Part 12: Cardiac Arrest in Special Situations

Abstract

HomeCirculationVol. 122, No. 18_suppl_3Part 12: Cardiac Arrest in Special Situations Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBPart 12: Cardiac Arrest in Special Situations2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Terry L. Vanden Hoek, Laurie J. Morrison, Michael Shuster, Michael Donnino, Elizabeth Sinz, Eric J. Lavonas, Farida M. Jeejeebhoy and Andrea Gabrielli Terry L. Vanden HoekTerry L. Vanden Hoek Search for more papers by this author , Laurie J. MorrisonLaurie J. Morrison Search for more papers by this author , Michael ShusterMichael Shuster Search for more papers by this author , Michael DonninoMichael Donnino Search for more papers by this author , Elizabeth SinzElizabeth Sinz Search for more papers by this author , Eric J. LavonasEric J. Lavonas Search for more papers by this author , Farida M. JeejeebhoyFarida M. Jeejeebhoy Search for more papers by this author and Andrea GabrielliAndrea Gabrielli Search for more papers by this author Originally published2 Nov 2010https://doi.org/10.1161/CIRCULATIONAHA.110.971069Circulation. 2010;122:S829–S861is corrected byCorrectionCorrectionCorrectionThis section of the 2010 AHA Guidelines for CPR and ECC addresses cardiac arrest in situations that require special treatments or procedures beyond those provided during basic life support (BLS) and advanced cardiovascular life support (ACLS). We have included 15 specific cardiac arrest situations. The first several sections discuss cardiac arrest associated with internal physiological or metabolic conditions, such as asthma (12.1), anaphylaxis (12.2), pregnancy (12.3), morbid obesity (12.4), pulmonary embolism (PE) (12.5), and electrolyte imbalance (12.6).The next several sections relate to resuscitation and treatment of cardiac arrest associated with external or environmentally related circumstances, such as ingestion of toxic substances (12.7), trauma (12.8), accidental hypothermia (12.9), avalanche (12.10), drowning (12.11), and electric shock/lightning strikes (12.12).The last 3 sections review management of cardiac arrest that may occur during special situations affecting the heart, including percutaneous coronary intervention (PCI) (12.13), cardiac tamponade (12.14), and cardiac surgery (12.15).Part 12.1: Cardiac Arrest Associated With AsthmaAsthma is responsible for more than 2 million visits to the emergency department (ED) in the United States each year, with 1 in 4 patients requiring admission to a hospital.1 Annually there are 5,000 to 6,000 asthma-related deaths in the United States, many occurring in the prehospital setting.2 Severe asthma accounts for approximately 2% to 20% of admissions to intensive care units, with up to one third of these patients requiring intubation and mechanical ventilation.3 This section focuses on the evaluation and treatment of patients with near-fatal asthma.Several consensus groups have developed excellent guidelines for the management of asthma that are available on the World Wide Web: http://www.nhlbi.nih.gov/about/naepphttp://www.ginasthma.comPathophysiologyThe pathophysiology of asthma consists of 3 key abnormalities: BronchoconstrictionAirway inflammationMucous pluggingComplications of severe asthma, such as tension pneumothorax, lobar atelectasis, pneumonia, and pulmonary edema, can contribute to fatalities. Severe asthma exacerbations are commonly associated with hypercarbia and acidemia, hypotension due to decreased venous return, and depressed mental status, but the most common cause of death is asphyxia. Cardiac causes of death are less common.4Clinical Aspects of Severe AsthmaWheezing is a common physical finding, although the severity of wheezing does not correlate with the degree of airway obstruction. The absence of wheezing may indicate critical airway obstruction, whereas increased wheezing may indicate a positive response to bronchodilator therapy.Oxygen saturation (Sao2) levels may not reflect progressive alveolar hypoventilation, particularly if oxygen is being administered. Note that Sao2 may fall initially during therapy because β2-agonists produce both bronchodilation and vasodilation and initially may increase intrapulmonary shunting.Other causes of wheezing are pulmonary edema,5 chronic obstructive pulmonary disease (COPD), pneumonia, anaphylaxis,6 foreign bodies, PE, bronchiectasis, and subglottic mass.7Initial StabilizationPatients with severe life-threatening asthma require urgent and aggressive treatment with simultaneous administration of oxygen, bronchodilators, and steroids. Healthcare providers must monitor these patients closely for deterioration. Although the pathophysiology of life-threatening asthma consists of bronchoconstriction, inflammation, and mucous plugging, only bronchoconstriction and inflammation are amenable to drug treatment.Primary TherapyOxygenOxygen should be provided to all patients with severe asthma, even