The lecture below can be accessed on the Disease Management section of the Cleveland Clinic, under Allergy and Immunology (to go to this link and see others in the series, please click here)
Published: September 2014
Cardiovascular emergencies are life-threatening disorders that must be recognized immediately to avoid delay in treatment and to minimize morbidity and mortality. Patients may present with severe hypertension, chest pain, dysrhythmia, or cardiopulmonary arrest. In this chapter, we review the clinician’s approach to these disorders and their treatments and provide links to other informative resources.
Cardiopulmonary arrest is a sudden and unexpected loss of perfusing pulsatile blood flow attributable to cessation of cardiac mechanical activity. It occurs as a result of a multitude of cardiovascular, metabolic, infectious, neurologic, inflammatory, and traumatic diseases.
These diseases can be generally classified into 5 H’s and 5 T’s (Hypovolemia, Hypoxemia, Hydrogen ion (acidosis), Hypo- or Hyperkalemia, Hypothermia, Tension pneumothorax, Tamponade, Toxins, and Thrombosis–both pulmonary and cardiac). The endpoint of these disorders is commonly pulseless ventricular tachycardia (VT) or ventricular fibrillation (VF), pulseless electrical activity, or asystole.
The incidence of out-of-hospital and in-hospital cardiac arrests assessed by emergency medical services (EMS) in the United States in 2013 was estimated to be 424,000 and 209,000, respectively. Among EMS-treated out-of-hospital cardiac arrests, 23% had an initial rhythm of VF or VT or were shockable by an automated external defibrillator. The value of early bystander cardiopulmonary resuscitation (CPR) and immediate defibrillation has been proven in many community-based studies.1-4 In addition, the increased use of automated external defibrillators by EMS, businesses, and airports for patients with VT or VF has improved survival.5-8 Without defibrillation, mortality from VT, VF, or both increases by approximately 10% per minute.9-12
Diagnosis and therapy
The American Heart Association and European Society of Cardiology have published revised resuscitation guidelines in 2010,7,13,14 which included some key changes from the 2005 guidelines. The new guidelines still include the major steps below:
- Activate EMS or the designated code team immediately.
- Perform basic life support (CPR).
- Evaluate heart rhythm and perform early defibrillation if indicated.
- Deliver advanced cardiac life support, such as intubation, establishment of intravenous (IV) access, and transfer to a medical center or intensive care unit.
The new changes are as follows:
- Changing the Airway (A) – Breathing (B) – Circulation (C) sequence to C-A-B. This change was made to emphasize the importance of rapid initiation of chest compressions because in the old guidelines, significant time is potentially wasted performing airway evaluation. Airway evaluation and initiation of mouth-to-mouth breathing may be a complex, time-consuming process for the layperson, and may delay chest compressions. The phrase “Look, listen and feel” has also been removed from the algorithm to prevent time delays.
- More emphasis on the quality of CPR performed, including the rate and depth of compressions, allowing complete chest recoil, and minimizing interruptions in compressions. Less emphasis on pulse checks.
- Highlighting the importance of professional healthcare rescue teams performing multiple tasks during CPR such as establishing an airway or delivering advanced cardiac life support drugs.
Pulseless VT or VF
- Start chest compressions as early as cardiopulmonary arrest is identified. Place airway device as soon as possible and confirm oxygenation and ventilation. Establish IV access, identify rhythm, and administer drugs appropriate for rhythm and condition. Search for and treat identified reversible causes (5 H’s and 5 T’s), with focus on basic CPR and early defibrillation.
- On arrival to an unwitnessed cardiac arrest or downtime longer than 4 minutes, five cycles (~2 min) of CPR (each cycle is 30 compressions at a rate of ~100 compressions per minute) are to be initiated before evaluation of rhythm. If the cardiac arrest is witnessed or downtime is shorter than 4 minutes, one shock may be administered immediately if the patient is in VF or pulseless VT followed by five cycles of CPR.
- If the patient is in VF or pulseless VT, shock the patient once using 200 J on biphasic (on equivalent monophasic, 360 J).
- Resume CPR immediately after attempted defibrillation, beginning with chest compressions. Rescuers should not interrupt chest compression to check circulation (e.g., evaluate rhythm or pulse) until five cycles or 2 minutes of CPR have been completed.
