Everything RTs need to know about pneumonia

Normally, a person's lungs are sterile, or completely free of bacteria, viruses, fungi, or any other little particles that might cause harm to them. However, on occasion, something might make it's way into the lungs and cause what is commonly known as pneumonia.

Pneumonia is the single most common diagnosis of all the patients that I take care of. I would guess that about at least 50 percent of all the patients I have taken care of in my career as an RT have been diagnosed with pneumonia. Likewise, according to my RT bosses, pneumonia is the most profitable diagnosis.

Granted, I assume that some of these so called pneumonia patients were diagnosed with this disorder even though they showed no clinical evidence of the disease. Doctor's don't do this out of ignorance (I hope), but because they feel the patient needs to be monitored in a hospital, but has to have a diagnosis that meets criteria for Medicaid.

That in mind, I'm certain that some pneumonia statistics might be altered.

According to Medicine.net, . "over 3 million people develop pneumonia each year in the United States. Over a half a million of these people are admitted to a hospital for treatment. Although most of these people recover, approximately 5% will die from pneumonia. Pneumonia is the sixth leading cause of death in the United States."

According to mayoclinic.com, that 5% comes to about 60,000 Americans who die of pneumonia in any given year, most of these patients were compromised in one way or another, be it that they were elderly or had some desease such as cancer, COPD or other chronic illness. And I didn't know this before now, but pneumonia is also the leading cause of death in children.

Pneumonia can be deadly, but it can also be treated. Personally, I've seen so many of these patients that I can do one quick assessment and have a pretty good idea if that patient has pneumonia or not. I'm certain most of my fellow RT and RN collegues can do the same. RT students and new RTs will be equally skilled at this in a few years.

Two common types of pneumonia are either viral or bacterial.

Here are the signs of symptoms:

1. Shortness of breath

2. Rapid, shallow breathing

3. Ausultation

• Crackles isolated to one lobe is usually bacterial
• Crackles/ rhonchi in bases or throughout is usually viral

4. SpO2 levels decreasing below patient normal value

5. Cough: either dry or productive (green, brown, yellow and/or bloody secretions if bacterial, and clear to white if viral)

6. Chest pain that worsens with deep breath or when coughing

7. Fever, shaking, chills

8. Lab values: Increased WBC and/or increased neutrophils (if bacterial)

9. X-Ray shows dense white patch in infected lobe (bacterial). Viral pneumonias produces faint, widely scattered white streaks or patches

10. Sputum sample: lab may isolate bacteria if caused by bacteria (According to Merck.com, the organism is not isolated in 50% of patients.)

11. Patient may be pale, dusky, blue

12. Patient may be Diaphoretic, loss of appetite, fatigue, and (in elderly) confusion

13. With bacterial pneumonia, elderly patients may even have a decreased temp

Aside from a good sputum sample, a good history from the patient or patient's family can help you determine which type of pneumonia the patient has. If the symptoms occured all of a sudden, then it may be bacterial or mycoplasma. On the other hand, if symptoms occured following a bout of flulike symptoms, than a virus is probably the culprit.

Was the patient drinking? He may have aspiration pneumonia. Is he immunocompromised? Perhaps he has Pneumocystis carinii. Is it community acquired? It's probably gram-positive bacterium Streptococcus pneumoniae. Was it hospital acuired? Then it's probably Staphylococcus aureus or a gram-negative bacterium such as Klebsiella pneumoniae or Pseudomonas aeruginosa.

A third type of pneumonia is called walking pneumonia, so called because most patients develop mild flulike symptoms and are usually not sick enough to seek medical help. This type of pneumonia is caused my Mycoplasma, and is rarely seen in hospitals.

However, this disease is very common among people who work or hang around where there are lots of other people, and it spreads easily. Walking pneumonia is treated the same way that bacterial pneumonia is treated, with the right antibacteria.

Another type of pneumonia, which is rare, is fungal pneumonia, which is usually less severe, but can cause a prolonged dry cough that might last for months. Patients with severely compromised imune systems may develop Pneumocystis carinii. This is usually reserved to patients who have AIDS, are receiving chemotherapy, and chronic lungers.

