4 Physiology of VentilationDuring Cardiac Arrest

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From: Contemporary Cardiology: Cardiopulmonary Resuscitation Edited by: J. P. Ornato and M. A. Peberdy © Humana Press Inc., Totowa, NJ

4 Physiology of Ventilation During Cardiac Arrest

Andrea Gabrielli, ^MD , A. Joseph Layon, ^MD , ^FACP , and Ahamed H. Idris, ^MD

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INTRODUCTION

Ventilation—the movement of fresh air or other gas from the outside into the lungs and alveoli in close proximity to blood for the efficient exchange of gases—enriches blood with oxygen (O

) and rids the body of carbon dioxide (CO

) by movement of alveolar gas from the lungs to the outside (1).

The importance of ventilation in resuscitation is reflected in the “ABCs” (Airway,

Breathing, Circulation), which is the recommended sequence of resuscitation practiced

in a broad spectrum of illnesses including traumatic injury, unconsciousness, and respi-

ratory and cardiac arrest (CA). Since the modern era of cardiopulmonary resuscitation

(CPR) began in the early 1960s, ventilation of the lungs of a victim of CA has been

assumed important for successful resuscitation.

Recently, this assumption has been questioned and is currently being debated (2).

Several laboratory studies of CPR have shown no clear benefit to ventilation during the early stages of CA (3–5). Furthermore, exhaled gas contains approx 4% CO

and 17% O

, thus making mouth-to-mouth ventilation the only circumstance in which a hypoxic and hypercarbic gas mixture is given as recommended therapy (6). The introduction of the American Heart Association’s (AHA) Guidelines 2000 for Cardiopulmonary Resuscita- tion emphasizes a new, evidence-based approach to the science of ventilation during CPR.

New evidence from laboratory and clinical science has led to less emphasis being placed on the role of ventilation following a dysrhythmic CA (arrest primarily resulting from a cardiovascular event, such as ventricular fibrillation [VF] or asystole). However, the classic airway patency, breathing, and circulation CPR sequence remains a fundamental factor for the immediate survival and neurological outcome of patients after asphyxial CA (CA primarily resulting from respiratory arrest).

This chapter reviews pulmonary anatomy and physiology, early studies of ventilation in respiratory and CA, the effect of ventilation on acid–base conditions and oxygenation during low blood flow states, the effect of ventilation on resuscitation from CA, manual, mouth-to-mouth, and newer techniques of ventilation, and current recommendations for ventilation during CPR.

HISTORY OF ARTIFICIAL VENTILATION AND CPR TECHNIQUES With the onset of CA, effective spontaneous respiration quickly ceases. Attempts to provide ventilation for victims of respiratory and CA have been described throughout history. Early descriptions are found in the Bible (7) and in anecdotal reports in the medical literature of resuscitation of victims of accidents and illness. Early examples of mouth-to-mouth ventilation are described in the resuscitation of a coal miner in 1744 (8), and in an experiment in 1796 demonstrating that expired air was safe for breathing (9).

In 1954, Elam and colleagues described artificial respiration with the exhaled gas of a rescuer using a mouth-to-mask ventilation method (10,11). Descriptions of chest com- pression to provide circulation (12) can be found in the historical literature of more than 100 years ago. Electrical defibrillation has been applied in animal laboratory research since the early 1900s, and by Kouwenhoven in 1928 (11).

The modern era of CPR began when artificial ventilation, closed-chest cardiac mas- sage, and electrical defibrillation were combined into a set of practical techniques to initiate the reversal of death from respiratory or CA. Resuscitation is associated with hypoperfusion and consequent ischemia. Recent studies suggest dual defects of hypoxia and hypercarbia during ischemia (13). Thus, the primary purpose of CPR is to bring oxygenated blood to the tissues and to remove CO

from the tissues until spontaneous circulation is restored. In turn, the purpose of ventilation is to oxygenate and to remove CO

from blood. The “gold standard” of providing ventilation during CPR is direct intubation of the trachea, which not only affords a means of getting gas to the lungs, but also protects the airway from aspiration of gastric contents and prevents insufflation of the stomach. Because this technique requires skill and can be difficult during CA, other airway adjuncts have been developed when intubation is contraindicated or impractical because of user skill.

Before the arrival of an ambulance, ventilation given by bystanders must employ

techniques that do not require special equipment. Manual methods of ventilation (i.e., the

Sylvester method, the Shafer prone pressure method, and so on) consisting of the rhyth-

mic application and release of pressure to the chest or back and lifting of the arms had been in widespread use for 40 to 50 years prior to the rediscovery of mouth-to-mouth venti- lation. These manual techniques were taught in Red Cross classes, to lifeguards, in the military, and in the Boy Scouts as recently as the 1960s, before being replaced by mouth- to-mouth ventilation as the standard for rescue breathing. Safar and Elam first showed that obstruction of the upper airway by the tongue and soft palate occurs commonly in victims who lose consciousness or muscle tone and that ventilation with manual tech- niques is markedly reduced or prevented altogether by such obstruction (14,15). Subse- quently, Safar and colleagues developed techniques that prevent obstruction by extending the neck and jaw and applying this in conjunction with mouth-to-mouth ventilation (16).

Although mouth-to-mouth ventilation has been studied extensively in human respiratory arrest and has been shown to maintain acceptable oxygenation and CO

levels, its evalu- ation in laboratory models of CA and in actual human CA has been limited.

PULMONARY PHYSIOLOGY

DURING LOW BLOOD FLOW CONDITIONS

Effects of Hypoxemia and Hypercarbia on Pulmonary Airways

During respiratory and CA, hypoxemia and hypercarbia gradually increase over time.

The concentrations of both oxygen and CO

affect ventilation and gas exchange. Hypox- emia has variable effects on airway resistance, which is the frictional resistance of the airway to gas flow and is expressed by:

Airway resistance (cm H₂O/L/s) = pressure difference (cm H₂O)/flow rate (L/s)

A number of studies in animals and humans, albeit with effective circulation, have shown that hypocapnia causes bronchoconstriction resulting in increased airway resis- tance, although the effect of hypercapnia on the airways is inconclusive (17–22). In one study, when end-tidal CO

was increased from between 20 and 27 mmHg to between 44 and 51mmHg, airflow resistance decreased to 29% of the initial mean (17). However, other studies have shown that hypercapnia causes an increase in airflow resistance through a central nervous system (CNS) effect mediated by the vagus nerve (18–22). It appears that hypocapnia causes bronchoconstriction and increased resistance to flow through a direct local effect on airways, although hypercapnia causes increased airway resistance through action on the CNS (18–22).

