More and more heart failure patients are being discharged from the hospital with ventricular assist devices (VADs).
VAD centers should notify local EMS agencies when a patient returns home with one of these devices to ensure responders are properly trained to deal with VAD-related emergencies.
Given our proximity to two major VAD centers - the University of Maryland Medical Center and Johns Hopkins - Baltimore County EMS providers will undoubtedly encounter patients with these devices with some frequency.
There is an excellent review article entitled "Prehospital Assessment and Management of Patients with Ventricular-Assist Devices" in the journal Prehospital Emergency Care (PEC 2013;17:223-229).
The Mid-Atlantic Regional Pre-Hospital Mechanical Circulatory Support Task Force 2009 Field Guide contains a FAQ sheet and emergency instructions for each of the devices listed below:
HeartWare HVAD
VentrAssist LVAD
HeartMate II
HeartMate XVE
Thoratec PVAD w/TLC II Driver
Jarvik 2000 FlowMaker
This emergency VAD field guide is available through the University of Maryland Heart Center Mechanical Heart and Lung Support home page found at:
http://www.umm.edu/heart/pdf/mechanical-circulatory-support.pdf
EMS 8 Lt. Barshinger coordinates an online training program to familiarize and educate Baltimore County EMS providers on VADs. Forward your name and email address to jbarshinger@baltimorecoutnymd.gov to register for this online training.
Sunday, June 16, 2013
Saturday, June 15, 2013
BCoFD Medical Director Notification Re: July 1, 2013 MIEMSS Protocol Changes (TRAUMA ARREST)
On June 10, 2013 the Baltimore County Fire Department EMS leadership staff convened for its bimonthly meeting. The EMS staff felt that it was very important to clarify some of the contents contained in the 'Trauma Arrest' protocol update:
o Trauma arrest:
• EMS providers can terminate without medical consult when there are no signs of life and the patient is in asystole
• EMS providers can terminate with medical consult
• Blunt trauma-- when there are no signs of life and the patient is in a rhythm other than asystole with no ROSC despite 15 minutes of EMS CPR and other appropriate treatment
• Penetrating trauma-- when there are no signs of life and the patient is in a rhythm other than asystole and there is no ROSC
o If less than 15 minutes from a trauma center, patient should be transported
o If greater than 15 minutes from a trauma center, provider should consult for orders to terminate
o Trauma arrest:
• EMS providers can terminate without medical consult when there are no signs of life and the patient is in asystole
• EMS providers can terminate with medical consult
• Blunt trauma-- when there are no signs of life and the patient is in a rhythm other than asystole with no ROSC despite 15 minutes of EMS CPR and other appropriate treatment
• Penetrating trauma-- when there are no signs of life and the patient is in a rhythm other than asystole and there is no ROSC
o If less than 15 minutes from a trauma center, patient should be transported
o If greater than 15 minutes from a trauma center, provider should consult for orders to terminate
- With both blunt and penetrating trauma when the patient is in a rhythm other than asystole and there are no obvious signs of death, priority should focus on MINIMAL ON-SCENE TIME and RAPID TRANSPORTATION to the receiving trauma center.
- Unless transport is delayed (i.e. an appropriate aviation request with prolonged MSP trooper ETA, heavily entrapped patient), on-scene time should always be kept to a minimum. On-scene time goal should be always be less than 10 minutes. Even after extrication (regardless of time required to extricate the patient), the patient should be transported immediately, without delay, and emergency care provided while enroute to the receiving trauma center.
- Blunt and penetrating trauma patients in cardiac arrest without obvious signs of death should be treated and transported rapidly to a trauma center. Providers should not remain on-scene to perform CPR or any other resuscitative measures for 15 minutes prior to transportation - the patient should be transported immediately and resuscitated enroute to the trauma center.
- Even if 'great than 15 minutes from a trauma center', transport immediately, and resuscitate enroute.
- Once treatment and transportation is initiated for patients in traumatic cardiac arrest, treatment should be continued to the receiving hospital and care should be transferred to the receiving facility. Termination of resuscitative efforts during transport should never occur.