those with normal oxygenation. As noted above, successful treatment with β2-agonists may cause an initial decrease in oxygen saturation because the resultant bronchodilation can initially increase the ventilation-perfusion mismatch.Inhaled β2-AgonistsShort-acting β-agonists provide rapid, dose-dependent bronchodilation with minimal side effects. Because the dose delivered depends on the patient's lung volume and inspiratory flow rate, the same dose can be used in most patients regardless of age or size. Studies have shown no difference in the effects of continuous versus intermittent administration of nebulized albuterol8,9; however, continuous administration was more effective in a subset of patients with severe exacerbations of asthma.8 A Cochrane meta-analysis showed no overall difference between the effects of albuterol delivered by metered-dose inhaler spacer or nebulizer.10 If prior use of a metered-dose inhaler has not been effective, use of a nebulizer is reasonable.Although albuterol is sometimes administered intravenously (IV) in severe asthma, a systematic review of 15 clinical trials found that IV β2-agonists, administered by either bolus or infusion, did not lead to significant improvements in any clinical outcome measure.9Levalbuterol is the R-isomer of albuterol. Comparisons with albuterol have produced mixed results, with some studies showing a slightly improved bronchodilator effect in the treatment of acute asthma in the ED.11 There is no evidence that levalbuterol should be favored over albuterol.One of the most common adjuncts used with β-agonist treatment, particularly in the first hours of treatment, include anticholinergic agents (see “Adjunctive Therapies” below for more detail). When combined with short-acting β-agonists, anticholinergic agents such as ipratropium can produce a clinically modest improvement in lung function compared with short-acting β-agonists alone.12,13CorticosteroidsSystemic corticosteroids are the only treatment for the inflammatory component of asthma proven to be effective for acute asthma exacerbations. Because the antiinflammatory effects after administration may not be apparent for 6 to 12 hours, corticosteroids should be administered early. The early use of systemic steroids hastens the resolution of airflow obstruction and may reduce admission to the hospital.14 Although there may be no difference in clinical effects between oral and IV formulations of corticosteroids,15,16 the IV route is preferable in patients with severe asthma. In adults a typical initial dose of methylprednisolone is 125 mg (dose range: 40 mg to 250 mg); a typical dose of dexamethasone is 10 mg.Adjunctive TherapiesAnticholinergicsIpratropium bromide is an anticholinergic bronchodilator pharmacologically related to atropine. The nebulizer dose is 500 mcg.15,16 Ipratropium bromide has a slow onset of action (approximately 20 minutes), with peak effectiveness at 60 to 90 minutes and no systemic side effects. The drug is typically given only once because of its prolonged onset of action, but some studies have shown that repeat doses of 250 mcg or 500 mcg every 20 minutes may be beneficial.17 A recent meta-analysis indicated a reduced number of hospital admissions associated with treatment with ipratropium bromide, particularly in patients with severe exacerbations.18Magnesium SulfateWhen combined with nebulized β-adrenergic agents and corticosteroids, IV magnesium sulfate can moderately improve pulmonary function in patients with asthma.19 Magnesium causes relaxation of bronchial smooth muscle independent of serum magnesium level, with only minor side effects (flushing, lightheadedness). A Cochrane meta-analysis of 7 studies concluded that IV magnesium sulfate improves pulmonary function and reduces hospital admissions, particularly for patients with the most severe exacerbations of asthma.20 The use of nebulized magnesium sulfate as an adjunct to nebulized β-adrenergic agents has been reported in a small case series to improve FEV1 and Spo2,21 although a prior meta-analysis demonstrated only a trend toward improved pulmonary function with nebulized magnesium.22 For those with severe refractory asthma, providers may consider IV magnesium at the standard adult dose of 2 g administered over 20 minutes.Epinephrine or TerbutalineEpinephrine and terbutaline are adrenergic agents that can be given subcutaneously to patients with acute severe asthma. The dose of subcutaneous epinephrine (concentration 1:1000) is 0.01 mg/kg, divided into 3 doses of approximately 0.3 mg administered at 20-minute intervals. Although the nonselective adrenergic properties of epinephrine may cause an increase in heart rate, myocardial irritability, and increased oxygen demand, its use is well-tolerated, even in patients >35 years of age.23 Terbutaline is given in a subcutaneous dose of 0.25 mg, which can be repeated every 20 minutes for 3 doses. There is no evidence that