December 4, 2023

‘Tis the Season

The tones dropped, and dispatch sent you to a private residence where the 40-year-old patient was complaining of a headache and feeling crummy. Having just cleared the ER, you knew it was a busy Sunday shift with many of the beds taken by patients with Influenza A (or B), Covid, RSV, and other viral syndromes. You pulled rank on your partner as you exited your squad and told him to put on a mask, as his flu shot was helpful, but it certainly wasn’t protective against the many viruses running rampant throughout the community.

Your patient explained that they had started feeling ill several days ago but that their symptoms had worsened over the weekend. They had a headache that wouldn’t go away despite their taking ibuprofen. They felt weak and had some nausea and dizziness. They didn’t think they had a fever, but they had been taking the ibuprofen on and off for the last several days. Your patient didn’t have a cough, chest pain, or shortness of breath. They were a little dizzy when they stood up, and you assisted them in walking to the cot. You figured you would start an IV and tank them up with some fluids once in the squad, as they were likely a little dehydrated from a fever and poor intake over the last several days.

Your partner put the patient on the monitor as you started explaining to them that you were going to start an IV and give them some fluids. And then it happened! The monitor started beeping an alarm, and a red box lit up on the display. Your patient’s carbon monoxide level was 28%.  You kicked yourself for having your blinders on and thinking the patient had the flu, a viral infection like “everyone else” in town. You knew it was important to think about all the possible causes for your patient’s presentation before fixing your mind on one single diagnosis, but it’s an easy trap to fall into. Your partner smiled at you as they took off their mask and threw it in the trash. After all, carbon monoxide poisoning isn’t contagious. Fortunately, they reframed from saying, “I told you so,” as they then placed the patient on a high-flow O2 mask.

As the weather turns cold and peoples’ furnaces run continuously, the incidence of CO poisoning increases. Under continuous load furnaces can fail, and small CO leaks can become significant. In this case, the patient was in their house over the weekend, giving them an increased exposure compared to during their work week, when they were often out of the house. 

At lower levels, the symptoms of CO poisoning reflect those of a simple viral syndrome. There are no specific symptoms that clearly distinguish between the two conditions. As the incidence of viral syndromes also increases during the cold weather months, it is easy to see how one could overlook CO poisoning for the much more prevalent viral syndrome. The carboxyhemoglobin level (HbCO%) is the percentage of blood that has carbon monoxide bound to it. The level at which a patient experiences specific symptoms is highly variable between patients. The table below, therefore, is a general guideline for one’s symptoms as a function of their level of CO poisoning.

The gas carbon monoxide (CO) is typically produced as the result of incomplete combustion. Propane, LPG, wood, and coal-burning furnaces and stoves, poorly ventilated fireplaces, sterno cans, space heaters, gas-powered vehicles, portable generators, and other non-electric heaters can all produce carbon monoxide gas. Ideally, the fumes from a furnace are exhausted to the outside. However, a crack in the furnace’s heat exchanger can allow the fumes from combustion to enter the dwelling’s interior air circulation, setting the stage for CO poisoning. As the gas is both colorless and odorless, one can be exposed to CO without even being aware of it.

Once inhaled, the carbon monoxide gas binds to the hemoglobin within the patient’s red blood cells. As more and more of the patient’s hemoglobin binds with carbon monoxide, there is less and less hemoglobin available to carry oxygen to the patient’s body. The body is essentially starved of oxygen. In addition to decreasing the amount of oxygen available to the body, carboxyhemoglobin also impairs many of the normal chemical reactions within the body’s cells. Once the carbon monoxide binds to the hemoglobin within the red blood cells, it forms carboxyhemoglobin, HbCO. Fortunately, carboxyhemoglobin levels can be easily measured non-invasively, i.e., with a clip-on finger sensor. The Masimo Rad-57 ® is a standalone, handheld, carboxyhemoglobin level monitor. It functions as a normal pulse oximeter, measuring a patient’s “oxygen level” (SpO2 reading), as well as measuring the patient’s carboxyhemoglobin level(HbCO level or SpCO%).  