Aspiration pneumonia is where a patient inhales a foreign object, such as vomit (sounds yummy, hey?) This is a major concern for our drug overdose patients or other patients who have lost their gag reflex. Likewise, a drunk, anebritated person who has passed out may also be at high risk of aspiration and, thus, aspiration pneumonia.

Okay, let's back up a second. What is pneumonia?

Say a bacteria makes it's way into the lungs. It is inhaled, goes down the trachea, takes a right or left turn at the corina, goes through the bronchioles, and to the tiny microscopic air sacs at the end of the air passages.

The bacteria infests the area where it lands and causes inflammation and fluid build up inside the alveoli, making it difficult or impossible for oxygen to cross into the blood stream.

Thus you can see why pneumonia may cause someone to become short of breath, and have a lower oxygen level. In essense, oxygen is shunted away from the infested area. And, if the pneumonia is untreated, or becomes large enough, can cause serious problems, and even death.

Anyone can get pneumonia, but normally it is reserved to patients who are compromised in one way or another. And, while it is normally treated on an outpatient pasis, occasionally a person has to be admitted, and these are the people we see.

The following is a list of who is at risk:

1. Chronic diseases such as COPD, AIDS, diabetes of whom are immunocompromised


2. Person's who've had spleen removed


3. Corticosteroids can impair the immune system


4. People who smoke. These people destroy their cilia, which is one of the bodies prime mechanisms for keeping the lungs sterile. Without cilia, a smoker has a weakened ability to remove secretions, and if they are not removed they can cause pneumonia.


5. People who drink too much


6. People exposed to chemicals or pollutents.


7. Post op patients who refuse to or are unable to take in a deep breath and cough up secretions (this is where scare tactics, cough and deep breathing excercises, incentive spirometers, CPT, and forcing the patient to go for a walk come in handy.)


8. Hospital acquired. This may or may not go hand in hand with #6. Intubated patients are at high risk of ventilator acquired pneumonia.


9. Patient's who's immune system is worn down by other illness, and this may also lead to nosocomial infections


10. Heart failure
11. broken ribs


12. Very old and very young


13. people who are debilitated, paralyzed, bedridedn, unconscious

What medicines or therapies to give the patient is up to the doctor. Usually all of these patients get an antibiotic, however an antibiotic will not benefit patient's with viral pneumonia. They will also get something to control fever (Tylenol), nausea, fluids and, voila, a Q4 breathing treatments and, occasionally, respiratory support if the pneumonia gets bad enough.

Just for the record, that first breathing treatment sometimes opens the patient up a bit, because that fluid breaking up may cause bronchospam and a wheeze, especially in COPD and asthma patients. But, despite what I have been told by many doctors, Albuterol will not cure pneumonia.

In fact, Albuterol does not even get into the Alveoli where the pneumonia is. And, it will not help break up the fluid. However, I am currently losing this battle.

Since nosocomial pneumonia is the most common infection acquired in hospitals, RTs and RNs have been given the responsibility of working together with patients to prevent pneumonia.

And this I will discuss tomorrow. Next week I will discuss every thing RTs need to know about VAP (Ventilator Acquired Pneumonia). There's been some changes in this area since I last attended Rt school.

That concludes today's class.

Everything RTs need to know about DIC

Tuesday is the day I'm setting aside to review things we learned in respiratory school but could stand a little review. Also, we will look into expanding our medical knowledge above and beyond what we are expected to know.

I will call these RT Wisdoms, and you can link to these posts at your convenience by clicking on the link RT Wisdoms near the top of this blog.

Today we will discuss DIC.

I worked a bunch of years in the hospital before I had a clue what DIC was. Of course I remember having patients in the critical care, most of them on ventilators, who seemed to be seeping fluid out their pores. But, considering it wasn't respiratory, I didn't think anything of it.