subcutaneous epinephrine or terbutaline has advantages over inhaled β2-agonists. Epinephrine has been administered IV (initiated at 0.25 mcg/min to 1 mcg/min continuous infusion) in severe asthma; however, 1 retrospective investigation indicated a 4% incidence of serious side effects. There is no evidence of improved outcomes with IV epinephrine compared with selective inhaled β2-agonists.24KetamineKetamine is a parenteral, dissociative anesthetic with bronchodilatory properties that also can stimulate copious bronchial secretions. One case series25 suggested substantial efficacy, whereas 2 published randomized trials in children26,27 found no benefit of ketamine when compared with standard care. Ketamine has sedative and analgesic properties that may be useful if intubation is planned.HelioxHeliox is a mixture of helium and oxygen (usually a 70:30 helium to oxygen ratio mix) that is less viscous than ambient air. Heliox has been shown to improve the delivery and deposition of nebulized albuterol28; however, a recent meta-analysis of clinical trials did not support its use as initial treatment for patients with acute asthma.29 Because the heliox mixture requires at least 70% helium for effect, it cannot be used if the patient requires >30% oxygen.MethylxanthinesAlthough once considered a mainstay in the treatment of acute asthma, methylxanthines are no longer recommended because of their erratic pharmacokinetics, known side effects, and lack of evidence of benefit.30Leukotriene AntagonistsLeukotriene antagonists improve lung function and decrease the need for short-acting β2-agonists for long-term asthma therapy, but their effectiveness during acute exacerbations of asthma is unproven.Inhaled AnestheticsCase reports in adults31 and children32 suggest a benefit of the potent inhalation anesthetics sevoflurane and isoflurane for patients with life-threatening asthma unresponsive to maximal conventional therapy. These agents may have direct bronchodilator effects. In addition, the anesthetic effect of these drugs increases the ease of mechanical ventilation and reduces oxygen demand and carbon dioxide production. This therapy requires expert consultation in an intensive care setting, and its effectiveness has not been evaluated in randomized clinical studies.Assisted VentilationNoninvasive Positive-Pressure VentilationNoninvasive positive-pressure ventilation (NIPPV) may offer short-term support for patients with acute respiratory failure and may delay or eliminate the need for endotracheal intubation.33–35 This therapy requires that the patient is alert and has adequate spontaneous respiratory effort. Bilevel positive airway pressure (BiPAP), the most common method of delivering NIPPV, allows for separate control of inspiratory and expiratory pressures.Endotracheal Intubation With Mechanical VentilationEndotracheal intubation is indicated for patients who present with apnea, coma, persistent or increasing hypercapnia, exhaustion, severe distress, and depression of mental status. Clinical judgment is necessary to assess the need for immediate endotracheal intubation for these critically ill patients. Endotracheal intubation does not solve the problem of small airway constriction in patients with severe asthma; thus, therapy directed toward relief of bronchoconstriction should be continued. Mechanical ventilation in the asthmatic patient can be difficult and associated risks require careful management. Intubation and positive-pressure ventilation can trigger further bronchoconstriction and complications such as breath stacking that result from incomplete expiration, air trapping, and buildup of positive end-expiratory pressure (ie, intrinsic or auto-PEEP). This breath stacking can cause barotrauma. Decreasing tidal volume may avoid auto-PEEP and high peak airway pressures. Optimal ventilator management requires expert consultation and ongoing careful review of ventilation flow and pressure curves. Although endotracheal intubation introduces risks, it should be performed when necessary based on clinical condition.Rapid sequence intubation is the technique of choice and should be performed by an expert in airway management. The provider should use the largest endotracheal tube available (usually 8 or 9 mm) to decrease airway resistance. Immediately after intubation, endotracheal tube placement should be confirmed by clinical examination and waveform capnography. A chest radiograph should then be performed.Troubleshooting After IntubationWhen severe bronchoconstriction is present, breath stacking (so-called auto-PEEP) can develop during positive-pressure ventilation, leading to complications such as hyperinflation, tension pneumothorax, and hypotension. During manual or mechanical ventilation, a slower respiratory rate should be used with smaller tidal volumes (eg, 6 to 8 mL/kg),36 shorter inspiratory time (eg, adult inspiratory flow rate 80 to 100 L/min), and longer expiratory