Cardiac Resuscitation

2012 ◽  
Author(s):  
Charles N. Pozner ◽  
Jennifer L Martindale ◽  
Brian C. Geyer
Keyword(s):  
Cardiac Arrest ◽  
Heart Association ◽  
The United States ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Chest Compressions ◽  
Neurologic Recovery ◽  
Cardiac Resuscitation ◽  
Postresuscitation Care ◽  
Large Pericardial Effusion

Over 1,000 people suffer sudden cardiac death every day in the United States. About half occur in the hospital, the remainder occurring in the home, outpatient medical environments, or public spaces. The ultimate goal of cardiac resuscitation is survival with full neurologic recovery. Interventions that have the greatest potential to provide this outcome are often those interventions that can be performed by trained laypersons. Delay in the initiation of compressions in a cardiac arrest is one of the leading predictors of mortality. This chapter deliberately opens with a discussion of one of the most vital, yet relatively under-appreciated aspects of cardiac resuscitation—teamwork. Following an overview of cardiac arrest, the chapter covers epidemiology and recognition of cardiac arrest, then activation of the emergency response system. Chest compressions, defibrillation and airway management are discussed, then end-tidal CO2, vascular access, rhythm analysis during cardiac arrest, and drugs used during cardiac resuscitation. The chapter concludes with a look at postresuscitation care, special considerations in cardiac arrest, and future directions. Figures include the foundations of cardiac resuscitation, a management algorithm for the initial treatment of cardiac arrest, coronary perfusion pressure as a function of time, an impedance threshold device incorporated into a bag-valve mask, a colorimetric CO2 detector, four basic phases of a capnogram, sample capnographs, a battery-powered intraosseous drill, electrocardiogram readouts of ventricular arrhythmias, a sonogram of large pericardial effusion, and electrocardiographic appearance of varying degrees of hyperkalemia. Tables summarize recommendations from the American Heart Association, the components of optimal and suboptimal chest compressions, and underlying causes of nonshockable rhythms and their management. This chapter contains 11 highly rendered figures, 3 tables, 138 references, 5 MCQs.

Cardiac Arrest and Resuscitation

2015 ◽  
Author(s):  
Charles N. Pozner ◽  
Jennifer L Martindale
Keyword(s):  
Cardiac Arrest ◽  
Ventricular Arrhythmias ◽  
Perfusion Pressure ◽  
Pulseless Electrical Activity ◽  
Coronary Perfusion Pressure ◽  
Spontaneous Circulation ◽  
Coronary Perfusion ◽  
Chest Compressions ◽  
Cardiac Resuscitation ◽  
Neurologic Function

The most effective treatment for cardiac arrest is the administration of high-quality chest compressions and early defibrillation; once spontaneous circulation is restored, post–cardiac arrest care is essential to support full return of neurologic function. This review summarizes the pathophysiology, stabilization and assessment, diagnosis and treatment, and disposition and outcomes of cardiac arrest and resuscitation. Figures show the foundations of cardiac resuscitation, ventricular arrhythmias, coronary perfusion pressure as a function of time, an algorithm for initial treatment of cardiac arrest, sample capnographs, and the electrocardiographic appearance of varying degrees of hyperkalemia. Tables include components of suboptimal cardiac resuscitation and corrective actions, recommended doses of medications commonly used in cardiac resuscitation, causes of pulseless electrical activity/asystolic arrest to consider, immediate post–return of spontaneous circulation checklist, and resuscitation goals during post–cardiac arrest care. This review contains 6 highly rendered figures, 5 tables, and 142 references.

scholarly journals The Physiologic Response to Rescue Therapy with Vasopressin versus Epinephrine during Experimental Pediatric Cardiac Arrest

2020 ◽  
Author(s):  
Julia Slovis ◽  
Ryan Morgan ◽  
William Landis ◽  
Anna L Roberts ◽  
Constantine Mavroudis ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Perfusion Pressure ◽  
Rescue Therapy ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Cerebral Vasculature ◽  
Chest Compressions ◽  
Rescue Dose ◽  
Physiologic Response ◽  
Hospital Cardiac Arrest