- If there is persistent or recurrent VT or VF despite several shocks and cycles of CPR, perform a secondary ABC survey with a focus on more advanced assessments and pharmacologic therapy. Pharmacologic therapy should include epinephrine (1 mg IV push, repeated every 3-5 min) or vasopressin (a single dose of 40 U IV, one time only).
- Consider using antiarrhythmics for persistent or recurrent pulseless VT or VF. These include amiodarone, lidocaine, magnesium, and procainamide
- Resume CPR and attempts to defibrillate
- If spontaneous circulation returns, start immediate post-cardiac arrest care. This includes optimization of oxygenation and ventilation with emphasis on avoiding hyperventilation, treating hypotension by starting vasopressor infusion or inserting intra-aortic balloon pump, assessing neurologic status and starting induced hypothermia if indicated and assessing need for coronary reperfusion if high suspicion for acute coronary syndrome.
Pulseless electrical activity or asystole
- Assess the patient and begin chest compressions immediately.
- Administer epinephrine (1 mg IV push repeated every 3-5 min). Consider transcutaneous pacing if asystole.
- Conduct a secondary ABC survey and consider reversible causes (5 H’s and 5 T’s).
- Resume immediate post-cardiac arrest care if there is a return of spontaneous circulation as above.
- Heart rate typically <50 beats per minute.
- Identify and treat underlying cause if patient is stable (5 H’s and 5 T’s).
- Check for serious signs of low cardiac output due to bradycardia such as hypotension, altered mental status, or acute heart failure.
- If serious signs or symptoms are present, begin the following intervention sequence:
- Atropine, 0.5 mg, up to a total of 3 mg IV
- Transcutaneous pacing, if available
- Dopamine, 5 to 20 µg/kg/min
- Epinephrine, 2 to 10 µ/min
- Isoproterenol, 2 to 10 µ/min
- Consider glucagon for beta-blocker toxicity, calcium infusion for calcium channel blocker toxicity.
- If no serious signs or symptoms are present, evaluate for a type II second-degree atrioventricular block or third-degree atrioventricular block.
- If neither of these types of heart block is present, observe.
- If one of these types of heart block is present, prepare for transvenous pacing.
- Resume immediate post-cardiac arrest care if there is a return of spontaneous circulation as above.
A hypertensive emergency is an acute, severe elevation in blood pressure accompanied by end-organ compromise. It is usually associated with a systolic blood pressure (SBP) equal to or higher than 180 mm Hg and/or a diastolic blood pressure (DBP) equal to or higher than 120 mm Hg.15,16
End-organ compromise includes acute renal failure due to nephrosclerosis, ocular involvement with retinal exudates, hemorrhages, or papilledema, hypertensive encephalopathy, acute stroke or intracranial hemorrhage, acute myocardial infarction, aortic dissection, and eclampsia. Hypertensive encephalopathy signals the presence of cerebral edema and loss of vascular integrity. If left untreated, hypertensive encephalopathy may progress to seizure and coma.17,18 Aortic dissection is associated with severe elevations in systemic blood pressure and wall stress, requiring immediate lowering of the blood pressure and emergent surgery for type A dissection to reduce morbidity and mortality. Eclampsia, the second most common cause of maternal death, occurs from the second trimester to the peripartum period. It is characterized by the presence of seizures, coma, or both, in the setting of preeclampsia. Delivery remains its only cure.19
Hypertensive emergencies result from an exacerbation of previously uncomplicated hypertension or have a secondary cause, including renal, vascular, pregnancy-related, pharmacologic, endocrine, neurologic, and autoimmune etiologies (Box 1).
|Box 1: Causes of Hypertensive Emergencies|
|Renal artery stenosis|
|Thrombotic thrombocytopenia purpura|
|Clonidine withdrawal, beta blocker withdrawal|
|Central nervous system trauma|
|Scleroderma renal crisis|
The prevalence of hypertension rises substantially with increasing age in the United States and is greater among blacks than among whites in every age group. 20,21Based on the third National Health and Nutrition Examination Survey (NHANES III), the prevalence of hypertension in those older than 70 years was found to be approximately 55% to 60% of the U.S. population. 22,23 A British study has revealed that less than 1% of patients with primary hypertension progress to hypertensive crisis. 24 This study also showed that despite increasingly widespread therapy, the number of patients presenting with hypertensive crises did not decline between 1970 and 1993.
