First Aid Express Forum (I) Prioritization of CPR
The existing guidelines recommend that when an out-of-hospital cardiac arrest is witnessed or when an in-hospital cardiac arrest occurs, first responders should perform CPR (chest compressions and artificial respiration) and use a defibrillator as soon as possible if an AED or manual defibrillator is immediately available at the scene; when an out-of-hospital cardiac arrest is not witnessed, especially if the rapid response time is more than 5 minutes, CPR is recommended before defibrillation. CPR followed by shock defibrillation is recommended when an out-of-hospital cardiac arrest is not witnessed, especially if the rapid response time is more than 5 minutes. In clinical practice, it is difficult to define the early and late stages of cardiac arrest, and it is difficult to define the order of priority defibrillation or CPR at a single point in time to reflect individual differences.
Recent advances in the study of ventricular fibrillation (VF) waveforms have provided new insights into the timing of defibrillation. Studies have shown that ECG waveforms correlate significantly with myocardial blood flow, allowing the decision between chest compressions and shock defibrillation to be made based on the VF waveform. If defibrillation is likely to terminate current VF, then defibrillation should be performed immediately; conversely, if current defibrillation has a low probability of terminating VF, then immediate CPR to improve coronary perfusion and prepare for defibrillation is the highest priority to improve resuscitation success.
The Weil Cardiology Institute of the EMS Express Forum has recently made a breakthrough in the analysis of VF waveforms, developing the Amplitude Spectral Area (AMSA) technique that combines the amplitude and frequency values of ECG waveforms to determine whether to prioritize defibrillation or CPR followed by defibrillation based on VF waveform analysis. As a result, defibrillation is no longer a simple estimate based on the time of the cardiac arrest event or the individual experience of the first responder. AMSA technology for defibrillation treatment is expected to be recommended in the 2010 CPR guidelines.
(ii) Sub-hypothermia Treatment Emergency Fast Track Forum
Hypothermia is a state in which the body temperature of a constant temperature animal is below normal. Unlike in vitro hypothermia, hypothermia treatment refers to the controlled reduction of body temperature.
Numerous studies have shown that hypothermia therapy has multiple protective effects and can act simultaneously on multiple targets of the cerebral ischemic cascade injury response. The main protective mechanisms include maintaining lipid membrane fluidity, inhibiting destructive enzyme reactions, reducing oxygen demand in the hypoperfused areas of the brain during reperfusion, inhibiting lipid peroxidation, and reducing brain edema and intracellular acidosis. It has been found that hypothermia not only reduces neuronal apoptosis after cerebral ischemia, but also reduces white matter damage and inhibits astrocyte proliferation. It has been reported that hypothermia treatment should be performed as early as possible after ischemic injury, and the later the start, the worse the therapeutic effect. On the other hand, since the post-ischemic injury process often lasts for several days, it may be beneficial to extend the duration of hypothermia treatment.
Currently, the quality of cardiopulmonary resuscitation, both out-of-hospital and in-hospital, is unsatisfactory, and brain injury is common after successful resuscitation. Hypothermia is expected to be one of the new resuscitation measures to improve the prognosis of cardiac arrest.
As early as 1959, researchers had already found that the use of hypothermia after resuscitation had the potential to significantly improve the prognosis. Unfortunately, the benefits of hypothermia were not identified sensitively at the time, and hypothermia did not receive much attention.
In 2002, the New England Journal of Medicine published two clinical studies of hypothermia in patients with out-of-hospital cardiac arrest in Austria and Europe that demonstrated that post-resuscitation hypothermia significantly improved post-resuscitation neurologic function, and hypothermia again gained widespread attention. The American Heart Association’s 2005 Guidelines for Cardiopulmonary Resuscitation explicitly recommended subcritical hypothermia for post-resuscitation patients, and hypothermia has again become a hot topic in the field of cardiopulmonary resuscitation, and will be further endorsed in the 2010 guidelines.
Problems with hypothermia
There are still many unanswered questions about hypothermia, such as whether systemic or local hypothermia (e.g., selective head cooling) is preferable. However, the brain is the most vulnerable organ during cardiac arrest and cardiopulmonary resuscitation, and it is important to consider head hypothermia first from this perspective. First Aid Express Forum
Secondly, is early or late hypothermia better? At present, in Europe, whole body hypothermia is usually used half an hour after successful resuscitation. However, because the tolerance of brain nerve cells to hypoxia is very limited, it is advisable to implement hypothermia as soon as possible, even at the beginning of cardiac arrest and resuscitation. What is the appropriate duration of third hypothermia treatment? European clinical studies have used 12-24 hours of hypothermia, is this the optimal duration of hypothermia? There is no clear clinical evidence. # Finally, what is the optimal temperature control for hypothermia? The existing clinical studies have used 32-34°C, but this is still debatable and the optimal temperature for hypothermia has not been clearly established. Pending the final publication of the 2010 guidelines, experts from the American Heart Association are discussing these issues in the context of evidence-based medicine, with the hope of providing more appropriate guidance.