Hypoxic Pulmonary Vasoconstriction

HPV is a physiologic mechanism that minimizes venous admixture by diverting blood from underventilated, hypoxic areas of the lung to areas that are better ventilated (23).

Pulmonary vessels perfusing underventilated alveoli are normally vasoconstricted. This effect is opposed by increases in the partial pressure of O

. HPV matches local perfusion to ventilation, increasing with low airway PO

and low mixed venous PO

. The greater the hypoxia, the greater the pulmonary vasoconstriction until a point is reached in which vasoconstriction becomes so intense and widespread that the response becomes patho- logic and pulmonary hypertension develops (24,25).

HPV is inhibited by respiratory and metabolic alkalosis and potentiated by metabolic

acidosis (26). Additionally, pulmonary vasoconstriction is more pronounced when pul-

monary artery pressure is low and is attenuated by increased pulmonary vascular pressure

(26). Hence, a consequence of low inspired O

concentration, as occurs during mouth- to-mouth ventilation, could be decreased blood flow caused by increased pulmonary vascular resistance. Whether HPV occurs during CA and CPR is unknown, and warrants evaluation because hypoxemia occurs commonly.

The Ventilation/Perfusion Ratio (V/Q Ratio): The Relationship of Blood Flow and Ventilation During Low-Flow Conditions

During normal cardiac output, ventilation is closely matched with perfusion through a series of physiologic mechanisms exemplified by the maintenance of alveolar and arterial PCO

within a range close to 40 mmHg at rest. However, during low blood flow states, the ventilation–perfusion relationship becomes altered.

When systemic blood flow decreases, the flow of blood through the lungs decreases as well. With less venous CO

delivered to the lungs, less is available for elimination via exhalation and the concentration of CO

in exhaled gas decreases. Because CO

elimi- nation is diminished, CO

accumulates in venous blood and in the tissues. Mixed venous PCO

thus reflects primarily systemic and pulmonary perfusion and is an indicator of the tissue acid–base environment. On the other hand, during low-flow conditions arterial PCO

and PO

reflect primarily the adequacy of alveolar ventilation. During low rates of blood flow, if alveolar ventilation is adequate, blood flowing through the pulmonary capillary bed is over-ventilated because of a large ventilation–perfusion mismatch. The relationship between alveolar ventilation and pulmonary blood flow is expressed in the ventilation–perfusion ratio equation (27):

V

Q

v

in which VA is alveolar ventilation; Q is the volume of blood flowing through the lungs each minute; 8.63 is a factor relating measurements made at body temperature, ambient pressure, and saturated with water vapor to measurements made at standard temperature, pressure, and dry; R is the respiratory exchange ratio (CO

minute production/O

con- sumption); CaO

is arterial oxygen content; CvO

is mixed venous oxygen content; and PACO

is the partial pressure of alveolar CO

.

This equation appears simple, but it can be solved only by numerical analysis with a computer because alveolar PO

is an implicit variable (i.e., alveolar PO

decreases when alveolar PCO

increases). The ventilation–perfusion ratio equation predicts that as pul- monary blood flow decreases (increasing VA/Q ratio), arterial PO

and mixed venous PCO

will increase and arterial PCO

will decrease. It predicts that as pulmonary perfu- sion is further reduced (VA/Q ratio approaches infinity), arterial PO

and PCO

approach the composition of inspired gas. In contrast, if blood flow is present, but alveolar venti- lation is absent (VA/Q ratio is 0), arterial PO

and PCO

approach the composition of mixed venous blood. A study of ventilation during precisely controlled low blood flow conditions found that arterial and mixed venous blood gases behaved as the equation predicts: as blood flow decreased, arterial PCO

decreased and PO

increased (28).

Although mixed venous gas provides more accurate information regarding flow status

during resuscitation, it can be obtained during CPR only rarely, when and if a pulmonary

artery catheter is already present. Animal laboratory work seems to suggest that the

intraosseous blood gas analysis can be a viable alternative to venous pH and PCO

measurements during cardiopulmonary resuscitation. In a swine pediatric model of

hypoxic CA, the intraosseous blood gas correlated closely to the mixed venous gas

within 15 minutes of CPR. Beyond this time, the intraosseous blood gas reflected more local acid–base conditions or the effect of intraosseous administration of medications than mixed venous blood gas (29).

Gas Exchange and the Transport of Oxygen and Carbon Dioxide in Blood Hemoglobin is the principle protein of red blood cells (RBCs) and functions impor- tantly in the transport of O

and in the elimination of CO

through the carbamate and bicarbonate pathways (30). Although hemoglobin is usually considered solely in its role as a carrier of oxygen from the lungs to the tissues, it has an equally important role as a carrier of CO

from the tissues to the lungs. Deoxyhemoglobin binds about 40% more CO

than oxyhemoglobin and, conversely, when hemoglobin becomes oxygenated dur- ing passage through the lungs, CO

is actively driven off. This mechanism is referred to as the Bohr-Haldane effect and is responsible for about 50% of the total CO

excreted by the lungs during each circulation cycle (31,32). The principle mechanism of the Bohr- Haldane effect is the binding of CO

as carbamate compounds to the _-amino groups of hemoglobin (33,34). When oxygen is released by hemoglobin in the tissues, a change takes place in the shape of the hemoglobin molecule making binding sites available for the uptake of CO

(35). When hemoglobin takes up O

in the lungs, the change in hemoglobin conformation repels CO

and promotes its excretion. Plasma proteins also function in the transport of CO

, but have only one-eighth the buffering capacity of hemoglobin (36).

A small amount of CO

dissolves in plasma (5–10% of total CO

) and a much larger amount (60%) is converted to carbonic acid intracellularly in RBCs through catalytic hydration. Cellular membranes are extremely permeable to CO

. As RBCs traverse the tissue capillary bed, CO

diffuses into RBCs and it is converted by carbonic anhydrase to carbonic acid, which then dissociates to bicarbonate and proton. The conversion of CO

to bicarbonate would soon stop if protons were not buffered by hemoglobin, and bicarbonate would otherwise be trapped within the RBC because of its polarity, prevent- ing diffusion through the RBC membrane. However, a membrane transport system rap- idly exchanges plasma chloride for intracellular bicarbonate and preserves the CO

-carbonic acid-bicarbonate gradient (36). Another important aspect of the interac- tion of proton with hemoglobin is its effect on lowering the affinity of hemoglobin for oxygen, and by the law of action and reaction, oxygenation of hemoglobin lowers its affinity for proton. When hemoglobin is exposed to higher concentrations of CO

from respiring tissues, the formation of protons helps unload O

, which becomes available to tissues. When hemoglobin is oxygenated in the pulmonary capillaries, protons are released from hemoglobin and bicarbonate is converted back to water and CO

, which then diffuses out of the blood into the alveoli. Thus, oxygenation of hemoglobin actively promotes the pulmonary excretion of CO

, and CO

from tissues promotes the release of O

from hemoglobin at the tissue level.

