After three minutes, global cerebral ischemia —the lack of blood flow to the entire brain—can lead to brain injury that gets progressively worse.
By nine minutes, severe and permanent brain damage is likely. After 10 minutes, the chances of survival are low. Even if a person is resuscitated, eight out of every 10 will be in a coma and sustain some level of brain damage. Simply put, the longer the brain is deprived of oxygen, the worse the damage will be. If you haven't learned CPR recently, things have changed.
You can usually find a two- to three-hour training course at a local community health center, or by contacting a Red Cross or American Heart Association office in your area. People are most likely to be successfully revived in a hospital or another site with quick access to defibrillators. These are devices that send electrical impulses to the chest to restart the heart.
These devices are found in many workplaces, sports arenas, and other public places. When a cardiac arrest is treated very quickly, a person may recover with no signs of injury. Others may have mild to severe damage. Memory is most profoundly affected by apoxia, so memory loss will often be the first sign of the damage.
Other symptoms, both physical and psychiatric, may be obvious, while some may only be noticed months or years later. For those who are resuscitated and are not in a coma, apoxia may cause:. Some symptoms may improve over time. Others, however, may be lasting and require a person to be under lifelong assisted care. Even when the heart is restarted and blood flow begins delivering oxygen to the cells again, most people will still have serious impacts.
These impacts, like memory loss or mobility issues, are worse the longer the brain is deprived of oxygen. People who are comatose after a cardiac arrest will often have damage to different parts of the brain, such as the:. Even the spinal cord will sometimes be damaged. People who are in a coma for 12 hours or more will usually have lasting problems with thinking, movement, and sensation. Recovery will often be incomplete and slow, taking weeks to months. The most severely affected people may end up in a vegetative state, more appropriately known as unresponsive wakefulness syndrome UWS.
The eyes may open in people with UWS, and voluntary movements may occur, but the person does not respond and is unaware of their surroundings. Unfortunately, those with UWS due to lack of oxygen more often don't.
Restoring the flow of blood through the body is called reperfusion. It is key to reviving the person and preventing or limiting brain damage. But when this occurs, the sudden rush of blood to areas of damaged tissues can cause injury.
It may seem counterintuitive because restarting the flow of blood is the critical goal. But the lack of oxygen and nutrients during the time of cardiac arrest means that when blood flow is restored, it places oxidative stress on the brain as toxins flood already-damaged tissues.
The inflammation and nerve injury this causes can trigger a cascade of symptoms, including:. Medical Review: Rakesh K. This information does not replace the advice of a doctor.
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Updated visitor guidelines. Top of the page. Immediately after your surgery General anesthesia is used during the CABG procedure, so you may be unconscious for several hours after surgery. Getting out of the intensive care unit When your condition has improved, you will be transferred from the specialized ward to a normal cardiac care unit, sometimes called a step-down unit. Most hospital step-down units have significantly fewer nurses and monitoring personnel, so you are usually transferred there when: Your breathing tube has been removed.
You are able to take medicines orally. Invasive tubes and monitoring requirements are reduced. Removing the breathing tube The tube from the ventilator to your lungs helps you breathe during your CABG surgery.
Taking oral medicines When your doctor thinks you are ready, your NG tube will be removed and you should be able to swallow food as well as medicines.
Removing other tubes and monitors You will have several tubes and monitors placed in and around your body to monitor your progress during recovery. What to think about After you have been transferred to a step-down unit, you will most likely be in the hospital only a few more days. Medical management of the patient undergoing cardiac surgery. In RO Bonow et al. Philadelphia: Saunders. Credits Current as of: August 31, Top of the page Next Section: Related Information. Cardiac arrest results in the cessation of spontaneous circulation, which causes hypoxic-ischemic encephalopathy, the severity of which is primarily related to the time from arrest to restoration of spontaneous circulation.
Prolonged intervals without spontaneous circulation result in death, long-term or permanent coma, persistent vegetative state, seizures, and myoclonus [ 1 ]. Predicting the outcome following cardiac arrest for survivors who are comatose following resuscitation is the source of much consternation among emergency room and intensive care unit ICU physicians, as well as family members.
As acute care resources have become increasingly scarce and costly, there has been increasing emphasis on identifying clinical, imaging, or molecular biomarkers that can reliably predict long-term outcome.
That evidence-based review found that pupillary light response, corneal reflexes, motor responses to pain, myoclonic status epilepticus, serum neuron-specific enolase NSE , and somatosensory evoked potential SSEP studies can reliably assist in accurately predicting poor outcomes in comatose patients.
NSE is an enzyme active in the glycolytic pathway and is released from peripheral and central neurons when they are damaged. The strongest predictors of outcome are the absence of the pupillary light response, absence of corneal reflexes, and extensor or no motor response to pain for at least 3 days after the arrest. Questions remain, however, about the sensitivity and specificity of serum biomarkers, as well as the role of imaging and electrophysiologic biomarkers.
There also has been intense interest in identifying therapies that may limit secondary brain injury after cardiac arrest. During the s several pre-clinical studies found that therapeutic resuscitative hypothermia was very effective in improving neurologic recovery after arrest for various lengths of time.
Based on the positive results of those trials, the advanced life support task force of the International Liaison Committee on Resuscitation recommended therapeutic moderate hypothermia for patients with OHCA and ventricular fibrillation as the initial rhythm [ 5 ].
