Cardiac Arrest

Pregnancy & Cardiac Arrest

Most anesthesiologists have received Advanced Cardiac Life Support (ACLS) certification. Does that mean we know how to resuscitate a parturient following cardiac arrest? American Heart Association (AHA) ACLS courses generally don’t spend much time, if any, teaching obstetric-specific interventions. The Society for Obstetric Anesthesia and Perinatology, have developed a consensus statement designed to expand AHA 2010 guidelines to focus on maternal resuscitation.

Treatment of Cardiac Arrest

Airway should be controlled as soon as possible. Ventilation should be accomplished by 8-10 inflations/min (1 second per inflation) with no pauses for chest compressions – high intrathoracic pressures are to be avoided because they reduce preload and diastolic coronary perfusion. Excessive tidal volumes are to be avoided, thus one-handed bag ventilation may be ideal. Compressions should be > 100/min (10:1 ratio). You must allow full recoil of the chest (for ventricular filling).

The survival rate for in-hospital cardiac arrest is 15% [J Am Board Fam Pract 6: 91, 1993 (19,955 subjects)]. The problem with CPR is that while systolic BP can be as high as 50 mm Hg, the arteriovenous difference is negligible. Active compression-decompression (suction) devices have not been shown to produce better outcomes than standard CPR. DC cardioversion is the single most effective measure for improving survival following cardiac arrest but is very time-dependent – a 5 min delay leads to a 40% survival, whereas a 20 min delay leads to a 10% survival [Ann Emerg Med 22: 1652, 1993]. The recommended doses are 200, 300, and 360 J, after which pharmacotherapy is initiated.

Pharmacotherapy should be initiated through the antecubital or external jugular veins as these do not interfere with chest compressions or intubation. Peripheral injections should always be bolused, followed by a 20 mL saline flush. If these fail, proceed to central cannulation, which reduces circulation time by ~ 2 minutes [JAMA 268: 2171, 1992]. If this fails, consider intraosseious (preferred) or endobronchial (epinephrine, vasopressin, atropine, lidocaine can be given endobronchially). In general, the endobronchial dose is 2x the IV dose although for epi it’s usually higher. Always dilute these drugs in 10 mL sterile water/saline prior to placing them endobronchially, followed by several manual breaths.

Note: there is no evidence that epinephrine or vasopressin increase survival in cardiac arrest [2005 AHA Guidelines for CPR…Part 7.2. Circulation 112SI: IV58, 2005]

ACLS Pharmacology

Vasopressors – Epinephrine and Vasopressin

The standard epinephrine dose in adults is 1 mg (10 mL of a 1:10,000 solution) q3-5 minutes as necessary. A randomized trial of 3327 patients comparing standard 1 mg to high (5 mg) dose epinephrine in resuscitation efforts showed an increase in return of spontaneous circulation (p=0.02) and in survival to be admitted to the hospital (p=0.05), but no change in the percent who survive to discharge (p=0.34) [NEJM 339: 1595, 1998]. A more recent study in children comparing high-dose epinephrine (0.1 mg/kg) with standard-dose epinephrine (0.01 mg/kg) as rescue therapy for in-hospital cardiac arrest trended towards a lower survival rate in the high dose group (p=0.08) [NEJM 350: 1722, 2004]

Although vasopressin has no cardiac effects and vasodilates the cerebrovasculature, a trial between epinephrine and vasopressin showed no difference between the two [AIM 165: 17, 2005]. Still, if endotracheal delivery is required, use vasopressin because epinephrine is poorly absorbed from airways and when given endobronchially preferentially overstimulates the heart.


Compared to placebo [NEJM 341: 871, 1999] or lidocaine [NEJM 346: 884, 2002], amiodarone improves survival to hospital (but not to discharge) in outside patients when given the drug in the field. Despite this, amiodarone (300 mg) is recommended for V-fib or unstable V-tach refractory to defibrillation and vasopressors [AHA 2005]. Lidocaine has no documented impact on survival and is now only offered as an alternative to amiodarone.