Any syndrome that produces an acute rise in blood pressure may lead to a hypertensive crisis. Cerebral vasomotor autoregulation is a key facet of a patient’s symptomatic presentation. Patients without chronic hypertension generally develop hypertensive crises at a lower blood pressure than those with chronic hypertension. Although the process is not completely understood, an initial rise in vascular resistance mediated by vasoconstrictors such as angiotensin II, acetylcholine, or norepinephrine is responsible for the acute increase in blood pressure. This cascade exceeds the vasodilatory response of the endothelium, mediated primarily by nitric oxide. Mechanical destruction of the endothelium by shear stress leads to further vasoconstriction, platelet aggregation, inflammation, and subsequent blood pressure elevation. The rate at which this occurs determines the rate of increase in systemic vascular resistance as well as the acuity of a patient’s presentation.
Understanding autoregulation is key to the safe management of hypertensive crises. In patients with chronic hypertension, the vascular bed auto-regulates at higher blood pressure ranges compared with those with newly diagnosed hypertension. Therefore, blood pressure should not be aggressively lowered in those with chronic hypertension, in whom a SBP of 130 mm Hg, for example, may cause end-organ hypoperfusion.
The symptoms and signs of a hypertensive emergency vary widely. Symptoms of end-organ involvement include headache, blurred vision, confusion, chest pain, shortness of breath, back pain (e.g., aortic dissection), seizures, and altered consciousness.15,16 Physical examination should assess end-organ involvement, including detailed fundoscopic, neurologic, and cardiovascular examinations, with emphasis on the presence of congestive heart failure and bilateral upper extremity blood pressure measurements. Laboratory evaluation should include measurement of the complete blood count with differential and smear evaluations, measurements of electrolyte, blood urea nitrogen, and creatinine levels, and electrocardiography, chest radiography, and urinalysis.
No large randomized clinical trials have assessed therapy in hypertensive emergency; therapeutic intervention is largely a result of expert opinion. All patients with end-organ involvement should be admitted for intensive monitoring and have an arterial blood pressure line placed.16
IV vasodilator therapy to achieve a decrease in mean arterial pressure (MAP) of 20% to 25% or a decrease in DBP to 100 to 110 mm Hg within the first 24 hours is recommended. Decreasing the MAP and DBP further should be done more slowly, over a period of days, because of the risk of decreasing perfusion of end organs.16Several drugs have proved beneficial in achieving this goal (Table 1).
Table 1: Intravenous Vasodilator Therapy for Hypertensive Crisis
|Sodium nitroprusside||2.5-10 µg/kg/min||1-2 min|
|Nitroglycerin||5-200 µg/min||3-5 min|
|Nicardipine||5-15 mg/h||1-4 hr|
|Labetalol||20- to 80-mg bolus, 2 mg/min drip||2-6 hr|
|Enalaprilat*||1.25- to 5-mg bolus||4-6 hr|
*Use specifically for angiotensin-converting enzyme-mediated hypertensive crises, such as scleroderma renal crisis. It is contraindicated in pregnancy.
At our institution, we focus on reducing shear forces and combine a beta-blocker with sodium nitroprusside (SNP). In cases of marked catecholamine level elevation, large doses of IV beta-blockers may be required to achieve blood pressure reduction. An exception to this rule is the treatment of cocaine-induced hypertension, for which beta-blockers can induce unopposed alpha-mediated vasoconstriction, so direct-acting vasodilators and benzodiazepines are instead the mainstays of therapy.
In addition to reducing MAP and DBP with medications as described above, early surgical intervention for type A dissection has been proven to reduce morbidity and mortality. Reduction in shear stress is best achieved with IV beta blockade and SNP.25,26
IV bolus hydralazine therapy is used occasionally in some institutions and departments to treat hypertensive urgency or emergency. We recommend against this practice, and using extreme caution with its use given the unpredictable pharmacodynamics and unpredictable blood pressure-lowering effects of IV hydralazine. It can cause large, abrupt drops in blood pressure, which may lead to stroke and other end-organ damage.