In summary, hemoglobin is the principle protein responsible for lung-to-tissue trans-

port of O

and tissue-to-lung transport of CO

. Hemoglobin transports CO

as carbamino

compounds and in the form of bicarbonate. It can be appreciated from these mechanisms

of CO

exchange and O

transport that alveolar oxygenation and ventilation as well as

pulmonary blood flow play crucial roles in the removal of CO

from the tissues. Because

pH and CO

levels affect the affinity of hemoglobin for O

, these issues are important

during the treatment of CA.

VENTILATION DURING LOW BLOOD FLOW CONDITIONS Effect of Ventilation on Acid–Base Conditions and Oxygenation Acid–base conditions and oxygenation are important issues in resuscitation from low blood flow states such as shock (37–42) and CA (43–48). Hypoxemia and hypercarbic acidosis critically reduce the force of myocardial contractions (49–53), make defibrilla- tion difficult (54,55), and are associated with poor outcome (54,55). It has been observed that, during CA, arterial blood gases do not reflect tissue conditions and that mixed venous blood has a level of CO

that is frequently twice the level of the arterial side (51,52,58).

Arterial and mixed venous metabolic acidosis and mixed venous hypercarbic acidosis are associated with failure of resuscitation from CA (43,46,48). Studies of both human and animal CA have shown that during CPR, the pH of blood is largely determined by the concentration of CO

(56–71) and that arterial blood is often alkalemic although mixed venous blood is acidemic because of differences in CO

levels. A recent Norwe- gian study measured arterial PCO

and pH in patients receiving tidal volumes of 500 mL vs 1000 mL several minutes after intubation during out-of-hospital CA (mean time of approx 15 minutes) (72). The study showed that mean PCO

was 28 and 56 mmHg with 1000 mL and 500 mL tidal volume, respectively. These results indicate that tidal volume affects arterial PCO

and pH significantly: larger tidal volume is associated with respi- ratory alkalosis and smaller tidal volume is associated with respiratory acidosis.

The arteriovenous PCO

gradient increases substantially during CPR and returns to near normal when spontaneous circulation is restored (13,38,57,62,64,73–75). The CO

gradient likely results from reduced blood flow through the lungs, decreased pulmonary elimination of CO

accumulation of CO

on the venous side of the circulatory system, and over-ventilation of blood entering the arterial side (13,56,62,73). A recent study showed that changes in ventilation could affect excretion of CO

even when blood flow rate is as low as 12% of normal (28). Additionally, with decreasing blood flow, the decrease in end-tidal CO

parallels the decrease in arterial PCO

. Thus, both arterial PCO

and end-tidal CO

vary directly with blood flow, although mixed venous PCO

varies inversely with blood flow.

Mixed venous PCO

and pH can be improved with proper ventilation and becomes worse with hypoventilation. Because mixed venous blood gases reflect tissue acid–base status, intracellular hypercarbia can be altered with ventilation, which emphasizes the potential importance of ventilation during low blood flow states.

Effect of Ventilation on VF and Defibrillation

Sudden death is thought to be a primary cardiac electrical event and may not be a result

of myocardial injury, although there is often underlying myocardial ischemia, which can

reduce electrical stability and lead to ventricular ectopy. The event is often fatal and is

probably initiated by ventricular tachycardia (VT), or VF. Investigations have shown that

hypoventilation, hypoxemia, hypercarbia, and metabolic acidosis can lower the thresh-

old for VF as well as affect the tendency of the heart to develop ventricular arrhythmias

(VAs). Furthermore, arterial hypoxemia has been shown to cause arrhythmia by excita-

tion of the autonomic nervous system and by affecting vagal tone (76). Both hyperven-

tilation and hypoventilation are associated with severe VA and supraventricular

arrhythmias (77). Hypoxemia and other issues such as hypoglycemia, hyper- and hypo-

kalemia cause VF by shortening the duration of the cardiac action potential (78).

Hypercarbia without hypoxemia lowers the VF threshold and respiratory alkalosis raises the VF threshold and enhances spontaneous recovery from VF (79). In another study, ischemia, but not hypoxemia, lowered the VF threshold (80).

The effect of ventilation on the defibrillation threshold, which is the minimum elec- trical energy required for defibrillation of a fibrillating ventricle, has not been studied directly. Instead, the defibrillation threshold has been investigated under conditions of hypoxemia, and metabolic and hypercarbic acidosis, either alone or in combination (46,48,54,81). The findings of different studies have been somewhat contradictory, but generally show the defibrillation threshold is unaffected by acid–base conditions existing either before or during CPR. However, more recent studies using animal models of CA suggest that hypercarbia is associated with VF refractory to defibrillation (46,52,55).

Coronary perfusion pressure, duration of untreated VF, and duration of CPR are critical issues known to affect success of defibrillation (82).

A human study of issues that influenced the success of defibrillation found that arterial hypoxemia and acidemia, and delay in defibrillation attempts were associated with fail- ure to defibrillate (54), but it was not possible to distinguish the effect of these issues independently because they tended to occur together. A canine study, in which ischemia, ventricular hypertrophy, hypoxemia, acidosis, and alkalosis were well-controlled inde- pendent variables, did not find an adverse effect of these issues on defibrillation threshold (81). Surprisingly, hypoxemia was found to lower the threshold for defibrillation. Another study found that metabolic acidosis, but not metabolic alkalosis or respiratory acidosis or alkalosis lowered the threshold for VF (83). More recent laboratory CPR studies of hypercarbic acidosis found a substantial reduction in rate of resuscitation. Although the defibrillation threshold was not investigated, four of six animals ventilated with 50% CO

had refractory VF (46). In other studies of acid–base conditions, most animals with sufficient coronary perfusion pressure during CPR were defibrillated, but only animals without substantial hypercarbia recovered adequate cardiac output (52,55,84–88). A recent study of human CPR also found that return of spontaneous circulation was asso- ciated with improved levels of arterial and mixed venous PO

and PCO

(44).

There are important differences in physiology during normal cardiac output and CPR that may not be widely appreciated. For example, high levels of arterial and mixed venous hypercarbia are usually tolerated well by humans (89) and animals (46,90–93) when there is normal spontaneous cardiac output. Nevertheless, during CA, hypercarbia substan- tially reduces success of resuscitation by adversely affecting myocardial contractility (46,52,55,84–88). At least one laboratory study found that hypercarbia was associated with refractory VF (55). In this rat model, very high levels of inspired and thus, myocar- dial PCO

were produced and may help explain the difference in findings of another study (81) that used more modest levels of hypercarbia and failed to find an effect on defibril- lation threshold.

