Critical Care Obstetrics part 11 pps

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Therapy with both magnesium and nifedipine does not increase the risk of serious magnesium - related maternal side effects in women with preeclampsia . Am J Obstet Gynecol 2005 ; 1 : 153 – 163 . 200 Anast CS , Winnacker JL , Forte LR , Burns TW . Impaired release of parathyroid hormone in magnesium defi ciency . J Clin Endocrinol Metab 1976 ; 42 : 707 – 717 . 201 Zaloga GP , Wilkens R , Tourville J et al. A simple method for determining physiologically active calcium and magnesium concentrations in critically ill patients . Crit Care Med 1987 ; 15 : 813 – 816 . 202 Zaloga GP , Chernow B . The multifactorial basis for hypocalcemia during sepsis. Studies of the parathyroid hormone - vitamin D axis . Ann Intern Med 1987 ; 107 : 36 – 41 . 203 Zaloga GP , Chernow B . Stress - induced changes in calcium metabo- lism . Semin Respir Med 1985 ; 7 : 56 . 204 Chernow B , Rainey TG , Georges LP , O ’ Brian JT . Iatrogenic hyper- phosphatemia: a metabolic consideration in critical care medicine . 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Disorders of calcium metabo- lism . In: Maxwell MH , Kleeman CR , Narins RG , eds. Clinical Disorders of Fluid and Electrolyte Metabolism , 4th edn . New York : McGraw - Hill , 1987 : 758 . 212 Mundy GR . Calcium Homeostasis: Hypercalcemia and Hypocalcemia . London : Martin Dunitz , 1989 : 1 . 213 Montoro MN , Paler RJ , Goodwin TM et al. Parathyroid carcinoma during pregnancy . Obstet Gynecol 2000 ; 96 ( 5 Part 2 ): 841 . 214 Mestamen JH . Parathyroid disorders of pregnancy . Semin Perinatol 1998 ; 22 ( 6 ): 485 – 496 . 215 Thomas AK , McVie R , Levine SN . Disorders of maternal calcium metabolism implicated by abnormal calcium metabolism in the neonate . Am J Perinatol 1999 ; 16 ( 10 ): 515 – 520 . 216 Illidge TM , Hussey M , Godden CW . Malignant hypercalcaemia in pregnancy and antenatal administration of intravenous pamidro- nate . Clin Oncol (R Coll Radiol) 1996 ; 8 ( 4 ): 257 – 258 . 174 Flakeb G , Villarread D , Chapman D . Is hypokalemia a cause of ventricular arrhythmias? J Crit Ill 1986 ; 1 : 66 . 175 Marino P . Potassium . In: Marino P , ed. The ICU Book . Philadelphia : Lea & Febiger , 1991 : 478 . 176 Smith JD , Bia MJ , DeFronzo RA . Clinical disorders of potassium metabolism . In: Arieff AI , DeFronzo RA , eds. Fluid, Electrolyte and Acid – Base Disorders . New York : Churchill Livingstone , 1985 : 413 . 177 Hartman RC , Auditore JC , Jackson DP . Studies in thrombocytosis. I. Hyperkalemia due to release of potassium from platelets during coagulation . J Clin Invest 1958 ; 37 : 699 . 178 Robertson GL . Abnormalities of thirst regulation . Kidney Int 1984 ; 25 : 460 – 469 . 179 Oster JR , Perez GO , Vaamonde CA . Relationship between blood pH and phosphorus during acute metabolic acidosis . Am J Physiol 1978 ; 235 : F345 – 351 . 180 Bismuth C , Gaultier M , Conso F et al. Hyperkalemia in acute digi- talis poisoning: prognostic signifi cance and therapeutic implica- tions . Clin Toxicol 1973 ; 6 : 153 – 162 . 181 Williams ME , Rosa RM . 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Am J Obstet Gynecol 1993 ; 168 : 1170 – 1177 . 194 Cruikshank DP , Pitkin RM , Donnelly E et al. Urinary magnesium, calcium and phosphate excretion during magnesium sulfate infu- sion . Obstet Gynecol 1981 ; 58 : 430 – 434 . 195 Cholst IN , Steinberg SF , Tropper PJ et al. The infl uence of hyper- magnesemia on serum calcium and parathyroid hormone levels in human subjects . N Engl J Med 1984 ; 310 : 1221 – 1225 . Chapter 6 92 231 Iseri LT , Freed J , Bures AR . Magnesium defi ciency and cardiac dis- orders . Am J Med 1975 ; 58 : 837 – 846 . 232 Burch GE , Giles TD . The importance of magnesium defi ciency in cardiovascular disease . Am Heart J 1977 ; 94 : 649 – 651 . 233 Rasmussen HS , McNair P , Norregard P et al. Intravenous magnesium in acute myocardial infarction . Lancet 1986 ; 1 : 234 – 236 . 234 Abraham AS , Rosenmann D , Kramer M et al. Magnesium in the prevention of lethal arrhythmias in acute myocardial infarction . Arch Intern Med 1987 ; 147 : 753 – 755 . 235 Flink EB . 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Magnesium metabolism. A review with special refer- ence to the relationship between intracellular content and serum levels . Arch Intern Med 1988 ; 148 : 2415 – 2420 . 