IV magnesium (frequently used as a tocolytic during preterm labor), hydralazine (a pregnancy category B drug that should be utilized cautiously as described above), and labetalol (category B) have value in the treatment of preeclampsia and prevention of eclampsia.19 Angiotensin-converting enzyme inhibitors (category D) are generally avoided during pregnancy because their use has been associated with an elevated risk of fetal congenital malformations.
Antihypertensive therapy in the context of ischemic stroke can be controversial in cases when recombinant tissue plasminogen activator is not used.27 For such cases, antihypertensive medications are generally not used during the first 24 hours, as long as the SBP does not exceed 220 mm Hg, and the DBP does not exceed 120 mm Hg. This is because maintenance of a moderately-high cerebral perfusion pressure theoretically could confer neurological benefits. On the other hand, for patients treated with recombinant tissue plasminogen activator, blood pressure should be controlled (SBP ≤185 mm Hg and DBP ≤105 mm Hg) to reduce the risk of hemorrhagic conversion.27 If not already involved in the patient’s care, the Neurology/Stroke team should be consulted.
Aortic dissection is a tear of the aortic intima that allows the shear forces of blood flow to dissect the intima from the media and, in some cases, penetrate the diseased media with resultant rupture and hemorrhage (Fig. 1).28 Sixty-five percent of dissections originate in the ascending aorta, 20% in the descending aorta, 10% in the aortic arch, and the remainder in the abdominal aorta.29,30
While some older classification systems of aortic dissection (such as Stanford and DeBakey) still exist and are used, they seem anachronistic in the current era of advanced imaging. We recommend describing aortic dissections anatomically by location of the intimal flap, the extent of vascular involvement and the organs supplied by the true and/or false lumens. This approach more specifically identifies the major vessels and organs involved, allowing for superior anticipation of complications and improved decision-making. The most commonly used old classification system is the Stanford system; a dissection that involves the ascending aorta is classified as type A, and one that does not, only affecting the aorta distal to the left subclavian artery, is classified as type B (Fig. 2). Dissections are further classified by chronicity as acute (<2 weeks) or chronic (>2 weeks); mortality peaks at 80% after 2 weeks, and then levels off.29
Any disease that weakens the aortic media predisposes patients to dissection. These include aging, hypertension, Marfan syndrome, Ehlers-Danlos syndrome, Loeys-Dietz syndrome, bicuspid aortic valve (associated with medial degeneration), coarctation, and Turner’s syndrome. Pregnancy poses a unique risk to women with any of these diseases because of increased blood volume, cardiac output, and shear forces on the aorta. In women younger than 40 years, 50% of dissections occur in the peripartum period.31 Iatrogenic trauma from catheters or intra-aortic balloon pumps may initiate dissection between the aortic intima and media.32 Aortic dissection can also be infrequently associated with blunt trauma or acceleration-deceleration injury, as can occur in motor vehicle accidents.
Most patients present with acute chest pain that peaks in intensity at onset, and is often self-described as “tearing” or “ripping” in nature. Uncommonly, patients present with congestive heart failure from accompanying acute aortic valve insufficiency, tamponade, or both. Also seen are cerebrovascular accidents due to involvement of the carotid artery or vertebrobasilar system, syncope from tamponade, or cardiac arrest.33,34 On physical examination, hypertension is usually present, either as the primary cause of dissection or secondary to renal artery involvement. Acute aortic valve insufficiency with a resultant diastolic murmur may complicate ascending dissections. Loss of pulse, decrease in blood pressure, or both (often asymmetric) are also found in many patients.33 Dissection into the spinal arteries, although rare, may produce secondary paraplegia.
Chest radiographs may reveal an abnormality in approximately 70% to 80% of patients, such as a widened mediastinum or loss of the demarcation of the aortic knob, pleural effusion, or pulmonary edema.33 Importantly, a normal chest radiograph does not rule out aortic dissection. The electrocardiogram (ECG) may reveal left ventricular hypertrophy, ST depression, T wave inversion, or ST elevation when the coronary arteries are involved. The right coronary ostium is involved in 1% to 2% of aortic dissection cases, leading to an inferior myocardial infarction.