Among issues that can affect the likelihood of defibrillation, the duration of VF is of great importance (94). In human CPR, the rate of successful defibrillation is approx 80%

if administered immediately after onset of VF, but the chance of success decreases approx

5% for each additional minute of VF (95,96). After 12 minutes of VF with CPR, the rate

of success is only about 20%. A similar effect of duration of VF is seen in laboratory CPR

models (97–99) and may be explained, in part, by the gradual depletion of myocardial

adenosine triphosphate, which is thought to be a marker for ischemic tissue damage and

the metabolic state of the myocardium (100). Additionally, potassium uptake by myocar-

dial cells is increased during VF and is related to hydrogen ion, CO

, and lactate produc-

tion (101). Earlier work found that the ratio of intracellular to extracellular potassium concentration affected the defibrillation threshold (102).

In summary, hypoxemia and hypercarbia decrease the threshold for VF. Hypoxemia and hypercarbia have a negligible effect on the defibrillation threshold when the duration VF is brief. Recent studies suggest that hypoxemia and hypercarbia make defibrillation more difficult when VF persists for several minutes or more.

Effect of Ventilation on Myocardial Force and Rate of Contraction Studies using an isolated heart model demonstrated that hypoxia and hypercarbia caused a profound decrease in myocardial force of contraction independent of pH (53,103–106). Studies examining the effect of hypercarbia on isolated spontaneously contracting myocytes have found that rate and force of contraction are inhibited by modestly increased concentrations of CO

, with pH held at 7.40 and PO

at 142 mmHg (107). The model demonstrated a rapid and profound effect of CO

independent of pH, PO

, vascular tone, neuroendocrine issues, or inflammatory mediators. In contrast, iso- lated decreased blood or perfusate pH is not associated with reduced ventricular force of contraction (49–53). The reason for these differences in myocardial response to extracel- lular CO

and hydrogen ion is that CO

is a nonpolar, lipid soluble molecule that is permeable to cellular membranes and diffuses rapidly into the intracellular space. Once CO

enters the cell, it lowers intracellular pH by dissociating to hydrogen ion and bicar- bonate. In contrast, hydrogen ion is polar, diffusing at a very slow rate through cell membranes, and this may account for its lack of effect on myocardial dynamics under most experimental conditions (108). There is accumulating evidence that reduced intra- cellular pH affects calcium ion flux, exchange, and binding and ultimately affects exci- tation–contraction coupling and myocardial contractility (108).

During VF, the heart continues to perform work and very likely has energy utilization greater than during normal contractions; metabolites in the form of hydrogen ion, lactate, and CO

continue to be produced. With the onset of VF, myocardial CO

tension increases rapidly from a normal value of approx 50 mmHg to 350 mmHg and there is a parallel increase in hydrogen ion concentration (74,103). As we have noted above, the removal of CO

from tissues is dependent on blood flow; thus, coronary blood flow is an important cofactor influencing levels of myocardial CO

. A coronary perfusion pressure of less than 10 mmHg was associated with myocardial CO

tensions 400 mmHg or more and failure of resuscitation, although a coronary perfusion pressure of greater than 10 mmHg was associated with myocardial CO

tensions 400 mmHg or less and successful resuscitation (109). Decreased intracellular pH is associated with changes to the structure and function of regulatory and enzyme proteins and if not corrected soon enough leads to irreversible loss of cell function and cell death (110).

In summary, both isolated hypoxemia and isolated hypercarbia have a negative ino-

tropic effect on the heart. Ischemia would be predicted to be a more injurious event than

hypoxemia or hypercarbia alone, because ischemia causes both decreased delivery of O

and decreased elimination of tissue CO

. To the extent that ventilation can affect the

elimination of CO

and enhance tissue oxygenation, it can likely provide some benefit

during CA and CPR. There are promising therapies that perfuse the heart with oxygen-

containing fluorocarbon compounds (SAPO: selective aortic arch perfusion and oxygen-

ation) resulting in higher rates of restoration of spontaneous circulation after prolonged

CA and CPR (111).

Hypoxemia, Hypercarbia, and the Vasopressor Effect of Catecholamines The importance of the administration of such catecholamines as epinephrine during CPR cannot be overstated. Numerous studies and years of experience treating CA have shown that epinephrine is often a pivotal factor in reversing sudden death by increasing coronary perfusion pressure and the likelihood of defibrillation (112). The interaction of ventilation and the vasopressor activity of epinephrine and other catecholamines need to be examined.

A number of studies have shown that increases in blood PCO

in animal models and in humans results in a decrement of the pressor response to epinephrine and norepineph- rine by more than 50% (113–115). The mechanism for the failure of blood pressure to increase is primarily decreased peripheral vasoconstriction and vascular resistance (113–

119) with a smaller contribution caused by a cardiac arrhythmia other than tachycardia (113–115). Metabolic acidosis (i.e., increased hydrogen ion concentration) has also been found to inhibit vasoconstriction, but to a much smaller degree than “respiratory” acidosis (i.e., increased PCO

; 119). With return of CO

to normal levels, the inhibitory effect of hypercarbia on epinephrine activity is reversed completely within 10 minutes in human volunteers with normal cardiac function (118).

Hypoxemia also has been found to decrease the pressor response to epinephrine (51).

Hypoventilation, through simultaneous hypoxemia and retention of CO

, causes greater peripheral vasodilation and loss of the pressor effect of epinephrine than isolated hypercarbia or hypoxemia alone (51). There are few studies specifically examining the effect of ventilation on the pressor response to catecholamines during CA and CPR.

Successful resuscitation is associated with epinephrine-induced increases in coronary perfusion pressure, and there are data suggesting that hypoxemia and hypercarbia may modulate the increase (120,121).

Hemodynamic Effects of Ventilation

Mean intrathoracic pressure is higher during positive pressure ventilation (PPV) than during spontaneous breathing. During normal heart function, increased intratho- racic pressure decreases right and left ventricular filling. If sufficient airway pressure is applied, pulmonary vascular resistance increases. The effect of lung inflation on pulmonary vessels is complex. At abnormally low lung volumes, vessels are collapsed and pulmonary vascular resistance is increased (27). When the lung is inflated, col- lapsed vessels open and resistance decreases. Alveolar capillaries are compressed and resistance increases at high inflation volumes. Underventilation and ventilation perfu- sion mismatch at low lung volumes results in a progressive decrease in lung compliance and an increase in alveolar-arterial oxygen tension difference. Because blood flow is related inversely to pulmonary vascular resistance, if the lungs are poorly inflated during CPR, pulmonary blood flow may possibly decrease further. The _-adrenergic effect of epinephrine during CA specifically depresses PaO

absorption and CO

elimi- nation of low V/Q lung units. Interestingly, vasopressin has significantly less adverse effect on pulmonary gas exchange, after CPR. It has been speculated that vasopressin could rehabilitate the pulmonary circulation through the agonist effect of the V

vasopressinergic receptor (122). However, there are little data available in this area.