222 Dacey MJ . Hypomagnesemic disorders . Crit Care Clin 2001 ; 17 ( 1 ): 155 – 173 . 223 Marino P . Magnesium: the hidden ion . In: Marino P , ed. The ICU ook . Philadelphia : Lea & Febiger , 1991 : 489 . 224 Ryan MP . Diuretics and potassium/magnesium depletion . Direction Am J Med 1987 ; 82 : 38A . 225 Zaloga GP , Chernow B , Pock A et al. Hypomagnesemia is a common complication of aminoglycoside therapy . Surg Gynecol Obstet 1984 ; 158 : 561 – 565 . 226 Elin RJ . Magnesium metabolism in health and disease . Dis Mon 1988 ; 34 : 161 – 218 . 227 Berkelhammer C , Bear RA . A clinical approach to common electro- lyte problems: hypomagnesemia . Can Med Assoc J 1985 ; 132 : 360 – 368 . 228 Brauthbar N , Massry SG . Hypomagnesemia and hypermagnesemia . In: Maxwell MH , Kleeman CR , Narins RG , eds. Clinical Disorders of Fluid and Electrolyte Metabolism , 4th edn . New York : McGraw - Hill , 1987 : 831 . 229 Kingston ME , Al - Siba ’ i MB , Skooge WC . Clinical manifestations of hypomagnesemia . Crit Care Med 1986 ; 14 : 950 – 954 . 230 Zaloga GP . Interpretation of the serum magnesium level . Chest 1989 ; 95 : 257 – 258 . 93 Critical Care Obstetrics, 5th edition. Edited by M. Belfort, G. Saade, M. Foley, J. Phelan and G. Dildy. © 2010 Blackwell Publishing Ltd. 7 Cardiopulmonary Resuscitation in Pregnancy Andrea Shields 1 & M. Bardett Fausett 2 1 Antenatal Diagnostic Center, San Antonio Military Medical Center, Lackland Airforce Base, Texas, USA 2 Obstetrics and Maternal - Fetal Medicine, San Antonio Military Medical Center and Department of Obstetrics and Gynecology, Wilford Hall Medical Center, Lackland Airforce Base, Texas, USA Introduction Sudden cardiac arrest (SCA) is a leading cause of death in the United States and Canada. An estimated 330 000 people die annu- ally in the United States from SCA in out - of - hospital and emer- gency department settings [1] . This translates to 0.55 per thousand people in the US, and 1 in 30 000 gravid women who will suffer SCA each year. Overall maternal mortality is signifi cantly higher in developing countries including mortality from SCA. Women of childbearing age are commonly healthy and the overall risk of death is low in developed nations. These facts, along with the additional life involved, make SCA in pregnancy unexpected and particularly devastating. Women are most likely to survive cardiopulmonary arrest when attended by providers skilled in basic and advanced cardio- pulmonary resuscitative techniques. The mechanical and physi- ologic changes of pregnancy impact every phase of the resuscitation process. In this chapter, we review the most recent American Heart Association (AHA) cardiopulmonary resuscitation (CPR) guidelines and emphasize pregnancy - specifi c modifi cations. We do not address infant and child resuscitation in this chapter but the practicing obstetrician should likewise be expert with neona- tal resuscitation. In this chapter, we will consider other relevant pregnancy - related issues such as perimortem cesarean section and the ethical dilemma of prolonged maternal life support for fetal maturation. The initial objective of CPR and emergency cardiac care (ECC) is to maintain adequate oxygenation and vital organ perfusion. CPR restores hemodynamic stability in 40 – 60% of arrested patients; however, prolonged survival is lower with underlying illness [2] . Overall outcome, particularly full neurologic recovery, is improved by early initiation of CPR and defi brillation. Most victims of SCA demonstrate ventricular fi brillation at some point leading to full arrest. Ventricular fi brillation is best treated by electrical cardioversion performed within the fi rst 5 minutes after collapse [3] . Since the majority of SCA occurs outside of the hospital setting, it is uncommon for emergency medical service personnel to be contacted and arrive at the victim ’ s side within these critical 5 minutes [4] . Thus, achieving a high survival rate depends upon public training in CPR and well - organized public access defi brillation programs. Considering all victims, out - of - hospital survival rates for SCA victims are only 6% but can improve to 75% when victims