clinical requiring of basic resuscitation - presentation.pptx

The clinical requiring of basic resuscitation procedures and sensitivity of brain cells to the stop of the circulation (hypoxia) Ass. Prof. Nataša Pejanović-Škobić, MD, PhD neurologist Clinic of Neurology, University Clinical Hospital Mostar • It is better to know first aid and not to need it th...

The clinical requiring of basic resuscitation procedures and sensitivity of brain cells to the stop of the circulation (hypoxia) Ass. Prof. Nataša Pejanović-Škobić, MD, PhD neurologist Clinic of Neurology, University Clinical Hospital Mostar • It is better to know first aid and not to need it than to need it and not to know it • A delay… can mean the difference between life and death Chain of survival Time is brain !!! • Failure of the circulation 3 - 5 minutes ➔ irreversible cerebral damage • Chances of successful CPR restoration of spontaneous circulation (ROSC) decreases by 10% with each minute following sudden cardiac arrest Cause of cardiac arrest and emergency system activation • Adults • Ischemic heart disease - AMI- with/or without ventricular fibrillation (> 80%) • Children • Suffocation or choking with hypoxemia or asphyxia. • Ventricular fibrillation is rare in children (only 5-8%) • Trauma CPR outcome • In first 4 minutes – brain damage is unlikely, if CPR started • 4 – 6 minutes – brain damage possible • 6 – 10 minutes – brain damage probable • > 10 minutes – severe brain damage certain • Cells of the brain cortex - most sensitive for the stop of perfusion and oxygenation • Without perfusion and oxygenation ➔ irreversibly damaged after 3-5 minutes Cardiac arrest and brain ischemia • Cardiac arrest induces the cessation of cerebral blood flow, which can result in brain damage • The primary intervention to salvage the brain under such a pathological condition is to restore the cerebral blood flow to the ischemic region • Ischemia is defined as a reduction in blood flow to a level that is sufficient to alter normal cellular function Hiroyuki et al. J Intensive Care. 2016; Cerebral hypoxia Cerebral hypoxia is a form of hypoxia (reduced supply of oxygen), specifically involving the brain When the brain is completely deprived of oxygen, it is called cerebral anoxia There are four categories of cerebral hypoxia, in order of severity: 1. diffuse cerebral hypoxia (DCH), 2. focal cerebral ischemia 3. cerebral infarction 4. global cerebral ischemia Prolonged hypoxia induces neuronal cell death via apoptosis, resulting in a hypoxic brain injury Malhotra R, et al. "Hypoxia induces apoptosis via two independent pathways in Jurkat cells: differential regulation by glucose". American Journal of Physiology. Cell Physiology. 2001. Cerebral hypoxia Cases of total oxygen deprivation are termed "anoxia", which can be hypoxic in origin (reduced oxygen availability) or ischemic in origin (oxygen deprivation due to a disruption in blood flow) Brain injury as a result of oxygen deprivation either due to hypoxic or anoxic mechanisms are generally termed hypoxic/anoxic injuries (HAI). Busl K. M.; Greer D. M. "Hypoxic-ischemic brain injury: pathophysiology, neuropathology and mechanisms". NeuroRehabilitation. 2010. Cerebral hypoxia Hypoxic ischemic encephalopathy (HIE) is a condition that occurs when the entire brain is deprived of an adequate oxygen supply, but the deprivation is not total While HIE is associated in most cases with oxygen deprivation in the neonate due to birth asphyxia, it can occur in all age groups, and is often a complication of cardiac arrest. Busl K. M.; Greer D. M. "Hypoxic-ischemic brain injury: pathophysiology, neuropathology and mechanisms". NeuroRehabilitation. 2010. Cerebral hypoxia • The brain requires approximately 3.3 ml of oxygen per 100 g of brain tissue per minute • Initially the body responds to lowered blood oxygen by redirecting blood to the brain and increasing cerebral blood flow. Blood flow may increase up to twice the normal flow but no more • However, if blood flow cannot be increased or if doubled blood flow does not correct the problem, symptoms of cerebral hypoxia will begin to appear. "Cerebral hypoxia". MedlinePlus Medical Encyclopedia. U.S. National Library of Medicine. 2007 Cerebral hypoxia • Mild symptoms include difficulties with complex learning tasks and reductions in short-term memory • If oxygen deprivation continues, cognitive disturbances, and decreased motor control will result • Continued oxygen deprivation results in fainting, longterm loss of consciousness, coma, seizures, cessation of brain stem reflexes, and brain death "Cerebral hypoxia". MedlinePlus Medical Encyclopedia. U.S. National Library of Medicine. 