A number of studies have shown that PPV can impair cardiac output in normally

functioning hearts, and that positive end-expiratory pressure can impair cardiac output

further because of increased intrathoracic pressure, which reduces venous return (123–

125). In fact, positive end-expiratory pressure has been used to create a model of func- tional hypovolemia to study the effect of conventional and high frequency jet ventilation on cardiac output and blood pressure (126). In this study, conventional ventilation during conditions of functional hypovolemia resulted in decreased cardiac output and arterial blood pressure, although high frequency jet ventilation did not affect hemodynamics, probably because of lower airway pressure, lower intrathoracic pressure, and improved venous return.

In contrast to the physiology of ventilation and blood flow during spontaneous cardiac circulation, the physiology of blood flow is somewhat different during CPR with external chest compression. Chandra et al. have shown convincingly that blood enters the lungs from the right heart during periods of low intrathoracic pressure corresponding to the release of pressure on the chest, although forward flow of blood from lungs to the left heart and then out to the systemic circulation takes place during chest compression and is associated with increased intrathoracic pressure (127). Furthermore, intrathoracic pressure can be increased even more with high airway pressure (70–80 mmHg) ventila- tion simultaneous with chest compression, which is associated with increases in carotid blood flow and cerebral perfusion (128–130). The application of negative airway pres- sure during the release phase further enhances carotid blood flow by increasing venous return to the chest. Another study showed that arterial pressure and blood flow during chest compressions is related directly to peak intrathoracic pressure up to pressures as high as 50 mmHg, beyond which no further increases in blood flow occur (131). Continu- ous positive airway pressure ventilation (CPAP or postive end-expiratory pressure [PEEP]) given during both the compression and release phase of chest compression would be expected to interfere with venous return and to decrease blood flow just as it does during spontaneous circulation (132). PEEP can also be the inadvertent result of excessive tidal volume, increased respiratory rate and reduced inspiratory time (auto- PEEP) and is associated with an increased incidence of pulseless electrical activity during resuscitation (133).

An impedance threshold device that causes negative intrathoracic pressure during CPR and hemorrhagic shock has been shown to increase venous return, right myocardial preload, blood pressure, and blood flow to the heart and brain (134–137). It also has been shown to improve survival from CA and hemorrhagic shock. The device is based on the physiologic principle that negative intrathoracic pressure enhances venous blood return to the chest and heart thus making increased cardiac output possible.

Another very important study was performed in the setting of hemorrhagic shock using PPV. This study showed that blood pressure decreased progressively as ventilation rate increased from 12 breaths to 30 breaths per minute (bpm; 138). More importantly, sys- tolic blood pressure improved from 66 to 84 mmHg when ventilation rate was decreased from 12 breaths to 6 bpm and the lower rate was associated with a significantly improved survival. The study emphasizes the principle that the duration of increased intrathoracic pressure is proportional to the ventilation rate when PPV is used. Another principle is that blood pressure is inversely proportional to ventilation rate.

Application of CPAP without active ventilation has been recently studied in CPR. In

a pig model of CA, CPAP titrated to achieve 75% of a baseline end-tidal CO

was

compared with intermittent PPV (139). A significant difference in both airway pressure

and diastolic blood pressure could be detected between the two techniques (27 ± 58 mmHg

in CPR vs 13 ± 11 mmHg in CPR

), and there was an improvement in arterial and mixed

venous pH, O

saturation, and CO

in the CPR

animals. Cardiac output did not change significantly between the two methods. This technique has the potential advan- tage of simplifying CPR, decreasing pulmonary atelectasis, and improving both oxygen- ation and ventilation. However, it can also have a negative effect on diastolic blood pressure and, thus, on both coronary and cerebral blood flow.

Despite the potential for decreased venous return, it is possible that very small amounts of positive airway pressure may decrease intrapulmonary shunting, pulmonary vascular collapse, and atelectasis without adverse hemodynamic effects. In fact, recent use of a multislice CT scanner to allow dynamic imaging of tridimensional volume of the lung during CPR suggested that CPAP was superior to simple volume controlled ventila- tions or no ventilations CPR in maintaining better lung distension and preventing atelectasis (140).

In conclusion, movement of venous blood into the lungs takes place during the release phase of external chest compression when intrathoracic pressure is low. When the chest is compressed, intrathoracic pressure rises and blood moves out of the lungs and heart and into the systemic circulation. Negative airway pressure enhances blood flow and venous return to the chest, although CPAP ventilation inhibits venous return and blood flow but decreases lung atelectasis. These studies emphasize the crucial relationship between ventilation mechanics and circulation.

The Effect of Ventilation on Outcome From Resuscitation

For more than 30 years, emergency ventilation has been considered an essential com- ponent of CPR. There are few studies and little direct evidence that ventilation affects outcome from CA, although it has been assumed crucial for resuscitation. Recommen- dations for ventilation were based on studies performed in the 1950s and 1960s in living humans with normal cardiac output (14–16). These studies presumed that the goal of ventilation during CPR was to achieve near “normal” tidal volumes and minute ventila- tion. However, substantially less ventilation may be sufficient for gas exchange during CPR because cardiac output and pulmonary blood flow are only 10%–15% of normal during manual chest compression (130). As a consequence, the amount of hemoglobin passing through the pulmonary bed is reduced and the amount of oxygen necessary to saturate hemoglobin is also reduced if there is not a large ventilation/perfusion mismatch.

Because venous return and thus the quantity of CO

delivered to the lungs are decreased, the amount of ventilation necessary to remove CO

is presumably reduced.

The time when ventilation must be initiated during CPR to achieve satisfactory results

and the ventilatory requirements during CPR is unclear. In a canine model of CA, arterial

pH, PCO

, and PO

had no significant change after 5 minutes of untreated VF (141),

although arterial PO

decreased from 81 to 69 mmHg under similar conditions in a swine

model (142). In the canine study, there was no significant change in arterial PO

and PCO

for 30 seconds after initiation of chest compressions without ventilation. At 45 seconds,

arterial PO

was 52 mmHg, a significant decline. Another canine study showed that chest

compression alone without assisted ventilation will produce a minute ventilation of 5.2 ±

1.1 L per minute and will maintain O

saturation at 90% or more for more than 4 minutes

(4). A murine study found that chest compression alone produced tidal volumes of 26% of

baseline and although arterial PCO

increased to 80 mmHg after 9 minutes, resuscitation

rate was not impaired (5,143). The animals were intubated in all of these studies. It is

likely that ventilation induced by chest compression would be less in nonintubated models,

but the way this would affect blood gases is unknown.