Then one day I remember one of our senior RTs told me in report she told the nurses to keep a particular close watch on this trauma patient because he was at high risk for DIC and ARDS, and I had no clue how she knew this. I knew what ARDS was, but how do you know someone is going to go into ARDS? And, what the heck is DIC?

I decided long ago I needed to educate myself, and make myself a more rounded RT. Which is nice, because instead of going into a room and having no clue what was going on with the patient other than his respiratory status, I was more focused on the Big Picture. And, as we learn in RT school, every organ can effect breathing.

So, that in mind, what do we RTs need to know about DIC.

First of all, DIC is an acronym for Disseminated Intravascular Coagulation and is always a secondary disease, or a consequence of other diseases.

This is a disease process when the proteins in the bloodstream that normally cause clotting in an injured area overreact, and form tiny clots all over the body, and then, clotting factors now exhausted, this causes the patient to bleed abnormally.

When you do an ABG, for example, you might hold the site for the recommended five minutes and the patient still has not stopped bleeding. Usually, when this happens, the RN will have to wrap gause around the puncture site and bind tape around the patients arm to act like a turniquate. I've seen this done on many occasions.

Technically speaking, on these patients, a doctor will want to limit the number of blood draws (ABGs included), because of the complication of bleeding. Another thing for us RTs to remember is to be very careful when suctioning. Ideally (and I think this should be standard procedure anyway), the catheter should not be advanced all the way to the corina so as not to puncture it and cause it to bleed.

In severe cases, the patient will seep ooze right out of the pores on his skin. This can be quite disgusting. But I've seen it quite a few times.

DIC can also cause sudden bruising, clotting, and, as I described, bleeding from multiply parts of the body, and can lead to severe bleeding, stroke, and lack of blood flow to arms, legs and organs.

How do you know what patients are at high risk for this disease process? Take note of the following:

1. Infection in blood (Sepsis, and I covered this in a previous post.)


2. Severe tissue injury, as in burns, trauma (particularly trauma to the head and brain)


3. Recent surgery or anesthesia


4. Reaction to transfusions


5. Labor and delivery problems


6. Liver disease

Trauma patients not only are at risk for getting DIC, but also Sepsis. And sepsis in itself is primary cause of DIC in the hospital setting. And, DIC may lead to acute renal failure and, ultimately, to miltiple organ failure -- including the lungs.

This is why it's also a good idea to do a thorough review of the chart, particularly lab results. The following are some lab results that might show DIC:

1. PTT: According to Medline Plus this is a test to determine how long it takes for the blood to clot. If a patient is on a blood thinner like coumadin the PTT may be therapeutically high. A high PTT is anything greater than 33, and >60 is considered critical, and may be indicative of DIC.


2. PT: Same as PTT, except for the the high value is >12.7 and >40 is critical


3. D-Dimer: >500 may be indicative of acute bleed, but can also indicative of PE and DVT.


4. Platelets: <80,000>


5. INR: >1.2 is considered high, but >6 is critical. This is indicative of DIC or acute bleed.

Now, keep in mind these critical values will vary from hospital to hospital, but at least this gives you an idea of what critical is, and what the labs of a patient in DIC might look like.

Also, you should know that there is a lot more involved in the DIC process than what I describe here, but this is pretty much all that an RT really needs to know about DIC. Now you can put this wisdom to good use and impress someone the next time you find one of these patients.

That concludes today's class.

Everything RTs need to know about Sepsis

What do we as RTs need to know about Sepsis?

For starters, we need to know that is is the leading cause of death in critical care units. According to the MUST protocol, "of the 750,000 patients it effects every year, 250,000 will die."

As I mentioned in my last post, these statistics have gone pretty much unchanged since the early 1980s. So, even with modern knowledge and technology, hospitals have been unable to break this trend.

But, I'm sure, that's not what initially opened up the eyes of hospital administrators to this problem: it was money. According to MUST, cost estimates nation wide tend to scale into the $17 billion category. I'm not sure what the data is for each individual hospital, but I imagine it's a lot of money, much of which more than likely goes un-paid.