- And a reminder: patients with isolated penetrating trauma do NOT require spinal immobilization - they DO require immediate and rapid transportation to the receiving trauma center.
- And finally: when in doubt, obtain a trauma consult.
BCoFD Medical Director Notification Re: July 1, 2013 MIEMSS Protocol Changes (MEDICAL ARREST)
On June 10, 2013 the Baltimore County Fire Department EMS leadership staff convened for its bimonthly meeting and made the following decision regarding EMS field operations as it pertains to medical cardiac arrest:
Termination of Resuscitation
o Exclusions: Arrest secondary to hypothermia/submersion, pregnant patient, patient not reached 18th birthday
o Medical arrest:
• EMS providers can terminate without medical consult when all of the following criteria are met
• Arrest not witnessed by EMS provider
• Non-shockable rhythm (AED), or manual monitor with asystole or PEA
• No ROSC despite 15 minutes of EMS CPR and other appropriate treatment
• EMS providers can terminate with medical consult if no ROSC despite 15 minutes of EMS CPR and other appropriate treatment in the presence of a shockable rhythm or an arrest witnessed by an EMS provider
- With regard to MEDICAL cardiac arrests, all providers must continue to obtain medical consultation prior to termination of resuscitation - even if there is no ROSC despite 15 minutes of EMS CPR and other appropriate treatments - regardless of the cardiac rhythm.
- This Baltimore County EMS specific directive is contrary to the bolded item highlighted in the new July 1, 2013 MIEMSS protocol update copied below.
- The new July 1, 2013 MIEMSS protocol allows the EMS provider to independently terminate resuscitation without consultation after 15 minutes of EMS CPR and treatment for patients that meet the three criteria of 1. arrest not witnessed by EMS provider; 2. non-shockable rhythm (AED) or manual monitor showing aystole or PEA; and 3. no ROSC despite 15 minutes of EMS CPR. In Baltimore County we will obtain medical consultation at 15 minutes (or sooner based on the clinical situation) for EVERY medical cardiac arrest where termination is being contemplated - regardless of cardiac rhythm.
- Medical consultation prior to termination of resuscitation will help ensure our providers have rendered all appropriate treatments and that the decision to terminate efforts is completely appropriate. In addition, medical consultation prior to termination of resuscitation in the presence of family members or bystanders often makes the act of stopping resuscitative efforts more acceptable to those parties as it shows we have done everything possible up to and including consultation with a base station physician.
- Termination of resuscitation during transportation of the patient should rarely and probably never occur. This can be prevented by resuscitating the medical arrest patient in the place they are found and obtaining medical consultation PRIOR to initiation of transportation.
- Baltimore County EMS providers are reminded that "medical consultation may be obtained at any time for any patient". When in doubt, consult.
Termination of Resuscitation
o Exclusions: Arrest secondary to hypothermia/submersion, pregnant patient, patient not reached 18th birthday
o Medical arrest:
• EMS providers can terminate without medical consult when all of the following criteria are met
• Arrest not witnessed by EMS provider
• Non-shockable rhythm (AED), or manual monitor with asystole or PEA
• No ROSC despite 15 minutes of EMS CPR and other appropriate treatment
• EMS providers can terminate with medical consult if no ROSC despite 15 minutes of EMS CPR and other appropriate treatment in the presence of a shockable rhythm or an arrest witnessed by an EMS provider
Monday, June 3, 2013
SpMet
The other day a DO called and advised me that SpMet functionality has been added to the LP15 monitors on the cars. His question was - what is the clinical significance of SpMet? And away we go . . .
What is methemoglobin (Met-Hb)? (I am going to abbreviate hemoglobin as Hb here forward)
Met-Hb: an altered state of Hb in which the FERROUS (Fe 2+) irons of heme are oxidized to the FERRIC (Fe 3+ state). (The heme portion of the Hb molecule is were oxygen binds).
FERRIC Hb CANNOT bind oxygen.
When there is a lot of FERRIC Hb around, the remaining 'good' FERROUS Hb has a HIGHER affinity for oxygen - that is - the remaining 'good' Hb will not let go of the oxygen it is carrying and oxygen delivery to the tissues is further impaired (if you have studied human physiology, this results in the oxygen dissociation curve shifting to the LEFT).