are given high - quality CPR [4] . Outside of the hospital, SCA is usually associated with cata- strophic trauma and is rarely a survivable event for pregnant women even in developed countries. In the hospital, SCA in pregnancy is usually associated with peripartum events [5] . In such circumstances delivery of high - quality CPR is likely to have a signifi cant impact on survival rates. Thus, hospital personnel involved in the care of pregnant women should be expertly trained and facile in techniques of cardiopulmonary resuscitation. Obstetrical units should have proper resuscitative equipment readily available and staff members be engaged in ongoing programs to train and maintain CPR competency. In one recent evaluation of obstetric training programs, the authors concluded that even basic life support knowledge and skills are inadequate and ongoing training is necessary [6] . Current c ardiac c are r ecommendations In December 2005, the American Heart Association published an update to the guidelines for lay and professional Basic and Advanced Cardiac Life Support (BLS/ACLS). A summary of the ABCDs of lay and provider rescuer BLS is shown in Table 7.1 . The primary changes to the 2005 resuscitation guidelines were meant to simplify algorithms and promote their early application to SCA victims. The new guidelines include four major changes relevant to women of reproductive age and are applicable to both lay and provider rescuer CPR [7] . These general changes are sum- marized in Table 7.2 . Chapter 7 94 Airway Head tilt/chin lift unless trauma then use jaw thrust Breathing : Initial 2 breaths at 1 second/breath Rescue breathing without chest compressions 10 – 12 breaths/min Rescue breaths with advanced airway 8 – 10 breaths/min Foreign body obstruction Abdominal thrusts Circulation Pulse check ( ≤ 10 s) Carotid Compression landmarks Lower half of sternum, between nipples Compression method Heel of one hand with the other on top; push hard and fast and allow complete recoil Compression depth 1 ½ to 2 inches Compression rate 100/min Compression : ventilation ratio 30 : 2 (either one or two rescuers) Defi brillation AED After 5 cycles of CPR if out of hospital Table 7.1 Summary of CPR ABCD s (modifi ed from “ Summary of BLS ABCD maneuvers for infants, children and adults ” ) [68] . Table 7.2 Summary of key changes in 2005 CPR guidelines [4] . Deliver more effective chest compressions Early, consistent, fast, hard Single compression : ventilation ratio for all but neonates 30 : 2 Rescue breaths Given over 1 second; 500 – 600 mL for adults Defi brillation After fi rst shock go directly to compression : ventilations × 2 min First, there is signifi cant emphasis on, and recommendations to improve, delivery of effective chest compressions. The key words are early, consistent, fast and hard. This emphasis is made because half of chest compressions (even by healthcare providers) are too shallow. The chest is often not allowed to recoil ade- quately between compressions and interruptions are too common. Complete chest wall recoil increases cardiac fi lling by increasing negative pressure, promoting venous return and maximizing cardiac output with the subsequent compression. The fi rst few compressions after interruption are not as effective as those that follow. Thus, inadequate compressions, incomplete chest recoil and frequent interruptions all signifi cantly decrease circulation and oxygen delivery and decrease survival [7] . The second new recommendation is for a single 30 : 2 compres- sion to ventilation ratio for all victims except newborns. The guideline authors note most cases of cardiac arrest in adults are not hypoxia - induced. Consequently, circulation is more critical than ventilation in the fi rst minute of CPR. Since the blood fl ow to the lungs is diminished (25 – 33%) during arrest/CPR, victims need less ventilation than normal. In contrast, newborn cardiac arrest is commonly related to hypoxia so more ventilations (5:1) to compressions are indicated and remain part of the new guide- lines [7] . The third recommendation is that each rescue breath should be given over 1 second (rather than 1 – 2 seconds) and produces a visible chest rise. The visible chest rise ensures effi cacy and the 1 - second breath