Other studies have shown that ventilation has an important role in resuscitation. An early study showed that well oxygenated dogs had better carotid artery blood flow than asphyxiated dogs. This was attributed to loss of peripheral vascular tone (144). Weil and colleagues showed that spontaneous gasping during CA in a swine model favored suc- cessful resuscitation and also showed that both the frequency and duration of gasps correlated with coronary perfusion pressure and predicted outcome (145).

More recent studies were designed specifically to test the effect of ventilation on outcome in swine models of CPR. One study compared a group receiving mechanical ventilation during CPR with a group receiving chest compression alone and a group without chest compression or ventilation. The duration of untreated VF was 30 seconds followed by 12 minutes of CPR in the treatment groups. All animals were successfully defibrillated and entered a 2-hour intensive care period. However, after 24 hours, only two of eight animals that had no CPR survived, although all 16 animals survived in the groups receiving chest compression with and without ventilation (3). Another study allocated 24 swine to groups with and without ventilation during 10 minutes of chest compression following 6 minutes of untreated VF. Nine of twelve ventilated animals and only 1 of 12 nonventilated animals had return of spontaneous circulation. The nonventilated animals died with significantly greater arterial and mixed venous hypox- emia and hypercarbia (146). A follow-up study was done to test whether hypoxemia or hypercarbia independently affects survival from CA. Using a swine model of isolated arterial and mixed venous hypoxemia without hypercarbia in one group and isolated hypercarbia without hypoxemia in another group, there was only one of ten animals with return of spontaneous circulation in each group (121).

Other experimental work in large animal survival and neurological outcome up to 48 hours were not different when ventilation was withheld during resuscitation. These initial studies, although clearly de-emphasizing the importance of ventilation during the first few minutes of CPR, were limited by the persistence of an “artificial” patent airway in the animal, which resulted from the presence of an endotracheal tube (ETT) allowing exchange of ventilations from gasping and chest compressions/decompressions (147,148).

More recent studies eliminated the possible influence of an artificial patent airway in animal models during CPR. When standard CPR was compared with compression-only CPR in a pig model in which the airway was occluded, no difference was found in 24-hour outcome (149). It is important to note that a supine, unconscious dog or pig usually has a patent airway, whereas a supine, unconscious human has an obstructed airway resulting from the kinked nature of the human airway. These model differences are rarely discerned in CPR ventilation experiments but do have fundamental clinical importance. These latest observations confirmed that ventilation for a few minutes after dysrhythmic CA was not fundamental and suggested the need to test the no-ventilation hypothesis in humans (150).

There are important differences between all these studies including duration of untreated VF, the use of 100% O

before CA, and whether or not agonal respirations were prevented with a paralytic agent. However, taken together, these studies provide some evidence that ventilation may possibly be withheld when chest compression is initiated promptly after CA, but that ventilation is important for survival when chest compression is delayed.

There are even fewer human studies of the role of ventilation during CA. Because

ventilation is such a well-accepted intervention, the ethical considerations of doing a

controlled study by withholding ventilation in one group has been difficult to overcome.

Indirect evidence pointing to a less important role of ventilation immediately after CA has existed since the early 1990s. For example, in Seattle, where ambulance response time is short, patients who were seen to have spontaneous agonal respiratory efforts immediately after CA had a higher rate of successful resuscitation (151). Another study found that hypoxemia and hypercarbia was associated with the use of the esophageal obturator airway in the field and also a lower resuscitation rate (65). Mixed venous oxygenation saturation is associated with prognosis for survival from CA; mixed venous pH, PO

, and PCO

measured during hemorrhagic shock and CA were significantly better in those with return of spontaneous circulation (44,152). In the Netherlands, clinical CPR is given in the order “CAB” (Chest Compression–Airway–Breathing) with ventilation being delayed and chest compression being initiated as soon as possible. Using “CAB,”

CPR survival data from the Netherlands is comparable to that reported in the United States (153). Human data also suggest that prompt chest compression following CA improves brain and heart perfusion and the success of defibrillation (154).

Related to this, more human studies became available in the last few years. In a prospective, observational study of CPR and ventilation, chest compression-only CPR, and no CPR, survival from CPR (i.e., return of spontaneous circulation) was found to be 16%, 15%, and 6% respectively (155). Although both forms of basic life support (BLS) were significantly better than no CPR, there were no differences between CPR with or without ventilation. Similar results were reported more recently in North America in a study of telephone dispatcher-assisted BLS-CPR in which survival of compression- only CPR vs ventilation CPR was 14% vs 10%, respectively, with a slight trend of survival favoring chest compression-only CPR (156). Although this study emphasized that CPR without ventilation is better than nothing, it presents several limitations in design. Mouth-to-mouth ventilation performed by a bystander was assessed by emer- gency medicine dispatcher only and not by the investigator at the scene; the patency of the airway was unclear in some patients, and primary respiratory arrests were excluded.

Additionally, if the bystander knew how to perform CPR, then the patient was excluded from the study. Nevertheless, the study suggested a need to reconsider BLS with a goal of minimizing the time to onset of CPR in the CA victim and maximizing the efficacy of chest compression. When the concept of this “simplified CPR” was tested in a man- nequin, effective compression was achieved an average of 30 seconds earlier than with the standard technique, and the number of compressions per minute were approximately doubled (157).

Despite the overall enthusiasm for the relatively positive results of dispatcher-assisted CPR instructions without ventilation as described by the providers (158,159), it has been emphasized by independent observers that the concept of no-ventilation CPR could be a misnomer, because, provided that the airway is open, patients undergoing VF often exchange a significant amount of air through gasping (160). Therefore, the term “CPR without assisted ventilation” has been suggested. Although the North American literature seems to de-emphasize the importance of ventilation in the first few minutes after CA, a recent Swedish report of 14,000 patients showed increased survival to one month for

“complete CPR” (both chest compressions and ventilation) vs “incomplete CPR” (com- pression only; survival, 9.7% vs 5.1%; p < 0.001; 161).