So, with the hope that hospitals would create sepsis protocols of their own, the MUST protocol was created to be used as a guideline protocol. According to the protocol itself most hospitals have not addapted it, but I do know that my hospital is looking into creating it's own sepsis protocol based mostly on recommendations of our hospitals keystone committee.

Basically, sepsis is an infection that has made its way into the blood stream. According to computorials.com, "it describe(s) a pathologic process involving widespread release of inflammatory mediators, with or without infection, leading to organ injury."

The basic theory here is early recognition and early treatment.

Here are the early signs of Sepsis:

A. Suspected Infection

B. Two of the following four:

1. Temperatuyre >100.4, <96.8
2. Fast heart rate >90
3. Fast respiratory rate (>20 or PCO2 <32>High white blood cell count (>12,000 or <4000,>10% bands)

C. Systemic blood pressure <90>

D. Lactate >4.0 or elevated LDH

E. Decreased platelets (watch for DIC)

F. Decreased PO2 below patient normal

G. Altered mental status not due to drugs may signify organ failure.

Here are the signs of Severe Sepsis:

A. Patient receiving antibiotics & needs Vasopressor (this is a dangerous sign).

B. Pt showing signs of organ failure in 2 + systems for <= 24 hrs.

C. Patient showing signs of Adult Respiratory Distress Syndrome, DIC, Multi System Organ Failure.

That's pretty much all you need to know. The basic signs you can pretty much determine by your basic assessment, but you may have to pick up the chart. We at the RT cave think it's a good idea to keep up on the patient's labs anyway, if we have time that is.

After early recognition, the nurse and the doctor must follow the rest of the protocol, or whatever is the standard for a particular hospital. The regimine usually includes vasopressor to control blood pressure, and central line placement to determine CVP and monitor fluids, and SVCO2 is used to titrate Dobutamine (if =>30%), or, if less than 30%, to determine if a transfusion is indicated.

And the administration of Activated Protein C, which is the only drug to show any efficacy in sepsis should be used. The keystone committe recommends this, but I'm not sure how widely used it is. In fact, I wonder if it's even used at our hospital.

Of course antibiotics and steroids are also standard therapy, but there is no evidence that this really does anything. More often than not, it's used just in case it might do something, kind of like Albuterol for CHF.

It's good to know all that stuff, but not essential for us RTs. If you want to know more you can simply refer to the MUST link above. It's actually pretty simple to follow. The hardest part about the whole thing is actually remembering all this when standing at the edge of the bed trying to figure out what's wrong with the patient We've all had moments where our memory seems to go blank, and that's when it's so important for us RTs to know more than just RT stuff.

There is a lot of pressure on the nursing staff as it is, and if your brain happens to click at the right moment, and you happen to notice the signs of sepsis, the nurse and/or doctor might be impressed with you. Heck, they might even thank you. Okay, so we won't go that far.

So, if I missed anything here, or if you find that I am incorrect on any of my information that I presented here, because I know many of you guys are a heck of a lot smarter than I am, please let me know.

The following is some additional information because sepsis often results in organ failure, which is why if it goes un-noticed can lead to death.

The following is criteria for organ failure:

A. Cardiovascular:

1. Systemic blood pressure <90
2. Mean Arterial Pressure <= 70 for 1 hour or CVP <8-12
3. CK, CKMB, Troponin elevated

B. Hemodynamics:

1. Platelets <80,000
2. 50% decrease in platelets over 3 days

C. Renal:

1. Urinary output <20cc/hour>
2. High creatinin and BUN, GFR <29
3. Increased electolytes (High K, MG, and Na)
4. Increased Uric Acid
5. Metabolic Acidosis
6. Increased blood pressure
7. Prolonged bleeding (DIC)

D. Hepatic:

1. Jaundice
2. High AST and ALT, Biliruben, Gamma-Gt
3. Decreased Albumin
4. Coagulation abnormalities

E. Metabolic:

1. Ph <7.30
2. BE > or = 5
3. Lactate >2.0 once CVP > 8-12

F. Respiratory:

1. PaO2/Fio2 <=250
2. Early ABG = Respiratory Alkalosis due to high respiratory rate
3. Later ABG = Metabolic Alkalosis due to low perfusion

Keystone Project to improve patient outcomes

As I have mentioned before, we at the RT Cave believe it is important for each respiratory therapist to be involved in the entire process of patient care as much as possible, as opposed to simply focusing on the respiratory side of the patient's needs.

