Cardiopulmonary arrest occurs in 1: 30 000 pregnancies. Although rare, optimal outcomes are dependent on the cause of the arrest, the rapid response team’s understanding of the physiological effects of pregnancy on the resuscitative efforts and application of the latest principles of advanced cardiac life support (ACLS). Anaesthesia-related complications, secondary to difficult or failed intubation, and inability to oxygenate and ventilate can result in adverse outcomes for mother and baby. Experience in advanced airway management has been shown to decrease the incidence of brain death and maternal mortality. Awareness of lipid resuscitation of local anaesthetic toxicity is important. The effects of lipid resuscitation and its interference with ACLS medications are also important. Peri-mortem caesarean delivery of the foetus greater than 24 weeks’ gestational age must be considered. Caesarean delivery should be performed no later than 4 min after initial maternal cardiac arrest. A foetus delivered within 5 min has the best chance of survival. Delivery of the baby helps in the maternal resuscitation efforts and recovery of circulation. Finally, the 2003 International Liaison Committee on Resuscitation (ILCOR) and the 2005 American Heart Association (AHA) advocate the provision of mild therapeutic hypothermia to the survivors of cardiac arrest. This will improve the neurological outcomes by decreasing cerebral oxygen consumption, suppression of the radical reactions and reduction of intracellular acidosis and inhibition of excitatory neurotransmitters.
Causes of cardiopulmonary arrest
Cardiopulmonary arrest in pregnant patients is rare. The estimated incidence is approximately 1:30 000 pregnancies and almost 10% of maternal deaths result from cardiopulmonary arrest. Optimal maternal and foetal outcomes are dependent on (1) the underlying cause of the arrest; (2) the speed of intervention by the response team; (3) an understanding of the principles of resuscitation during pregnancy; and (4) the specific challenges of dealing with two potential lives, that is, mother and baby. Cardiac arrest with widespread cerebral ischaemia leads to severe neurological impairment. Haemodynamic instability and devastating neurological injury contribute to mortality, despite the restoration of circulation. Functional survival to discharge after cardiac arrest in all victims is estimated at 6.4%. Success is also dependent on addressing therapeutic interventions to optimise neurological outcomes. Until recently, there was no therapy with documented efficacy in preventing brain damage after cardiac arrest. On the basis of the published evidence to date, the Advanced Life Support (ALS) Task Force of the International Liaison Committee on Resuscitation (ILCOR) has made a specific recommendation for the institution of therapeutic hypothermia after return of spontaneous circulation (ROSC). Therapeutic hypothermia after cardiac arrest has been demonstrated to improve functional recovery and increase the likelihood of a neurologically intact survival in patients. There is a recent case report of successful outcome using hypothermia in pregnancy. Induction of moderate hypothermia after ROSC following cardiac arrest has been associated with improved functional recovery and reduced cerebral histological deficits in various animal models of cardiac arrest.
There are many causes of cardiac arrest in the general population; however, the causes of cardiac arrest during pregnancy include direct causes of pregnancy as well as pre-existing disease states. Major causes of cardiac arrest are listed in Table 1 . The available epidemiological data on maternal mortality in the United States of America and the United Kingdom are shown in Figures 1 and 2 .
| Obstetric causes | Nonobstetric causes |
|---|---|
| Hemorrhage (17%) | Pulmonary embolism (29%) |
| Pregnancy induced hypertension (2.8%) | Infection/sepsis (13%) |
| Idiopathic peripartum cardiomyopathy (8%) | Stroke (5%) |
Anesthetic complications (2%)
| Myocardial infarction Cardiac disease
|
| Amniotic fluid embolism | Trauma |
The causes and management of cardio-respiratory maternal arrest include venous thrombo-embolism, pre-eclampsia, sepsis, amniotic fluid embolism, haemorrhage, trauma, cardiomyopathy and congenital or acquired cardiac disease. Iatrogenic causes include anaesthesia-related complications, such as failed or difficult intubation and local anaesthetic toxicity. Following amniotic fluid embolism (AFE), patients often either die or suffer permanent neurologic damage. Chanimov et al., in discussing AFE, make a plea for better brain protection in survivors of AFE. This article also deals with post-resuscitation management and brain protection. Several of the causative factors of maternal cardio-respiratory arrest are discussed in detail in other articles.