The first and foremost treatment for carbon monoxide poisoning is to exit the environment that has the carbon monoxide gas! This stops ongoing exposure and worsening of the patient’s condition. It also limits the EMS crew’s exposure to the gas. The next step is to place the patient on a high-flow O2 mask to provide them with close to “100%” oxygen. 

When the patient is no longer exposed to carbon monoxide, their body will slowly eliminate that which has already been bound to their hemoglobin.   If the patient is breathing normal fresh air,, they would eliminate ½ of their carbon monoxide load in about 5 hours and 20 minutes.  

Patients who are unconscious, who have markedly elevated HbCO levels, or who have moderate HbCO levels and are pregnant might be treated with hyperbaric oxygen. In this case, the patient is placed into a chamber pressurized to three times the normal atmospheric pressure, with oxygen, so as to reduce their HbCO level to 50% of its initial level in only 23 minutes (14 times faster than fresh air alone).

Seizures would usually be treated with a benzodiazepine medication (e.g., Versed, midazolam). Airway management with an OP/NP airway, SGA, or ETT might be indicated, in addition to ventilation with a bag valve mask. Remember that all patients with an altered mental status require a blood glucose level measurement. EKG and EtCO2 monitoring are also indicated in these patients. Remember that capnography measures EtCO2, which is the patient’s carbon dioxide levels, not their carbon monoxide levels.

Don’t be fooled by a “good” pulse oximetry level in your patient with carbon monoxide poisoning! An EMS clip-on pulse oximeter reads the combined oxygen level (HbO2) and carboxyhemoglobin level (HbCO), but it can’t distinguish between them. In one’s usual patient, without carboxyhemoglobin poisoning, the monitor is essentially reading their HbO2 level as their HbCO level is very low. In a patient with carboxyhemoglobin poisoning, the monitor displays the total of BOTH the patient’s HbO2 level and their HbCO level. These are both measures, in percentage, of the amount of hemoglobin that has either oxygen or carbon monoxide attached to it. If, as in this case scenario, the patient has a carboxyhemoglobin level of 28%, then 28% of their hemoglobin has carbon monoxide attached to it. It means that, at the very most, only 72% of their blood could possibly have oxygen attached to it. The pulse oximeter monitor, however, would give one a false sense of security by displaying 100% (72% HbO2 plus the 28% HbCO).

Ideally, everyone’s home and work environment should have a carbon monoxide monitor, similar to a smoke/fire detector. The monitor can measure the colorless and odorless CO gas and alert one if the levels exceed safe limits. Again, the exact symptoms vary from person to person, but the table below shows typical symptoms as a function of the amount of CO gas in the environment. It is measured in parts per million of CO in the atmosphere.

Many EMS personnel are equipped with a small, handheld, 4-gas meter that includes measuring the CO gas level in the environment. They carry this on their belt or have it clipped to an entry gear bag that they take with them to the patient’s side. In this way, the crew is immediately alerted to the unsafe, toxic environment as they enter an area with an elevated CO level.  

Jay Carter, MSEE, MD, FACEP, FAEMS

EMS Physician

December 11, 2023

It wasn’t even a motorcycle!

“What did you get for a pressure?” I asked. I was riding in the back of the squad with the medic. Our patient was a 38-year-old male who was riding an electric bicycle right up until the moment he crashed. I was busy putting EKG patches on the patient and applying the EtCO2 nasal cannula. The medic had done a quick secondary exam, including listening to breath sounds, and was now working on a line. Our patient, who fortunately had been wearing a helmet, was A&O x3. He had an obvious left wrist fracture and pain in his left shoulder. He also had scattered abrasions everywhere. The good news was that he was alert, talking to us, and neurologically intact. The bad news was that the medic noted some tenderness on his abdominal exam.

The monitor was cycling (no pun intended!) the BP again, and eventually, we had a full set of vital signs: BP 86/56, HR 124, RR 24, SaO2 98% RA, EtCO2 36. The patient was now actively complaining of abdominal pain, in addition to his left wrist and shoulder hurting.