time (eg, inspiratory to expiratory ratio 1:4 or 1:5) than generally would be provided to patients without asthma.37 Management of mechanical ventilation will vary based on patient-ventilation characteristics. Expert consultation should be obtained.Mild hypoventilation (permissive hypercapnia) reduces the risk of barotrauma. Hypercapnia is typically well tolerated.38,39 Sedation is often required to optimize ventilation, decrease ventilator dyssynchrony (and therefore auto-PEEP), and minimize barotrauma after intubation. Because delivery of inhaled medications may be inadequate before intubation, the provider should continue to administer inhaled albuterol treatments through the endotracheal tube.Four common causes of acute deterioration in any intubated patient are recalled by the mnemonic DOPE (tube Displacement, tube Obstruction, Pneumothorax, Equipment failure). Auto-PEEP is another common cause of deterioration in patients with asthma. If the asthmatic patient's condition deteriorates or if it is difficult to ventilate the patient, check the ventilator for leaks or malfunction; verify endotracheal tube position; eliminate tube obstruction (eliminate any mucous plugs and kinks); evaluate for auto-PEEP; and rule out a pneumothorax.High-end expiratory pressure can be reduced quickly by separating the patient from the ventilator circuit; this will allow PEEP to dissipate during passive exhalation. If auto-PEEP results in significant hypotension, assisting with exhalation by pressing on the chest wall after disconnection of the ventilator circuit will allow active exhalation and should lead to immediate resolution of hypotension. To minimize auto-PEEP, decrease the respiratory rate or tidal volume or both. If auto-PEEP persists and the patient displays ventilator dyssynchrony despite adequate sedation, paralytic agents may be considered.In exceedingly rare circumstances, aggressive treatment for acute respiratory failure due to severe asthma will not provide adequate gas exchange. There are case reports that describe successful use of extracorporeal membrane oxygenation (ECMO) in adult and pediatric patients40–43 with severe asthma after other aggressive measures have failed to reverse hyoxemia and hypercarbia.BLS ModificationsBLS treatment of cardiac arrest in asthmatic patients is unchanged.ACLS ModificationsWhen cardiac arrest occurs in the patient with acute asthma, standard ACLS guidelines should be followed.Case series and case reports describe a novel technique of cardiopulmonary resuscitation (CPR) termed “lateral chest compressions”; however, there is insufficient evidence to recommend this technique over standard techniques.44–50The adverse effect of auto-PEEP on coronary perfusion pressure and capacity for successful defibrillation has been described in patients in cardiac arrest without asthma.51,52 Moreover, the adverse effect of auto-PEEP on hemodynamics in asthmatic patients who are not in cardiac arrest has also been well-described.53–56 Therefore, since the effects of auto-PEEP in an asthmatic patient with cardiac arrest are likely quite severe, a ventilation strategy of low respiratory rate and tidal volume is reasonable (Class IIa, LOE C). During arrest a brief disconnection from the bag mask or ventilator may be considered, and compression of the chest wall to relieve air-trapping can be effective (Class IIa, LOE C).For all asthmatic patients with cardiac arrest, and especially for patients in whom ventilation is difficult, the possible diagnosis of a tension pneumothorax should be considered and treated (Class I, LOE C).Part 12.2: Cardiac Arrest Associated With AnaphylaxisAnaphylaxis is an allergic reaction characterized by multisystem involvement, including skin, airway, vascular system, and gastrointestinal tract. Severe cases may result in complete obstruction of the airway and cardiovascular collapse from vasogenic shock. Anaphylaxis accounts for about 500 to 1000 deaths per year in the United States.57The term classic anaphylaxis refers to hypersensitivity reactions mediated by the immunoglobulins IgE and IgG. Prior sensitization to an allergen produces antigen-specific immunoglobulins. Subsequent reexposure to the allergen provokes the anaphylactic reaction, although many anaphylactic reactions occur with no documented prior exposure. Pharmacological agents, latex, foods, and stinging insects are among the most common causes of anaphylaxis described.Signs and SymptomsThe initial symptoms of anaphylaxis are often nonspecific and include tachycardia, faintness, cutaneous flushing, urticaria, diffuse or localized pruritus, and a sensation of impending doom. Urticaria is the most common physical finding. The patient may be agitated or anxious and may appear either flushed or pale.A common early sign of respiratory involvement is rhinitis. As respiratory compromise becomes more severe, serious upper airway (laryngeal) edema may cause stridor