There is now a consensus that subcritical treatment during and after resuscitation improves the prognosis and neurological function of patients in cardiac arrest, the sooner the better!
Sub-hypothermia in cardiac arrest patients
Animal studies in the EMS Express Forum have shown that the neurological prognosis of animals treated with hypothermia at the onset of cardiac arrest is better than that of animals treated with hypothermia after successful resuscitation, and that the combination of hypothermia and chest compressions improves the neurological prognosis after prolonged cardiac arrest. It has also been found that hypothermia has a protective effect on myocardium in cardiac arrest, but the rapid induction of hypothermia during cardiopulmonary resuscitation remains a challenge. For hypothermia during resuscitation and reperfusion, animal studies have demonstrated that subhypothermia after normothermic resuscitation can reduce brain tissue damage. If the duration of hypothermia treatment is extended to 48 hours, the neuroprotective effect may last for more than 1 month. In recent years, multicenter randomized controlled clinical trials in Europe and Australia have demonstrated that hypothermia significantly reduces mortality and improves neurological prognosis. 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation evaluated the evidence for manual subhypothermia treatment and stated that spontaneous mild hypothermia (>33°C) is not required in patients who are hemodynamically stable after resuscitation from cardiac arrest. No rewarming therapy is required. In prehospital and in-hospital cardiac arrests caused by ventricular fibrillation, the recovery of patients who remain unconscious but hemodynamically stable after resuscitation should be facilitated by lowering their body temperature to 32-34°C for a total of 12-24 hours (Class Ea). Similar therapy can be used for out-of-hospital and in-hospital cardiac arrests not caused by ventricular fibrillation (level Eb).
Contraindications to artificial subcooling include <18 years of age, pregnancy, coma due to medication or central nervous system disease, cardiogenic shock, mean arterial pressure <90 mmHg, and body temperature <30 °C.
Clinical methods of hypothermia include the use of ice packs, ice blankets with circulating coolant, cooling fluid infusion through the carotid artery, extracorporeal cooling blood infusion through one carotid artery, helmets with chemical cooling, ice caps with -30 °C solution, and nasal irrigation with ice water. However, the ideal method and time of hypothermia induction is still inconclusive, and is the main direction of research at present.
(iii) Post-resuscitation management
The recommendations of many cardiopulmonary resuscitation guidelines, including the 2005 guidelines, do not focus on the post-resuscitation treatment process. The 2010 guidelines will emphasize the importance of post-resuscitation management and make clear recommendations.
The vast majority of patients in cardiac arrest have coronary artery disease, but there is a lack of clear recommendations on how to manage them. In the past, we have used a passive approach to the management of patients after resuscitation: open venous access, administration of vasoactive drugs, and symptomatic management. In a clinical study currently underway in Europe, patients with cardiac arrest, whether resuscitated or not, or in the process of resuscitation, are first admitted to the cardiac catheterization laboratory for PCI. The results of this study showed that revascularization significantly improved the prognosis of patients in cardiac arrest and confirmed that proactive treatment significantly improved the prognosis of patients compared to traditional passive treatment. microcirculatory perfusion. The 2010 guidelines for comprehensive therapeutic management after resuscitation will be described. It is well recognized that the mechanisms of cardiac arrest and cardiopulmonary resuscitation are poorly understood and that existing clinical practice is largely empirical, due in part to the paucity of scientific research. Therefore, there is a long way to go.
The American Heart Association 2010 CPR Guidelines development process (Note LCOR (IrItemadonal Liaison Committee on Resusciudon) Emergency Express Forum)
(IV) Status and progress of malignant arrhythmias after CPR
Under normal conditions, cardiac excitation originates in the sinoatrial node and travels downward in a certain frequency and speed sequence, finally reaching the ventricular muscle for depolarization. If the origin, frequency, speed, and sequence of conduction of cardiac excitation are abnormal, this is called an arrhythmia.2 1.
2 1. Types and causes of arrhythmias
Arrhythmias can be both a cause of cardiac arrest and a complication of successful cardiopulmonary resuscitation. They can be simply divided into malignant arrhythmias and nonmalignant arrhythmias according to their degree of hemodynamic impact. The former can cause severe hemodynamic disturbances and endanger the patient’s life within a short period of time, while the latter is usually asymptomatic or mildly symptomatic, hemodynamically stable, and generally non-life-threatening with a good prognosis.