I asked him if he knew what happened or why he crashed, a good question to assess how well they are faring; some are unaware. My concern in those cases is that they likely experienced a loss of consciousness, even if they don’t recall. In this case, our patient said a car was passing him and didn’t leave him enough room to avoid a storm sewer grate on the side of the road. The next thing he knew, he was flying through the air. 

When he finished his description of the accident, he told me his pain was getting worse.   I am a strong advocate for treating a patient’s acute traumatic pain, but he was tachycardic and hypotensive. We have three analgesics in the drug box: Fentanyl, Ketamine, and Toradol. Fentanyl would be 25 – 100 mcg IV, IN, IM, or IO. Toradol would be contra-indicated for a trauma patient with bleeding (otherwise, it would be 15 mg IV, single dose). Ketamine has an easy dose to remember, 10 mg iv, with a repeat x 2 if needed. Unfortunately, diluting it before administration is required, which is an extra step that takes time and is error-prone. I knew that our patient was in a lot of pain, but I told the patient that he would have to wait until we got to the ER for any pain medicine as his blood pressure was too low to give him anything at this time.  

If you have a patient who warrants analgesics but you can’t administer them, it is appropriate to explain WHY they can’t have any pain meds at the moment. The pain management protocol lists several contra-indications to their administration: altered mentation, traumatic abdominal pain, head trauma, and hypovolemia.  

The medic placed a 16 g IV in the patient’s right forearm and made it look easy. Ironically, the medic was sitting in the CPR seat on the patient’s right side; was it pure luck that he was on the patient’s uninjured side or the perfect plan? He looked up and said: “How much fluids do you want him to have?” My answer? “Run it wide open until we get his systolic BP over 90 mmHg.” Truth be known, I wasn’t sure if we would even get his pressure up to 90 mmHg before we arrived at the ER. I was worried about the possibility of a splenic injury from his abdomen hitting the handlebars as he went flying earlier. The goal, however, was simple: a SBP of 90 mmHg.  

This number is based on years and years of injury and survival data on trauma patients. The best solution for replacing acute, hemorrhagic blood loss is blood, as blood has red blood cells to carry oxygen to the tissues, platelets and clotting factors to help control the bleeding, and the right pH (acid-base balance) to match what the body needs. Our bag of salt water is a poor man’s second choice for blood when resuscitating a patient in hemorrhagic shock. It doesn’t have RBCs to carry oxygen, it dilutes the platelets and clotting factors, and it makes the patient both hypothermic and acidotic.

We administer IV fluids (NS, LR, Plasmalyte, etc.) to provide enough blood volume for the heart to perfuse the heart itself, the brain, and other critical organs that require O2 and glucose. Pumping cold, acidotic, diluted blood is better than not pumping any blood at all! However, how much fluid to administer is a tradeoff, and obtaining a systolic BP of 90 mmHg is a reasonable goal to balance maintaining some perfusion against the detrimental effects of salt water fluid resuscitation. In the ER, patients with hemorrhagic shock are typically resuscitated with blood products. Our goal in the pre-hospital setting is to maintain a viable patient until we get them to the ER, where the optimal resuscitation fluid can be initiated.

There is a caveat to the fluid resuscitation goal of 90 mmHg for acute adult trauma patients. Those with an isolated head injury and shock do better with higher pressures to better perfuse the injured brain. Also, in these particular patients, any episode of hypotension portends a poor outcome. Avoiding hypotension in head injury patients is critical.     

Repeat vital signs after a 500 ml NS fluid bolus showed improvement, with an increased blood pressure and improvement in the tachycardia. The patient’s vital signs were now: BP 96/64, HR 112, RR 20, SaO2 99 % RA, and EtCO2 36 with a good waveform. The patient remained alert and was talking throughout the transport, a good indicator that his mentation was fine and that he was adequately perfusing his brain.

As the medic placed a SAM® splint on the patient’s left wrist fracture, I attempted to distract the patient’s attention by asking him how fast he thought he was going when he hit the drainage grate in the road. Although it wasn’t a clinically important question, it helped to take his mind off the pain he experienced while splinting his wrist. 