Subsequent clinical studies have documented as much as a twofold increase in the rate of good outcomes for this subgroup of OHCA patients treated with therapeutic hypothermia [ 6 ]. Several questions remain, however, about the long term efficacy of hypothermia, and its benefit for other subgroups of patients with cardiac arrest, such as those with post-arrest rhythms of asystole or electro-mechanical dissociation.
Clinical risk factors associated with poor outcome after cardiac arrest continue to be extensively studied in the search for one or a combination of features with high enough specificity and sensitivity to be clinically reliable. In one cohort of patients with OHCA who had initiation of professional cardiopulmonary resuscitation and who survived long enough to be hospitalized, The strongest predictors for long-term survival were age under 70 years, ventricular fibrillation as the initial rhythm, cardiopulmonary resuscitation without atropine, and ST-segment elevation myocardial infarction.
In fact, the subgroup with ST-segment elevation myocardial infarction had a 1-year survival of Other recent studies also show that clinical findings independently associated with death or severe disability are older age, the presence of chronic obstructive pulmonary disease, the absence of corneal and pupillary reflexes, myoclonus, and, to a lesser extent, extensor or absent motor responses to painful stimuli [ 8 - 10 ].
In addition, duration of cardiac arrest greater than 25 minutes, defined as time from collapse to return of spontaneous circulation, is strongly associated with such poor outcomes [ 11 , 12 ] Table 1. The early onset of generalized myoclonic status is an ominous sign, although there is at least one case report of a patient who regained consciousness after successful treatment of the status [ 13 ].
Seizures may contribute to mortality, morbidity, and to increased ICU length of stay. In addition, most agree that a neurologic assessment-based prognosis of patients should be considered unreliable for at least the first 72 hours after the arrest, and particularly for those patients receiving therapeutic hypothermia [ 14 ].
Some have also raised concerns that subclinical or nonconvulsive status epilepticus may be an important cause of prolonged coma after cardiac arrest.
But electroencephalograms EEGs obtained from patients admitted alive but comatose after OHCA found only two patients with EEG evidence of generalized myoclonic status without clinical manifestations [ 15 ].
Cardiac arrest and loss of spontaneous circulation causes global cerebral ischemia. Molecular markers of neuronal distress might be expected to be elevated in proportion to the severity of ischemia, and thereby reflect the likelihood of prolonged coma.
Amaraz et al. There is some preliminary evidence that NSE may be unreliable as a predictor of poor outcome when patients have been treated with hypothermia, however. NSE serum levels obtained from 12 to 36 hours after the arrest also have been found to be predictive of 6-month outcomes for patients with in-hospital cardiac arrest [ 19 ].
SB is a relatively non-specific biomarker of neuronal distress, and serum levels are elevated in a variety of stress related conditions. Threshold levels of serum SB at hours after OHCA have been identified that predict moderate to severe memory impairment.
The relationship between the clinical manifestations of hypoxic-ischemic encephalopathy following cardiac arrest, and anatomic brain injury, is not entirely clear. In some cases at least, prolonged coma or vegetative state may be more due to a disruption of cerebral physiology than to anatomic injury.
In one post-mortem study of 41 patients who fulfilled standard clinical criteria for brain death prior to discontinuation of life-support measures, only mild histologic change was present in one-third of the patients, though it should be noted that only two of these patients had cardiac arrest as their primary diagnosis — the rest were traumatic brain injury [ 23 ].
No distinctive neuropathologic features of brain death could be identified. However, there also is evidence for pathognomonic ischemic histopathology. For example, diffuse axonal injury is more common after traumatic brain injury; cytotoxic edema is most common after ischemic stroke; and cortical laminar necrosis is most common after cardiac arrest.
As a result, there is some rationale for using magnetic resonance imaging MRI to identify early ischemic injury and distinguish the cause [ 24 ]. In a study of 80 comatose patients with cardiac arrest who underwent diffusion-weighted MRI, a reduction of the whole-brain apparent diffusion coefficient ADC was a significant predictor of death or severe disability [ 25 ]. The differences in ADC between those with a good versus those with a poor outcome were most prominent in the occipital and parietal lobes.
Others also have found that the largest number of diffusion changes indicative of acute ischemia are seen in patients who die, and such changes are most common in the parietal lobes [ 26 ].
Diffusion-weighted MRI-based ADC thresholds for recovery of function and survival were defined in a very recent paper by Christine et al. Timing of the MRI relative to seizures is very important because seizures can cause reversible changes in the ADC map that are not related to prognosis. A recent study of functional MRI also found a correlation between the level of BOLD blood oxygenation-level dependent activation of the primary sensory cortex following stimulation of the palm of the hand, and survival at 3 months [ 28 ].
In particular, the bilateral absence of the N20 potential is a very good predictor of death or persistent vegetative state. The PROPAC study of patients from the Netherlands found that bilaterally absent early cortical responses N20 following stimulation of the median nerve is the most reliable predictor of poor outcome, and especially the likelihood that the patient will not regain consciousness [ 10 ].
However, SSEPs are not very useful for predicting good outcomes, such as who will regain normal or near normal neurologic and cognitive functioning. In one study of 14 patients with coma after cardiac arrest, all 11 patients who had BIS values of zero either died or had severe neurologic deficits at 6 months after the arrest [ 30 ]. Again, however, BIS monitoring was not useful for predicting who would have complete neurologic and functional recovery, and 11 out of 31 patients with BIS values higher than zero died, while 17 had no or minor neurologic deficits 6 months after cardiac arrest.
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