In this study, ventilation, and duration of less than 2 minutes between patient collapse

and the beginning of lay bystander CPR, were both powerful modifying issues on survival

at 30 days, emphasizing the need for better and earlier CPR. A limitation of these out-of-

hospital studies is the lack of proper neurological examination during or immediately

after resuscitation. Therefore, the relative influence of ventilation on cerebral perfusion is unclear. In swine models, pupillary diameter light reaction was used and found to have a reasonable correlation with cerebral perfusion pressure. However, the animal was ventilated during resuscitation with a tidal volume of 15 mL/kg at an FiO

of 1.0. It is unknown if these clinical findings could be used in a human prospective randomized study during CPR to evaluate the level of influence of ventilation on neurological out- come (162).

In summary, the standards for ventilation during CPR are based on studies that are somewhat contradictory and inconclusive. The amount of ventilation required during CPR is still unclear. It is likely that the number of bpm needed during conventional CPR is less than currently recommended. It is logical that ventilation should be matched with perfusion of blood through the lungs and the systemic circulation. Thus, when blood flow is 0, ventilation is unnecessary because it would not affect tissue oxygenation and CO

removal. However, with CPR techniques that improve blood flow, such as use of device adjuncts for chest compression, more ventilation may be necessary.

The duration of VF before the start of chest compression is likely to be of signifi- cance regarding the need for ventilation, although the importance of ventilation in CPR has been de-emphasized in favor of the need for more effective chest compression and early defibrillation. In fact, it is likely that time of defibrillation is an important factor in determining whether ventilation is necessary for successful resuscitation. The etiol- ogy of CA is another very important factor related to the role of ventilation in CPR.

Ventilation has primary importance when CA occurs from asphyxia, such as in drown- ing, and is the most frequent cause of pediatric CA.

TECHNIQUES OF VENTILATION DURING CPR

Ventilation Techniques That Can Be Used for Basic CPR by the Lay Public:

Manual, Mouth-to-Mouth, and Mouth-to-Mask Ventilation

In the 1950s and early 1960s, alternative methods of artificial respiration were inves- tigated additionally to mouth-to-mouth ventilation. A number of studies showed that the application of external pressure to the chest during manual maneuvers in normal volun- teers caused substantial respiratory tidal volumes that ranged from 50 to 1114 mL (10,14–

16,163–168). The rate of manual ventilation was 10–12 compressions per minute and

total minute ventilation (the product of tidal volume and respiratory rate per minute)

provided by these techniques was 0.5–11.1 L per minute. When these techniques were

applied to patients with pre-existing pulmonary disease, tidal volumes were considerably

less (50–540 mL) than in healthy subjects (168). These studies also noted that tidal

volumes generated by actively expanding the chest with arm-lift or hip-lift techniques

were 20–40% greater when compared with passive chest expansion (166). Techniques

that relied exclusively on passive chest expansion were ineffective for adequate ventila-

tion and resulted in mean arterial oxygen saturations of 67% in normal volunteer subjects

(163). Manual techniques that included active chest expansion produced mean arterial

oxygen saturations of 93% in human subjects, and thus were able to maintain acceptable

gas exchange without PPV (163). In contrast with the manual techniques previously

mentioned, pressure applied directly over the sternum of curarized, intubated volunteers

produced mean tidal volumes of only 156 mL. Furthermore, without intubation sternal

pressure produced no tidal exchange because of airway obstruction by the tongue (15).

However, with the head extended to prevent airway obstruction, five of six patients had tidal volumes greater than 340 mL and three of six had tidal volumes in excess of 500 mL.

Simultaneous with studies of manual ventilation techniques, mouth-to-mouth venti- lation was also studied extensively. Several research projects were funded by the Depart- ment of the Army because of the urgency of problems of resuscitation in nerve gas poisoning. In one study, 29 volunteers were paralyzed with curare, and mouth-to-mask resuscitation was started before the onset of cyanosis (169). The arterial oxygen satura- tion of the volunteers receiving artificial ventilation was never below 85% and the mean oxygen saturation was 94%. Alveolar CO

tensions, measured in 21 patients, were main- tained at or below 50 mmHg. The mean alveolar CO

concentration was 5.6% before resuscitation and 3.9% during resuscitation. Expired gas resuscitation produced a fall in alveolar CO

concentration in all 12 patients. The authors concluded that with mild hyperventilation, the rescuer readily converted his exhaled gas to a suitable resuscitation gas. These experiments were designed to simulate a respiratory arrest and only healthy volunteers were studied. Whether exhaled gas would benefit a patient who suffers CA was not considered and has not been investigated.

Because exhaled gas contains CO

, it may have adverse cardiovascular effects during CPR, but few investigations have addressed this issue. A study of the effect of ventilation on resuscitation during CPR using an animal model showed that both hypoxemia and hypercarbia independently have an adverse effect on outcome from CA. Swine were ventilated with experimental gas mixtures consisting of 85% oxygen in a control group, 95% O

and 5% CO

in a hypercarbic group, and 10% O

and 90% N

in a hypoxic group.

The model succeeded in producing isolated hypoxemia without hypercarbia and isolated hypercarbia without hypoxemia. Only 1 of 10 (10%) animals could be resuscitated in each of the hypercarbic and hypoxic groups, although 9 of 12 (75%) animals were resus- citated in the control group (121).

A study of the isolated effect of CO

on spontaneously contracting chick myocytes showed that myocytes perfused with 4.6% or 9.6% CO

had inhibition of both rate and force of contraction with both concentrations. The model demonstrated a rapid and profound effect of CO

independent of pH, PO

, vascular tone, neuroendocrine issues, or inflammatory mediators (107).

A study of the composition of gas given by mouth-to-mouth ventilation during simu- lated one- and two-rescuer CPR showed that the rescuers exhaled a mean concentration of CO

of 3.5% to 4.1% and a mean concentration of O

of 16.6% to 17.8% (6). Therefore, the gas given by mouth-to-mouth ventilation has a similar concentration of CO

and is more hypoxic than the gas shown to be deleterious in the above-cited animal study. When compared with mouth-to-mouth ventilation, room air is a superior gas for ventilation because it contains 21% oxygen and a negligible amount of CO

(0.03%).

Furthermore, when these gas concentrations were used in a swine model with 6 mL/

kg ventilation, profound arterial desaturation was noted and was shortly followed by

hemodynamic instability (170). This instability and desaturation were not observed if the

tidal volume was increased to 12 mL/kg, or if a fraction of inspired oxygen of 0.70 was

used with a tidal volume of 6 mL/kg. Two main features make older human studies

different from more recent animal laboratory experiences: the patients described in

the original case reports were typically paralyzed, and the rescuer hyperventilated to the

point of feeling dizzy, an arterial partial pressure of CO

of about 20 mmHg (10). These

differences highlight the need for more controlled human studies before recommending

withholding mouth-to-mouth ventilation during CA.