In addition, I was surprised to learn that many states have classes for electric bicycles and that his class 3 can go 28 MPH. He thought he was cruising at about 15 MPH when his accident occurred.

Given the patient’s traumatic injuries, uncontrolled hemorrhage (presumed intra-abdominal injury with bleeding), and his initial HR > 120 BPM and (or) SBP < 90 mmHg, he was a great candidate for TXA (Tranexamic Acid). The medic mixed 2 gms in a 100 ml D5W IV bag, and we ran them in over 10 minutes, which finished upon arrival.

In the ER, a chest X-ray demonstrated a fractured left clavicle, which accounted for the patient’s left shoulder pain. Fortunately, he did not have pneumothorax or widened mediastinum. The patient received two units of packed red blood cells and two units of fresh frozen plasma while he had a CAT Scan of his head, C-spine, chest, and abdomen performed. The extensive splenic injury and its resultant intra-abdominal hemorrhage resulted in the patient being taken to surgery.

Jay Carter, MSEE, MD, FACEP, FAEMS

EMS Physician

December 18, 2023

It’s just a vein!

The squad was responding to a 68-year-old female in a car in the parking lot of a local restaurant. Dispatch said that she was in and out of consciousness and was bleeding. The caller was the patient’s daughter, and she sounded hysterical. Dispatch was sending the police as well, as it wasn’t clear what was going on.

In this case,  it wasn’t clear from dispatch what the true nature of the call might be. An update from dispatch revealed that the patient had just finished lunch at the restaurant and gotten in the car. There was no car crash, no entrapment, no report of any altercation or gunshots fired, and yet the patient’s daughter didn’t know where “all the blood” was coming from.

Having confirmed no obvious scene threats, the crew approached the patient’s car, and upon opening the front passenger door, they saw a large puddle of blood on the floor. The patient was awake, and her eyes opened when the crew asked her questions, but she certainly wasn’t alert. She appeared to be breathing adequately and was mumbling some answers to the crew’s questions. A quick check of her radial pulse revealed that it was rapid and weak. There was no blood on the patient’s shirt (chest and abdomen) or in the pelvic region or the car seat, but her pants were saturated with blood in the calf region of her leg.

The EMT quickly cut the patient’s pants up from the bottom towards the knee and exposed a small wound on the back of the patient’s calf that was gushing blood, which was instantly stopped by pressing her thumb against the small wound’s hole as she clamped her hand around the patient’s lower leg.

The hazy scenario painted by dispatch was now becoming crystal clear. The elderly patient had brushed her calf against the car seat as she got into the car and had ruptured a varicose vein in her calf. Who knew a little vein could bleed so much, or could mimic an arterial bleed, or a life could be saved with a little thumb pressure on a wound?

Varicose veins are superficial veins typically in the legs that are swollen, bulging, and full of blood. They are quite common, with 30% of the population experiencing them with increasing age. They can sometimes cause discomfort, but they are often asymptomatic, at least until the thin skin overlying them breaks down and the vein ruptures. Although the venous system is the “low-pressure side” of the circulatory system, the bleeding from a small, ruptured varicose vein can be quite significant. One can model the system as a pipe (vein) with a column of fluid (blood), with the height of the fluid column being the distance from the wound to the patient’s heart. This column of fluid has hydrostatic pressure based on the height of the fluid column, and this hydrostatic pressure helps to squirt the blood out with significant force. If the patient was lying down flat in bed, there would be no hydrostatic pressure from a column of blood, and the bleeding would be much less pronounced. In our patient, who remained sitting upright in the car, there was a continuous, significant, ongoing hemorrhage until direct pressure was applied to the bleeding site. 

Although the bleeding was significant, our patient’s bleeding was easily stopped with direct pressure to the wound. The crew placed a rather tightly wrapped pressure dressing on the wound, which stopped the bleeding, and a tourniquet was neither indicated nor needed. Likewise, although the patient was shocked by her blood loss, TXA was not indicated. The bleeding was from a small superficial wound and was easily controlled. There was no ongoing, uncontrollable hemorrhage, such as one might see in a patient with a GSW or a major trauma motorcycle accident patient.

