Rounds October 2015

Sheila Silva and Trauma Update Update from the State

Safer IntubationAvoiding Disaster after Intubation

OxygenMiscellaneous

Update From the State

• SPW’s • 1. Sepsis, • 2.BLS LMA with CCR , • 3.Surgical Cricothyroidotomy to replace Cric Kits,

Epi Kits, • 4.TXA and Multiple Trauma. • These are all special project waivers and are NOT

in the state treatment protocols, they are waivers

Sepsis SPW

• Basically the medics will draw blood for a serum lactate level and if it is > 2 the protocol calls for administering 2 liters of saline. The waiver may prove very useful for alerting the hospital that they have a septic patient en route. We will rarely have the time to give 2 liters of fluid in our area.

BLS LMA ,Supraglottic Airway

• With cardiac arrests in Dracut ,Patriot ambulance has applied for waiver to use LMA’s for the airway . The emphasis will remain on chest compressions and CCR. They want to use a supraglottic airway to replace the OPA feeling that it is safer and more effective.

EPI Kits

• The cost of Epipens has skyrocketed and Pro Ems has proposed a way to markedly decrease the cost of epi and still make the likelihood of administering IV epi very unlikely. Basically they are purchasing a kit from Seattle at $5 per kit [ versus $700 for epi pens] . The needles on the epi syringe are NOT REMOVABLE and the IV tubing is needless. There may be an increase in the risk of needle stick exposures .

TXA and Trauma

• This project is one I am very interested in pursuing. It is low cost and almost certainly will save lives. It is currently approved for use by St Lukes Hospital, in conjunction with the New Bedford Fire Department.

• Tranexamic acid is a cheap generic medication that has been in use for many years. It inactivates plasmin which lyses clots and thus it helps to allow the body to clot after major trauma when patients are bleeding out.

TXA Continued• There are 3 major studies. Crash 2 from Europe with 20,000

patients and a decrease in mortality of 1.5 % with no significant adverse effects . In those patients with a BP of 75 or less the decrease was 15 %.

• The Matters study from the US military experience in Afghanistan with 900 combat injuries and massive hemorrhage with a 7x increase in survival !

• There was also a study on pediatric trauma patients in Afghanistan from a US military hospital that showed a 3x increase in survival . The drug is helpful when given in the first hour and probably harmful when given more than 3 hours after the trauma.

TXA Cont’d

• There is a study ongoing in the US in Ohio and thus far it appears to be working.

• Researchers using the available data have estimated that we could save 4,000 victims of trauma per year in the US if we were using this drug.

• The WHO [not the rock group] has recently added this rx to the list of essential drugs that every health care system should have.

Update on Toxicology

Reduced Nicotine Cigarettes

• In a recent NEJM article a study was discussed on the use of low nicotine cigarettes and it seems likely that if we move in that direction we can markedly decrease the number of people who smoke.

• “People smoke for the nicotine and die from the tar”

• “Smoking kills half the people who engage in it long term” [per the CDC] . We can expect 20 million Americans to die prematurely from smoking if they continue .

Proposal on IVDA

• Governor Baker has proposed that hospitals have the authority to hold addicts against their will for 3 days and evaluate whether to file a section 35 that will mandate 90 days of rx.

Bath Salts

• Derivatives of cathinone . Low doses produce euphoria , higher doses result in tachycardia , hallucinations, delirium, hyperthermia, psychosis rarely death. The drugs are available over the internet and at head shops and even gas stations. Think of them as “legal cocaine, amphetamines and ecstasy”. Snorting is the most common method of use, although they are injected and taken by mouth as well.

Bath Salts Cont’d• They are derived from the khat plant from Africa

which has been chewed by the locals for generations.

• The drugs interfere with the reuptake of neurotransmitters serotonin , dopamine, and norepinephrine. They result in an agitated delirium.

• The toxic screen is usually negative and the toxicity may last for a few days!

• The treatment is symptomatic, usually lorazepam 2 mg IM. More may be required and at times Haldol may be needed as well.

Safer Intubation

Preoxygenation and Prevention of Desaturation During Emergency Airway Management

• Based on the article by Scott Weingart and Richard Levitan , Ann. Emerg. Med. 2012:59:165-175

• Patients requiring emergency airway management are at great risk of hypoxemia. They often have lung pathology, increased metabolic demands with fever and anemia, and are at high risk of aspiration. You can minimize the risk of critical hypoxia while securing a tracheal tube rapidly.

