival. A meta-analysis of 4162 patients in 10 out-of-hospital trials and 826 patients in 2 in-hospital trials found no difference in early or late survival with ACD-CPR compared to standard CPR.51
The Lund University Cardiac Arrest System (LUCAS) is a gas (oxygen or air) or electric powered piston-type device that produces a consistent chest compression rate of 100/min and a maximum compression depth of 5 cm, and incorporates a suction cup attached to the sternum to return the sternum to the starting position or to cause active decompression.52 Case series have reported variable success with the device.
Impedance Threshold Device
The impedance threshold device (ITD) is a valve that limits the flow of air into the lungs during the relaxation phase of chest compressions, reducing intrathoracic pressure during chest recoil and enhancing venous return.53 Originally designed for use with an endotracheal tube, it has been adapted for use with a face mask, assuming the maintenance of a tight seal with the face. It has frequently been studied in association with ACD-CPR in the belief that the 2 techniques would act synergistically to improve venous return. One meta-analysis using data from randomized trials of both standard CPR and ACD-CPR found an improved short-term outcome with the use of an ITD but no significant improvement in survival to discharge.54 Recently, a randomized trial (ROC PRIMED) involving 11500 patients was stopped for futility because "researchers found that ITD use did not significantly improve or worsen survival rates for cardiac arrest patients" (https://roc.uwctc.org/tiki/tiki-index.php; statement released Nov. 6, 2009).
Pneumatic Vest CPR and Load-Distributing Band CPR
Pneumatic vest CPR is a method of increasing intrathoracic pressure by phasically inflating a bladder around the chest (with or without simultaneous ventilation) yet without significantly changing the dimensions of the chest.55,56 Experimental animal studies show excellent hemodynamics and the ability to maintain viability for prolonged periods. The technique continues to be investigated with a number of modifications from the original method. One modification of this technique is the load-distributing band (LDB) device consisting of a pneumatically or electrically actuated constricting band and backboard.57 A multicenter randomized controlled trial comparing this device against manual CPR demonstrated no improvement in 4-hour survival.58
In contrast to the closed chest techniques, invasive methods have been able to maintain cardiac and cerebral viability during long periods of cardiac arrest. In animal models, open-chest cardiac massage can provide better hemodynamics and myocardial and cerebral perfusion than closed chest techniques.59,60 When performed after 15 minutes of closed-chest CPR, open-chest CPR significantly improves coronary perfusion pressure and the rate of successful resuscitation.61 Furthermore, when initiated early (probably within 20-30 min of arrest) following failure of closed-chest CPR, open-chest CPR may improve resuscitation.62-64 However, if open-chest massage is begun after 30 minutes of ineffective closed-chest compressions, there is no better survival even though hemodynamics are improved.65 This may be a useful technique when the chest or abdomen is already open in the operating room or early in the postoperative period after cardiothoracic surgery.
Preliminary trials of percutaneous cardiopulmonary bypass (through the femoral artery and vein using a membrane oxygenator) for refractory human cardiac arrest have been reported66 and this is a technique available in some institutions. In canines, prompt restoration of blood flow and perfusion pressure with cardiopulmonary bypass can provide resuscitation with minimal neurologic deficit after 20 minutes of fibrillatory cardiac arrest.67
Assessment of the patient during CPR is similar to that in other clinical situations; Box 82-4 lists the major points. A basic clinical examination and adherence to basic principles, including inspection, palpation, and auscultation of the patient, are performed. The chest is carefully observed for adequacy of expansion with artificial ventilation and for equal and normal breath sounds. In addition, the depth of compression and the position of the rescuer's hands in performing chest compressions should be reevaluated constantly.
Box 82-4 ||Download (.pdf)
Assessment of Patient During Cardiopulmonary Resuscitation
Depth of compression
Position of rescuer's hands
Assess peripheral pulses
Central venous catheter
Physiologic variables associated with successful resuscitation are listed in Table 82-2. When they are available, these variables should be used to guide resuscitation efforts. The use of an indwelling arterial catheter is an invaluable monitor in assessing the arterial blood pressure and estimating these critical perfusion pressures. In addition, an arterial line allows for the determination of arterial blood gases. If pressures are below the critical levels, adjustments should be made to improve chest compressions and/or additional epinephrine should be administered. Greater pressures do not ensure success. Damage to the myocardium from underlying disease may preclude survival no matter how effective the CPR efforts. However, inadequate vascular pressures consistently result in poor outcomes.
Although invasive pressure monitoring may be the ideal, exhaled end-tidal CO2 is an excellent noninvasive guide to the effectiveness of standard CPR.68 Carbon dioxide excretion during CPR with an endotracheal tube in place is dependent primarily on flow rather than ventilation. Because alveolar dead space is large during low-flow conditions, end-tidal CO2 is very low (frequently <10 mm Hg). If cardiac output increases, more alveoli are perfused and end-tidal CO2 rises (usually to >20 mm Hg during successful CPR). When spontaneous circulation resumes, the earliest sign is a sudden increase in end-tidal CO2 to greater than 40 mm Hg. Within a wide range of cardiac outputs, end-tidal CO2 during CPR correlates with coronary perfusion pressure,69 cardiac output,70 initial resuscitation,71,72 and survival.73 End-tidal CO2 measured during human CPR has been used to predict outcome. No patient with an end-tidal CO2 of less than 10 mm Hg could be successfully resuscitated.73 In the absence of invasive pressure monitoring, end-tidal CO2 monitoring can be used to judge the effectiveness of chest compressions, and quantitative waveform capnography is encouraged for use during all resuscitations. Attempts should be made to maximize the value by alterations in technique or drug therapy. Sodium bicarbonate administration results in the liberation of CO2 in the venous blood and a temporary rise in end-tidal CO2. Therefore, end-tidal CO2 monitoring will not be useful for judging the effectiveness of chest compressions for 3 to 5 minutes following bicarbonate administration.