The main reasoning for this is that, as we learned in respiratory school, "all the organs of the body combined effect the respiratory system in one way or another." Not only is it important for nurses to pick up on the early signs that a patient is failing, it is the job of the respiratory therapist. After all, we are a team, we are all responsible for taking care of the patient.

Most doctors agree that most people do not go into respiratory failure without showing early signs that this is going to happen. It is our job as part of the hospital team to pick up on these early signs and prevent a patient from getting so bad that he or she has to be moved to the critical care unit (CCU).

And, once in the patient is admitted to the CCU, it is our job, along with the nurses, that we continue to monitor the patient for signs of impending failure, besides treating the patient for the critical issue that landed the patient in the CCU.

According to the MHA Keystone Center, "It is estimated that, "over 5 million people are admitted annually (to the CCU) in the U.S., consuming approximately 30% of acute care costs or $180 billion annually. In addition to consuming health care costs, these patients suffer preventable morbidity and mortality. Previous studies suggest that nearly every one of the 5 million patients admitted to an ICU suffer a potentially life threatening adverse event (emphasis added)."

It was the goal of the Keystone Project make recommendations based on the most up to date research to improve costs and, most important, recommend steps that hospitals can take to improve patient outcomes regarding illnesses that do show early signs. And the project recommends each hospitals voluntarily create its own Keystone Team to implement these recommendations.

One of the early recommendations was to create a rapid response team , which would get nurses and respiratory therapists on the patient floors to be on the look out for early signs, and to call the rapid response team into action, to generate early intervention, and thus to prevent the patient's illness from progressing to the point that a move to the CCU is necessary.

Creating ventilator protocols is another recommendation of the Keystone Project in order for the doctors and the respiratory therapists to begin thinking about weaning the moment the patient is placed on the ventilator. Since we have initiated our ventilator protocol, we have seen patient length of time on a ventilator decline sharply.

The Keystone Team at Shoreline where I work has decided that the next step they want to tackle is creating a Sepsis protocol.

I'm not sure what steps we will take, but a few years ago I went to an MSRC conference and one doctor gave a presentation "Everything a respiratory therapist needs to know about Sepsis." And he made us aware that the number one killer in the CCU is sepsis. But people do not get spontaneous sepsis any more than they get spontaneous DIC or ARDS, so it is very important for nurses and RTs to pick up on the early signs.

I couldn't remember everything this doctor said because he went so fast I couldn't keep up with my notes, so as soon as I had a slow night at work I looked this up on the Internet, and was surprised at how much I found.

I found that the MUST protocol was created to make hospital staff aware that sepsis, according to aacnjournals.org, "affects more than 750,000 patients and accounts for more than 215,000 deaths in the United States each year at a cost of $16 billion. Mortality to septic shock has decreased only slightly between 1970 and the late 1990s; it remains the most frequent cause of death in noncardiac intensive care units (emphasis added)."

The MUST protocol makes recommendations in making hospital staff aware of the early signs of sepsis and what to do in the event these signs are prevalent. And while sepsis is not necessarily a respiratory illness, if it progresses, it may result in respiratory failure. Thus, when the RT is present with the patient, or part of the rapid response team, it is essential that he or she knows what the early signs of sepsis are.

While I'm not going to get into the nursing end of sepsis (and you RNs can check out the links above if you are interested), I will address everything that an RT needs to know about Sepsis in the next few days. It's also to know which patients are at risk for Sepsis, ARDS, DIC and PE so they can be closely monitored. At some point in the future I will address all of these as well.