ConceptsEmphasis must be on maintaining good oxygenation at all times . Both the O2 saturation and the ETCO2

must be monitored. Pulse oximetry will lag 30-60 seconds and as the sats

are dropping this must be considered. The O2 saturation should not be permitted to drop to < 90 %.Try to get the O2 saturation as high as possible prior

to attempting intubation, if possible.Remember that the key is preventing hypoxia , not

getting in a tube. We are intubating to prevent hypoxia and /or to prevent severe hypoventilation

Oxyhemoglobin Dissociation Curve

Hypoxic below 60% High Risk Below 89%• Weingart SD. AnnEmergMed 2013.

Safer IntubationWhen patients are being intubated the key to decreasing mortality is

avoiding hypoxemia. When the O2 mask is removed the patient is at risk for hypoxia and a respiratory arrest. How can we minimize the chance of

this occurring ?

Concepts cont’d

• Safe Apnea is a term that refers to how long a patient will take to desaturate while they are paralyzed. Obese patients will desaturate more quickly. Sick , anemic, volume depleted patients will desaturate more quickly than normal patients.

• On room air a normal patient will desaturate in 45-60 seconds while paralyzed. They utilize 250 ml of O2 per minute and there are 450 mls of oxygen in the lungs. A non paralyzed patient will use more O2 and will desaturate must faster.

Concepts

• KEY :Delaying the time until the patient will become hypoxic , maximize the oxygen in the blood stream and lungs.

• Positioning• Preoxygenation and Denitrogenation• Positive pressure Devices• Passive Apneic Oxygenation

Position the patient

• Putting the head of the patient up to 20 degrees

• Why? When we are flat it is harder to take a full breath and more of the posterior lung becomes atelectatic. The diaphragms are higher and the total lung volume is less. This will increase the safe apnea time.

Maximize the O2

• We have approximately 5 liters of air in our lungs , only 16 % is oxygen. By getting rid of the nitrogen [over 80 % of the lungs is filled with nitrogen] and filling the lungs with oxygen prior to intubating the patient we can markedly decrease the risk of hypoxemia.

• Preoxygenate the patient . When the Oxygen saturation is up to 100% we need to continue BVM for 3 more minutes to get rid of all the nitrogen and fill the air spaces in the lungs with oxygen , giving us close to 5 liters of oxygen.

Preoxygenation and Denitrogenation• How to maximize the O2 in the lungs prior to

intubation• 1.High Flow O2 via a nasal cannula• 2.Non rebreather mask, crank up the oxygen

as high as possible. • 3.With Tidal Volume breathing [normal

inspirations]

How to give the O2

• A nonrebreather face mask will deliver only 60-70 % O2 when it is set at 15 LPM. If you turn the flow rate up to 30-60 LPM you can deliver 90 % FIO2. A tight seal must be achieved to deliver more than ambient O2, [21 % ] .

• A standard reservoir facemask with theflow rate set as high as possible is the best source of O2

Add a Nasal Cannula

• When we remove the mask to intubate the patient we should always place a nasal cannula and turn the oxygen on the wall to maximum.

• The keys are that the patient has No O2 when the mask is removed and by placing a nasal cannula and turning up the O2, now the oxygen is under pressure and is being forced into the lungs and across the alveoli during your intubation. This will prolong the time it takes to desaturate. They will become hypoxic more slowly.

More Benefits of Nasal O2

• “Nasal O2 boosts the FiO2 ,flushes the nasopharynx, and fills the upper airway with a high concentration of oxygen available for the next breath. Combining nasal and mask oxygen increases the volume of oxygen available for the patient to inspire.” This may decrease CPAP or mask intolerance.

Use Of CPAP or Positive Pressure Devices

• If patients are unable to achieve an O2 sat > 95 % then they are likely to desaturate during your intubation. There are alveoli that are perfused but not ventilated . Open the alveoli with positive pressure to increase the O2 sat.

