This is a summary of my lecture on recent advances on Cardiocerebral resuscitation (CCR). It is related to the new poll of the site.
• Cardiocerebral resuscitation (CCR) is a new approach for resuscitation of patients with cardiac arrest.
• It is composed of 3 components:
• 1) continuous chest compressions for bystander resuscitation; the "lay component" for the public,
• 2) a new emergency medical services (EMS) algorithm; and
• 3) aggressive post-resuscitation care.
The major changes of 2005 AHA Guidelines for CPR for the lay rescuer might be summarized as follows:
• Start CPR as soon as collapse occurs,
• Activate the EMS system by calling 911.
• Use an AED if available.
• Push hard, push fast, allow full chest recoil, and minimize interruptions of chest compressions.
• “A single (universal) chest compression: ventilation ratio of 30:2 for single rescuers of victims.
Three Time-Sensitive Phases of VF Basis for Changes:
• The first, or electrical, phase of VF, lasts for about 4 to 5 minutes.
• The second, or circulatory, phase of untreated VF lasts for a variable period of time, but typically from about 5 to 15 minutes after the onset of VF.
• The third or metabolic phase of VF follows the circulatory phase.
So, What is new in CCR?
• The CCR method advocates continuous chest compressions without mouth-to-mouth ventilations for witnessed cardiac arrest.
• For bystanders with access to an automated external defibrillator (AED) and EMS personnel who arrive during the electrical phase (i.e., the first 4 or 5 min of VF arrest), prompt defibrillator shock is recommended.
• However, EMS personnel most often arrive after the electrical phase—in the circulatory phase of VF arrest .
• Endotracheal intubation is delayed, excessive ventilations are avoided, and early administration of epinephrine is advocated .
• For comatose patients postresuscitation, hypothermia and early cardiac catheterization (unless contraindicated), even in the absence of classic ECG signs of infarction or ischemia, are recommended.
• CCR is not recommended for individuals with respiratory arrest.
• Arterial blood is almost always fully oxygenated at the time of cardiac arrest, and cardiac arrest secondary to respiratory failure, in which the initially normal cardiac output in spite of the lack of ventilation leads to severe hypoxemia, hypotension, and secondary cardiac arrest.
Bystander-Initiated Resuscitation Efforts Are Critical
• The initiations of bystander resuscitations, especially when begun within 1 min of the arrest, markedly improve survival.
• In 1 analysis, survival was more than 4 times greater in patients who received early bystander CPR.
“Rescue Breathing” for Cardiac Arrest Is a Misnomer
• This requirement dramatically decreases the survival chances of patients with witnessed cardiac arrest receiving bystander-initiated resuscitation.
• The bystander attempts at assisted ventilation have been shown to decrease the chance of survival in the subset of subjects with cardiac arrest who have the greatest chance of survival—namely those with witnessed cardiac arrest and shockable rhythm.
• It decreases the number of individuals with cardiac arrest who receive prompt bystander resuscitation efforts.
• Even the best attempts by laypersons to do “rescue breathing” result in inordinately long interruptions of chest compressions during cardiac arrest , and long interruptions of chest compressions decrease neurologically normal survival.
Mouth-to-mouth ventilations has several major drawbacks for patients with cardiac arrest.
• Even if chest compressions are not interrupted, positive-pressure ventilation during cardiac arrest increases intrathoracic pressure, thereby decreasing venous return to the thorax and subsequent perfusion of the heart and the brain.
• The recommended ventilations do not increase arterial saturation—they only further delay the onset of critical chest compressions .
• If chest compressions are initiated early, many subjects who are not gasping will begin to gasp.
• Because of these facts, it is important that bystanders be taught that “abnormal breathing” is either no or abnormal respirations and that abnormal respirations are apnea or gasping.
• Witnesses a sudden collapse of an adult.
• If there is no response, assess the breathing: is it normal or abnormal?
• Abnormal breathing means either no breathing at all or intermittent gasping.
• Snoring or gurgling respirations are types of gasping or agonal breathing. Such a victim should be treated as a cardiac arrest . If someone collapses after obviously choking at a restaurant.
• If someone is rescued from the water.
• A person who has a drug or drug and alcohol overdose, who is obtunded.
Decreasing Chest Compression Interruptions :
• Without such immediate postshock hemodynamic support provided by chest compressions, the aortic pressure will decline and soon be truly asystolic. Therefore, CCR calls for an additional 200 chest compressions immediately after the shock without a pause to assess the post-shock rhythm.
• Interruptions in chest compressions were frequent when EMS personnel were following the previous guidelines.
• Endotracheal intubation has adverse effects due to the relatively long interruptions of chest compressions during placement and adverse effects of positive-pressure ventilation and frequent hyperventilation
Excessive Positive-Pressure Ventilations Eliminated
• Inversely proportional relationship between mean intrathoracic pressure, coronary perfusion pressure, and survival from cardiac arrest.
• positive-pressure ventilation causes increase in intrathoracic pressure and the inability to develop a negativeintrathoracic pressure during the release phase of chest compression.
• Positive-pressure ventilation inhibits venous return to the thorax and right heart and decreased coronary and cerebral pressures.
• Another aspect of hyperventilation and increased intrathoracic pressure is its adverse effect on intracranial pressure and cerebral perfusion pressure.
• Survival after cardiac arrest was more likely in cold water drowning or hypothermic states, suggesting a protective effect of hypothermia. Therapeutic, controlled mild hypothermia (89.6 to 93.2°F [32 to 34°C]) appears to be beneficial for preserving cerebral function.
• Hypothermia activates shivering, and in postcardiac arrest comatose patients. Shivering-produced thermogenes are deleterious.
• Uncontrolled hypothermia results in catecholamine release, and vasoconstriction. Seizures, myoclonus, or shivering may occur, necessitating sedation and intermittent or continuous neuromuscular blockade. There may be hyperglycemia.
Importance of Therapeutic Hypothermia
• The use of mild (32°C to 34°C) therapeutic hypothermia for
• comatose post-resuscitated cardiac arrest victims is accepted
• Should nearly everyone who is successfully resuscitated from OHCA be taken to the cath. Lab. for CA and potential emergency PCI?
• Among 13 patients with OHCA, they achieved a 54% survival to hospital discharge with aggressive early cardiac catheterization and angioplasty (Quintero-Moran et al., 2006).
• Survival to hospital discharge was achieved in 67% (Gorjup et al., 2007).
• Prior to cardiac catheterization, all of these patients were sedated and given neuromuscular blockage, hence their precatheterization neurologic status was not known.
• Aggressive post-resuscitation care (therapeutic hypothermia and emergent cardiac catheterization and PCI) when appropriate must be included.
• Reperfusion therapy, either PCI or coronary artery bypass graft, had the most profound effect on outcome.
• Many of these patients were transported directly from the emergency department to the PCI suite upon arrival to the hospital (i.e., in an aggressive manner paralleling the current recommendation for certain STEMI patients.