Post-Resuscitation Management in the ICU Case File
Eugene C. Toy, MD, Manuel Suarez, MD, FACCP, Terrence H. Liu, MD, MPH
Case 39
A 56-year-old man was at a mall, where he had a sudden witnessed cardiac arrest. He received immediate cardiopulmonary resuscitation (CPR) from bystanders. When the paramedics arrived, they noted that the patient was in ventricular fibrillation and initiated cardioversion and continued CPR. After several rounds of cardioversion, the patient's rhythm returned to sinus tachycardia with a rate of 120 beats/minute and a blood pressure of 96/40 mm Hg. In the emergency center he was noted to have sinus tachycardia with rate of 115 beats/minute, BP of 98/60 mm Hg, and Glasgow coma score (GCS) of 7T. You have been called to see the patient, since he has been admitted to the ICU.
⯈What are your priorities in this patient's management?
⯈What are post-resuscitation treatment strategies that have shown to improve outcome?
ANSWER TO CASE 39:
Post-Resuscitation Management in the ICU
Summary: A 56-year-old man with witnessed ventricular fibrillation-induced cardiac arrest has been successfully resuscitated following CPR, cardioversions, and pharmacological interventions. He is now intubated and admitted to the ICU for further care.
- Priorities in patient's mamagement: Minimizing post-cardiac arrest brain injury, addressing his post-cardiac arrest myocardial dysfunction, minimizing his systemic ischemia/reperfusion responses, addressing the problem that caused his cardiac arrest in the first place, and lastly prognostication of outcome.
- Post-resuscitation strategies that improve outcome: Coronary reperfusion with either percutaneous intervention and/or thrombolytic therapy has shown to improve survival in cardiac arrest survivors if acute change in coronary plaque morphology is the underlying cause for the cardiac arrest. Other strategies that have shown to improve neurologic outcome in post-cardiac arrest patients include controlled reoxygenation, therapeutic hypothermia, and glucose management.
ANALYSIS
Objectives
- To learn the post-cardiac arrest syndrome and strategies directed toward its management, including optimization of neurological outcome, optimization of myocardial function, glucose management, and controlled reoxygenation.
- Describe the use the therapeutic hypothermia to reduce the neurological injury after resuscitation.
Considerations
This 56-year-old man is admitted to the ICU after successful resuscitation from an apparent ventricular fibrillation (VF)-induced cardiac arrest. Neurological and cardiac dysfunction are common complications. Therapeutic hypothermia (TH) is defined as lowering the core temperature to 32°C to 34°C, which can help both postresuscitation neurological and myocardial dysfunction. Maintaining oxygen saturation in the 96% to 98% range also decreases post-resuscitation sequelae. Finally, hyperglycemia is very common following resuscitation. While prior interventions attempted to more strictly control serum glucose levels, more recent evidence has found that moderate hyperglycemia correlates to better prognosis. Thus, target glucose levels of 144 to 180 mg/dL are sought.
Approach To:
The Post-Resucitation Patient
DEFINITIONS
POST-CARDIAC ARREST SYNDROME: This syndrome includes post-cardiac arrest brain injury, post-cardiac arrest myocardial dysfunction, ischemia/reperfusion injuries, and the underlying disease process that contributed to the event.
THERAPEUTIC HYPOTHERMIA (TH): Therapeutic maneuvers to improve neurological outcomes by reducing core body temperature to 32°C to 34°C following cardiac arrest, with hypothermia maintained for 24 to 48 hours.
POST-CARDIAC ARREST MYOCARDIAL DYSFUNCTION: This is a biventricular dysfunction from multiple reasons that occurs transiently following resuscitation from cardiac arrest.
POST-CARDIAC ARREST ENCEPHALOPATHY: Ischemic brain injury in which the 2 main issues are depressed level of consciousness and seizures.
CLINICAL APPROACH
Introduction
Survival after in-hospital and out-of-hospital cardiac arrest is poor. For the subset of patients with return of spontaneous circulation following resuscitation, the probability of survival is significantly improved. Approximately one-third of patients admitted to an ICU following cardiac arrest survive to discharge from the hospital. Post-cardiac arrest syndrome describes a number of complex pathophysiologic processes, which are grouped into 4 major categories: post-resuscitation brain injury, ischemia/reperfusion injuries, myocardial dysfunction, and persistence of the precipitating cause of the cardiac arrest. Neuronal susceptibility to ischemia is not uniform within the brain. These differential responses may be related to the different brain regions' cellular energy requirements and adaptive heat-shock responses. The hallmark of anoxic encephalopathy is disorder of consciousness and arousal. In addition to depressed levels of arousal, 10% to 40% of post-cardiac arrest patients develop seizure activities that have to be monitored and treated.
Most of the treatment strategies and rationale are based on recent post-arrest resuscitation literature and include TH and early cardiac intervention. Several organizations now recommend bundling of post-resuscitation care to include therapeutic hypothermia, early coronary angiography and PCI, hemodynamic support with inotropes or vasopressors, and rapid extubation.