Abstract Background: While epinephrine is the mainstay of therapy during cardiopulmonary resuscitation, it is potentially detrimental to the cerebral vasculature and ineffective in certain populations. This study compares a rescue dose of vasopressin to a rescue dose of epinephrine after ineffective initial doses of epinephrine in diverse models of pediatric in-hospital cardiac arrest. 67 one- to three-month old female swine (10-30kg) in six experimental cohorts from one laboratory received hemodynamic-directed CPR, a resuscitation method where high quality chest compressions are provided and vasopressor administration is titrated to coronary perfusion pressure (CoPP) ³20 mmHg. Vasopressors are given when CoPP is <20 mmHg, in sequences of two doses of 0.02 mg/kg epinephrine separated by minimum one-minute, then a rescue dose of 0.4 U/kg vasopressin followed by minimum two-minutes. Invasive measurements were used to evaluate and compare the hemodynamic and neurologic effects of each vasopressor dose. Results: Increases in CoPP and cerebral blood flow (CBF) were greater with vasopressin rescue than epinephrine rescue (CoPP: +8.16 [4.35, 12.06] mmHg vs. +5.43 [1.56, 9.82] mmHg, p=0.022; CBF: +14.58 [-0.05, 38.12] vs. +0.00 [-0.77, 18.24] perfusion units (PFU), p=0.005). Twenty animals (30%) failed to achieve CoPP ³20 mmHg after two doses of epinephrine; 9/20 (45%) non-responders achieved CoPP ³20 mmHg after vasopressin. Among all animals, the increase in CBF was greater with vasopressin (+14.58 [-0.58, 38.12] vs. 0.00 [-0.77, 18.24] PFU, p=0.005).Conclusions: CoPP and CBF rose significantly more after rescue vasopressin than after rescue epinephrine. Importantly, CBF increased after vasopressin rescue, but not after epinephrine rescue. In the 30% that failed to meet CoPP of 20mmHg after two doses of epinephrine, 45% achieved target CoPP with a single rescue vasopressin dose.

Cardiac massage and blood flow management during cardiac arrest

2016 ◽  
Author(s):  
Gavin D. Perkins
Keyword(s):  
Blood Flow ◽  
Cardiac Arrest ◽  
Essential Element ◽  
Coronary Perfusion Pressure ◽  
Cardiac Massage ◽  
Coronary Perfusion ◽  
Chest Compressions ◽  
Term Survival

When cardiac arrest occurs, blood flow to the vital organs diminishes rapidly. Chest compressions are an essential element of cardiopulmonary resuscitation (CPR), yet they achieve, at best, one-third of the normal cardiac output. The speed of initiating CPR, as well as its quality is critical to patient outcomes. Optimal chest characteristics of compressions are defined as pushing hard (depth > 5 cm) and fast (compression rate 100–120/min). Pressure should be released fully between sequential chest compressions and interruptions in chest compressions should be minimized. Even short interruptions in CPR around the time of attempted defibrillation can be harmful. CPR feedback and prompt devices can be used to monitor the quality of CPR. Studies have shown these devices can improve the quality of CPR, but do not improve overall survival. Mechanical chest compression devices may be usefully deployed when it is difficult or unsafe to perform manual CPR, but there is no evidence that the routine deployment of these devices improves outcome. Vasoactive drugs improve coronary perfusion pressure and increase the chances of return of spontaneous circulation. However, there is no definitive evidence that they improve long-term survival. Recent data have raised the possibility that adrenaline may worsen long-term outcomes.

scholarly journals Even Four Minutes of Poor Quality of CPR Compromises Outcome in a Porcine Model of Prolonged Cardiac Arrest

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Heng Li ◽  
Lei Zhang ◽  
Zhengfei Yang ◽  
Zitong Huang ◽  
Bihua Chen ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Porcine Model ◽  
Coronary Perfusion Pressure ◽  
Poor Quality ◽  
Spontaneous Circulation ◽  
Coronary Perfusion ◽  
Chest Compressions ◽  
Yorkshire Pigs ◽  
Anterior Posterior

Objective. Untrained bystanders usually delivered suboptimal chest compression to victims who suffered from cardiac arrest in out-of-hospital settings. We therefore investigated the hemodynamics and resuscitation outcome of initial suboptimal quality of chest compressions compared to the optimal ones in a porcine model of cardiac arrest.Methods. Fourteen Yorkshire pigs weighted 30 ± 2 kg were randomized into good and poor cardiopulmonary resuscitation (CPR) groups. Ventricular fibrillation was electrically induced and untreated for 6 mins. In good CPR group, animals received high quality manual chest compressions according to the Guidelines (25% of animal’s anterior-posterior thoracic diameter) during first two minutes of CPR compared with poor (70% of the optimal depth) compressions. After that, a 120-J biphasic shock was delivered. If the animal did not acquire return of spontaneous circulation, another 2 mins of CPR and shock followed. Four minutes later, both groups received optimal CPR until total 10 mins of CPR has been finished.Results. All seven animals in good CPR group were resuscitated compared with only two in poor CPR group (P<0.05). The delayed optimal compressions which followed 4 mins of suboptimal compressions failed to increase the lower coronary perfusion pressure of five non-survival animals in poor CPR group.Conclusions. In a porcine model of prolonged cardiac arrest, even four minutes of initial poor quality of CPR compromises the hemodynamics and survival outcome.