provides adequate tidal volume (500 – 600 mL) while avoiding hyperinfl ation. Rescuers are to take a normal breath before giving the rescue breath. Frequent rescue breathing interrupts and delays chest compressions. Hyperinfl ation increases intrathoracic pressure leading to decreased blood return to the chest. This results in diminished effi cacy of the next several compressions and increases the risk of gastric insuffl ation. The fi nal new major recommendation is that during ventricu- lar fi brillation (VF) cardiac arrest, a single shock should be given followed by immediate CPR. CPR is to begin even before the fi rst rhythm check 2 minutes later. Historically, rhythm analysis by automated defi brillators available before 2005 resulted in delays of more than 30 seconds before giving the fi rst post - shock com- pressions. Current defi brillators eliminate VF more than 85% of the time. Thus, in a case where the fi rst shock fails, CPR is likely to convey greater value than a second shock. Even when a shock eliminates VF, it usually takes several minutes for a normal effec- tive rhythm to return. A brief period of CPR can increase energy and oxygen to the heart, increasing the likelihood that the heart will be able to continue effective blood fl ow. There is no evidence that postdefi brillation chest compressions provoke recurrent VF. For similar reasons, lay rescuer CPR recommendations now eliminate the initial check for pulse after giving the initial two rescue breaths [7] . Key changes to recommendations for provider - level and hos- pital - based adult BLS include use of the 30 : 2 ventilation to com- pression ratio (even with two rescuers) until an advanced airway is in place. As noted in the general guidelines above, before an advanced airway is in place, rescuers should perform 5 cycles of CPR after shock before the next rhythm check. Even once the advanced airway is in place, rescuers should perform 2 minutes Cardiopulmonary Resuscitation in Pregnancy 95 of CPR after shock before the next rhythm check. With two or more rescuers and an advanced airway in place, rescuers no longer provide cycles of compressions with pauses for ventila- tion. One rescuer provides 8 – 10 breaths per minute (1 every 6 – 8 seconds) while the other rescuer provides continuous compres- sions. Where possible, rescuers should rotate the compressor role every 2 minutes, taking no more than 5 seconds to do so. After 2 – 3 minutes of CPR, rescuers typically perform chest compres- sions less effectively [7] . The general provider BLS algorithm is shown in Figure 7.1 and the pulseless arrest ACLS algorithm in Figure 7.2 . Algorithms for tachycardia and bradycardia are not included here but are usually available on all “ code carts ” . Patient p opulation and e tiologies of SCA in p regnancy Of women who suffer SCA during pregnancy, most have throm- boembolic - , followed by hemorrhage - , related events [8] . The most common causes of SCA during pregnancy are listed in Table 7.3 . Victims of SCA in pregnancy are younger and have fewer underlying medical conditions than non - pregnant victims [8] . However, maternal age and underlying medical problems con- tinue to increase in developed countries due to elective delayed childbearing and advanced reproductive technologies. Pregnancy increases the risk of venous thromboembolic disease (VTE) due to hormonally stimulated increases of virtually all of the procoagulant proteins. The risk of VTE is amplifi ed by condi- tions necessitating bed rest such as gestational hypertensive dis- orders and preterm labor. The risk is highest in the immediate postpartum period, [9] probably due to the tissue trauma and decreased physical activity associated with delivery. Lipo - oxidative injury to the coronary vessels is the most common cause of SCA in non - pregnant individuals but is an uncommon cause of SCA in pregnancy. However, the added physiologic stress of pregnancy can unveil underlying congenital or acquired valve disease. Pregnancy does increase the risk of myocardial infarction 3 – 4 - fold over otherwise comparable non - pregnant women. The pregnancy - related MI risk is signifi cantly greater in women older than 30 years [10] . Additionally, pregnant women have a relatively increased risk of