Apneic oxygenation• This clearly works, article on RSI in Australia

with decreased desaturation times• Tolerance of high flow nasal O2 seen in a study• Remember 3 bits of info :1. get the nitrogen

out of the lungs by maintaining 100 % Sat for 3 minutes , if possible,2. nasal O2 at high flow before the mask removed to intubate the patient, 3. if unable to get sats up use of PEEP or CPAP

NEJM 6/14/2015• Newest study on the use of high flow O2 via nasal

cannula• The study was in 313 patients in ICU’s in France

and Belgium between 2011-2013. • They studied High flow O2 [50L/min] vs mask O2

[>10L/min] vs NIPPV [PEEP 2-10 cm].• Over 90 days the High flow O2 delivered by Nasal

cannula was safest. The mortality was 2 -2.5 higher in the other 2 groups.

• Of interest is that they reported that most patients had relief of their dyspnea within one hour.

Another New Study on NC and O2

• JAMA June 16,2015• They used High Flow 60 L/min O2 by nasal

cannula on postoperative respiratory failure patients versus NIV [BIPAP] and found them to be essentially equivalent for care. Again a study that was longer term and not prehospital.

• The O2 is heated and and humidified• Get used to this concept and begin to use it.

SUMMARY

• Position the patient at 20 Degrees• Tight seal with Non rebreather• Turn Flow rate to maximal• Try to get O2 Sat to 100%• Keep the O2 sat at 100% for 3 Minutes• If Unable to get sat to 100%, Use CPAP• Prior to Intubating, Use a NC at MAX FLOW

Avoiding Disaster After Intubations• Oxygenation: “ Preoxygenate with Nasal Cannulas and a face

mask”, intubate as upright as you can. Try to avoid a high pressure face mask when the patient is in a flat position. Get the head higher than the stomach.

• Try to mimic the minute ventilation of the patient prior to intubation.

• In the severely ill asthma or COPD patient start with 500ml and 6 breaths /min, going slow and allowing the maximal time for expiration. Increase the minute ventilation slowly. “Permissive Hypercapnia” .

• Avoid overinflation, which will lead to gastric distention and vomiting.

Minute Ventilation

• The amount of air a patient breathes in one minute . It is simply the tidal volume x the respiratory rate. Normally it is 7 L/min. With heavy exercise it may exceed 40L/min . The only way we can increase our oxygen is to increase our TV and respiratory rate. Therapeutically we can increase the oxygen concentration or add PEEP [keep alveoli open] .

Minute Ventilation• When patients are experiencing respiratory distress it

may be that they have a problem with obstruction. They cannot get the CO2 out fast enough to bring in more oxygen. If we turn up the O2 that may relieve the problem, if we try to breathe faster than they can get the air out because of obstruction they will have “stacking”, Autopeep. They will have hyperinflation . They run the risk of barotrauma .They may develop a pneumothorax. Also these patients may become severely hypotensive [from decreased cardiac return] . Postintubation hypotension is often due to this .

Oxygen ?

Is oxygen a useful treatment ? High flow, low flow or no flow? What evidence do

we have that it is harmful?

It Is Time

We must use our knowledge of the potential harm from the use of O2 and only use it where it is

indicated. O2 should not be used on patients with chest pain or possible CVA’s unless the O2 sats are

<94 %

Oxygen and Cardiac Harm

• There have been multiple studies that have examined the effects of oxygen and it seems clear that oxygen increase coronary resistance and decreases coronary blood flow. It decreases cardiac output.

Cochrane Database• The Cochrane database review in 2010 and in

2013 reported that there are 4 trials of AMI and O2 that looked at 430 patients. You are more than 3 times more likely to die if O2 is given when you are having an acute MI if the O2 saturation is >than 94 % [you don’t need it ] .

Oxygen in other settings• There is data that high concentrations of oxygen

are harmful to neonates needing resuscitation, and in exacerbations of COPD.

• In a study of 405 patients with an acute exacerbation of COPD in Australia [BMJ 2010] the mortality was more than twice as high with high flow O2 [8-10 LPM] compared to titrated O2 [sat kept between 88-92%].

• Again more is not better. There is no good reason to have an O2 saturation greater than 94%. I would suggest that oxygen should be titrated in almost all situations to <100%.

Oxygen in the Post cardiac arrest setting

• There is good data that after a resuscitation from cardiac arrest that the O2 sat should not be 100%. The AHA recommends that oxygen be used at the lowest level to keep the O2 sat at 94% [or higher ].