Anaesthesia-related causes of cardio-pulmonary arrest
Anaesthesia -related complications are the seventh leading cause of maternal death in the United States and United Kingdom. Such complications are mainly related to difficult or failed intubation and inability to ventilate or oxygenate. The first national study of anaesthesia-related maternal mortality in the United States was presented in 1997. The majority of the anaesthesia-related deaths (82%) took place during caesarean section (C/S). Death rates during C/S increased from 20 per million to 32.3 per million for general anaesthesia (GA). Conversely, the death rate for regional anaesthesia (RA) declined from 8.6 to 1.9 per million. The risk ratio for GA increased to 16.7 times from 1985 to 1990, despite the wide use of pulse oximetry and end-tidal CO 2 monitoring. The risk ratio of GA mortality was 2.3 times that of regional anaesthesia.
In the United Kingdom, in the Confidential Enquiry into Maternal and Child Health (CEMACH) 2000–2002 study, there were six direct deaths, all related to GA. Maternal deaths from complications of GA included a risk of one maternal death in 20 000. These cardiopulmonary arrests and deaths were related to difficult or failed intubation, difficult pulmonary ventilation resulting in failure to oxygenate, pulmonary aspiration and acute respiratory distress syndrome (ARDS). In all of these cases, the anaesthesia care that was rendered was considered substandard.
Since difficult or failed intubation during pregnancy can lead to hypoxic cardio pulmonary arrest and complicate the situation, it is important to be skilled in the use of various advanced airway devices. The recent Closed Claims Study, published in the USA, revealed that obstetric anaesthesia claims for injuries from 1990 to 2003 had declined compared with obstetric claims for injuries before 1990. In case of the obstetric claims from 1990 to 2003, the proportion of maternal death/brain damage and newborn death/brain damage decreased. Respiratory causes of injuries also decreased from 24% to 4% in claims from 1990 or later. Claims related to inadequate oxygenation/ventilation and aspiration also decreased. However, the claims related to difficult intubation did not change. The improvement in the statistics and decline in anaesthesia-related maternal mortality in the past few years is due to the invention and use of various supraglottic devices in these difficult situations. Recently, other newer airway adjuncts such as videolaryngoscopes have been introduced. There is also a heightened awareness of difficult obstetric airway amongst all anaesthesia practitioners. The laryngeal mask airways (Classic, Intubating, and ProSeal) have been shown to be life-saving rescue devices during failed intubation in obstetrical patients.
The Combitube ( ™ ) , which is included in the advanced cardiac life support (ACLS) resuscitation and laryngeal tube devices have also been shown to be useful in establishing ventilation and oxygenation in a difficult or failed intubation situation in obstetrics.
Videolaryngoscopy (VL) is the latest frontier in airway management. Currently available videolaryngoscopes include Glidescope, Storz C-MAC, Airtraq, McGrath and Pentax AWS-S-100. Several studies have shown that videolaryngoscopes can provide better laryngeal exposure than conventional laryngoscopy in routine and in difficult intubation. In obstetric patients, VL has also been shown to provide enhanced glottic view and decrease the risk of failed intubation. The Airtraq was shown to be useful in establishing ventilation and oxygenation in morbidly obese parturients during emergency C/S. Advantages of VL include a high-illumination, high-resolution view of the glottis and an improvement in viewing angle as the line of sight is different. Alignment of oral, pharyngeal and laryngeal axes is not required.