Therapeutic Hypothermia
TH, lowering the patient's core temperature to 32°C to 34°C, has been shown in several randomized controlled trials to improve neurological recovery in patients following VF-induced cardiac arrest. TH should be instituted as soon as possible with surface cooling using cooling blankets and ice packs. This approach has been definitively shown to improve neurologic outcomes in patients suffering from out-of-hospital VF arrest. Some experts have proposed applying this strategy more broadly to include patients with cardiac arrest from other causes; however, the beneficial effects in these groups have not been demonstrated. TH has been incorporated into the International Consensus Guidelines for Resuscitative Care since 2005. During hypothermia, magnesium, phosphate, potassium, and calcium should be replaced to higher end of normal values. During the rewarming phase, core temperature should increase at a rate of 0.25 °C to 0.5°C/h, with continued monitoring and replacement of electrolytes. Rapid rewarming is associated with increased catabolism and can worsen outcomes. The potential complications associated with hypothermia include increased infections from leukocyte dysfunction, increased bleeding from platelet and clotting factors dysfunction, and arrhythmias (predominantly atrial fibrillation).
Post-resuscitation myocardial dysfunction is a transient reduction in left and right ventricular function that presents after cardiac arrest for up to 24 to 48 hours. It is now believed that TH also may have beneficial effects in reducing post-resuscitation myocardial dysfunction. Because the majority of out-of-hospital cardiac arrests occur as the result of acute coronary syndrome, patients with successful resuscitation from out-of-hospital cardiac arrest should be considered for intervention. For those candidates, early coronary angiography and percutaneous coronary interventions (PCI) may improve outcome.
Oxygenation
Observations from experimental models suggest that ventilation during and after resuscitation with minimal oxygen fractions to maintain O2 saturations of 94% to 96% or PAO2 ~ 100 mm Hg would lead to reduction in reperfusion injuries. In addition, in a multicenter cohort study, it was observed that adult patients with non-trauma-related cardiac arrests had a mortality odds ratio of 1.8 when hyperoxia (PAO2 > 300 mm Hg) was recorded as the initial blood gas values following arrest. Based on these principles and clinical evidence, the target oxygenation for this patient during resuscitation and immediately following resuscitation should be 94% to 98% saturation, and not higher.
Fluids and Vasopressors
The resuscitation of patients with hemodynamic instability from hemorrhagic shock and sepsis are discussed in detail in other sections of this book. The Surviving Sepsis Campaign is a multinational sponsored effort to standardize the approach to the early management of patients with sepsis and septic shock. Fluids and vasopressor support strategies have been well defined based on these efforts. Similarly, recent clinical observations from the casualty management during the ongoing military conflicts in the Middle East have led to developments in the resuscitation of patients with hemorrhagic shock. What remains relatively undefined is management strategies to minimize the harm associated the initial aggressive resuscitation of patients with sepsis, septic shock, and hemorrhagic shock.
The amount of fluids and blood products required to resuscitate patients with hemorrhagic shock or sepsis may produce generalized edema with excess loss of fluid into the extracellular tissue spaces. These fluid shifts produce edema and organ dysfunction, especially in the lungs and gastrointestinal tract. Resuscitation efforts directed at optimizing tissue oxygenation are most valuable during the initial few hours following the septic or hemorrhagic insults, whereas extended periods of excess fluid administration in these patients is potentially harmful. Strong efforts should be made to limit fluid administration; those who have had excessive fluids should receive timely diuretic treatment as soon as shock has been corrected. Early fluid restriction to avoid hypervolemia is associated with improved recovery from acute lung injury and acute respiratory distress syndrome. Early fluid restriction has been demonstrated to be associated with improved lung injury scores, reduced ventilator days, and reduced ICU lengths of stay. Similarly, judicious fluid management in patients following resuscitation from sepsis or hemorrhage is beneficial as it is associated with improved GI functions and improved tolerance to early (within 24 hours) enteral nutritional support, which has been shown to be associated with immunological and physiological benefits.
Glucose Levels
Hyperglycemia is a common encounter in post-cardiac arrest patients. Recent observations suggest that strict glycemic control in the ICU patient leads to increase in neurological complications, and a randomized controlled trial has shown that there was no difference in mortality among out-of-hospital arrest patients managed with glucose values of 72 to 108 mg/dL versus those maintained with glucose levels of 108 to 144 mg/dL. Therefore, suggesting that controlling glucoses to "normal" levels may be harmful. The 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care now recommends moderate glycemic control targeting glucose values between 144 and 180 mg/dL, to avoid possible hypoglycemia.
CLINICAL CASE CORRELATION
- See also Case 3 (Scoring Systems and Patient Prognosis), Case 4 (Hemodynamic Monitoring), and Case 40 (Postoperative Care in ICU).