It is essential to recognize several key signs in the imaging of aortic dissection, because they dramatically affect treatment and outcome:
- Involvement of the ascending aorta
- Location of dissection flap, intimal tear and the major vessels involved
- Presence of pericardial effusion or cardiac tamponade
- Involvement of coronary ostia
The sensitivity of computed tomography angiography (CTA) for detecting aortic dissection is approximately 83% to 100%, and its specificity ranges from 87% to 100%, depending on the study.35,36 In the current age of ECG-gated CTA, the sensitivity and specificity for detecting dissections approaches 100%, and thus it is the diagnostic imaging modality of choice. Transesophageal echocardiography has a sensitivity of approximately 98%; however, its lower specificity of 77% to 97%, reflects differences in operator experience.30,36 Magnetic resonance imaging has a sensitivity and specificity of approximately 98% for detection of dissection but its lack of portability, limited access, and long duration of imaging make this a less favorable option in the care of acute aortic dissection.37 Choice of testing should be based on the medical center’s expertise, hemodynamic stability of the patient, and access to the imaging modality.35-37
Surgical therapy is the best option for acute aortic dissection involving the ascending aorta. Studies have shown that delaying surgical intervention, even to carry out left heart catheterization, aortography, or both, results in worse outcomes.38-40 Mortality increases by 1% per hour while waiting for surgery. Surgical repair in patients with type B dissection is generally reserved for those with end-organ compromise or those who do not respond to medical therapy.
Medical therapy should be initiated in all patients with acute dissection. Reductions of shear force and blood pressure should be the primary goals. Beta-blockers should be given intravenously and titrated to the desired effect. In our institution, we typically start by using boluses of IV metoprolol to achieve a heart rate of 50 to 60 beats/min, which may require very high doses of 200 to 1,000 mg. We then add SNP if needed because of its rapid onset and ease of titration, aiming for a MAP of 65 to 75 mm Hg.
In the hypotensive patient, diagnoses of pericardial tamponade, aortic rupture, aortic insufficiency, myocardial infarction, or a combination of these should be suspected and tested for. Volume replacement and early surgical intervention should be pursued. Pericardiocentesis should be avoided if tamponade is present, because immediate surgical intervention is the therapy of choice. If hypotension persists, norepinephrine and phenylephrine are the vasopressors of choice because of their limited effects on increasing cardiac contractility. Endovascular stenting, a rapidly growing field, remains investigational in this acute setting and is sometimes used in very high-risk surgical patients with type B aortic dissections or aneurysms.
Acute pulmonary edema
Acute pulmonary edema is an emergency that necessitates admission to the hospital. It has two major forms, cardiogenic and noncardiogenic. We focus on cardiogenic pulmonary edema, which generally is more reversible than the noncardiogenic form.
Cardiogenic pulmonary edema results from an absolute increase in left atrial pressure, with resultant increases in pulmonary capillary and venous pressures. In the setting of normal capillary permeability, this increased pressure causes extravasation of fluid into the alveoli and overwhelms the ability of the pulmonary lymphatics to drain the fluid, thus impairing gas exchange in the lung.41,42
Etiology and pathophysiology
Left ventricular systolic dysfunction, left ventricular diastolic dysfunction, and obstruction of the left atrial outflow tract are the primary causes of increased left atrial pressure. Left ventricular systolic dysfunction is the most common cause of cardiogenic pulmonary edema.41 This dysfunction can be the result of coronary artery disease, hypertension, valvular heart disease, cardiomyopathy, toxins, endocrinologic or metabolic causes, or infections.
Diastolic dysfunction results in impaired left ventricular filling and elevation in left ventricular end-diastolic pressure. In addition to myocardial ischemia, left ventricular hypertrophy, hypertrophic obstructive cardiomyopathy, and infiltrative or restrictive cardiomyopathy are all causes of diastolic dysfunction.
Left atrial outflow obstruction is often a result of valvulopathy, such as mitral stenosis or mitral regurgitation, but also can be caused by tumors (atrial myxoma), dysfunctional prosthetic valves, thrombus, and cor triatriatum. It is imperative to distinguish between mitral regurgitation and mitral stenosis, given their very different treatments.