coronary artery and aortic dissections compared to non - pregnant women with other- wise similar demographic characteristics [11] . This may be due to progesterone - mediated relaxation of smooth muscle. Pregnancy - s pecifi c c onditions a ssociated with SCA Turning now to pregnancy - specifi c conditions associated with SCA, we fi rst highlight the anaphylactoid syndrome of pregnancy also called amniotic fl uid embolus (AFE). This disorder is char- acterized by an anaphylaxis - like syndrome that is associated with cardiac depression, cardiopulmonary collapse and coagulopathy. The disorder is highly lethal with a 50 – 65% risk of cardiac arrest and maternal death [12 – 15] . This catastrophic condition is discussed in detail in Chapter 35 but the reader is encouraged to remember that this disorder is associated with profound vascular leak, and over - resuscitation with crystalloid fl uids can result in massive pulmonary edema. Therapy targeted to support the cardiovascular system and correct the coagulopathy while avoiding over - resuscitation with crystalloid fl uid may be helpful [16] . Gestational hypertensive disorders occur more frequently than thromboembolic disorders and both occur more commonly than anaphylactoid syndrome of pregnancy [14] . Women with hyper- tensive disorders of pregnancy are at increased risk of SCA for several reasons including the associated underlying endothelial injury and infl ammatory response. Hypertension may necessitate medical therapy and magnesium is often used for seizure prophy- laxis. Both may be associated with cardiac compromise leading to SCA [17 – 20] . Profound hypotension and SCA can occur in women with pre - eclampsia treated concurrently with calcium channel antagonists and magnesium sulfate. In cases of cardio- pulmonary compromise due to magnesium sulfate toxicity, resuscitation must include calcium rescue. The typical dose is 1 g of intravenous calcium carbonate. ABCD s in p regnancy If breathing stops fi rst, then the heart often continues to pump for several minutes usually providing enough oxygen in the lungs and bloodstream to support life for up to 6 minutes [21] . In contrast, when the heart stops fi rst, oxygen in the lungs and bloodstream cannot be circulated to vital organs. The patient whose heart and respirations have stopped for less than 4 minutes has an excellent chance of recovery if CPR is administered imme- diately and is followed by ACLS within 4 minutes [22] . By 4 – 6 minutes, brain damage may occur, and after 6 minutes, brain damage will almost always occur. Therefore, the initial goals of CPR are to deliver oxygen to the lungs and provide a means of circulation to the vital organs. Initially circulation is provided via closed - chest compression followed by ACLS, with restoration of the heart as the mechanism of circulation. These goals are achieved by remembering the “ ABCDs ” of the primary and sec- ondary survey (Table 7.1 ). The primary survey consists of airway management using non - invasive techniques, breathing with pos- itive - pressure ventilations, and performing CPR until equipment for external defi brillation arrives. Out - of - hospital and BLS tools required include gloved hands, a barrier device for CPR, and an automated external defi brillator (AED) for defi brillation. A sec- ondary survey requires the use of advanced, invasive techniques as the rescuer attempts to resuscitate, stabilize, and transfer the patient to a higher level of care if indicated (i.e. hospital or inten- sive care setting). Potentially reversible causes of cardiopulmo- nary arrest should also be considered and addressed at this stage (Table 7.4 ). Chapter 7 96 If not breathing, give 2 BREATHS that make chest rise Denite Pulse Shockable Not Shockable If no response, check pulse: Do you DEFINITELY feel pulse within 10 seconds? No movement or response PHONE 911 or emergency number Get AED or send second rescuer (if available) to do this Open AIR WAY, check BREATHING Resume CPR immediately for 5 cycles Check rhythm every 5 cycles; continue until ALS providers take over or victim starts to move Give cycles of 30 COMPRESSIONS and 2 BREATHS until AED/debrillator arrives, ALS providers take over, or victim starts to move Push hard and fast (100/min) and release