What is the net effect of Met-Hb formation (increasing Met-Hb levels compared to normal Hb) in the bloodstream?
The patient becomes functionally anemic. Oxygen delivery to the tissues and organs becomes even more impaired in that the remaining 'normal' Hb won't let go of the oxygen it is carrying.
Do normal healthy individuals produce Met-Hb?
Yes. We auto-oxidize some of our Hb (from ferrous to ferric form) every day and maintain a steady-state level of about 1% Met-Hb.
What is the disease state know as methemoglobinemia?
There are actually 2 types of methemoglobinemia: CONGENITAL and ACQUIRED.
What is congenital methemoglobinemia?
As the name implies, it is a genetic disease - the patient is born with the condition. In congenital methemoglobinemia the patient can have Met-Hb levels as high as 40% (of total Hb). Most of these patients, despite having a high SpMet reading will be asymptomatic. They may have a headache or complain of easy fatigability. These patients will be chronically cyanotic (bluish discoloration of the skin and mucous membranes).
What is acquired methemoglobinemia?
This is what we are on the look-out for. It is a rapid increase in Met-Hb levels. Oxygen binding and oxygen delivery to the tissues is acutely impaired and the patient becomes rapidly cyanotic and symptomatic. Early symptoms include headache, fatigue, dyspnea, and lethargy. As Met-Hb levels rise, respiratory depression, decreased LOC, shock, seizures, and death can occur.
What medications or exposures can cause (acute) acquired methemoglobinemia?
2. The mother of a 27-year-old HIV positive patient calls 911 after she finds her son unconscious on the couch in his downstairs apartment. He was recently started on all of his HIV medications 4 weeks ago after being discharged from a local hospital where he was treated for pneumonia. He has been on Truvada, Kaletra, zidovudine, dapsone, and azithromycin for only the past 4 weeks. His skin is cool, he appears pale with some bluish discoloration about his lips and fingers, and he is minimally responsive. Room air Spo2 is 86%. SpMet is 14%. SpCO is 21%. Upon starting an IV, the paramedic comments that the blood has a 'chocolate' appearance. Even after the 100% NRB face mask was on the patient's face for 10 minutes, the Spo2 still read 86%. An engine crew is called to evaluate the elevated SpCO reading and gets no CO readings on their meter. The mother who lives in the home has no symptoms.
A few caveats about SpMet on the LP15 monitor:
SpMet levels > 20% are associated with clinical symptoms. However, the SpMet measurement range on the LP15 Masimor Rainbow sensor is only 0-15%. It is normal to have an SpMet reading of 1-2%. Anything above 3% with the right clinical scenario, drug exposure, or toxic exposure is abnormal and should heighten your suspicion for methemoglobinemia. Very sick patients can have as high as 40-70% Met-Hb in their blood - but again - the SpMet probe will only read up to 15%.
Elevated SpMet levels can give you a FALSE HIGH SpCO level. The LP15 SpCO measurement range is 0-40%. A CO meter can be used to verify absence of detectable atmospheric CO readings. Again, you need to use common sense here and look at your environment and the clinical situation. A patient at an urgent care center in a confined space small examination room surrounded by multiple asymptomatic care givers who is turning blue and did not have respiratory complaints a few minutes ago probably has methemoglobinemia and not CO toxicity.
Elevated SpMet levels can give you FALSE LOW SpO2 level. It is very common for the SpO2 to sit in the mid 80% range and not change with O2 administration. The bottom line - give all of these patient's high flow oxygen.
Is there anything we can do to treat suspected methemoglobinemia in the field?
ABCs. High flow O2 +/- intubation. IV. ECG. SpO2. SpMet. FS. Good history. Get med list. Consult. Communicate your suspicion during consultation. Rapid transport to the ED.
Think about at risk patients and the more common offending drugs: HIV, travel to areas with malaria, industrial chemicals, dapsone, sulfa drugs.
It is important to try to identifying and remove the patient from the offending agent (this is where your history and observation of the scene will be important).