Extricating the patient from the vehicle is a routine and necessary step in caring for this patient. In this case, however, it was also part of the specific treatment for the patient’s condition. Transitioning her from the sitting (vertical) position to the supine (flat) position eliminated the hydrostatic pressure that was initially helping the wound to bleed profusely. 

This patient’s first set of vital signs were obtained in the squad: BP 92/56, HR 110, RR 24, SaO2 97% RA, EtCO2 36 mmHg.   Surprisingly, she does NOT warrant an IV fluid bolus. Remember that when treating acute hemorrhagic shock, the goal is to provide IV fluids until the patient’s systolic BP > 90 mmHg. When treating acute hemorrhagic shock, a higher blood pressure is NOT better, and over-hydration with salt water is detrimental to the patient’s outcome. In the ER, the patient can be further resuscitated with the fluid of choice, blood, and blood products (fresh frozen plasma). Had the patient been experiencing ongoing blood loss, then IV fluid resuscitation would have been indicated until one reached the desired goal: an SBP > 90 mmHg.

While discussing wound care, it is also worth reminding NOT to remove a dressing to re-check a wound, as its removal will also dislodge a clot forming at the wound site. Applying a fresh, new dressing means that the clotting process has to start over from the beginning.

En route to the ER, this patient also warrants an IV (saline lock), EKG monitoring, pulse oximetry, and capnography monitoring. A blood glucose level is indicated due to her transiently altered, but now improved, mental status. A 12-lead EKG is indicated for any shocked, elderly patient. In this case, the patient’s hypotension and tachycardia were the result of hemorrhage, not cardiogenic shock. But know the patient could also have cardiac ischemia secondary to her shock state and the increased cardiac workload from her hypotension, tachycardia, and acute anemia.  

A deep venous thrombosis (DVT) is also a potentially fatal condition that frequently originates from the veins within the legs. A clot that forms in the deep veins of the legs, pelvis, or arms can break loose and travel back to the heart and lungs. There, it can cause a pulmonary embolism or a saddle pulmonary embolism, both of which can be fatal. The primary risk factors for experiencing a DVT include immobility, long-distance travel, cancer, pregnancy, smoking, and genetic conditions.

Veins certainly don’t get much attention in anatomy class, nly later in one’s career, they learn that “those little veins” can be the source of such life-threatening calamities!      

Jay Carter, MSEE, MD, FACEP, FAEMS

EMS Physician

December 25, 2023

Don’t miss the easy stuff!

An Altered Mental Status (Altered Mentation, Altered Level of Consciousness) is a sign of an underlying and often serious problem. It is not, itself, a specific disease process. Our job in EMS is to treat the patient symptomatically AND to recognize and treat many of the specific causes for this patient presentation since the condition list is almost endless.

The global protocol addressing a patient who is not alert and oriented is the Altered Level of Consciousness protocol. It specifies a number of general treatments that EMS should undertake. Then, it has a lengthy laundry list pointing one to more specific protocols based on one’s suspicion of the underlying cause.

General care:

o  Universal patient care protocol, including:

• Scene safety

• Patient assessment

• Airway/breathing assessment and care

• Circulation assessment and care

• Spinal motion restriction assessment and care

• Vital signs and monitoring (EKG, SaO2, EtCO2)

o  12-Lead Protocol

o  Blood glucose assessment

o  IV access

Specific Protocols:

• Seizure

• Hypoxia

• Anaphylaxis

• Sepsis

• Hypotension

• Arrhythmia

• Psychiatric / Behavioral Health

• Hypoglycemia / Hyperglycemia

• Hypothermia / Hyperthermia

• Stroke / TIA

• Overdose / Toxin exposure

• Head trauma

When caring for a patient with an altered level of consciousness, the ultimate goal is to identify a specific cause for the patient’s presentation and then provide a specific treatment for that cause. When the specific cause isn’t clear, general, symptom-based care is provided.  

