drive is responsible for 90% of our drive to breathe.
The goal of hyperventilating or the increased rate of breathing is to reduce the amount of carbon dioxide that accumulates and to restore normal levels of oxygen as a result of low oxygen states, such as when Hal stopped breathing for approximately 90 seconds. High levels of carbon dioxide and low oxygen states cause the bloodstream to become acidic, which is bad for the body. When there are low oxygen states in the body, the cells cease to produce ATP, the chemical energy storage battery system needed to keep us going.
When the chemoreceptors in the brain stem responsible for breathing and the systems responsible for arousal are suppressed or damaged, the will to breathe is reduced or completely suppressed. To ensure survival, an organism must rely on mechanical means to continue breathing, hence the need for ongoing mechanical ventilation (ventilator or breathing machine) in persons with severe TBI, where there is suppression of the chemoreceptors in the brain stem. Patients who are unable to restart their breathing due to severe TBI (causing damage to the hypercarbia chemoreceptors centers in the brain stem) will need external/mechanical or artificial respiratory support, such as mouth-to-mouth resuscitation or with an ambu-bag or ventilator. It should be noted that in Hal’s case, he was spontaneously hyperventilating after he came to himself.
These measures are critical to preserve brain function in severely brain-injured victims and avoid a cascade of further injury.
Another system that was important in Hal’s case was the RAS, located at the back of the brain stem (midbrain and pons), which allows for arousal and unconsciousness. This system was also temporarily injured due to Hal’s concussion, but within 90 seconds after injury, he was aroused from his state.
Addressing the issue of blood supply
Mario (Case #1) experienced a common phenomenon that is seen in individuals with severe TBI called bradycardia. Bradycardia is the slowing down of the heart rate, usually to a level that impairs blood flow. Bradycardia in TBI is caused when there is an expanding mass in the brain, causing increased intracranial (inside the skull) pressure. The increased pressure in the brain caused the stimulation of the vagus nerve, which ultimately slowed down the heart rate. The vagus nerve originates in the brain stem (lower portion of the brain), and by its connection to the heart, it can influence the rate and extent of heart muscle contractility. When the heart rate is slow, it means the pumping capacity of the heart is reduced, and blood supply to the brain and other organs becomes compromised. In the normal human brain, cerebral blood flow (CBF) is approximately 50–60 cc/100 g/minute. When CBF drops between 20–30cc/100g/min, there is a loss of electrical activity due to diminished production of energy. Neuronal cell death occurs when the CBF falls below 10 cc/100g/min. (Bullock 1996) Low blood pressure and blood flow ultimately cause diminished tissue perfusion, which can be caused by bleeding, cardiac arrest, slow or irregular heart rate, diminished ability of the heart to pump (heart failure), medications, infections, and the lack of fluid intake.
Addressing increase intracranial pressure
While Mario was given drugs to speed up his heart and increase his blood pressure, relieving the intracranial pressure in the brain was the only assured way to gain control of the low heart rate (bradycardia) and prevent the continuous dropping of his heart rate and blood pressure in the period following his injury.
| Image # 7 – Vagus nerve ICP and the heart |
As a result, the next intervention to preserve the brain was performing a craniectomy to give the brain room to expand and reduce the pressure. Given the restricted space within the skull, there was not much room for the brain to accommodate the swelling. The increased pressure (increased intracranial pressure or increased ICP) was caused by massive swelling in the brain. Increased ICP was also the result of a subdural hematoma (bleeding in the space between the covering of the brain called the dura and the brain itself), causing the brain to shift from the right to left. The shift was due to the “mass effect,” i.e., the subdural hematoma caused it. Increased ICP results in diminished blood supply and oxygen to the brain cells, as the heart has to pump blood into a high-pressure system and has to work harder to do so. Mario’s emergency craniectomy was lifesaving, as it helped to mechanically relieve the pressure in the brain ultimately eliminating the bradycardia and allowing for the restoration of blood supply to the brain. In this case, the goal was to preserve nerve cells by mitigating further cell death. His heart rate and blood pressure improved to normal levels following the craniectomy as the vaso-vagal response caused by the vagus nerve stimulation ceased, and the additional work required by the heart to pump blood into a high-pressure system was reduced.
A review of the literature performed by Barthelemy et al. and published in World Neurosurgery showed decreased mortality (death) and improved outcomes in patients aged 50 and under when decompressive craniectomies were performed in less than 5 hours following TBI (Barthelemy 2016).
For persons with more severe injuries such as a TBI, where hemorrhaging causes the mass effect (pressing on other brain structures), an emergency craniectomy (removal of portion of the skull) or craniotomy (opening of skull) for the removal of blood products or a craniostomy, creating a hole for the placement of a catheter in the ventricular (fluid channel in the brain) can result in the reduction or elimination of increased intracranial pressure in the brain. These measures, if implemented in a timely manner, can reduce or eliminate cellular edema and cell death in the brain and preserve brain hierarchical organization.
Neuroprotection through primary and secondary prevention
You must have heard, “An ounce of prevention is better than a pound of cure”. Our ability to preserve the brain hierarchical organization starts with measures to prevent and mitigate injury in the first instance. Such preservation and prevention of injury are called primary prevention. In this fight, prevention is our first line of defense. Primary prevention includes safety education and prevention measures, such as the use of helmets and seat belts, the development of safer cars, and regulatory policies that promote personal safety and the safety of others to avoid injury or to mitigate the severity of any injury. Drunk driving, seatbelt, and helmet laws have heightened standards for safer cars and reduced the number of traffic accidents over the years. These laws have increased the chance of surviving an accident and preserving brain organization.
Primary prevention related to the wearing of helmets to really protect American football players was not established until 1973 by the National Operating Committee on Standards for Athletic Equipment (NOCSAE) (Clarke 1979).
Shortly thereafter, in 1976, rules for leading with the head when blocking and tackling were established. After helmet standards were adopted, fatalities dropped by 74%, decreasing head injuries from 4.5/100,000 to 0.69/100,000. So yes, contrary to popular beliefs, better helmet technology can make a difference (Levy 2004).
In the state of Florida, there was a time when helmet laws were fully enforced. Effective July 1st, 2000, Florida’s Universal Helmet Law was amended to exclude riders ages 21 and older with insurance coverage of at least $10,000. I still cannot fathom how legislators could respond to the pressures of financial gain in this way. Word on the street has it that the short-sighted legislators in Florida felt threatened that bikers would pull out of the famous “bike week” during which riders from all over the world came to Florida and pour a significant amount of dollars into the state’s coffers. A study by Kyrychenoko and McCartt in 2006 showed that helmet use declined from almost 100% in 1998 when the helmet law was fully in effect to 53% when the law was amended. The rates of death from motorcycle crashes in Florida before the law changed (1998–1999) was 30.8 per 1000 crash, and that changed to 38.8 deaths per 1000 crash between 2001 and 2002 after the law was changed (Kyrychenko 2006).
In this period, in the trauma center at Jackson Memorial Hospital, we saw a decline in the number of motorcyclists