COMPREHENSION QUESTIONS
39.1 Which of the following strategies has been shown to improve recovery from the post-cardiac arrest syndrome?
A. Early echocardiography
B. Cooling of core temperature to 28°C to 30°C
C. Maintaining O2 saturation of 100%
D. Cooling of core temperature of 32°C to 34°C
E. Swan-Ganz catheter-directed goal resuscitation
39.2 Which of the following is the most accurate statement regarding glucose management in the post-cardiac arrest patient?
A. Hypoglycemia is a common cause of in-hospital cardiac arrest.
B. Glycemic control does not play a role in the management of patients following cardiac arrest.
C. Glycemic control to target glucose at 80 to 110 mg/dL is optimal.
D. Glycemic control to serum glucose values of 144 to 180 mg/dL is preferred.
E. Avoidance of glucose-containing intravenous solutions.
39.3 A 64-year-old man, who was being treated in the hospital for acute cholecystitis, is found to be unresponsive. He was found to be in VF and underwent chest compression for several minutes and resuscitated successfully. Which of the following is an important treatment for this patient?
A. Target oxygen saturation for 93%
B. Target glucose level at 110 mg/dL
C. Percutaneous coronary angiography
D. Target core body temperature for 37°C
E. Extended and prolonged fluid resuscitation
ANSWERS
39.1 D. Therapeutic hypothermia to core temperatures of 32°C to 42 °C for 24 to 48 hours has been shown to improve neurological outcomes in patient following V-fib arrests. Cooling of patients to 28°C to 30°C is associated with increased risk of arrhythmia without additional improvement in neurological outcomes. Maintaining PAO2 of 100% could result in hyperoxia and has been shown to increase mortality. Even though maintaining euvolemia improves post-cardiac arrest patient outcomes, the use of Swan-Ganz catheter goal-directed therapy has not been proven to have survival benefits in these patients.
39.2 D. Hyperglycemia and hypoglycemia are common following resuscitation from cardiac arrest and if unaddressed can contribute to worse neurological outcomes. The AHA guidelines currently recommend moderate glycemic control targeting values of 144 to 180 mg/dL. Randomized trial comparing glycemic control targeting levels of 80 to 110 mg/dL versus target levels of 110 to 140 mg/dL for post-cardiac arrest patients did not demonstrate a survival difference in the ICU setting. Hypoglycemia in the post-resuscitation patient contributes to worsening neurological outcome; therefore, glucosecontaining solutions may be indicated if the patient is hypoglycemic.
39.3 C. This patient likely has acute coronary syndrome. Early cardiac intervention has been shown to improve prognosis. TH may also help with target core temperature of 32 °C to 34°C. Glucose levels should be in the range of 144 to 180 mg/dL. Resuscitation to achieve early hemodynamic goals (first 6 hours) has been shown to improve survival in septic patients; however, prolongation of resuscitation has not been shown to provide survival advantages. Intolerance to feeding, decreased pulmonary compliance, decreased oxygenation, and the development of abdominal compartment syndrome are associated with excess fluid administration and failure to reduce excess fluid administration following initial resuscitation from septic shock.
CLINICAL PEARLS
⯈ The 4 major categories involving post-resuscitation care include post-resuscitation brain injury, ischemia/reperfusion injuries, myocardial dysfunction, and persistence of precipitating cause of the cardiac arrest.
⯈ Core temperature cooling to 32°C to 34°C for 24 to 48 hours has been shown to improve neurologic recovery after successful resuscitation from cardiac arrest ca used by VF.
⯈ Core temperature cooling to 32°C to 34°C has been shown in animal models to improve cardiac recovery following cardiac arrest resuscitation.
⯈ Oxygen saturation targets should be in the 96% to 98% range.
⯈ Hyperglycemia is common after resuscitation and glucose levels should not be strictly controlled but allowed to be in the 144 to 180 mg/dl range.
⯈ Goal-directed resuscitation has been shown to be of benefit during the initial 6-hour window.
References
BernardS. Hypothermia after cardiac arrest: expanding the therapeutic scope. Crit Care Med. 2009;37 (7 suppl):S227 -S233.
Kilgannon JH, Jones AE, Shapiro NI, et al. Association between arterial hyperoxia following resuscitation from cardiac arrest and in-hospital mortality. ]AMA. 2010;303:2165-2171.
Nolan JP, Soar J. Postresuscitation care: entering a new era. Curr Opin Crit Care. 2010;16:216-222.
Sagalyn E, Band RA, Gaieski DF, Abella BS. Therapeutic hypothermia after cardiac arrest in clinical practice: review and compilation of recent experiences. Crit Care Med. 2009;37(7 suppl):S223-S226.
The National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome (ARDS) Clinical Trial Network. Comparison of two fluid-management strategies in acute lung injury. N Engl] Med. 2006;354:2564-2575.
Xiong W, Hoesch RE, Geocadin RG. Post-cardiac arrest encephalopathy. Semin Neural. 2011 ;31 :216-225.
Zia A, Kern KB. Management of postcardiac arrest myocardial dysfunction. Curr Opin Crit Care . 2011;17: 241-246.
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