Magnesium is useful in Torsades (1-2 g over 5 min)

Others (atropine, bicarb, Ca++, dextrose)

Atropine is probably the least effective drug in the ACLS armementarium. It is most useful for bradycardia but also recommended for PEA and ventricular asystole. It has not been proven to work.

Bicarbonate is still a source of debate – in the 1992 version of the ACLS guidelines, bicarbonate may be indicated in cases of protracted arrest or long resuscitative efforts or with preexisting metabolic acidosis. The 2000 ACLS guidelines do not offer any new discussion of buffer therapy and their section on bicarbonate use is basically a copy of the 1992 version.

Class I (definitely beneficial)

  • Hyperkalemia

Class IIA (probably beneficial)

  • Bicarbonate-responsive acidosis
  • Tricyclic overdose
  • Urinary alkalinization

Class IIB (possibly beneficial)

  • Prolonged cardiac arrest
  • Post-resuscitation acidosis

Class III (harmful)

  • Anaerobic lactic acidosis

Calcium is only indicated in cases of acute hyperkalemia, ionized hypocalcemia, and CCB overdose. Otherwise it should be considered dangerous, as it may disrupt cell membranes.

Dextrose can have deleterious effects on critically-ill patients [Crit Care Clin 12: 667, 1996] by enhancing lactic acid production, thus this is a class III (harmful) intervention.

Clinical Monitoring During Cardiac Arrest

Palpable pulses or arterial pressure waves are NOT indications of blood flow. Changes in end-tidal CO2 indicate changes in cardiac output and should be followed as it has important prognostic value [JAMA 262: 1347, 1989; Ann Emerg Med 25: 762, 1995]. If end-tidal CO2 does not rise above 10 mm Hg after 20 minutes of resuscitation, the effort is not likely to be successful.

Venous blood gases should be measured, as opposed to arterial blood gases, because venous blood more accurately represents the oxygenation and acid-base status of the peripheral tissues [NEJM 315: 153, 1986; Arch Emerg Med 9: 169, 1992]. Unfortunately, the time it takes to do this limits its utility in a CPR situation.

In witnessed arrest, if arrest time is less than 6 minutes CPR can be continued for 30 minutes (50% of survivors have a satisfactory neurologic recovery if they are revived in under 30 min), otherwise it should be stopped in 15. Furthermore, while some coma is expected, coma that lasts > 4 hours after CPR carries a poor prognosis for full neurologic recovery. At 24 hours of coma, the satisfactory recovery rate is 9%, and at 3 days it is 5% [Ann Intern Med 94: 293, 1981]. Absence of pupillary light response after one or more days indicates little or no chance of neurologic recovery.

Post-resuscitation management should pay homage to several principles: 1) increased body temperature is associated with decreased survival rates during CPR [AIM 161: 2007, 2001], although the value of intervention has not been studied. Do not use cooling blankets because they can induce shivering and/or coronary vasospasm [Circulation 77: 43, 1987] 2) Therapeutic hypothermia to 32 – 34 C for 12 – 24 hours has been shown to improve neurologic outcome in a very small subset of cardiac arrest patients who survived CPR (~ 8%) [NEJM 346: 549 and 557, 2002], hopefully the inclusion criteria can soon be expanded. These patients require NMJ blockade to prevent shivering 3) hyperglycemia is associated with worse neurologic outcomes in cardiac arrest patients [Circulation 112S: IV84, 2005], however intervening has not been proven to help. Still, given the ICU data on hyperglycemia [NEJM 345: 1359, 2001], it is probably a good idea to institute strict control and avoid dextrose in all IV fluids.