Where is the data? • In the Impact study at 120 U.S. hospitals between

2001 and 2005 with 6,326 post cardiac arrest patients and the group that had “hyperoxia” [Pa O2 > than 300 mm] had almost a twofold risk of death compared to those patients who had a “normal oxygen sat” [Pa O2 > than 60mm and < than 300mm]. This data is retrospective , but until there is better data the o2 sat SHOULD NOT BE 100%.

Post Cardiac Arrest and O2•Providers should titrate oxygen during the post-cardiac arrest phase to the lowest level required to achieve an oxygen saturation of >94 %. •This helps to avoid any potential complications associated with oxygen toxicity.

More on O2• Other studies reveal that at cath that coronary

blood flow will decrease by 30 % with 100% FIo2 compared to RA.

• Hyperoxia will decrease cerebral blood flow, shown in a 1988 study.

• These studies make it clear that O2 is a vasoactive drug and that it should be given only to patients who need it…. Per the AHA 2010 guidelines

Oxygen Toxicity

• There is a great deal of animal and human data that high concentrations of oxygen are deleterious, injuring the airways and resulting in tracheobronchitis and diffuse alveolar damage, similar to ARDS.

Why is oxygen harmful?

• High concentrations of oxygen cause damage to airways and pulmonary parenchyma. Erythema and edema of large airways is seen on bronchoscopy as early as 6 hours after high flow O2. High concentrations of oxygen also cause washout of alveolar nitrogen which causes atelectasis of the alveoli. Shunting of blood will result and in older healthy adults shunting as high as 11 % after only 30 minutes of breathing 100 % FIO2 has been seen . This absorptive atelectasis is not quickly reversed. Decrements of up to 20 % of vital capacity can be the result.

The Mechanism for Harm

• Even 1 hour after breathing 28 % FiO2 there is an increase in reactive oxygen species. These oxygen free radicals promote an inflammatory response leading to secondary tissue damage. Those cells exposed to the highest concentration of oxygen are at the highest risk for damage –those cells that line the tracheobronchial tree and the alveoli. These are the cells that manifest the injury. Thus even a short exposure to high flow O2 may be deleterious.

Summary of O2 and Cardiopulmonary Effects

• High flow oxygen is harmful to both the cardiac and pulmonary systems.

• It is harmful to both the pulmonary parenchyma [the alveoli and the tracheobronchial tree] and the cardiovascular system by a decrease in the cardiac output .

Oxygen and Acute MI, CVA and ACS

• The 2010 ACLS guidelines suggest that EMS care include oxygen only if the O2 saturation is < 94 % for all patients with acute MI, CVA and ACS patients.

• The use of oxygen is also suggested for patients with dyspnea, obvious heart failure, or if the oxygen saturation is unknown.

Harm

• “ There is no single threshold of FiO2 defining a safe upper limit for prevention of oxygen toxicity .” [UPTODATE 2011] How long the patient is exposed to a high FiO2 , and the concentration of the oxygen determines how likely the patient is to suffer harm.

Preshock Pauses

• Remember that a preshock pause of <20 seconds is associated with improved survival in cardiac arrests. The less interruption of compressions the better the patient will do. All defibrillators should always be on manual mode . The automatic mode should not be used.

Intranasal Narcan

• Remember it is faster to administer [no IV required], but it less potent . Frequently we need 6-8 mg of narcan for complete reversal of obtundation.

Intranasal fentanyl

• A recent study looked at kids and the use of intranasal fentanyl. 5 Minutes after its use the pain was rated as only half as severe. It works quickly, and it should be kept in mind both for adults and children, especially if an IV is problematic.

Anaphylaxis

• Definition: remember skin plus either upper or lower respiratory involvement with shortness of breath , hypoxemia, wheezes , or stridor .

• OR • Skin or mucosa, plus decreased BP, or

respiratory symptoms, or syncope, or GI symptoms.

Anaphylaxis contd

• The Rx of choice is epinephrine.It should be given in the thigh IM. Do not give it in the arm, do not give it sub Q.

• Benadryl is slow in onset and has no effect on BP, upper airways and lower airways.

• If the BP does not rise with the epinephrine a fluid bolus of 1-2 liters is indicated.