and lower airway edema (asthma) may cause wheezing. Upper airway edema can also be a sign in angiotensin converting enzyme inhibitor-induced angioedema or C1 esterase inhibitor deficiency with spontaneous laryngeal edema.58–60Cardiovascular collapse is common in severe anaphylaxis. If not promptly corrected, vasodilation and increased capillary permeability, causing decreased preload and relative hypovolemia of up to 37% of circulating blood volume, can rapidly lead to cardiac arrest.61,62 Myocardial ischemia and acute myocardial infarction, malignant arrhythmias, and cardiovascular depression can also contribute to rapid hemodynamic deterioration and cardiac arrest.63 Additionally, cardiac dysfunction may result from underlying disease or development of myocardial ischemia due to hypotension or following administration of epinephrine.64,65There are no randomized controlled trials evaluating alternative treatment algorithms for cardiac arrest due to anaphylaxis. Evidence is limited to case reports and extrapolations from nonfatal cases, interpretation of pathophysiology, and consensus opinion. Providers must be aware that urgent support of airway, breathing, and circulation is essential in suspected anaphylactic reactions.Because of limited evidence, the management of cardiac arrest secondary to anaphylaxis should be treated with standard BLS and ACLS. The following therapies are largely consensus-based but commonly used and widely accepted in the management of the patient with anaphylaxis who is not in cardiac arrest.BLS ModificationsAirwayEarly and rapid advanced airway management is critical and should not be unnecessarily delayed. Given the potential for the rapid development of oropharyngeal or laryngeal edema,66 immediate referral to a health professional with expertise in advanced airway placement is recommended (Class I, LOE C).CirculationThe intramuscular (IM) administration of epinephrine (epinephrine autoinjectors, eg, the EpiPen™) in the anterolateral aspect of the middle third of the thigh provides the highest peak blood levels.67 Absorption and subsequent achievement of maximum plasma concentration after subcutaneous administration is slower than the IM route and may be significantly delayed with shock.67Epinephrine68 should be administered early by IM injection to all patients with signs of a systemic allergic reaction, especially hypotension, airway swelling, or difficulty breathing (Class I, LOE C). The recommended dose is 0.2 to 0.5 mg (1:1000) IM to be repeated every 5 to 15 minutes in the absence of clinical improvement (Class I, LOE C).69 The adult epinephrine IM auto-injector will deliver 0.3 mg of epinephrine and the pediatric epinephrine IM auto-injector will deliver 0.15 mg of epinephrine. In both anaphylaxis and cardiac arrest the immediate use of an epinephrine autoinjector is recommended if available (Class I, LOE C).ACLS ModificationsAirwayEarly recognition of the potential for a difficult airway in anaphylaxis is paramount in patients who develop hoarseness, lingual edema, stridor, or oropharyngeal swelling. Planning for advanced airway management, including a surgical airway,70 is recommended (Class I, LOE C).Fluid ResuscitationIn a prospective evaluation of volume resuscitation after diagnostic sting challenge, repeated administration of 1000-mL bolus doses of isotonic crystalloid (eg, normal saline) titrated to systolic blood pressure above 90 mm Hg was used successfully in patients whose hypotension did not respond immediately to vasoactive drugs.61,71 Vasogenic shock from anaphylaxis may require aggressive fluid resuscitation (Class IIa, LOE C).VasopressorsThere are no human trials establishing the role of epinephrine or preferred route of administration in anaphylactic shock managed by ACLS providers.68 In an animal study of profound anaphylactic shock, IV epinephrine restored blood pressure to baseline; however, the effect was limited to the first 15 minutes after shock, and no therapeutic effect was observed with the same dose of epinephrine administered IM or subcutaneously.72 Therefore, when an IV line is in place, it is reasonable to consider the IV route as an alternative to IM administration of epinephrine in anaphylactic shock (Class IIa, LOE C).For patients not in cardiac arrest, IV epinephrine 0.05 to 0.1 mg (5% to 10% of the epinephrine dose used routinely in cardiac arrest) has been used successfully in patients with anaphylactic shock.73 Because fatal overdose of epinephrine has been reported,64,71,74,75 close hemodynamic monitoring is recommended (Class I, LOE B).In a study of animals sensitized by ragweed, a continuous IV infusion of epinephrine maintained a mean arterial pressure at 70% of preshock levels better than no treatment or bolus epinephrine treatment (IV, subcutaneous, or IM).76 Furthermore, a recent human study suggests that careful titration of a continuous infusion of IV epinephrine (5 to 15 mcg/min), based