Hemodynamic Drugs



Dobutamine: ionotrope of choice in acute management of severe systolic heart failure but should not be used as monotherapy in shock. Strong β1 effects but also has mild β2 effects (vasodilation, thus do not use as monotherapy in shock). Stroke volume increases, filling pressures decrease, and SVR decreases leading to enhanced cardiac output with no major changes in blood pressure. Dobutamine increases myocardial O2 consumption and cardiac work, and for these reasons vasodilators are now the preferred agents for acute management of decompensated heart failure [Am J Cardiol 96S: 47G, 2005]. When used, dobutamine is effective in both left and right heart failure. Effectiveness can vary significantly in critically-ill patients (for instance, elderly patients may seem to be resistant), thus dobutamine should be titrated based on hemodynamic endpoints and NOT based on preselected doses [Crit Care Med 22: 1926, 1994]. Do not infuse with bicarbonate or other alkaline solutions as they inactivate catecholamines. Dobutamine is contraindicated in patients with HOCM, is no longer first line in systolic left heart failure, and is not indicated in diastolic heart failure. According to 1987 data it is, however, still first line in right heart failure.


Amrinone: PDE inhibitor that has ionotropic and vasodilatory actions. Despite its dual activity is has not been proven superior to dobutamine [Am Heart J 1212: 1871, 1991]. As it has a different mechanism of action, it can be complementary to dobutamine. It is not affected by beta-blockers. Its primary use is add-on therapy with dobutamine. It is degraded by dextrose and light and thus cannot be infused in D5 and must be protected from light. Amrinone should not be infused with furosemide because the two precipitate. Thrombocytopenia occurs in 2 – 3% of patients. Hypotension can occur but usually only in hypovolemic patients. Amrinone is contraindicated in hypertrophic cardiomyopathy and possibly if platelets < 50,000


Dopamine: at 0.5 – 3.0 μg/kg/min activates D receptors in the renal, mesenteric, and cerebral circulation and increases blood flow there as well as increasing urinary sodium and water secretion. At 3.0 – 7.5 μg/kg/min activates β1 and β2 receptors, but its ionotropic response is modest compared to dobutamine. At > 7.5 μg/kg/min activates α receptors, attenuating increases in cardiac output and elevating the PCWP – the wedge pressure is thus significantly less reliable in patients on dopamine. Dopamine is indicated as second-line therapy in septic shock (norepinephrine is first) and is known for its ability to vasoconstrict while at the same time maintain cardiac output, making it useful for cardiogenic shock. As in dobutamine, dopamine should not be infused with alkalemic fluids. It is not effective at preventing renal failure [Crit Care Med 29: 1526, 2001]


Epinephrine: activates β1 and β2 receptors at 0.005 – 0.02 μg/kg/min but also activates α receptors at higher doses. Doses above 0.1 μg/kg/min can produce severe vasoconstriction. In addition to its cardiovascular effects, epinephrine causes hypermetabolism, hyperglycemia, lipolysis and increase ketoacids, lyperlactatemia (without ischemia), decreased serum potassium, and can block the release of inflammatory mediators from mast cells and basophils [Chest 100: 1676, 1991]. It is indicated in cardiac arrest and for severe anaphylactic reactions (but not first line for low cardiac output or circulatory shock). It is available as a 1:1000 solution. It is inactivated by alkaline solutions. Epinephrine is arrhythmogenic, especially in combination with halothane or electrolyte abnormalities [Am J Cardiol 119: 891, 1990]. It can cause serious hypertension in patients on β-blockers (unopposed α action) and ischemic renal failure if accidentally overdosed. Epinephrine increases resting metabolic rate by 35%, which can be an issue in patients with poor tissue oxygenation [Am Rev Resp Dis 147: 25, 1993]. Dobutamine, by contrast, is relatively metabolically neutral.


Labetalol:α and β antagonist that lowers SVR and blood pressure without reflex tachycardia or increased CO. Unlike nitroglycerin or nitroprusside, labetalol does not increase ICP [Lancet 344: 1335, 1994]. It is indicated for severe hypertension in the face of adequate cardiac output and is particularly useful in aortic dissection. It can be given IV but should only be bolused in supine patients (orthostatic hypotension). Side effects include orthostatic hypotension, myocardial depression, and bronchospasm. Avoid this drug in patients with heart failure or asthma.