Try to get an updated and accurate list of medications (including over the counter meds) as this will often contain the offending agent.
Rapid transport to the ED (for definitive treatment with administration of methylene blue 1-2 mg/kg IV).
Am I ever going to see this?
In an article from JAMA (April 2013) the overall prevalence of methemoglobinenmia during or after hospital procedures was only 0.035%. The medical literature is dotted with case reports of methemoglobinemia in every age group with every type of exposure I listed above. Masimo has the following bold statement on its website:
What is methemoglobin (Met-Hb)? (I am going to abbreviate hemoglobin as Hb here forward)
Met-Hb: an altered state of Hb in which the FERROUS (Fe 2+) irons of heme are oxidized to the FERRIC (Fe 3+ state). (The heme portion of the Hb molecule is were oxygen binds).
FERRIC Hb CANNOT bind oxygen.
When there is a lot of FERRIC Hb around, the remaining 'good' FERROUS Hb has a HIGHER affinity for oxygen - that is - the remaining 'good' Hb will not let go of the oxygen it is carrying and oxygen delivery to the tissues is further impaired (if you have studied human physiology, this results in the oxygen dissociation curve shifting to the LEFT).
What is the net effect of Met-Hb formation (increasing Met-Hb levels compared to normal Hb) in the bloodstream?
The patient becomes functionally anemic. Oxygen delivery to the tissues and organs becomes even more impaired in that the remaining 'normal' Hb won't let go of the oxygen it is carrying.
Do normal healthy individuals produce Met-Hb?
Yes. We auto-oxidize some of our Hb (from ferrous to ferric form) every day and maintain a steady-state level of about 1% Met-Hb.
What is the disease state know as methemoglobinemia?
There are actually 2 types of methemoglobinemia: CONGENITAL and ACQUIRED.
What is congenital methemoglobinemia?
As the name implies, it is a genetic disease - the patient is born with the condition. In congenital methemoglobinemia the patient can have Met-Hb levels as high as 40% (of total Hb). Most of these patients, despite having a high SpMet reading will be asymptomatic. They may have a headache or complain of easy fatigability. These patients will be chronically cyanotic (bluish discoloration of the skin and mucous membranes).
What is acquired methemoglobinemia?
This is what we are on the look-out for. It is a rapid increase in Met-Hb levels. Oxygen binding and oxygen delivery to the tissues is acutely impaired and the patient becomes rapidly cyanotic and symptomatic. Early symptoms include headache, fatigue, dyspnea, and lethargy. As Met-Hb levels rise, respiratory depression, decreased LOC, shock, seizures, and death can occur.
What medications or exposures can cause (acute) acquired methemoglobinemia?
- Benzene derivatives: common industrial chemical, also a principal product of combustion of PVC (polyvinyl chloride)
- Chloroquine: a drug used for malaria treatment and prophylaxis
- Dapsone: a drug used to treat PCP pneumonia (which primarily affects patients with HIV/AIDS),
- Local anesthetics (benzocaine, lidocaine):
- Metoclopramide (Reglan)
- Napthoquinone: found in diesel exhaust particles
- Napthalene: was once the primary ingredient in moth balls
- Nitrites
- Amyl nitrite: component of the Lily Cyanide antidote kit, abused as "poppers"
- Nitroglycerin: an old friend
- Nitric oxide: this is NOT nitrOUS oxide = laughing gas; nitric oxide is used mostly in the ICU setting for patients with severe pulmonary hypertension and ARDS in the setting of right ventricular failure
- Phenacetin: used to be a component of Vicks, used to be sold in pill form as an anti-pyretic, US FDA ordered the drug to be removed from all substances in 1983 due to carcinogenic and kidney damaging properties
- Phenazopyridine: aka Pyridium - a urinary tract analgesic
- Primaquine: a drug used to treat PCP pneumonia and malaria
- Sulfonamides: most medications with contain 'sulfa'
OK. So that is a long list. What are some examples of typical clinical scenarios where I might encounter a patient with acute/acquired methemoglobinemia?
