I HAVE NOTICED WHEN GIVING A MECH. VENT PT. A HHN INLINE. THE ICP PRESSURE DROPS APROX BY 8-12. I HAVE LEFT THE BLEED-IN ON ATC AND THE PRESSURES ARE LOWER THAN THAT WITH IT OFF. DOES NOT WORK WITH ALL PTS, SEEMS THE 16-30 Y/O RESPOND BETTER. MY DIRECTOR DID A SHORT STUDY ABG WITH 4-5L BLEED-IN
ABG W/O BLEED IN

SMALL DIFFRENCE IN CO2 LOWER W/BLEED IN

HOPE THIS MIGHT HELP SOMEONE

Ok

Wolf,

Can you tell us exactly which ventilator you were using, mode and settings?

Could it be that the patient was, without the added continuous flow, pulling in volume off the exp. side? I'm trying to find a reason for the increased PaCO2 without the added "flow-by". ? It seems to me you would want to fix that.

Further hyperventilating for reduce PaCO2 has been found to affect outcomes negatively. I don't have the exact references handy, but we had a lecture from an MD last name Manley whom published in some Trauma Journal.

One of the latest issue of SCCM Clinical Currents had a very good article about this (author was Branson I recall).

Found this prior posting I did on RC World archives...

This is actually an area of controversey amongst neurologists. Basically
it's the "Perfusionsists" (raise the systolic BP high enough to "blast
through the high ICP, "damn the torpedoes"), vs. the "ICPers--optimized
hyperventilation camp" (lower ICP such that a more normal BP can then
perfuse the brain).

The problem with the Perfusionist approach, one of them anyway, is that
there is a real increase in ARDS and pulmonary edema. And there is also
cerebral edema which is worsened with increased vascular driving pressures.

The problem with the ICPers approach, the part of using lower PaCO2's to
achieve it anyway, is that it only works where arterial blood is going--the
perfused areas. So O2 delivery is curtailed to the perfused areas causing
them to then also swell later, release evil humors, etc. Kind of like
getting better temporary ABG's in severe ARDS at the cost of using high VTs
and ventilating for normal PaCO2's. The healthy tissue gets whacked in the
quest for better global numbers.

There is actually fairly compelling evidence that reducing the PaCO2 may be
very deleterious. I remember a lecture by a Dr. Manley at SF General in
which he implored us all not to do this, even suggesting that in the future
we may want to even increase the PaCO2....

Brain Tissue Oxygenation during Hemorrhagic Shock, Resuscitation, and
Alterations in Ventilation by Manley, et al in the Journal of Trauma,Injury,
Infection and Critical Care Vol.46 Number 2

They directly measured the cerebral PO2 (PbO2) during shock and under
hyperventilation, hypoventilation, and hyperoxia.

Hyperventilation had a very detrimental effect on PbO2. Hyperoxia had a
marked effect on raising the PbO2, almost a linear one going from RA to 100%
O2. But, hypoventilation was even more effective at raising the PbO2 than
hyperoxia.

It could be that we will eventually be hypoventilating neuro patients in
order to augment cerebral O2 tension. And keeping them on 100% O2 for
awhile no matter what the sat (or even perhaps if they're a "retainer" and
they may already have some protection then).
If an effective, non-hyperventilation, method is found to lower ICP, raising
CO2 levels may be a way to then augment flow through perfused regions of the
brain. ??

Ahh here is the text of that Currents article.

Respiratory Care of the Neurologic Patient

Richard Branson, RRT, FCCM
University of Cincinnati
Medical Center
Cincinnati, Ohio, USA



Jay Johannigman, MD
University of Cincinnati
Medical Center
Cincinnati, Ohio, USA



Lori Shutter, MD
University of Cincinnati
Medical Center
Cincinnati, Ohio, USA

Traumatic brain injury (TBI) is a major cause of disability and death in Western nations and results in healthcare costs of nearly $100 billion annually in the United States. The management of TBI has evolved dramatically in the last decade. This is in part due to improved understanding of events leading to secondary neurologic injury (hypotension, hypoxemia, etc.). Neurointensive care is dedicated to preventing this secondary injury through aggressive monitoring and optimization of variables, which may improve outcome.

Respiratory care and mechanical ventilation of the patient with neurologic injury have evolved from the rather haphazard and injudicious use of hyperventilation to therapy directed at maximizing brain tissue oxygen. The head injured patient also presents a host of other respiratory care challenges to the critical care team including prevention and treatment of pneumonia, airway management and weaning.