Anaesthetic-related causes of arrest due to systemic toxicity resulting from local anaesthetic administration
Both the incidence of local anaesthetic toxicity and the occurrence of death due to local anaesthetic toxicity have declined in recent years. Data estimates the incidence of epidural anaesthesia-associated local anaesthetic toxicity to be 1 to 1.3 per 10 000 epidural anaesthetics. This decline may be attributed to several factors, which include the use of low concentration anaesthetics in parturients, an increased awareness of toxicity by anaesthesia providers, and the use of improved safety measures during neuraxial anaesthetic techniques. Albeit a rare entity, the effects of local anaesthetic systemic toxicity can be quite deleterious if they do occur. Therefore, it is prudent that anaesthesia providers understand its prevention and appropriate treatment.
Systemic toxicity may result from high circulating plasma levels of local anaesthetics as a result of unintentional intravenous injection or from absorption after neural blockade. In particular, parturients are at increased risk. This is because pregnancy represents one of several clinical settings in which local anaesthetic toxicity may be potentiated. At higher doses, local anaesthetic toxicity may cause hypoxia leading to respiratory arrest as well as cardiovascular depression. Cardiovascular manifestations of local anaesthetic toxicity may include hypotension, bradycardia, contractile dysfunction and ventricular dysrhythmias. Perhaps the most devastating manifestation of local anaesthetic overdose is complete cardiovascular collapse.
Local anaesthetic toxicity has the potential to be quite catastrophic if it occurs. It has been asserted that creation of a definitive plan to manage this clinically significant event is necessary. The establishment of uniform guidelines in this area is greatly needed but continues to be a challenge to develop. A recently conducted survey of academic anaesthesiology departments demonstrated wide variability in preparedness for local anaesthetic toxicity and lack of consensus for treatment. The creation of a universally accepted protocol for treating systemic local anaesthetic toxicity would reduce treatment variance and improve physician preparedness and overall patient safety.
At the earliest sign of toxicity, immediate intervention must be executed to improve the chances of the most favourable patient outcomes. Particularly in the setting of obstetric anaesthesia, rapid resuscitation of the parturient provides the best chance of survival for both mother and foetus. Conventional treatments must follow without delay. Clinicians must immediately discontinue the use of the inciting agent. Effective airway management that includes the provision of adequate oxygenation and ventilation must be ensured. Intubation with a tracheal tube may be necessary. Adequate lung ventilation and delivery of 100% oxygen is vital because hypoxaemia and resulting acidosis enhance the neurologic and cardiac toxicities of local anaesthetics. Securing of a definitive airway also serves to protect against aspiration of gastric contents in parturients, who are at increased risk for this event.
The establishment or confirmation of appropriate intravenous access is also a key therapeutic intervention. It may be necessary to suppress seizure activity via intravenous administration of anticonvulsants and other pharmacologic agents (benzodiazepines, barbiturates and propofol) in small incremental doses.
It is also important to assess cardiovascular status throughout. In the setting of cardiac arrest, ACLS protocols should be initiated immediately. This includes cardiac compression, defibrillation, cardioversion and pressor support as deemed necessary. Evidence favours the use of sympathomimetics to restore haemodynamic stability. Specifically, “ACLS guidelines recommend the use of vasopressin (40 units intravenous, once) in place of, or in addition to, epinephrine. This appears logical in the setting of bupivacaine toxicity because epinephrine may exacerbate local anaesthetic-induced arrhythmias”. Current data support the use of amiodarone to treat bupivacaine-induced severe ventricular dysrhythmias.
It has been demonstrated that cardiac toxicity caused by local anaesthetics (namely bupivacaine) is extremely resistant to most conventional resuscitative techniques and drugs. Until recently, the institution of cardiopulmonary bypass was the only known treatment shown to be effective in treating the refractory cardiac arrest that occurred as a result of local anaesthetic overdose. Therefore, its possible role must be seriously considered early in this clinical setting.