Abstract 254: Synchronized Chest Compressions for Pseudo-PEA: Proof of Concept and Synching Algorithm

Circulation ◽  
2019 ◽  
Vol 140 (Suppl_2) ◽  
Author(s):  
Keith Marill ◽  
James J Menegazzi ◽  
Allison C Koller ◽  
Matthew Sundermann ◽  
David D Salcido
Keyword(s):  
Cardiac Arrest ◽  
Chest Compression ◽  
Porcine Model ◽  
Pulseless Electrical Activity ◽  
Compression Therapy ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Compression Rate ◽  
Proof Of Concept ◽  
Chest Compressions

Introduction: Pulseless electrical activity (PEA) is a common rhythm in cardiac arrest with a persistently poor outcome. This report describes our successful development of a synchronized compression device and algorithm to treat PEA with or without intrinsic myocardial contractions. Methods: We adapted our previously developed signal-guided CPR system to provide synchronized compressions in a porcine model of cardiac arrest. We describe the first comparison of unsynchronized to synchronized compressions in a single animal as a proof-of-concept. We developed an algorithm to provide optimal synchronized chest compressions regardless of intrinsic heartrate while simultaneously maintaining the chest compression rate within a desired range. We tested the algorithm with computer simulations measuring the proportion of intrinsic and compression beats that were synchronized, and the compression rate and its standard deviation, as a function of intrinsic heartrate and heartrate jitter. Results: We demonstrate and compare unsynchronized versus synchronized chest compressions in a single porcine model with an intrinsic rhythm and hypotension. Synchronized, but not unsynchronized, chest compressions were associated with increased blood pressure and coronary perfusion pressure (Figure). Our synchronized chest compression algorithm is able to provide synchronized chest compressions to over 90% of intrinsic beats for most heartrates while maintaining an average compression rate between 95 and 135 BPM with relatively low variability. Conclusion: Synchronized chest compression therapy for pulseless electrical rhythms is feasible. A high degree of synchronization can be maintained over a broad range of intrinsic heart rates while maintaining the compression rate within a satisfactory range. Further investigation to assess benefit for treatment of PEA is warranted.

scholarly journals Cardiac arrest complicating cardiogenic shock: from pathophysiological insights to Impella-assisted cardiopulmonary resuscitation in a pheochromocytoma-induced Takotsubo cardiomyopathy—a case report

2021 ◽  
Vol 5 (3) ◽  
Author(s):  
Filippo Zilio ◽  
Simone Muraglia ◽  
Roberto Bonmassari
Keyword(s):  
Cardiac Arrest ◽  
Cardiopulmonary Resuscitation ◽  
Left Ventricle ◽  
Cardiogenic Shock ◽  
Takotsubo Cardiomyopathy ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Coronary Perfusion ◽  
Refractory Cardiac Arrest

Abstract Background A ‘catecholamine storm’ in a case of pheochromocytoma can lead to a transient left ventricular dysfunction similar to Takotsubo cardiomyopathy. A cardiogenic shock can thus develop, with high left ventricular end-diastolic pressure and a reduction in coronary perfusion pressure. This scenario can ultimately lead to a cardiac arrest, in which unloading the left ventricle with a peripheral left ventricular assist device (Impella®) could help in achieving the return of spontaneous circulation (ROSC). Case summary A patient affected by Takotsubo cardiomyopathy caused by a pheochromocytoma presented with cardiogenic shock that finally evolved into refractory cardiac arrest. Cardiopulmonary resuscitation was performed but ROSC was achieved only after Impella® placement. Discussion In the clinical scenario of Takotsubo cardiomyopathy due to pheochromocytoma, when cardiogenic shock develops treatment is difficult because exogenous catecholamines, required to maintain organ perfusion, could exacerbate hypertension and deteriorate the cardiomyopathy. Moreover, as the coronary perfusion pressure is critically reduced, refractory cardiac arrest could develop. Although veno-arterial extra-corporeal membrane oxygenation (va-ECMO) has been advocated as the treatment of choice for in-hospital refractory cardiac arrest, in the presence of left ventricular overload a device like Impella®, which carries fewer complications as compared to ECMO, could be effective in obtaining the ROSC by unloading the left ventricle.