Mechanical Ventilation Goals

Traumatic brain injury is often seen in conjunction with pulmonary contusion and other life-threatening injuries. Hypoxemia associated with pulmonary contusion and lung dysfunction has been shown to adversely affect neurologic outcome. Historically, mechanical ventilation in TBI featured hyperventilation to produce hypocarbia, cerebral vasoconstriction and reduce intracranial pressure. However, realization that cerebral vasoconstriction also resulted in cerebral ischemia has caused hyperventilation to fall into disfavor. Neurological injuries due to trauma, stroke, subarachnoid and intracerebral hemorrhages involve complex pathophysiology. Hypoxia, hypotension and associated cerebral ischemia play key roles in both initial and secondary injury. The focus of critical care management of the brain-injured patient revolves around avoiding secondary injuries, which may ultimatelyworsen clinical outcomes. Monitoring intracranial pressure (ICP) and cerebral perfusion pressure (CPP) are standards of care, but they are at best an indirect measure of secondary injury. Recent advances in neuromonitoring devices have introduced the ability to directly measure partial brain tissue oxygenation (PbtO2), thus providing direct information regarding cerebral hypoxia.

PbtO2monitoring presently is accomplished with a Licox system (GMS, Kiel, Germany) using fiberoptic technology. The sensor is 0.8 mm in diameter with a sensing area of 13 mm 2. An additional temperature sensor probe is required to correct PbtO2measurements for temperature variations. The Licox system may be placed in the intensive care unit (ICU) through a burr hole. It uses a multi-lumen bolt system that allows for placement of both sensors through one access,as well as providing stability and reliable positioning. The optimal placement of the catheter should be in a region that is considered salvageable but vulnerable to ischemia.

The brain consumes 15% of the body's cardiac output and 20% of available oxygen to meet its energy demands. This requires a constant cerebral blood flow (CBF) with sufficient oxygen delivery. Brain tissue becomes ischemic with oxygen levels below 15 mm Hg, and tissue infarction occurs at levels below 5 mm Hg. Studies examining the relationship of clinical outcome to PbtO2have shown correlation between duration and severity of low PbtO2values and poor outcome.

Hyperventilation has been commonly used to treat acute elevations in ICP by causing hypocapnic vasoconstriction and reduced intracranial blood volume. The resultant decrease in ICP has been presumed to cause increased CPP and cerebral oxygenation. This concept has recently been questioned, and studies have shown that CBF and PbtO2 actually decrease with hyperventilation, thus potentially leading to secondary tissue ischemia. This supports the concept that use of hyperventilation should be limited to the acute management of cerebral herniation while more definitive ICP treatments are being initiated.

Animal studies suggest that hypoventilation-induced hypercarbia may be effective in optimizing PbtO2. Arterial CO2is a potent cerebral vasodilator,resulting in increased CBF. Hypercarbia also shifts the hemoglobin-O2 saturation curve, thus facilitating O2 delivery into cerebral tissues. This raises the question that permissive hypercarbia may have a role in management of neurologic injuries. (see Respiratory Care of the Neurologic Patient, page 8)T raumatic brain injury (TBI) is a major cause of disability and death in Western nations and results in healthcare costs of nearly $100 billion annually in the United States. The management of TBI has evolved dramatically in the last decade. This is in part due to improved understanding of events leading to secondary neurologic injury (hypotension, hypoxemia, etc.). Neurointensive care is dedicated to preventing this secondary injury through aggressive monitoring and optimization of variables, which may improve outcome.

Despite adequate arterial oxygen saturation, occult cerebral hypoxia may occur in TBI patients. Increased FiO2 has consistently been shown to increase PbtO2, although the mechanism is unclear. Microdialysis studies have suggested an effect on reducing lactate levels thus improving oxidative metabolism. A recent study demonstrated that episodes of cerebral hypoxia were infrequently associated with ICP elevations or CPP decreases. Instead, systemic hypoxia and elevated PEEP were related to cerebral hypoxia. Researchers have also shown that marked oxygen reactivity in the first 24 hours after injury correlates with poorer outcome. It has been suggested that this represents a loss of cerebral vasoregulation and implies a possible prognostic role for O2 reactivity testing. At this time, the optimal level of oxygen therapy is not yet clear, and further studies of hyperoxic therapy are warranted.

The use of elevated FiO2 to meet brain tissue oxygen goals and supranormal PaO2 is in contradiction with the current oxygenation goals in patients with respiratory failure without TBI. Certainly concerns over exposure to elevated FiO2 and the potential for pulmonary oxygen toxicity are warranted. However, in light of the importance of adequate TbO2 in preventing secondary neurologic injury, these concerns must take a backseat to improved cognitive outcomes. Additionally, while pulmonary oxygen toxicity has a sound basis in animals and normal man, the evidence in critically ill mechanically ventilated patients is less compelling.