Pulmonary edema is diagnosed by the presence of various signs and symptoms, including tachypnea, tachycardia, crackles (reflecting alveolar edema), hypoxia (secondary to alveolar edema), and the S3 or S4 heart sounds, individually or in combination. Additionally, if hypertension is present, it may represent diastolic dysfunction, decreased left ventricular compliance, decreased cardiac output, and increased systemic vascular resistance. The presence of increased jugular venous pressure indicates increased right ventricular filling pressure secondary to right ventricular or left ventricular dysfunction. Finally, the presence of peripheral edema indicates a certain degree of chronicity to the patient’s condition.
Laboratory data associated with pulmonary edema include hypoxemia on arterial blood sampling and a chest radiograph showing bilateral perihilar edema and cephalization of pulmonary vascular marking. Cardiomegaly, pleural effusion, or both may be present. Two-dimensional transthoracic echocardiography is usually helpful in the acute setting to assess biventricular size and function, to identify valvular stenosis or regurgitation, and to determine the presence or absence of pericardial pathology. The ECG may reflect ongoing ischemia, injury, tachycardia, and atrial or ventricular hypertrophy. In many cases, differentiating cardiogenic and noncardiogenic pulmonary edema can be challenging and requires the insertion of a pulmonary artery catheter to measure the pulmonary capillary wedge pressure.
Mainstays of immediate therapy include improving oxygen delivery to end organs, decreasing myocardial oxygen consumption, increasing venous capacitance, decreasing preload and afterload (with careful attention to MAP), and avoiding hemodynamic compromise. All patients should receive supplemental oxygen to maximize hemoglobin oxygen saturation. Administration of continuous positive airway pressure can increase gas exchange, and may perhaps decrease preload via increased intrathoracic pressure.43,44 In our experience, however, repeated attempts to improve oxygenation with noninvasive positive pressure ventilation often prove inadequate. In such cases, restoration of oxygenation is best achieved via prompt endotracheal intubation and initiation of mechanical ventilation.
The pharmacologic agents most commonly used in the treatment of acute pulmonary edema are nitroglycerin, SNP, and diuretics.45
Nitroglycerin acts immediately to decrease preload and afterload.46 It should be used for the management of patients with pulmonary edema who are not hypotensive. Sublingual administration allows rapid delivery, which is often required to decrease preload. IV administration of nitroglycerin also should be used in the nonhypotensive patient and, based on symptoms, titrated to a MAP of approximately 70 to 75 mm Hg.
SNP is an effective vasodilator that is often required for the treatment of the hypertensive patient with pulmonary edema.47 Due to the rapid and potent effects of SNP, its use requires continuous invasive monitoring of arterial blood pressure. The issues of methemoglobinemia, cyanide, and thiocyanate toxicity rarely become significant, but since patients receiving continuous infusions will often develop tachyphylaxis—a progressive resistance to the drug’s effects—frequent blood testing is necessary. SNP should be used with caution in the setting of hepatic dysfunction, since the liver is responsible for transformation of the cyanide radical into thiocyanate. Patients with renal dysfunction will tend to accumulate thiocyanate more rapidly than those with normal kidney function, since thiocyanate is excreted in the urine. Finally, through its effects on coronary arteriolar resistance vessels, SNP can potentially cause coronary “steal,” drawing blood flow away from ischemic myocardium. We generally co-administer nitroglycerin along with SNP to dilate conductance vessels and lessen this theoretical risk.
IV diuretics are most helpful for the treatment of volume overload in chronic congestive heart failure. Their vasodilative and diuretic properties also are useful in the management of pulmonary edema. Diuretics should be used with caution in the euvolemic patient to avoid compromising cardiac output and oxygen delivery.
IV morphine can be used in certain select patients to decrease their “air hunger,” anxiety, and sympathetic tone, which can in turn help reduce their afterload.
Cardiovascular emergencies are common in the practice of medicine and quick action is necessary.