Nitroglycerin: active in both systemic and pulmonary vascular beds. Venodilation is prominent at low doses (< 40 μg/min), leading to a decrease in cardiac filling pressures (CVP, PCWP) without affecting cardiac output. Arteriodilatation is prominent at high doses (> 200 μg/min), leading to increased CO. Further increases lead to a drop in blood pressure. Rapid onset, short duration. Can inhibit platelet aggregation [Cardiol Clin 12: 73, 1994]. Useful for relieving chest pain, lowering filling pressures (low dose), augmenting cardiac output (medium dose), or lowering blood pressure (high dose). Nitroglycerin binds to soft plastics like PVC (up to 80%), but not glass or hard plastic – this must be taken into account when infusing. Adverse effects include increased cerebral blood flow (headache, elevated ICP, IC-HTN [Crit Care Clin 7: 555, 1991]), increases in pulmonary blood flow (hypoxemia if a shunt is present, especially in ARDS [Anesthesiology 70: 112, 1989]), worsened hypotension in right heart patients (infuse them with volume first), methemoglobinemia at very high doses (look for brown blood or on cooximetry, missed by pulse oximetry, abnormal MetHb is 3%, 40% produces ischemia and 70% is lethal, give methylene blue to counteract), and solvent toxicity (must be dissolved in ethanol or propylene glycol, screen with an osmol gap and worry if > 10 mOsm/L). Tolerance can develop after 24 hours, so the drug should be discontinued for 6 – 8 hours each day if possible.


Nitroprusside: very similar actions as nitroglycerin (uses the same NO molecule) but 50% of its molecular weight is cyanide. It is more of an arterial dilator and less of a venous dilator compared to nitroglycerin. One should infuse 500 mg thiosulfate for each 50 mg of nitroprusside. Besides the potential for toxicity, nitroprusside can also elevate ICP and is contraindicated in patients with hypertensive encephalopathy.


Norepinephrine: α agonist which is the vasopressor of choice in septic shock despite not being shown to increase survival [Crit Care Med 32S: S455, 2004] and is often used in response to circulatory shock. In non-septic states it decreases blood flow to various organ systems, especially the kidneys. In addition to α-receptors, it can also stimulate β receptors but does not affect CO except for a mild increase at low doses. Adverse effects include hypoperfusion and/or ischemia.


[Curr Opin Crit Care 8: 212, 2002] Advanced life support drugs: do they really work?

Epinephrine – high dose is no longer recommended

Despite a lack of robust data demonstrating improved long-term outcome, epinephrine (adrenaline), in a “standard” dose of 1 mg every 3 minutes, continues to be advocated during resuscitation. Its [alpha]-adrenergic receptor–stimulating properties should result in improved CPP, but the [beta]-adrenergic effects of epinephrine are potentially harmful. These include increased myocardial oxygen consumption [3], ventricular arrhythmias [4], and increased intrapulmonary shunting caused by reduced hypoxic pulmonary vasoconstriction [5]. High-dose (up to 0.2 mg/kg) epinephrine may further enhance CPP but does not seem to improve long-term survival after out-of-hospital [6] or in-hospital cardiac arrest [7]. Its use is therefore no longer recommended [8,9,10].

9. Latorre F, Nolan J, Robertson C, et al.: European Resuscitation Council Guidelines 2000 for Adult Advanced Life Support. A statement from the Advanced Life Support Working Group and approved by the Executive Committee of the European Resuscitation Council. Resuscitation 2001, 48:211–221. A summary of the European Resuscitation Council ALS guidelines, updated following publication of the International CPR Guidelines 2000. Bibliographic Links Library Holdings [Context Link]

10. Babbs CF, Berg RA, Kette F, et al.: Use of pressors in the treatment of cardiac arrest. Ann Emerg Med 2001, 37(suppl 4):S152–S162. An account of the data presented at the 1999 Evidence Evaluation Conference, which formed the basis for recommendations on the use of vasopressors in the Guidelines 2000. Ovid Full Text Bibliographic Links Library Holdings [Context Link]