Risk of Pneumonia

TBI is often associated with loss of consciousness at the accident scene and altered consciousness throughout the hospital course. Alcohol is also a factor in nearly 40% of motor vehicle accidents resulting in TBI. These factors conspire to increase the risk of pneumonia in the mechanically ventilated patient with TBI. While it is tempting to consider this as ventilator-associated pneumonia (VAP), patients with TBI suffer from an early onset of pneumonia, frequently a consequence of aspiration. The TBI patient continues to be at risk in the ICU for the development of pneumonia due to the multiple factors including coma, gastric ulcer prophylaxis and the use of nasogastric tubes.

Bronchard et al recently reviewed 109 patients with TBI over a two-year period to evaluate risk factors for pneumonia. They found that nasal carriage of Staphylococcus aureus on admission, aspiration prior to intubation and barbiturate use were independent risk factors for early onset pneumonia in TBI. They also found important consequences of pneumonia in TBI patients. Patients with early onset pneumonia had lower PaO2/FiO2, more febrile days, more frequent hypotension, and increased intracranial pressures. These factors are known to adversely affect neurologic outcome. Interestingly, these authors also demonstrated a reduced incidence of early onset pneumonia in patients concomitantly treated with antibiotics for orthopedic injuries.

The challenge for the critical care team is to prevent pneumonia through elimination of risk factors, early diagnosis, and early, appropriate antibiotic treatment. Prevention of risk factors in this population is difficult. Selective decontamination of the digestive tract might play a role, and early antibiotic administration could prove useful. However, concerns about the emergence of resistant bacteria cannot be ignored. As with all critically ill patients, strict attention to appropriate airway management principles and hand washing is mandatory.

Effective Airway Management

Tracheostomy has long been used Airway management is an integral component in the care of the TBI patient from accident scene to discharge. At the scene, the ABC's of trauma care take precedence. First responders must establish a patent airway and, if possible, prevent aspiration. Studies report that over half of head injured patients are hypoxemic in the field. This hypoxemia is associated with increased mortality. A recent retrospective study suggests that early endotracheal intubation in the field reverses hypoxemia and improves outcome. Despite the limited number of patients (n=44) in this trial, data indicated that patients with a Glasgow Coma Scale (GCS) of < 8 should be intubated.

Tracheostomy has long been used to facilitate secretion removal, airway management and speed ventilator discontinuation in the TBI patient. The appropriate timing of tracheostomy remains unclear. However, this is often dictated by the severity of illness. In our experience, TBI patients who pass spontaneous breathing trials, but remain at a GCS of 28, benefit from early tracheostomy. Percutaneous tracheostomy is typically done when ventilatory support is minimized (PEEP < 8, FIO2 < 0.50) and neurologic function has stabilized.

Critical care of the TBI injured patient with respiratory failure represents an ongoing challenge for the multiprofessional critical care team. Appropriate care in the field, transfer to a center with neurosurgical expertise, VAP prevention, airway management, sedation, and optimization of mechanical ventilation and TbO2 are hallmarks of good care. The economic and personal losses due to TBI are devastating"”prevention is our best treatment. References are available at SCCM's Web site, www.sccm.org/criticalconnections

BTW, the latest supplement of CCM is all about HFOV.

THE VENT IS A PB840, OR BEAR 1000. THE MODE EITHER AC OR BILEVEL. I KNOW THAT SOME TRAUMA DOCS WANT THE C02 30-35, SOME WANT TO KEEP IT AT 35-40 FOR ICB. WHEN THE ICP STARTS CREEPING UP TO AROUND 25+, THATS APROX WHEN WE WILL START TO TREND ICP'S WITH BLEED-IN, OR WHILE GIVING HHN. IF I NOTICE A DROP IN ICP, I INFORM THE MD AND GO FROM THERE. YOU MISSED UNDERSTOOD ME ABOUT THE PaC02 IT WAS LOWER WITH THE THE 4-5 LITER BLEED-IN. {NOT SURE THE ACT #} I KNOW THAT MORE MDS ARE GOING BACK TO NORMAL PaC02 LEVELS WITH ICB'S. I SEE ALOT OF ICB'S AND WANTED TO SHARE THIS WITH OTHER RRT'S. ITS NOT 100%, BUT IT WORKS SOMETIME...