Abstract 17334: The Detrimental Effect of Chest Compression Interruptions on Coronary Perfusion Pressure Dynamics

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Norman A Paradis ◽  
Karen L Moodie ◽  
Christopher L Kaufman ◽  
Joshua W Lampe
Keyword(s):  
Blood Flow ◽  
Chest Compression ◽  
Detrimental Effect ◽  
Perfusion Pressure ◽  
Vena Cava ◽  
Coronary Perfusion Pressure ◽  
Right Atrial ◽  
Coronary Perfusion ◽  
Chest Compressions ◽  
Over Time

Introduction: Guidelines for treatment of cardiac arrest recommend minimizing interruptions in chest compressions based on research indicating that interruptions compromise coronary perfusion pressure (CPP) and blood flow and reducing the likelihood of successful defibrillation. We investigated the dynamics of CPP before, during, and after compression interruptions and how they change over time. Methods: CPR was performed on domestic swine (~30 Kg) using standard physiological monitoring. Blood flow was measured in the abdominal aorta (AAo), the inferior vena cava, the right common carotid and external jugular. Ventricular fibrillation (VF) was electrically induced. Mechanical chest compressions (CC) were started after four minutes of VF. CC were delivered at a rate of 100 compressions per minute (cpm) and at a depth of 2” for a total of 12 min. CPP was calculated as the difference between aortic and right atrial pressure at end-diastole per Utstein guidelines. CPP was determined for 5 compressions prior to the interruption, every 2 seconds during the CC interruption, and for 7 compressions after the interruption. Per protocol, 12 interruptions occurred at randomized time points. Results: Across 12 minutes of CPR, averaged CPP prior to interruption was significantly greater than the averaged CPP after the interruption (22.4±1.0 vs. 15.5±0.73 mmHg). As CPR continued throughout the 12 minutes, CPP during compressions decreased (First 6 min = 24.1±1.4 vs. Last 6 min = 20.1±1.3 mmHg, p=0.05), but the effect of interruptions remained constant resulting in a 20% drop in CPP for every 2 seconds irrespective of the prior CPP. The increase (slope) of CPP after resumption of compressions was significantly reduced over time (First 6 min = 1.47±0.18 vs. Last 6 min = 0.82±0.13 mmHg/compression). Conclusions: Chest compression interruptions have a detrimental effect on coronary perfusion and blood flow. The magnitude of this effect increases over time as a resuscitation effort continues. These data confirm the importance of providing uninterrupted CPR particularly in long duration resuscitations.

Abstract 167: Epinephrine Plus Chest Compressions May Be Superior to Epinephrine Alone in a Hypoxia-Induced Porcine Model of Lifeless Shock

Circulation ◽  
2019 ◽  
Vol 140 (Suppl_2) ◽  
Author(s):  
Felipe Teran ◽  
Claire Centeno ◽  
Alex L Lindqwister ◽  
William J Hunckler ◽  
William Landis ◽  
...  
Keyword(s):  
Chest Compression ◽  
Porcine Model ◽  
Contractile Activity ◽  
Coronary Perfusion Pressure ◽  
Spontaneous Circulation ◽  
Swine Model ◽  
Coronary Perfusion ◽  
Chest Compressions ◽  
Fraction Of Inspired Oxygen ◽  
External Chest Compressions

Background: Lifeless shock (LS) (previously called EMD and pseudo-PEA) is a global hypotensive ischemic state with retained coordinated myocardial contractile activity and an organized ECG. We have previously described our hypoxic LS model. The role of standard external chest compressions remains unclear in the setting of LS and its associated intrinsic hemodynamics. Although it is known the patients with LS have better prognosis compared to PEA, it is unclear what is the best treatment strategy. Prior work has shown that chest compressions (CC) when synchronized with native systole results in significant hemodynamic improvement, most notably coronary perfusion pressure (CPP), and hence it is plausible that standard dyssynchronous CC may be detrimental to hemodynamics. Furthermore, retrospective clinical data has shown that LS patients treated with vasopressors and no CC, may have better outcomes. We compared epinephrine only versus epinephrine and chest compression, in a porcine model of LS. Methods: Our porcine model of hypoxic LS has previously been described. We randomized pigs to episodes of LS treated with epinephrine only (control) (0.0015 mg/kg) versus epinephrine plus standard external chest compressions (intervention). Animals were endotracheally intubated and mechanically ventilated, and the fraction of inspired oxygen (FiO 2 ) was gradually lowered from room air (20-30% O 2 ) to a target FiO 2 of 3-7% O 2 . This target FiO 2 was maintained until the systolic blood pressure (SBP) dropped to 30 mmHg for 30 seconds, or the animal became bradycardic (HR less than 40), which was defined as the start of LS. FiO 2 was then raised to 100%, and then animal would receive control or intervention. Return of spontaneous circulation (ROSC) was defined as SBP 60 mmHg, stable after 2 minutes. Results: Twenty-six episodes of LS in 11 animals received epinephrine only control and 21 episodes the epinephrine plus chest compression intervention. The rates of ROSC in two minutes or less were 5/26 (19%) in the control arm vs 14/21 (67%) in the intervention arm (P=0.001;95% CI 19.7 %-67.2%). Conclusions: In a swine model of hypoxia induced LS, epinephrine plus CPR may be superior to epinephrine alone.

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