Here are a few clinical examples:
1. You are dispatched to a local urgent care center where a patient has developed acute onset respiratory distress. The patient presented to the urgent care center 30 minutes ago with complaints of a sore throat and fever. The patient did not have any respiratory distress. The doctor discovered an abscess on the right tonsil. He arranged for the patient to be transported by private ambulance to the University Medical Center for drainage of the abscess by an ENT physician. Up to this point, the patient was not having any respiratory distress whatsoever. In the meantime, in an effort to make the patient feel better, he sprayed the back of the oropharynx with Hurricaine Spray. Within a few minutes the patient developed generalized cyanosis, respiratory distress, and decreased LOC.
2. The mother of a 27-year-old HIV positive patient calls 911 after she finds her son unconscious on the couch in his downstairs apartment. He was recently started on all of his HIV medications 4 weeks ago after being discharged from a local hospital where he was treated for pneumonia. He has been on Truvada, Kaletra, zidovudine, dapsone, and azithromycin for only the past 4 weeks. His skin is cool, he appears pale with some bluish discoloration about his lips and fingers, and he is minimally responsive. Room air Spo2 is 86%. SpMet is 14%. SpCO is 21%. Upon starting an IV, the paramedic comments that the blood has a 'chocolate' appearance. Even after the 100% NRB face mask was on the patient's face for 10 minutes, the Spo2 still read 86%. An engine crew is called to evaluate the elevated SpCO reading and gets no CO readings on their meter. The mother who lives in the home has no symptoms.
A few caveats about SpMet on the LP15 monitor:
SpMet levels > 20% are associated with clinical symptoms. However, the SpMet measurement range on the LP15 Masimor Rainbow sensor is only 0-15%. It is normal to have an SpMet reading of 1-2%. Anything above 3% with the right clinical scenario, drug exposure, or toxic exposure is abnormal and should heighten your suspicion for methemoglobinemia. Very sick patients can have as high as 40-70% Met-Hb in their blood - but again - the SpMet probe will only read up to 15%.
Elevated SpMet levels can give you a FALSE HIGH SpCO level. The LP15 SpCO measurement range is 0-40%. A CO meter can be used to verify absence of detectable atmospheric CO readings. Again, you need to use common sense here and look at your environment and the clinical situation. A patient at an urgent care center in a confined space small examination room surrounded by multiple asymptomatic care givers who is turning blue and did not have respiratory complaints a few minutes ago probably has methemoglobinemia and not CO toxicity.
Elevated SpMet levels can give you FALSE LOW SpO2 level. It is very common for the SpO2 to sit in the mid 80% range and not change with O2 administration. The bottom line - give all of these patient's high flow oxygen.
Is there anything we can do to treat suspected methemoglobinemia in the field?
ABCs. High flow O2 +/- intubation. IV. ECG. SpO2. SpMet. FS. Good history. Get med list. Consult. Communicate your suspicion during consultation. Rapid transport to the ED.
Think about at risk patients and the more common offending drugs: HIV, travel to areas with malaria, industrial chemicals, dapsone, sulfa drugs.
It is important to try to identifying and remove the patient from the offending agent (this is where your history and observation of the scene will be important).
Try to get an updated and accurate list of medications (including over the counter meds) as this will often contain the offending agent.
Rapid transport to the ED (for definitive treatment with administration of methylene blue 1-2 mg/kg IV).
Am I ever going to see this?
In an article from JAMA (April 2013) the overall prevalence of methemoglobinenmia during or after hospital procedures was only 0.035%. The medical literature is dotted with case reports of methemoglobinemia in every age group with every type of exposure I listed above. Masimo has the following bold statement on its website:
"Acquired Methemoglobinemia is fairly common and causes morbidity and mortality in both the inpatient and outpatient settings. Acquired methemoglobinemia is often unrecognized and thus untreated."
Dr. Rachel Ash-Bernal
and other researchers at Johns Hopkins Hospital
and other researchers at Johns Hopkins Hospital
Acquired methemoglobinemia is probably not as common as Masimo would like you to think it is. The statement is correct, however, in that you have to have your feelers up for this condition when you respond to a doctor's office, outpatient surgery center, or any health care facility as it is more likely to occur in these settings.
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