Human studies In a prospective, randomized study, 40 patients with out-of-hospital ventricular fibrillation resistant to shocks were given either 1 mg epinephrine or 40 U vasopressin [34]. Significantly more patients receiving vasopressin were alive at 24 hours, but this very small study lacked the power to demonstrate any significant differences in long-term survival. A prospective, randomized study involving 200 patients with in-hospital cardiac arrest (all rhythms) who were given either 40 U vasopressin or 1 mg epinephrine as the initial vasopressor [35]. The study was powered to allow detection of a 20% absolute difference in survival to 1 hour, assuming the baseline survival at 1 hour to be 30%, was undertaken. Forty (39%) of the vasopressin group survived to 1 hour versus 34 (35%) of the epinephrine group (P = 0.66). The difference in the findings between these two studies is not readily explained at present. It could be postulated that vasopressin may be more beneficial than epinephrine in the presence of severe acidosis [36]. A European multicenter study to determine the effect of vasopressin, 40 U, versus epinephrine, 1 mg, on short-term survival after out-of-hospital cardiac arrest (all rhythms) had recruited 1135 of the planned 1500 patients by December 2001 (Volker Wenzel, Personal communication, December 2001)

Vasopressin and current cardiopulmonary resuscitation guidelines The International Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care [8] was the culmination of a series of detailed, evidence-based reviews and discussions amongst experts from around the world [37]. The role of vasopressin in CPR was debated intensely. The lack of data from large-scale human studies was a concern to many experts. The final decision mandated a Class IIb recommendation (acceptable, safe, and useful—an optional or alternative intervention) for vasopressin to be used as an alternative to epinephrine for shock refractory ventricular fibrillation [8,10]. There were inadequate data to support the use of vasopressin in patients with asystole or pulseless electrical activity (Class Indeterminate) or in infants and children (Class Indeterminate). Not all experts agree with the decision to recommend vasopressin for shock refractory ventricular fibrillation [35], and the Advanced Life Support Working Group of the European Resuscitation Council did not include vasopressin in the European Resuscitation Council Guidelines 2000 for adult ALS [9].

35. Stiell IG, Hébert PC, Wells GA, et al.: Vasopressin versus epinephrine for in-hospital cardiac arrest: a randomised controlled trial. Lancet 2001, 358:105–109. An important study that failed to detect a survival advantage for vasopressin after in-hospital cardiac arrest. Bibliographic Links Library Holdings [Context Link] [NEJM 350: 105, 2004] A comparison of vasopressin and epinephrine for out-of-hospital cardiopulmonary resuscitation.

We randomly assigned adults who had had an out-of-hospital cardiac arrest to receive two injections of either 40 IU of vasopressin or 1 mg of epinephrine, followed by additional treatment with epinephrine if needed. The primary end point was survival to hospital admission, and the secondary end point was survival to hospital discharge. RESULTS: A total of 1219 patients underwent randomization; 33 were excluded because of missing study-drug codes. Among the remaining 1186 patients, 589 were assigned to receive vasopressin and 597 to receive epinephrine. The two treatment groups had similar clinical profiles. There were no significant differences in the rates of hospital admission between the vasopressin group and the epinephrine group either among patients with ventricular fibrillation (46.2 percent vs. 43.0 percent, P=0.48) or among those with pulseless electrical activity (33.7 percent vs. 30.5 percent, P=0.65). Among patients with asystole, however, vasopressin use was associated with significantly higher rates of hospital admission (29.0 percent, vs. 20.3 percent in the epinephrine group; P=0.02) and hospital discharge (4.7 percent vs. 1.5 percent, P=0.04). Among 732 patients in whom spontaneous circulation was not restored with the two injections of the study drug, additional treatment with epinephrine resulted in significant improvement in the rates of survival to hospital admission and hospital discharge in the vasopressin group, but not in the epinephrine group (hospital admission rate, 25.7 percent vs. 16.4 percent; P=0.002; hospital discharge rate, 6.2 percent vs. 1.7 percent; P=0.002). Cerebral performance was similar in the two groups. CONCLUSIONS: The effects of vasopressin were similar to those of epinephrine in the management of ventricular fibrillation and pulseless electrical activity, but vasopressin was superior to epinephrine in patients with asystole. Vasopressin followed by epinephrine may be more effective than epinephrine alone in the treatment of refractory cardiac arrest