The release of recent data provides evidence that lipid infusion therapy may have a promising role in the treatment of toxicity from local anaesthetics. There now exist a growing number of case reports that document successful resuscitation from local anaesthetic toxicity via lipid emulsions. It is purported that institution of lipid infusion therapy will attenuate progression of the local anaesthetic toxicity syndrome. Given this information, it seems reasonable to stock lipid emulsion rescue kits in obstetric units, operating rooms, and other perioperative areas where local anaesthetic overdoses may occur.
The exact mechanism of lipid emulsion reversal of local anaesthetic toxicity is unclear but recent data propose the theory of a ‘lipid sink’. This theory is based on the predominant view that “exogenous lipid provides an alternative source for binding of lipid soluble local anaesthetics”. It has also been proposed that the lipid may affect the heart in a ‘metabolically advantageous’ way.
This commentary does in no way advocate the use of lipid therapy as a substitution or alternative for standard resuscitative techniques. Instead, it recommends its role as an adjunct therapy for a toxicity that is often times resistant to traditional resuscitative measures. Anaesthesia providers must be cognizant of some of the limiting factors associated with the institution of lipid therapy in this setting. The appropriate dose, duration and optimal timing of lipid therapy for resuscitation remain unknown. Further, excess lipid may impair the action of lipophilic ACLS drugs. Possible complications or adverse effects of lipid infusion must also be considered. Despite these concerns, respondents from 90 academic anaesthesiology departments revealed that 26% would consider using lipid rescue in the setting of local anaesthetic toxicity.
An example protocol for the use of lipid emulsions as a treatment for local anaesthetic toxicity as proposed by Weinberg is described below. With acknowledgement of the limitations noted previously, this protocol should be considered along with standard resuscitation methods to re-establish sufficient circulatory stability when local aesthetic toxicity is suspected.
- (1)
Administer 1.5 ml kg −1 of Intralipid 20% as an initial bolus. The bolus can be repeated 1–2 times if persists.
- (2)
Start an intravenous infusion of Intralipid 20% at 0.25 ml kg −1 min −1 for 30–60 min. Increase the infusion rate up to 0.5 ml kg −1 min −1 for refractory hypotension.
- (3)
The infusion should be continued until a stable and adequate circulation has been restored.
In conclusion, the primary therapy for local anaesthetic toxicity should adhere to standard measures. That is, emphasis should remain on several factors: (1) appropriate patient monitoring, (2) proper dosing and use of local anaesthetic agents, (3) extreme vigilance by anaesthesia providers, (4) immediate means to support ventilation, (5) proper cardiac resuscitative efforts and (6) appropriate application of proven ALS techniques. Once these conventional measures have been followed, the use of lipid infusion should be considered as an adjunct to the therapeutic algorithm.
Maternal anatomy and physiology
Changes in maternal anatomy and physiology that occur throughout pregnancy affect the incidence and presentation of certain diseases as well as their management. Physicians dealing with obstetric patients should have a thorough knowledge of these physiologic changes to determine the severity of the illness, institute timely intervention, and provide appropriate resuscitation interventions when needed.
The cardiovascular and respiratory changes that occur during pregnancy are discussed in detail elsewhere in this publication, but they are summarised here to discuss in the context of appropriate resuscitation following cardiac arrest. One of the most important interventions during cardiac arrest includes securing the airway, and a thorough knowledge of the anatomic and physiological changes during pregnancy is important. Anatomic and physiologic factors alter the airway during pregnancy, placing the parturient at risk for difficult intubation. An effect of oestrogen on the ground substance of connective tissue leads to an increase in interstitial water resulting in oedema of the respiratory tract, including the oral and nasal pharynx, larynx and trachea. An increase in nasal mucosal congestion predisposes the patient to epistaxis with the passage of a nasogastric or nasotracheal tube. Pharyngolaryngeal and vocal cord oedema may hinder the passage of an ETT that would pass easily in a non-pregnant female. Furthermore, tongue enlargement and immobility of the floor of mouth can result in difficult laryngoscopy. A pregnant patient with pre-eclampsia/eclampsia who sustains a cardiopulmonary arrest may also be at high risk for difficult intubation because of reduced plasma proteins and marked fluid retention, especially in the head and neck region. Oedema makes the tongue larger and less mobile, making identification of landmarks more difficult. An expert in airway management is preferable to secure the airway.