completely Minimize interruptions in compressions AED/debrillator ARRIVES Check Rhythm Shockable rhythm? Give 1 shock Resume CPR immediately for 5 cycles -Give 1 breath every 5 to 6 seconds -Recheck pulse every 2 minutes 5A 1 2 3 4 5 6 7 8 910 No Pulse Figure 7.1 ACLS Adult BLS Provider Algorithm. Modifi ed from Circulation 2005; 112: IV - 58 – IV - 66. Cardiopulmonary Resuscitation in Pregnancy 97 Figure 7.2 ACLS Adult Pulseless Arrest Algorithm. Modifi ed from Circulation 2005; 112: IV - 58 – IV - 66. Shockable Not Shockable Shockable Give 5 cycles of CPR* Give 5 cycles of CPR* Shockable Give 5 cycles of CPR* Not Shockable Shockable Check rhythm Shockable rhythm? PULSELESS ARREST • BLS Algorithm: Call for help, ve CPR • Give oxygen when available • Attach monitor/debrillator when available Continue CPR while debrillator is charging Give 1 shock • Manual biphasic: device specic (typically 120 to 200 J) • AED: device specic • Monophasic: 360 J Resume CPR immediately after the shock When IV/IO available, give vasopressor during CPR (before or after the shock) • Epinephrine 1 mg IV/IO Repeat every 3 to 5 minutes or • May give 1 dose of vasopressin 40 U IV/IO to replace rst or second dose of ephinephrine VF/VT Asystole/PEA Give 1 shock • Manual biphasic: device specic (typically 120 to 200 J) • AED: device specic • Monophasic: 360 J Resume CPR immediately Check rhythm Shockable rhythm? Continue CPR while debrillator is charging Give 1 shock • Manual biphasic: device specic (typically 120 to 200 J) • AED: device specic • Monophasic: 360 J Resume CPR immediately after the shock Consider antiarrhythmics; give during CPR (before or after the shock) amiodarone (300 mg IV/IO once, then consider additional 150 mg IV/IO once) or lidocaine (1 to 1.5 mg/kg rst dose, then 0.5 to 0.75 mg/ kg IV/IO, maximum 3 doses or 3 mg/kg) Consider magnesium, loading dose 1 to 2 g IV/IO for torsades de pointes After 5 cycles of CPR,* go to Box 5 above Check rhythm Shockable rhythm? • If asystole, go to Box 10 • If elecrical activity, check pulse, If no pulse, got to Box 10 • If pulse present, begin postresuscitation care Resume CPR immediately for 5 cycles When IV/IO available, give vasopressor • Epinephrine 1 mg IV/IO Repeat every 3 to 5 minutes or • May give 1 dose of vasopressin 40 U IV/IO to replace rst or second dose of ephinephrine Consider atropine 1 mg IV/IO for asystole or slow PEA rate Repeat every 3 to 5 min (up to 3 doses) Check rhythm Shockable rhythm? Go to Box 4 During CPR • Push hard and fast (100/min) • Ensure full chest recoil • Minimize interruptions in chest compressions • One cycle of CPR; 30 compressions then 2 breaths; 5 cycles takes about 2 min •Avoid hyperventilation • Secure airway and conrm placement After an advanced airway is placed, rescuers no longer deliver “cycles” of CPR, Give continuous chest com- pressions with pauses for breaths. Give 8 to 10 breaths/minute. Check rhythm every 2 minutes • Rotate compressors every 2 minutes with rhythm checks • Search for and treat possible contributing factors: •Hypovolemia •Hypoxia •Hydogen ion (acidosis) •Hypo-/hyperkalemia •Hypoglycemia •Hypothermia •Toxins •Tamponade, cardiac •Tension pneumothorax •Thrombosis (coronary or pulmonary) •Trauma No No 1 2 3 4 5 6 7 8 9 10 11 12 13 Airway Delivery of oxygen is achieved by positioning the patient, opening the airway, and delivering rescue breaths. In the absence of muscle tone, the tongue and epiglottis frequently obstruct the airway. The head tilt with the chin - lift maneuver (Figure 7.3 ) or the jaw thrust maneuver (Figure 7.4 ) facilitates airway access. If foreign material appears in the mouth, it should be removed. If air does not enter the lungs with rescue breathing, reposition the head and repeat the attempt at rescue breathing. Persistent obstruction may require the Heimlich maneuver (subdiaphrag- matic abdominal thrusts), chest thrusts, removal of foreign body if now visualized, and rescue breathing. The Heimlich maneuver cannot be used in the late stages of pregnancy or in the obese choking victim. Airway obstruction may occur in a choking victim as well as the patient experiencing a cardiopulmonary arrest. The conscious women with only partial airway obstruction should be allowed to attempt to clear the