2007 Cerebral hypoxia • Blood oxygen saturation may be used for hypoxic hypoxia, but is generally meaningless in other forms of hypoxia. • In hypoxic hypoxia 95–100% saturation is considered normal; 91–94% is considered mild and 86–90% moderate • Anything below 86% is considered severe The Maryland Medical Protocols for Emergency Medical Services Providers" Maryland Institute for Emergency Medical Services Systems (2004) Cerebral hypoxia • It should be noted that cerebral hypoxia refers to oxygen levels in brain tissue, not blood • Even in hypoxic hypoxia blood measures are only an approximate guide; the oxygen level in the brain tissue will depend on how the body deals with the reduced oxygen content of the blood The Maryland Medical Protocols for Emergency Medical Services Providers" Maryland Institute for Emergency Medical Services Systems (2004) Sensitivity of brain cells to stop circulation (hypoxia) • Brain tissue is highly sensitive to ischemia, such that even brief ischemic periods in neurons can initiate a complex sequence of events that may ultimately culminate in cell death • However, paradoxically, restoration of blood flow can cause additional damage and exacerbate the neurocognitive deficits in patients who suffered a brain ischemic event, which is a phenomenon referred to as “reperfusion injury.” Hiroyuki et al. J Intensive Care. 2016; Sensitivity of brain cells to stop circulation (hypoxia) • The pathophysiology of post-cardiac arrest brain injury involves a complex cascade of molecular events, most of which remain unknown • Many lines of evidence have shown that mitochondria suffer severe damage in response to ischemic injury. Hiroyuki et al. J Intensive Care. 2016; Sensitivity of brain cells to stop circulation (hypoxia) • Patients who achieve return of spontaneous circulation (ROSC) after out-of-hospital cardiac arrest (OHCA) show significant morbidity and mortality due to the cerebral and cardiac dysfunction that leads to prolonged whole-body ischemia. • This syndrome, called the post-cardiac arrest syndrome (PCAS), comprises anoxic brain injury, post-cardiac arrest myocardial dysfunction, systemic ischemia/reperfusion response, and persistent precipitating pathology • Cardiac arrest is often associated with neurological deterioration. Hiroyuki et al. J Intensive Care. 2016; Mechanisms which might precipitate organ arrest and the dying process Sam David Shemie et al. Front. Cardiovasc. Med., 2018 Mechanisms which might precipitate organ arrest and the dying process • Primary or secondary brain event with cessation of brain function, most often associated with intracranial hypertension and cessation of brain blood flow, leading to apnea, hypoxemia, cardiac arrest and cessation of circulation • Primary or secondary respiratory event causing hypoxemia resulting in cardiac arrest and cessation of circulation to all organs including the brain • Primary or secondary cardiac event resulting in cardiac arrest and cessation of circulation to all organs including the brain Sam David Shemie et al. Front. Cardiovasc. Med., 2018 Hypoxic-Ischemic Brain Injury: Imaging Findings from Birth to Adulthood. Benjamin Y. Huang. RadioGraphics 2008 Questions ? Hypoxia and consequences Ass. Prof. Nataša Pejanović-Škobić, MD, PhD neurologist Clinic of Neurology, University Clinical Hospital Mostar Hiroyuki et al. J Intensive Care. 2016; Hiroyuki et al. J Intensive Care. 2016; Cerebral hypoxia and consequences Cerebral hypoxia is typically grouped into four categories depending on the severity and location of the brain's oxygen deprivation: 1. Diffuse cerebral hypoxia 2. Focal cerebral ischemia 3. Global cerebral ischemia 4. Cerebral infarction Cerebral hypoxia and consequences 1. Diffuse cerebral hypoxia – A mild to moderate impairment of brain function due to low oxygen levels in the blood 2. Focal cerebral ischemia – A stroke occurring in a localized area that can either be acute or transient. This may be due to a variety of medical conditions such as an aneurysm that causes a hemorrhagic stroke, or an occlusion occurring in the affected blood vessels due to a thrombus (thrombotic stroke) or embolus (embolic stroke) 3. Global cerebral ischemia – A complete stoppage of blood flow to the brain 4. Cerebral infarction – A "stroke", caused by complete oxygen deprivation due to an interference in cerebral blood flow which affects multiple areas of