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Standard CPR consists of manual chest compressions to maintain blood flow and positive pressure ventilation to maintain oxygenation until spontaneous circulation returns.
It is a method of external chest compressions and artificial respirations the provides perfusion to vital organs during cardiac arrest until definitive treatment is available.
Chest compressions are int2242upted by ventilations on an intermittent basis as rescue breathing during the treatment of cardiac arrest.
Interruptions reduce blood flow and reduce the effectiveness theoretically of effectiveness of CPR.
Only 19% of adults that sustain a cardiopulmonary arrest on presentation to a prehospital system can be resuscitated on arrival at an emergency hospital department.
Only 4% of patients arriving at a hospital emergency department in cardiopulmonary arrest are discharged from the hospital alive.
Early initiation of CPR by a layperson can increase chances of survival and long-term neurologic recovery.
A cardiac cause is the most common mechanism of cardiac arrest, but respiratory causes may be an important contributing factor.
In a randomized trial of bystanders performing CPR with random assignment to chest compression vs. chest compression plus rescue breathing: no significant difference between the two groups with 12.5% of patients surviving hospital discharge with chest compression alone and 11% with chest compression plus rescue breathing (Rea TD).
Provision of cardiopulmonary resuscitation for approximately 90 seconds before defibrillation with autonomic external defibrillation is associated with improved survival when response time is four minutes or longer.
Epinephrine is the vasopressor of choice for cardiopulmonary resuscitation, the prognosis for patients who require this agent is extremely poor, regardless of the dose given.
Epinephrine use during advanced cardiac life support is associated with little or no improvement in survival to hospital discharge.
In a prospective, randomized control trial of consecutive adult patients with out of hospital cardiac arrest treated with emergency service and advanced cardiac life support patients who received intravenous drug administration compared to patients without intravenous drug administration resulted in significant improvement in survival to hospital discharge, quality of CPR, all long-term survival (Olasveegen TM).
Use of epinephrine during CPR associated with increased myocardial oxygen consumption, ventricular dysfunction and arrhythmias.
As compared to epinephrine alone, the addition of vasopressin to epinephrine does not improve outcomes.
Vasopressin acts via V1 receptors on vascular contractile elements.
Vasopressin is released during cardiac arrest as an adjunct to epinephrine.
Among patients with cardiac arrest that require vasopressors, combinations of vasopressin-epinephrine and methylprednisolone during CPR and stress dose hydrocortisone in post resuscitation shock compared with epinephrine/saline placebo resulted in improved survival to hospital discharge with favorable neurologic status (Mentzelopoulos SD et al).
Return of spontaneous circulation is associated with increased cytokines, endotoxemia, coagulopathy and adrenal insufficiency, all which contribute to post resuscitation shock.
Two basic approaches to CPR: conventional chest compressions and ventilations, and compression only CPR, perform with only chest compressions.
Closed chest massage generates blood flow by direct cardiac compression and by cyclic changes in the intrathoracic pressure.
Conventional closed chest CPR is, at best, a holding measure, providing hemodynamic changes as seen in cardiogenic shock, with low systemic arterial pressure, significantly reduced cardiac output, and high left ventricular filling pressure.
Quality related to the depth, force and duration of chest compression, completeness of chest wall decompression during the upstroke, maintenance of chest compression at a rate of approximately 100 per minute and avoidance of hyperventilation.
Three physiological phases: electrical, circulatory and metabolic (Weisfeldt and Becker).
Cerebral microcirculation flow is reduced by approximately 60% during chest compression-only CPR.
When cardiac arrest due to ventricular fibrillation occurs myocardial ATP levels decline as myocardial cells continue to consume ATP at normal rate.
The first few minutes after an arrest, the electrical phase, the circulation can be restored with prompt defibrillation.
Following ventricular fibrillation myocardial ATP stores are critically depleted soon after the event and defibrillation shock will result in either asystole or pulse less electrical activity as cell run out of high energy phosphate.
During the circulatory phase, 90 seconds to 3 minutes of effective chest compression boosts myocardial ATP and increases the likelihood that a perfusing rhythm will result after defibrillation.