However an important factor might affect the feasibility of such studies: a widespread fear of acquiring contagious diseases from victims of CA that has recently resulted in reluctance among the lay public, and even some health professionals, to perform mouth- to-mouth ventilation.

Infectious disease concerns published in the literature include Helicobacter pylori, Salmonella, Herpes simplex virus, tuberculosis, HIV, and the hepatitides (171–174).

Being repulsed by the sight of a victim in agony and the fear of doing harm may also affect the decision to provide mouth-to-mouth ventilation. Recent surveys of CPR instructors reported that all would perform mouth-to-mouth ventilation on a 4-year-old drowned child, but only 54% on a college student, 35% on a hemophiliac, 18% on a stranger in a bus in San Francisco, and 10% on a person who had overdosed on heroin (175,176). Awareness of new infectious disease issues, if not new infectious diseases, has resulted in the current recommendation of the AHA to use barrier devices to protect the rescuer against contamination with any infective secretions (174). Effective barri- ers against contamination increase efficacy and effectiveness of CPR, helping the rescuer to overcome fear of contamination and to start resuscitation immediately.

However, the overall willingness to perform bystander CPR is disappointingly low in the United States, Europe, and Japan, both for lay bystanders and health care providers alike. Different reasons are likely responsible for this widespread attitude. In the United States and Europe, the factor deterring performance of mouth-to-mouth ventilation by a bystander or health care provider is fear of contracting infectious diseases. This does not seem to be the case in Japan, where unwillingness to perform mouth-to-mouth ventilation is mostly a result of lack of confidence in one’s ability to properly perform CPR (177). The difference may be related to the 200-fold lower incidence of HIV in Japan, as compared with the United States (178).

Education and increased retention of proper mouth-to-mouth ventilation technique is fundamental but difficult to apply to all populations. The use of television spots as a means of teaching basic skills of CPR in at-risk populations has been explored in Brazil. Although television spots seem to increase skill retention over 1 year, mouth- to-mouth ventilation and effective external cardiac compression are recognized as skills that are dependent on supervised practice with mannequins. Although the study is limited, it makes sense to use an alternative methodology to promote resuscitation skills in the lay population, including the use of educational clips or scenarios in entertaining and motivating television spots (179).

Although recent evidence-based literature acknowledges the importance and effi- cacy of CPR without ventilation, the need for assisted ventilation in CA with asphyxia (CA primarily resulting from respiratory arrest) or in pediatric populations (generally younger than 8 years of age) cannot be overemphasized (180). CA with asphyxia was originally illustrated in the first case of external chest compressions (181). The ratio- nale of ventilation during CPR for CA is based on the assumption that CPR delays brain death in no-flow situations, and that hypoxia and respiratory acidosis can aggra- vate the injury. A critical decrease of brain ATP of 25% below the normal level has been observed after 4 minutes in an animal model of decapitated normothermic dog (182).

In general, arterial partial pressure of oxygen is maintained within the normal range for approx 1 minute in a dog model of chest compressions without ventilation (183).

Furthermore, when asphyxia is the cause of CA, oxygen consumption has proceeded

to near complete exhaustion, and CO

and lactate have significantly accumulated just

before CA. This is in contrast with VF, in which hypoxemia and acidemia become significant only several minutes after the onset of CA. In a model of resuscitation after asphyxia (clamping of the ETT in an anesthetized pig), the animal subjects were ran- domly selected to receive resuscitation with and without simulated mouth-to-mouth ventilation. Return of spontaneous circulation was noted only when ventilation was added to chest compression (184). Successful chest compressions and mouth-to-mouth rescue breathing allowed complete neurological recovery in 90% of the animals.

The presence of a foreign body obstructing the airway is an uncommon, but impor- tant, cause of CA with asphyxia, with an incidence of 0.65 to 0.9 per 100,000 CAs (185). A recent study seems to support the original investigation of Ruben and MacNaughton (186), in that abdominal thrust is not necessary in foreign body choking, and that chest compressions can achieve higher airway pressure than the Heimlich maneuver (187). In fact, when CPR was performed and compared with an abdominal thrust in the cadaver, median and peak airway pressure (PAP) reached a value of 30 cm H

O vs 18 cm H

O and 41 cm H

O vs 26 cm H

O, respectively. The mean airway pressure produced by the Heimlich maneuver was higher than that produced with chest compression only in a moderately obese cadaver. The European Resuscitation Council (ERC) has recently addressed acute asphyxia from airway obstruction (188).

Despite recent knowledge that occurrence of VF in children may be more frequent

than previously thought (189), asphyxia is still the most common cause of CA in the

pediatric population. The Pediatric Resuscitation Subcommittee of the Emergency

Cardiovascular Care Committee of the AHA worked with the Neonatal Resuscitation

Program Steering Committee (American Academic of Pediatrics) and the Pediatric

Working Group of the International Liaison Committee on Resuscitation to review

recommendations on oxygenation and ventilation in neonatal resuscitation (190). The

approach to the recommendations has been the same as that described in the AHA

Guidelines 2000 for adults, which uses five classes of recommendations centered on

evidence-based medical data. Up to 10% of newborn infants require resuscitation at

birth. The majority, because of meconium airway obstruction/aspiration, require imme-

diate intervention and assisted ventilation. Because of their unique physiology, the

importance of ventilation/oxygenation in newborns cannot be overemphasized. Fluid-

filled lungs and intracardiac as well as extracardiac shunts at birth are physiologically

reversed in the first few minutes of extrauterine life with either spontaneous or assisted

vigorous chest expansion. Failure to normalize this function may result in persistence

of right-to-left, intracardiac and extracardiac shunt, pulmonary hypertension, and sys-

temic cyanosis. Bradycardia usually follows, with severe hemodynamic instability and

rapid deterioration to CA. Although these physiologic characteristics are typical of the

newborn (minutes to hours after birth), similar events can be triggered by hypoxia in

neonates (first 28 days of life) and infants (up to 12 months of age). The importance of

proper ventilation/oxygenation and the small margin of safety resulting from the unique

physiology and high oxygen consumption of the newborn mandate the need for imme-

diate ventilation and the presence of skilled personnel at the bedside to perform proper

basic steps of resuscitation. Clearance of meconium fluid should be the immediate

maneuver performed on birth and providing PPV should be considered within 30 sec-

onds when bradycardia or apnea is present. Tracheal intubation remains the gold stan-

dard for providing immediate ventilation/oxygenation to the newborn. European and

American guidelines have essentially the same sequence of resuscitative events in neo-

nates, recommending a chest compression-to-ventilation ratio of 3:1, with about 90