the brain Cerebral hypoxia and consequences • Because of their high demand for energy, the nerve cells of the brain are particularly sensitive to lack of oxygen • Although anoxia may produce damage to cells throughout the brain, some areas are more vulnerable than others Cerebral hypoxia and consequences • The cerebral cortex (especially the parietal lobes and occipital lobes), the hippocampus, the basal ganglia and the cerebellum are particularly sensitive to anoxia • Severe anoxic brain injury may occasionally cause damage to the hypothalamus and pituitary gland Cerebral hypoxia and consequences • Damage to the cerebral cortex, the cerebellum and the basal ganglia may lead to limb weakness and disturbances of movement, balance and coordination, spasticity or rigidity, with increased muscle tone Cerebral hypoxia and consequences • Anoxic injury to the basal ganglia may lead to abnormal movements, including tremor, involuntary writhing movements (athetosis) and brief, jerky movements (chorea). Cerebral hypoxia and consequences • The occipital lobe contains the main visual centres and it is particularly susceptible to anoxia, which may cause a loss of visual function referred to as cortical blindness Cerebral hypoxia and consequences • The hippocampus is an important structure for memory function and it is sensitive to anoxic injury. Memory problems are very common following cerebral anoxia and they may be quite severe • Damage to the frontal lobes may lead to disturbances in executive function - the ability to think and reason, to synthesize and integrate complex information and make considered judgements and decisions about what to do in a particular situation Cerebral hypoxia and consequences • Frontal lobe injury may produce changes in personality, including irritability, poor tolerance of frustration, impulsiveness and impairments in social perception and conduct. There may be apathy and lack of insight, as well as intermittent agitation and mood swings, or more sustained periods of depression Hypoxic-Ischemic Brain Injury: Imaging Findings from Birth to Adulthood. Benjamin Y. Huang. RadioGraphics 2008 Hypoxic-Ischemic Brain Injury: Imaging Findings from Birth to Adulthood. Benjamin Y. Huang. RadioGraphics 2008 Hypoxic-Ischemic Brain Injury: Imaging Findings from Birth to Adulthood. Benjamin Y. Huang. RadioGraphics 2008 Hypoxic-Ischemic Brain Injury: Imaging Findings from Birth to Adulthood. Benjamin Y. Huang. RadioGraphics 2008 Hypoxic-Ischemic Brain Injury: Imaging Findings from Birth to Adulthood. Benjamin Y. Huang. RadioGraphics 2008 Cerebral hypoxia and consequences • If there has been very severe anoxic damage to the brain, there may be a transition from coma into a persistent vegetative state (PVS) • In PVS the basic brain functions of breathing spontaneously, maintaining the heartbeat and blood pressure, digesting food and producing urine all continue Cerebral hypoxia and consequences • However, even though there may still be a cycle of sleeping and waking and the eyes may open spontaneously, there is no real evidence of consciousness in any meaningful sense and no response to what is going on in the environment Cerebral hypoxia and consequences • More recently, the possibility of a minimally conscious state has been recognised Cerebral hypoxia and consequences • This is distinct from PVS, because although it is still a state of profoundly altered consciousness, there is minimal but definite evidence of some limited selfawareness or awareness of the surroundings Cerebral hypoxia and consequences • The long-term consequences will depend on the severity of the cerebral anoxia and on how much irreversible damage has occurred in the brain • If there has only been mild or short-lived anoxia, there may well be recovery back to a normal or near normal level of functioning Cerebral hypoxia and consequences • However, if the anoxic injury has been more marked the outcome is less certain and there are likely to be long-term effects, unfortunately Questions ? Basic resuscitation procedures Ass. Prof. Nataša Pejanović-Škobić, MD, PhD neurologist Clinic of Neurology, University Clinical Hospital Mostar HISTORICAL REVIEW • 5000 - 3000 BC - first artificial mouth to mouth ventilation • 1780 – first attempt of newborn resuscitation by blowing • 1874 – first experimental direct cardiac massage • 1901 – man first successful direct cardiac massage in • 1946 – first experimental indirect cardiac massage and defibrillation • 1960 – • 1980 – development of cardiopulmonary resuscitation