The most common malignant arrhythmias after successful CPR are ventricular tachycardia (including tip-twist ventricular tachycardia) and ventricular fibrillation, which can still cause the heart to stop again and reduce the success rate of CPR if not treated promptly or properly. There are many causes of arrhythmias. Patients with cardiac arrest usually have underlying cardiac pathology, such as coronary artery disease, stroke, myopathy, or myocarditis. Primary heart disease itself can induce arrhythmias, and some conditions during resuscitation, such as myocardial hypoxia, acidosis, electrolyte disturbances, especially hypothermia, application of large amounts of cardiac stimulants and ischemia and repeated perfusion injury can also induce or aggravate arrhythmias.
2. Pharmacological treatment of malignant arrhythmias
In the process of CPR resuscitation, in addition to the conventional procedures, timely and accurate treatment of various rapid ventricular arrhythmias is the key to successful CPR. DC resuscitation remains an effective treatment for ventricular tachycardia and ventricular fibrillation.2005 The American Heart Association Guidelines for Cardiopulmonary Resuscitation recommend that antiarrhythmic drugs should be considered if ventricular tachycardia and ventricular fibrillation persist after 24 shocks, continuous CPR, and vasopressors during CPR.
It is important to note that all antiarrhythmic drugs have arrhythmogenic effects and inhibit myocardial systolic function. Patients in the early post-resuscitation period have varying degrees of cardiac dysfunction, and antiarrhythmic drugs should be administered with caution.
Lidocaine is a traditional drug for the treatment of ventricular arrhythmias, but it has certain inhibitory effects on the myocardium. Recently, various guidelines have recommended amiodarone as the drug of choice for the treatment of malignant arrhythmias to stop ventricular tachycardia episodes, essentially replacing lidocaine.
Other indications for amiodarone include: primary prevention in patients at high risk of sudden death; ejection fraction (EF) <35% in infarction or heart failure; microvoltage T-wave alternans; and patients with frequent nonsustained ventricular tachycardia who are not eligible for automatic defibrillator (ICD) implantation therapy. The combination of amiodarone and magnesium sulfate has also been reported to reduce the incidence of ventricular arrhythmias after cardiopulmonary resuscitation.
{The myocardium in acute ischemia and failure stress is susceptible to electrical instability, which often leads to malignant arrhythmias. The nature of these arrhythmias is accompanied by sympathetic activation, manifested as sympathetic storm, and recurrent episodes of ventricular tachycardia/ventricular fibrillation. Therefore, the application has a broad spectrum and multiple electrophysiological effects. Receptor blockers are effective. Slowly administered metoprolol can completely block sympathetic effects over a period of time. Receptor blockers have effects on a variety of ion channels and can inhibit arrhythmias of three mechanisms: autoregulation, triggering, and folding, and also have systemic anti-sympathetic effects, which can improve myocardial ischemic tolerance, and have good effects on complex refractory sympathetic arrhythmias.
3. extracorporeal membrane pulmonary oxygenation (ECMO)
Patients with cardiac arrest caused by coronary artery disease often develop intractable and malignant arrhythmias after cardiopulmonary resuscitation, mainly because the blood supply to the heart is not improved. In recent years, some scholars have applied extracorporeal pulmonary oxygenation (ECPO) to expand the “window of care” for patients in cardiac arrest, i.e., emergency coronary stenting for patients with acute myocardial infarction with the support of ECPO to address the blood supply to the myocardium.
Extracorporeal membrane pulmonary oxygenation is a respiratory and circulatory support technique, which is based on the principle of drawing venous blood outside the body through a catheter, oxygenating it through a membrane oxygenator under the drive of a blood pump, and returning it to the patient’s body, providing both left and right ventricular assist, and replacing pulmonary function, allowing the heart and lungs to rest while providing a stable amount of circulating blood for cardiopulmonary resuscitation patients, and restoring blood and oxygen supply to the heart, brain and other vital organs in a timely and effective manner. It can restore blood and oxygen supply to the heart and brain in a timely and effective manner. However, extracorporeal membrane pulmonary oxygenation itself is only a short-term life support method. Only by taking comprehensive therapeutic measures based on maintaining the stability of systemic hemodynamics, including emergency coronary intervention, active treatment of the primary disease, restoring the pumping function of the heart and correcting the disturbance of the body’s internal environment as soon as possible, can malignant arrhythmias be effectively reduced or avoided.
Early detection and timely management of malignant arrhythmias can reduce the early mortality of cardiopulmonary resuscitation to a certain extent, but it is a remedial measure after all. If possible arrhythmias can be predicted in advance by ECG monitoring or ECG examination, and then appropriate preventive measures can be taken, it will have a positive impact on further reducing early mortality after resuscitation.