The underlying cause for a patient’s altered mentation might be readily apparent. For example, a patient who is unconscious and found to be in VTach has an arrhythmogenic cause for their altered mentation. Their heart is simply not pumping effectively and is not supplying the patient’s brain with sufficient oxygen and glucose to maintain consciousness. In this case,  the specific treatment to correct the patient’s altered mentation is cardioversion (synchronized defibrillation).  

Likewise, a rather dramatic and attention-getting cause for an altered level of consciousness is a grand mal seizure. In this case, the usual pre-hospital intervention to treat the underlying cause for the patient’s altered level of consciousness is to administer a benzodiazepine medication (e.g., Versed (Midazolam): 2.5 mg iv/IO or 5 mg IM/IN).

However, other treatments might also be indicated depending on the underlying cause for the seizure. If the patient were seizing because of marked hypoglycemia, then treating the true underlying cause would require the administration of glucose. Similarly, if the cause for the seizure were a carbon monoxide exposure, then the patient would require the administration of the “100%” oxygen and perhaps the CyanoKit (Hydroxocobalamin) if the scene was suggestive of a coexistent cyanide exposure. These would be in addition to the benzodiazepine medication. 

Hypoglycemia is a common cause for a patient to present with an altered level of consciousness. It is such a common cause and an easily corrected condition that obtaining a blood glucose level is REQUIRED for every patient who presents with an altered level of consciousness. Sustained hypoglycemia can cause permanent brain injury or even death. Given the dire consequences of missing this diagnosis, obtaining a blood glucose level is even required when one has another reason to explain the patient’s condition. Hypoglycemia can easily precipitate other disease states, such as a seizure, an arrhythmia, or an MVA. Patients can have multiple reasons for their altered mental status. Check the glucose level on all your patients who are not fully alert and oriented. 

An opioid overdose is another cause for a patient to present with an altered mental status. Most EMS personnel have treated opioid overdose patients with Narcan (naloxone). Typical opioid overdoses involve heroin, fentanyl, oxycodone, hydrocodone, and other compounds that may or may not have approved clinical indications. When observing an opioid overdose patient who is lethargic, has depressed respirations, or is unconscious, it is reasonable to administer Narcan to reverse the effects of the opioid upon the patient’s mental status and respiratory system. In these known or suspected patient presentations, it is wise to carefully and incrementally titrate up the dose of Narcan administered. In theory, one can partially awaken the patient without suddenly, totally reversing their depressed mental state. Sudden, complete reversal can often lead to a highly agitated or combative individual.  

Narcan isn’t a magic cure-all medication. It won’t have any impact on non-opioid overdoses or other causes for an altered mental status. However, it will sometimes awaken an individual in whom an opioid overdose was not originally suspected. Examples of this include a nursing home patient who was erroneously administered another patient’s medications or, an elderly patient who mistakenly takes the wrong medication from the numerous bottles of medications they have collected over the years, or who forgets that they already took their medication and takes an additional dose. Administering a dose of Narcan to a patient who is not experiencing an opioid overdose does not cause any harm. When treating a patient with an altered mental status or unconsciousness, certainly consider administering a dose of Narcan as a trial, even if the call doesn’t present itself as “an obvious overdose” patient.

While discussing Narcan, is it worth remembering that an opioid overdose can result in unconsciousness and respiratory depression. Respiratory depression (hypoventilation or even apnea) can then lead to hypoxia. The hypoxia can then lead to an oxygen-starved heart that results in cardiac arrhythmias and death. It is certainly appropriate to administer Narcan to a patient who is in extremis (i.e., in critical condition and on the verge of death) to reverse an opioid-mediated cause for the patient’s condition. Narcan, however, is not itself a cardiac resuscitation medication. Once a patient is in cardiac arrest, EMS assumes control of the patient’s ventilation and oxygenation as part of one’s resuscitation. Even if an opioid was the underlying cause for the cardiac arrest, Narcan won’t reverse the cardiac arrest. If, following the standard cardiac arrest protocols, one’s patient has ROSC (Return Of Spontaneous Circulation) but remains unconscious, then once again, a trial of Narcan to assess its impact on the patient’s mental and respiratory status is reasonable.    

Jay Carter, MSEE, MD, FACEP, FAEMS

EMS Physician