If a patient remains in cardiac arrest longer than 8-10 minutes increasing injury occurs during the metabolic phase indicating that additional cellular protecfibrillation management is to shock initially and add cardiopulmonary resuscitation, defibrillation and postresuscitation care.
Even if spontaneous circulation returns after in hospital cardiac arrest, approximately 60% of patients will not survive hospital discharge.
Current standards for standard CPR measures call for 30 compressions followed by two ventilations.
Compression-only CPR is a reasonable alternative to standard CPR.
Evidence suggests that int2242uptions in chest compressions, even for providing artificial ventilation, are detrimental.
The forward flow of blood stops very soon after chest compressions are halted, and it takes several compressions to reestablish perfusion when compressions are resumed.
Multiple studies reveal standard CPR and compression-only CPR have similar outcomes.
Compression only CPR is associated with better acceptance by lay rescuers.
Lay rescuers are concerned about victims regurgitating during mouth-to-mouth ventilation, and or anxiety regarding disease transmission.
In a comparison of EMS management of a brief period of manual chest compressions and ventilations with prompt initiation of rhythm analysis and defibrillation versus a longer period of compressions and ventilations before the first analysis of cardiac rhythm in patients with out of hospital cardiac arrest: no differences were noted in outcomes ( Resuscitation Outcomes Consortium).
In the above study patients were assigned to receive 30-60 seconds of EMS administered CPR and those in the later analysis group assigned to receive 180 seconds of CPR, before initial electrocardiographic analysis- both groups had a primary outcome of survival to hospital discharge of 5.9%.
High mortality after CPR associated with postcardiac arrest syndrome involving global ischemic reperfusion injury, myocardial stunning, and anoxic brain injury (Negovsky VA).
Following resuscitation from cardiac arrest, arterial hypoxemia hypoxemia is independently associated with increased in-hospital compared with hypoxia or normoxia (Kilgannon JH).
Central oxygen saturation levels are likely to be normal at the moment of cardiac arrest as it takes several minutes before oxygen saturations fall to critical levels and this makes immediate initiation of ventilation, not to be necessary.
Bystander mouth-to-mouth ventilations are often ineffective and unlikely to provide meaningful oxygenation for the patient but can produce excessive intrathoracic pressure with negative effects on perfusion.
Ventilations early in cardiac arrest can detract from high-quality chest compressions and timely defibrillation.
The benefits of lay rescuer ventilations early in cardiac arrest, particularly if delivered by Untrained bystanders, are questionable.
There is markedly higher survival among patients with out of hospital cardiac arrest who receive bystander CPR than among those who did not (16.1% versus 3.9%) in a study of 142,740 patients in a metanalysis.
Bystander CPR can prolong the time in which successful resuscitation can occur and allow for longer EMS response times.
Bystander CPR increases the percentage of shockable rhythm cases.
The number needed to treat to save one life among persons receiving bystander CPR ranges from 24 to 36.
Patients who receive conventional CPR versus those who receive compression only CPR have no significant difference in survival.
Following resuscitation from cardiac arrest too little oxygen delivered may potentiate anoxic injury and too much oxygen may increase oxygen free radical production that can trigger cellular injury and apoptosis (Becker LB).
Reperfusion after an ischemic event is associated with a surge of reactive oxygen species which can overwhelm antioxidant defenses.
Current American Heart Association guidelines for adult cardiopulmonary resuscitation suggests the utilization of 100% inspired oxygen during the procedure for the return of spontaneous circulation.
Among patients treated with cardiopulmonary resuscitation the presence of arterial hyperoxemia was independently associated with increased in hospital mortality compared with either hypoxia or normoxia (Kilgannon JH).
Impedance threshold device to enhance venous return and cardiac output during CPR by increasing the degree of negative intrathoracic pressure does not significantly improve survival in patients with out of hospital cardiac arrests (Aufderheide TP et al).
In witnessed out of hospital cardiac arrest, Black and Hispanic persons are less likely than white persons to receive potentially lifespan life-saving by standard CPR, at home and in public locations regardless of racial or ethnic make up or income level of the neighborhood with the cardiac arrest occurred.