The heart rate increases throughout pregnancy. By the end of pregnancy, it is 15–20% higher than in the non-pregnant state. Progesterone-induced smooth muscle relaxation results in decreased vascular resistance leading to a decrease in systolic and diastolic blood pressures during the first two trimesters. The blood pressure returns to prepregnancy values during the third trimester. In addition, pregnant patients have a dilutional anaemia due to a 50% increase in plasma volume accompanied by a 30% increase in red blood cell mass; this leads to a 35–40% expansion of blood volume. Depending on the patient’s prepregnancy values, all of these changes have the potential to mimic shock in an otherwise stable patient. At term, the placenta alone receives approximately 13% of the circulating blood volume. The increase in circulating volume means that a substantial amount of haemorrhage can take place before signs of maternal hypovolaemia become apparent. At the end of the second trimester, cardiac output increases by 30–50% in response to the increasing demands of the growing uterus. ( Table 2 ) There is a 10-fold increase in the blood flow to the pregnant uterus. The mother’s total blood volume flows through the uterus every 8–11 minutes. Thus, placental disruption or trauma to the uterus or pelvis can result in extensive maternal haemorrhage.
| Pre-pregnancy | 1st trimester | 2nd trimester | 3rd trimester | |
|---|---|---|---|---|
| Heart rate (beats/min) | 70 | 78 | 82 | 85 |
| Systolic blood pressure (mm/Hg) | 125 | 112 | 122 | 115 |
| Diastolic blood pressure (mm/Hg) | 70 | 60 | 63 | 70 |
| Central Venous pressure (mm/Hg) | 9.0 | 7.5 | 4.0 | 3.8 |
| Femoral venous pressure (mm/Hg) | 6 | 6 | 18 | 18 |
| Cardiac output (L/min) | 4.5 | 4.5 | 6.0 | 6.0 |
| Blood volume (mL) | 4000 | 4200 | 5000 | 5600 |
| Uterine blood flow (mL/min) | 60 | 600 | 600 | 600 |
| Hematocrit (%) | 40 | 36 | 34 | 36600 |
By 20 weeks’ gestation, the gravid uterus has reached the level of the inferior vena cava. In the supine position, the gravid uterus can cause compression of the vena cava resulting in decreased venous return and hypotension.
The compression of pelvic veins by the enlarging uterus can cause an increase in venous pressure below the uterus. Increased venous pressure can result in rapid blood loss from injuries to the pelvis or lower extremities. Due to the increased pressure and poor venous return to the heart, intravenous lines in the lower extremities should be avoided because any medication administered through that route will have a limited return to the heart and arterial circulation.
In addition to the haemodynamic changes, there are also alterations in the respiratory system, which can affect the patient’s ability to compensate for respiratory distress. The enlarging gravid uterus pushes the diaphragm more cephalad. This decreases the functional residual capacity and makes the parturient more vulnerable to the effects of hypoxia. There is a 15–20% increase in maternal oxygen requirements. The combination of these changes causes a 40% increase in tidal volume with a resultant 35% decrease in residual volume and functional residual capacity. Therefore, hypoxia can occur quickly with respiratory arrest. The increase in tidal volume and minute ventilation result in respiratory alkalosis.
While renal compensation usually maintains a near-normal pH, arterial blood gas values may reflect an increase in PaO 2 and a decrease in both PaCO 2 and bicarbonate. Consequently, the parturient is less able to buffer pH changes or to compensate for respiratory compromise, thereby increasing the risk of maternal hypoxaemia and acidaemia.