Amiodarone has now replaced lidocaine as the drug of choice for patients who remain in ventricular fibrillation/pulseless ventricular tachycardia after three shocks

Data from the Amiodarone versus Lidocaine in pre-hospital refractory Ventricular fibrillation Evaluation (ALIVE) study have been published recently [55]. Drugs were given by the paramedics in the Toronto Emergency Medical Service system. Following the administration of 5 mg/kg amiodarone, 41 (22.7%) of 179 patients survived to hospital admission versus 18 (11.0%) of patients given 1.5 mg/kg lidocaine (P < 0.0043). In comparison with the Seattle study, the mean interval to first defibrillation was 2.5 minutes longer and the interval to study drug administration was 4 minutes longer. The results of this study support the choice of amiodarone instead of lidocaine for shock refractory ventricular fibrillation, but the uncertainty of the impact of amiodarone on long-term outcome remains.


The antiarrhythmic action of magnesium is through activation of membrane sodium-potassium adenosine triphosphatase and blocking of slow calcium channels [56]. Despite being supported by only two uncontrolled case series [57,58], magnesium is a universally accepted therapy for torsades de pointes [8,9,41]. Magnesium sulphate, 2 g (8 mmol), is also recommended for shock refractory ventricular fibrillation when hypomagnesemia is suspected [9]; however, its routine use in cardiac arrest is contentious. There are anecdotal reports of the successful use of magnesium in shock refractory ventricular fibrillation [59], but a randomized, double-blind, placebo-controlled trial of 2 g (8 mmol) magnesium sulphate in 116 patients with out-of-hospital ventricular fibrillation arrest failed to show any benefit [60]. Other small, prospective, randomized trials of magnesium after in-hospital [61] and out-of-hospital [62] cardiac arrest have also failed to show any survival benefit. On the basis of these data, magnesium is not recommended for routine use in cardiac arrest. [8]

Cardiac Arrest (usually PE or MI)

In the past, because of the fear of severe bleeding complications [65,66], the need for CPR has been a relative contraindication to fibrinolysis. However, there are several case series documenting the safety of fibrinolysis in patients with acute myocardial infarction who have undergone CPR [67,68]. Most clinicians would now consider fibrinolysis to be frequently appropriate after CPR based on the relative risks and benefits in individual patients.

There are several reports on the use of fibrinolysis during CPR in patients with massive pulmonary embolism [69,70,71,72]. Of the 80 patients studied, 42 (53%) survived to hospital discharge, and only one of these patients died from intracerebral hemorrhage after ROSC. Inevitably, there is a considerable reporting bias, and the true chances of survival after the use of fibrinolysis during CPR for pulmonary embolism are less than this. A prospective, randomized trial would provide an indication of the true efficacy of fibrinolysis for cardiac arrest after pulmonary embolism, but, following these case series, few clinicians would be prepared to withhold fibrinolysis during CPR if there is good evidence of pulmonary embolism. Recombinant tissue plasminogen activator (rt-PA) given as two 100-mg bolus doses 30 minutes apart is a simple fibrinolytic technique to use during CPR [71].