due to the works of Peter Safar indirect cardiac massage Background • Approximately 700,000 cardiac arrests per year in Europe • Outcome: • Survival to hospital discharge present in approximately 10 - 14% • Bystander CPR = vital intervention before arrival of emergency services • Early resuscitation and prompt defibrillation (within 1-2 minutes) can result in >60% survival CPR = CPCR Cardio Pulmonary Cerebral Resuscitation Diagnosis of cardiac arrest BLS • Basic life support (BLS) is a level of medical care which is used for victims of life-threatening illnesses or injuries until they can be given full medical care at a hospital. It can be provided by trained medical personnel, including emergency medical technicians, paramedics, and by qualified bystanders Before starting CPR, check: • Is the environment safe for the person? • Is the person conscious or unconscious? • If the person appears unconscious, tap or shake his or her shoulder and ask loudly, "Are you OK?" • If the person doesn't respond and two people are available, have one person call 911 or the local emergency number and get the AED, if one is available, and have the other person begin CPR • If you are alone and have immediate access to a telephone, call 911 or your local emergency number before beginning CPR. Get the AED, if one is available • As soon as an AED is available, deliver one shock if instructed by the device, then begin CPR ALS • Advanced Life Support (ALS) is a set of lifesaving protocols and skills that extend Basic Life Support to further support the circulation and provide an open airway and adequate ventilation (breathing) Compressions: Restore blood circulation • Put the person on his or her back on a firm surface • Kneel next to the person's neck and shoulders • Place the heel of one hand over the center of the person's chest, between the nipples. Place your other hand on top of the first hand. Keep your elbows straight and position your shoulders directly above your hands Compressions: Restore blood circulation • Use your upper body weight (not just your arms) as you push straight down on (compress) the chest at least 2 inches (approximately 5 centimeters) but not greater than 2.4 inches (approximately 6 centimeters). Push hard at a rate of 100 to 120 compressions a minute. • If you haven't been trained in CPR, continue chest compressions until there are signs of movement or until emergency medical personnel take over. If you have been trained in CPR, go on to opening the airway and rescue breathing. Airway: Open the airway • If you're trained in CPR and you've performed 30 chest compressions, open the person's airway using the head-tilt, chin-lift maneuver. Put your palm on the person's forehead and gently tilt the head back. Then with the other hand, gently lift the chin forward to open the airway Breathing: Breathe for the person • Rescue breathing can be mouth-to-mouth breathing or mouth-to-nose breathing if the mouth is seriously injured or can't be opened • With the airway open (using the head-tilt, chin-lift maneuver), pinch the nostrils shut for mouth-to-mouth breathing and cover the person's mouth with yours, making a seal • Prepare to give two rescue breaths. Give the first rescue breath — lasting one second — and watch to see if the chest rises. If it does rise, give the second breath. If the chest doesn't rise, repeat the head-tilt, chin-lift maneuver and then give the second breath. Thirty chest compressions followed by two rescue breaths is considered one cycle. Be careful not to provide too many breaths or to breathe with too much force Breathing: Breathe for the person • Resume chest compressions to restore circulation • As soon as an automated external defibrillator (AED) is available, apply it and follow the prompts. Administer one shock, then resume CPR — starting with chest compressions — for two more minutes before administering a second shock. If you're not trained to use an AED, a 911 or other emergency medical operator may be able to guide you in its use • Continue CPR until there are signs of movement or emergency medical personnel take over Drugs used in CPR • Atropine – can be injected bolus, max 3 mg to block vagal tone, which plays significant role in some cases of cardiac arrest • Adrenaline – large doses have been withdrawn from the algorithm. The recommended dose is 1 mg in each 3-5 min. • Vasopresine – in some cases 40 U can replace adrenaline • Amiodarone - should be included in algorithm • Lidocaine – should be used only in ventricular fibrillation Questions ?