Gastrointestinal motility decreases and the gastric sphincter response is reduced, resulting in an increased likelihood of aspiration with an altered level of consciousness during resuscitative efforts. Moreover, increased gastric acid production during pregnancy increases the pulmonary damage following aspiration.
Because of the risks of rapid development of hypoxaemia and aspiration, securing the airway during maternal cardiopulmonary arrest is critical.
Changes in maternal physiology impact some laboratory values and this has to be taken into account when interpreting the results (see Table 3 ). Laboratory values can be normal, falsely elevated, or falsely decreased indicating the presence of a disease process. Haemoglobin and haematocrit will be decreased due to haemodilution. Platelets may also be decreased due to haemodilution, increased consumption, or pre-eclampsia/HELLP (haemolytic anaemia, elevated liver enzymes, low platelet count) syndrome. White blood cells, erythrocyte sedimentation rate and fibrinogen levels may all be increased in pregnancy.
| Pregnancy values | Normal values | |
|---|---|---|
| Hematocrit (%) | 32–42 | 35–47 |
| White blood cell count (M/μL) | 5,000–32,000 | 4,500–22,000 |
| ESR (mm/hr) | 78 | <20 |
| Arterial pH | 7.40–7.45 | 7.35–7.44 |
| Bicarbonate (mEq/L) | 17–22 | 22–28 |
| PCO (mmHg) | 25–30 | 35–45 |
| Fibrinogen (mg/dL) | >400 | 200–400 |
| Prothrombin time (sec) | 11.2 | 23.5 |
| Platelets (x 10 3 μL) | No change or decreased | 130–400 |
Arterial blood gas values provide valuable information about a patient’s respiratory status. A PaCO 2 of 40 mmHg is normal for a non-pregnant patient. However, it is a cause for concern in a pregnant patient where it may indicate poor ventilation and possible respiratory acidosis – both of which may lead to foetal compromise.
Maternal anatomy and physiology
Changes in maternal anatomy and physiology that occur throughout pregnancy affect the incidence and presentation of certain diseases as well as their management. Physicians dealing with obstetric patients should have a thorough knowledge of these physiologic changes to determine the severity of the illness, institute timely intervention, and provide appropriate resuscitation interventions when needed.
The cardiovascular and respiratory changes that occur during pregnancy are discussed in detail elsewhere in this publication, but they are summarised here to discuss in the context of appropriate resuscitation following cardiac arrest. One of the most important interventions during cardiac arrest includes securing the airway, and a thorough knowledge of the anatomic and physiological changes during pregnancy is important. Anatomic and physiologic factors alter the airway during pregnancy, placing the parturient at risk for difficult intubation. An effect of oestrogen on the ground substance of connective tissue leads to an increase in interstitial water resulting in oedema of the respiratory tract, including the oral and nasal pharynx, larynx and trachea. An increase in nasal mucosal congestion predisposes the patient to epistaxis with the passage of a nasogastric or nasotracheal tube. Pharyngolaryngeal and vocal cord oedema may hinder the passage of an ETT that would pass easily in a non-pregnant female. Furthermore, tongue enlargement and immobility of the floor of mouth can result in difficult laryngoscopy. A pregnant patient with pre-eclampsia/eclampsia who sustains a cardiopulmonary arrest may also be at high risk for difficult intubation because of reduced plasma proteins and marked fluid retention, especially in the head and neck region. Oedema makes the tongue larger and less mobile, making identification of landmarks more difficult. An expert in airway management is preferable to secure the airway.