- Cardiopulmonary arrest has several possible causes, all of which require prompt resuscitative efforts. The 2010 American Heart Association guidelines have proposed changes that make chest compressions a priority before assessment of airway and breathing, in order to minimize time delays. All healthcare professionals need to be aware of these changes.
- Hypertensive emergency causes end-organ damage and warrants admission for intensive monitoring, including continuous arterial blood pressure measurement, and treatment.
- Aortic dissection categorized as Stanford type A requires emergent surgery, whereas type B is generally managed medically unless end-organ damage can be demonstrated.
- Acute pulmonary edema should be treated by improving oxygen delivery to end organs, decreasing myocardial oxygen consumption, and safely decreasing preload and afterload.
- Go AS, Mozaffarian D, Roger VL, et al; on behalf of the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics—2014 update: a report from the American Heart Association [published online ahead of print December 18, 2013]. Circulation 2014; 129:e28–e292. doi:10.1161/01.cir.0000441139.02102.80
- Li H, Hu C, Xia J, et al. A comparison of bilevel and continuous positive airway pressure noninvasive ventilation in acute cardiogenic pulmonary edema [published online ahead of print August 6, 2013]. Am J Emerg Med 2013; 31:1322–1327. doi:10.1016/j.ajem.2013.05.043
- Stub D, Bernard S, Duffy SJ, Kaye DM. Post cardiac arrest syndrome: a review of therapeutic strategies. Circulation 2011; 123:1428–1435.
- Varon J, Acosta P. Therapeutic hypothermia: past, present, and future. Chest 2008; 133:1267–1274.
- Sedgwick ML, Watson J, Dalziel K, Carrington DJ, Cobbe SM. Efficacy of out of hospital defibrillation by ambulance technicians using automated external defibrillators: the Heartstart Scotland Project. Resuscitation 1992; 24:73–87.
- Herlitz J, Bång A, Axelsson A, Graves JR, Lindqvist J. Experience with the use of automated external defibrillators in out of hospital cardiac arrest. Resuscitation 1998; 37:3–7.
- Wik L, Hansen TB, Fylling F, et al. Delaying defibrillation to give basic cardiopulmonary resuscitation to patients with out-of-hospital ventricular fibrillation: a randomized trial. JAMA 2003; 289:1389–1395.
- Berg RA, Hilwig RW, Ewy GA, Kern KB. Precountershock cardiopulmonary resuscitation improves initial response to defibrillation from prolonged ventricular fibrillation: a randomized, controlled swine study. Crit Care Med 2004; 32:1352–1357.
- Eisenberg MS. Is it time for over-the-counter defibrillators? JAMA 2000; 284:1435–1438.
- Balady GJ, Chaitman B, Foster C, Froelicher E, Gordon N, Van Camp S. Automated external defibrillators in health/fitness facilities: supplement to the AHA/ACSM recommendations for cardiovascular screening, staffing, and emergency policies at health/fitness facilities. Circulation 2002; 105:1147–1150.
- Field JM, Hazinski MF, Sayre MR, et al. Part 1: executive summary: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation 2010; 122(18 suppl 3):S640–S656.
- Hanefeld C, Lichte C, Mentges-Schröter I, Sirtl C, Mügge A. Hospital-wide first-responder automated external defibrillator programme: 1 year experience. Resuscitation 2005; 66:167–170.
- Larsen MP, Eisenberg MS, Cummins RO, Hallstrom AP. Predicting survival from out-of-hospital cardiac arrest: a graphic model. Ann Emerg Med 1993; 22:1652–1658.
- Swor RA, Jackson RE, Cynar M, et al. Bystander CPR, ventricular fibrillation, and survival in witnessed, unmonitored out-of-hospital cardiac arrest. Ann Emerg Med 1995; 25:780–784.
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- Ko PC, Ma MH, Yen ZS, Shih CL, Chen WJ, Lin FY. Impact of community-wide deployment of biphasic waveform automated external defibrillators on out-of-hospital cardiac arrest in Taipei. Resuscitation 2004; 63:167–174.
- Nolan JP, Soar J, Zideman DA, et al; on behalf of the ERC Guidelines Writing Group. European Resuscitation Council Guidelines for resuscitation 2010 Section 1. Executive summary. Resuscitation 2010; 81:1219–1276.
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