Fibrinolysis has also been used successfully during CPR in patients with acute myocardial infarction. Of 23 such patients, 12 (52%) survived to hospital discharge [70]. The successful use of fibrinolysis in hospital during and after CPR has led to studies of its efficacy during CPR after out-of-hospital cardiac arrest [73,74]. In the first of these studies, 40 patients with out-of-hospital cardiac arrest and with no ROSC after 15 minutes of CPR were given 50 mg rt-PA over 2 minutes [73]. In comparison with a historical control group of 50 patients, patients receiving rt-PA were more likely to achieve ROSC (68%vs 44%, P = 0.026) and to be admitted to an intensive care unit (58%vs 30%, P = 0.009). There was no CPR-related bleeding, but upper gastrointestinal hemorrhage occurred in two patients in the rt-PA group. The second study retrospectively compared 108 patients who were given rt-PA during out-of-hospital CPR with 216 matched control subjects [74]. Patients given rt-PA were more likely to achieve ROSC (70.4%vs 51%, P = 0.001) and to survive to hospital discharge (25.0%vs 15.3%, P = 0.048). Massive intracranial hemorrhage occurred in one patient who had received rt-PA and in two control subjects. The small number of patients, lack of randomization, and historical controls makes it very difficult to draw firm conclusions on the routine use of fibrinolysis in out-of-hospital cardiac arrest from these studies. A randomized trial is essential [75] and is now being planned. Four percent of out-of-hospital cardiac arrests are caused by spontaneous subarachnoid hemorrhage, which is exacerbated by fibrinolysis. However, even in the absence of fibrinolysis, the chances of long-term survival under these circumstances are very poor [76].

55. Dorian P, Cass D, Gelaznikas R, et al.: Alive: a randomized, blinded trial of intravenous amiodarone versus lidocaine in shock resistant ventricular fibrillation. Circulation 2001, 104(suppl 2):765. An abstract of a study showing that amiodarone leads to higher rates of survival to hospital admission than lidocaine in patients with out-of-hospital shock refractory ventricular fibrillation.

68. Ruiz-Bailen M, Aguayo de Hoyos E, Serrano-Corcoles MC, et al.: Efficacy of thrombolysis in patients with acute myocardial infarction requiring cardiopulmonary resuscitation. Intensive Care Med 2001, 27:1050–1057. This study demonstrated no increase in hemorrhagic complications in 67 patients given fibrinolytic therapy after acute myocardial infarction and CPR.

70. Böttiger BW, Martin E: Thrombolytic therapy during cardiopulmonary resuscitation and the role of coagulation activation after cardiac arrest. Curr Opin Crit Care 2001, 7:176–183. An excellent overview of the use of fibrinolytics during CPR. It includes a discussion on the possible mechanisms for their benefit.

71. Ruiz-Bailen M, Aguayo De Hoyos E, Serrano-Corcoles MC, et al.: Thrombolysis with recombinant tissue plasminogen activator during cardiopulmonary resuscitation in fulminant pulmonary embolism. A case series. Resuscitation 2001, 51:97–101. The use of fibrinolysis in six patients in cardiac arrest secondary to pulmonary embolism. A simple double bolus technique for giving rt-PA is described.

72. Ruiz-Bailen M, Cuadra JA, Aguayo De Hoyos E, et al.: Thrombolysis during cardiopulmonary resuscitation in fulminant pulmonary embolism: a review. Crit Care Med 2001, 29:2211–2219. A review of the literature on the use of fibrinolysis during CPR for patients with massive pulmonary embolism. The safety of this therapy under these circumstances is inferred.

73. Böttiger BW, Bode C, Kern S, et al.: Efficacy of thrombolytic therapy after initially unsuccessful resuscitation: a prospective clinical trial. Lancet 2001, 357:1583–1585. A study showing increased survival to hospital admission for patients given rt-PA during CPR for out-of-hospital cardiac arrest. The findings are weakened by the use of historical controls.

74. Lederer W, Lichtenberger C, Pechlaner C, et al.: Recombinant tissue plasminogen activator during cardiopulmonary resuscitation in 108 patients with out-of-hospital cardiac arrest. Resuscitation 2001, 50:71–76. A retrospective chart review that concludes that fibrinolytic therapy given during CPR may increase survival after out-of-hospital cardiac arrest. Its retrospective nature makes firm conclusions impossible.

76. Kurkciyan I, Meron G, Sterz F, et al.: Spontaneous subarachnoid hemorrhage as a cause of out-of-hospital cardiac arrest. Resuscitation 2001, 51:27–32. In this study, 4% of out-of-hospital cardiac arrests were caused by spontaneous subarachnoid hemorrhage.