The heart rate increases throughout pregnancy. By the end of pregnancy, it is 15–20% higher than in the non-pregnant state. Progesterone-induced smooth muscle relaxation results in decreased vascular resistance leading to a decrease in systolic and diastolic blood pressures during the first two trimesters. The blood pressure returns to prepregnancy values during the third trimester. In addition, pregnant patients have a dilutional anaemia due to a 50% increase in plasma volume accompanied by a 30% increase in red blood cell mass; this leads to a 35–40% expansion of blood volume. Depending on the patient’s prepregnancy values, all of these changes have the potential to mimic shock in an otherwise stable patient. At term, the placenta alone receives approximately 13% of the circulating blood volume. The increase in circulating volume means that a substantial amount of haemorrhage can take place before signs of maternal hypovolaemia become apparent. At the end of the second trimester, cardiac output increases by 30–50% in response to the increasing demands of the growing uterus. ( Table 2 ) There is a 10-fold increase in the blood flow to the pregnant uterus. The mother’s total blood volume flows through the uterus every 8–11 minutes. Thus, placental disruption or trauma to the uterus or pelvis can result in extensive maternal haemorrhage.
| Pre-pregnancy | 1st trimester | 2nd trimester | 3rd trimester | |
|---|---|---|---|---|
| Heart rate (beats/min) | 70 | 78 | 82 | 85 |
| Systolic blood pressure (mm/Hg) | 125 | 112 | 122 | 115 |
| Diastolic blood pressure (mm/Hg) | 70 | 60 | 63 | 70 |
| Central Venous pressure (mm/Hg) | 9.0 | 7.5 | 4.0 | 3.8 |
| Femoral venous pressure (mm/Hg) | 6 | 6 | 18 | 18 |
| Cardiac output (L/min) | 4.5 | 4.5 | 6.0 | 6.0 |
| Blood volume (mL) | 4000 | 4200 | 5000 | 5600 |
| Uterine blood flow (mL/min) | 60 | 600 | 600 | 600 |
| Hematocrit (%) | 40 | 36 | 34 | 36600 |
By 20 weeks’ gestation, the gravid uterus has reached the level of the inferior vena cava. In the supine position, the gravid uterus can cause compression of the vena cava resulting in decreased venous return and hypotension.
The compression of pelvic veins by the enlarging uterus can cause an increase in venous pressure below the uterus. Increased venous pressure can result in rapid blood loss from injuries to the pelvis or lower extremities. Due to the increased pressure and poor venous return to the heart, intravenous lines in the lower extremities should be avoided because any medication administered through that route will have a limited return to the heart and arterial circulation.
In addition to the haemodynamic changes, there are also alterations in the respiratory system, which can affect the patient’s ability to compensate for respiratory distress. The enlarging gravid uterus pushes the diaphragm more cephalad. This decreases the functional residual capacity and makes the parturient more vulnerable to the effects of hypoxia. There is a 15–20% increase in maternal oxygen requirements. The combination of these changes causes a 40% increase in tidal volume with a resultant 35% decrease in residual volume and functional residual capacity. Therefore, hypoxia can occur quickly with respiratory arrest. The increase in tidal volume and minute ventilation result in respiratory alkalosis.
While renal compensation usually maintains a near-normal pH, arterial blood gas values may reflect an increase in PaO 2 and a decrease in both PaCO 2 and bicarbonate. Consequently, the parturient is less able to buffer pH changes or to compensate for respiratory compromise, thereby increasing the risk of maternal hypoxaemia and acidaemia.
Gastrointestinal motility decreases and the gastric sphincter response is reduced, resulting in an increased likelihood of aspiration with an altered level of consciousness during resuscitative efforts. Moreover, increased gastric acid production during pregnancy increases the pulmonary damage following aspiration.
Because of the risks of rapid development of hypoxaemia and aspiration, securing the airway during maternal cardiopulmonary arrest is critical.
Changes in maternal physiology impact some laboratory values and this has to be taken into account when interpreting the results (see Table 3 ). Laboratory values can be normal, falsely elevated, or falsely decreased indicating the presence of a disease process. Haemoglobin and haematocrit will be decreased due to haemodilution. Platelets may also be decreased due to haemodilution, increased consumption, or pre-eclampsia/HELLP (haemolytic anaemia, elevated liver enzymes, low platelet count) syndrome. White blood cells, erythrocyte sedimentation rate and fibrinogen levels may all be increased in pregnancy.