on severity of reaction and in addition to crystalloid infusion, may be considered in treatment of anaphylactic shock.71 Therefore, IV infusion of epinephrine is a reasonable alternative to IV boluses for treatment of anaphylaxis in patients not in cardiac arrest (Class IIa, LOE C) and may be considered in postarrest management (Class IIb, LOE C).Recently vasopressin has been used successfully in patients with anaphylaxis (with or without cardiac arrest) who did not respond to standard therapy.77–79 Other small case series described successful results with administration of alternative α-agonists such as norepinephrine,80 methoxamine,81,82 and metaraminol.83–85 Alternative vasoactive drugs (vasopressin, norepinephrine, methoxamine, and metaraminol) may be considered in cardiac arrest secondary to anaphylaxis that does not respond to epinephrine (Class IIb, LOE C). No randomized controlled trials have evaluated epinephrine versus the use of alternative vasoactive drugs for cardiac arrest due to anaphylaxis.Other InterventionsThere are no prospective randomized clinical studies evaluating the use of other therapeutic agents in anaphylactic shock or cardiac arrest. Adjuvant use of antihistamines (H1 and H2 antagonist),86,87 inhaled β-adrenergic agents,88 and IV corticosteroids89 has been successful in management of the patient with anaphylaxis and may be considered in cardiac arrest due to anaphylaxis (Class IIb, LOE C).Extracorporeal Support of CirculationCardiopulmonary bypass has been successful in isolated case reports of anaphylaxis followed by cardiac arrest.90,91 Use of these advanced techniques may be considered in clinical situations where the required professional skills and equipment are immediately available (Class IIb, LOE C).Part 12.3: Cardiac Arrest Associated With PregnancyScope of the ProblemThe Confidential Enquiries into Maternal and Child Health (CEMACH) data set constitutes the largest population-based data set on this target population.92 The overall maternal mortality rate was calculated at 13.95 deaths per 100 000 maternities. There were 8 cardiac arrests with a frequency calculated at 0.05 per 1000 maternities, or 1:20 000. The frequency of cardiac arrest in pregnancy is on the rise with previous reports estimating the frequency to be 1:30 000 maternities.93 Despite pregnant women being younger than the traditional cardiac arrest patient, the survival rates are poorer, with one case series reporting a survival rate of 6.9%.93,94During attempted resuscitation of a pregnant woman, providers have 2 potential patients: the mother and the fetus. The best hope of fetal survival is maternal survival. For the critically ill pregnant patient, rescuers must provide appropriate resuscitation based on consideration of the physiological changes caused by pregnancy.Key Interventions to Prevent ArrestThe following interventions are the standard of care for treating the critically ill pregnant patient (Class I, LOE C): Place the patient in the full left-lateral position to relieve possible compression of the inferior vena cava. Uterine obstruction of venous return can produce hypotension and may precipitate arrest in the critically ill patient.95,96Give 100% oxygen.Establish intravenous (IV) access above the diaphragm.Assess for hypotension; maternal hypotension that warrants therapy has been defined as a systolic blood pressure <100 mm Hg or <80% of baseline.97,98 Maternal hypotension can result in reduced placental perfusion.99–102 In the patient who is not in arrest, both crystalloid and colloid solutions have been shown to increase preload.103Consider reversible causes of critical illness and treat conditions that may contribute to clinical deterioration as early as possible.Resuscitation of the Pregnant Patient in Cardiac Arrest (Figure 1)Download figureDownload PowerPointFigure 1. Maternal cardiac arrest algorithm.There are no randomized controlled trials evaluating the effect of specialized obstetric resuscitation versus standard care in pregnant patients in cardiac arrest. There are reports in the literature of patients not in arrest that describe the science behind important physiological changes that occur in pregnancy that may influence treatment recommendations and guidelines for resuscitation from cardiac arrest in pregnancy.BLS ModificationsPatient PositioningPatient position has emerged as an important strategy to improve the quality of CPR and resultant compression force and output. The pregnant uterus can compress the inferior vena cava, impeding venous return and thereby reducing stroke volume and cardiac output. Reports of noncardiac arrest parturients indicate that left-lateral tilt results in improved maternal hemodynamics of blood pressure, cardiac output, and stroke volume96,98,104; and improved fetal parameters of oxygenation, nonstress test, and fetal heart rate.100–102Although chest compressions in the left-lateral tilt position are fea