obstruction herself. Rescuers should avoid the fi nger sweep in a conscious patient. In the fi rst half of pregnancy, airway obstruction can be relieved with the Heimlich maneuver or abdominal thrusts. From a stand- ing position the rescuer wraps his arms around the victim ’ s waist, making a fi st with one hand and placing the thumb side of the fi st against the victim ’ s abdomen in the midline slightly above the umbilicus and well below the top of the xiphoid process. The rescuer grasps the fi st with the other hand and presses the fi st into the victim ’ s abdomen with quick, distinct, upward thrusts. The thrusts are continued until the object is expelled or the victim is unconscious. The unconscious victim is placed supine, the heel of one hand remains against the victim ’ s abdomen, in the midline slightly above the umbilicus but below the top of the xiphoid. The Chapter 7 98 second hand lies directly on top of the fi rst, and quick upward thrusts are administered. In the latter half of pregnancy, the gravid uterus or maternal habitus may necessitate the use of chest thrusts instead of abdom- inal thrusts. Chest thrusts in a conscious sitting or standing victim require placing the thumb side of the fi st on the middle of the sternum, avoiding the xiphoid and the ribs. The rescuer then grabs his or her own fi st with the other hand and performs chest thrusts until either the foreign object is dislodged or the patient loses consciousness. The unconscious patient is placed supine. The rescuer ’ s hand closest to the patient ’ s head is placed 2 fi nger- breadths above the xiphoid. The long axis of the heel of the provider ’ s hand rests on the long axis of the sternum and the other hand lies over the fi rst, with the fi ngers either extended or interlaced. The elbows are extended and the chest is compressed 1.5 – 2 inches. Up to 5 abdominal or chest thrusts are given fol- lowed by repetition of the jaw - lift, foreign body visualization, and attempted ventilation. These steps are repeated until effective or until a surgical airway can be obtained by emergency cricothy- rotomy or jet - needle insuffl ation. If, after clearing any obstruction, the patient is unresponsive but breathing spontaneously, she is placed in the recovery posi- tion to keep the airway open. The pregnant victim is placed on her left side. The left arm is placed at a right angle to the victim ’ s torso, while the right arm is placed across her chest with the back of her hand under the lower cheek. The victim ’ s right thigh is fl exed at a right angle to the torso, across the left leg, with the right knee resting on the surface. The victim ’ s head is tilted back to maintain the airway, using the right hand to maintain the head tilt. Fetal monitoring should begin as soon as possible and breath- ing is monitored regularly. If breathing does not resume after clearing the airway or if it stops, the emergency medical system is activated and the BCDs of CPR continued. Table 7.3 Causes of cardiac arrest during pregnancy [69] . Venous thromboembolism Pregnancy - induced hypertension Sepsis Amniotic fl uid embolism Hemorrhage Placental abruption Placenta previa Uterine atony Disseminated intravascular coagulation Trauma Iatrogenic Medication errors or allergy Anesthetic complications Hypermagnesemia Pre - existing heart disease Congenital Acquired Table 7.4 Potentially reversible causes of cardiac arrest. Hypovolemia Hypoxia Hydrogen ion acidosis Hyper - or hypokalemia, other metabolic Hypothermia Tablets (drug overdose) Trauma Tamponade, cardiac Tension pneumothorax Thrombosis, coronary Thrombosis, pulmonary Toxins (e.g. amniotic fl uid) Figure 7.3 Head tilt, chin lift. Figure 7.4 Jaw thrust. . hyper- phosphatemia: a metabolic consideration in critical care medicine . Crit Care Med 1981 ; 9 : 772 – 774 . 205 Zaloga GP . Phosphate disorders . Probl Crit Care 1990 ; 4 : 416 . 206 Nagant De. hypomagnesemia . Crit Care Med 1986 ; 14 : 950 – 954 . 230 Zaloga GP . Interpretation of the serum magnesium level . Chest 1989 ; 95 : 257 – 258 . 93 Critical Care Obstetrics, 5th edition : 228 – 230 . 110 Maurer PH , Berardinelli B . Immunologic studies with hydroxyethyl starch (HES): a proposed plasma expander . Transfusion 1968 ; 8 : 265 – 268 . 111 Ring J , Seifert