We have met resistance in every step of the way in initiating these protocols, but so far at Shoreline we have managed to create our own rapid response team and a ventilator protocol, and we are currently in the process of creating a sepsis protocol.

While it's not the RTs role to insert catheters, central lines and pulmonary artery catheters, the Keystone Project believes it's the role of every person at the bedside to make sure nurses and doctors are in compliance with infection control techniques to "reduce or eliminate catheter related blood stream infections in ICUs." Since we RTs are often at the bedside, we need to be aware of proper technique.

And, while it's not our role to check sugars, an RT must be one of the team members thinking about this, especially when a patient has sudden mental changes, which may also be an early indicator of sepsis. Does the patient all of a sudden have significant change in respiratory rate, heart rate and blood pressure? Is the patient suddenly filled with Rhonchi or crackles. These are not things to be ignored, as they may be signs of impending failure.

As a respiratory therapist, I like to see the big picture above and beyond my role as an RT. Due to the recommendations of the Kestone Team, I know that it is important to do oral care on a regular basis to prevent VAP (ventilator acquired pneumonia), and to have inline suction as opposed to bag and suction, and to make sure the head of the bead is up 30 degrees, and to make sure the patient is still rotated from side to side even though he or she is on a vent.

And, while it was once recommended not to exceed 20 cwp of cuff pressure in the ETT, , it is now recommended not to let the pressure become anything less than 20. The reason for this is to prevent aspiration and VAP.

I'm not sure if this was a recommendation by Keystone or not, but while I was taught to use 1-15ml/kg ideal body weight when I was in RT school in the mid-199s, it is now recommended to go with a lower tidal volume of 6-10ml/kg ideal body weight to prevent barotrauma. And, in cases of chronic or severe pulmonary illness, it is recommended to start on the low end.

If these things are not being done, it is my responsibility as an RT to either do them, or to at least make sure the nurses or other RTs are doing them.

Not only is is a good idea to generate these teams, and these protocols, but it's also a good idea for respiratory therapists to continue to research, to attend seminars and in services, to stay up to date on all the latest research and recommendations to improving patient care. I think this is necessary even if protocols are not available.

Personally, I don't need a protocol to make me participate in the patient's care this way, but the use of protocols provide RTs with more leeway in what we are allowed to do regarding the patient, especially regarding early intervention. If the patient looks bad now, why not get a quick ABG, EKG and, perhaps, order a STAT x-ray while the nurse is calling the doctor.

When we RTs are called to the patient room to give a breathing treatment, and we observe that the patient is not having bronchospasm but is wet, and then we notice that the IV is running at 500, we would naturally make the RN aware of this. And then we would recommend a diuretic, instead of a bronchodilator.

It's not that the nurses are incapable of finding this out on their own, because they are and they do. But if we are a team, we all must be vigilant all the time. What one of us does not pick up on right away, the other hopefully will.

By keeping up on our research, participating in protocols, and making recommendations that work to benefit the patient, we are not just helping the patient, we are using the skills and education that we have accumulated. This is good for our RT morale.

We are a team, and we must all work together to the benefit of the patient, and to the benefit of ourselves and our institutions.

Rapid Response Teams are awesome

I just want you guys to know I absolutely love our new Rapid Response Team. If you don't have one at your hospital you ought to order one up right now, because it is really cool.

I can't even count how many times I've had a patient who doesn't look good to me or the nurses, only for the nurse to call the doctor and the doctor say, "Mumble, mumble, mumble... Give 20 of Lasix, mumble, mumble, mumble."

Click.

That's okay sometimes, but I know there have been many times we've stressed out the rest of the night about the patient, especially if the lasix didn't work. Sometimes these patients end up in the CCU and we saw it coming.

Now if a patient doesn't look good the nurse pages the RRT and an RT, a CCU nurse and the RN supervisor go STAT to the patient's room. We assess the patient and perform procedures and tests we feel are appropriate.

Tonight I had such a call. The patient was sitting on the edge of the bed, arms spread across the bedside table, paradoxically breathing. I arrived and took charge.

"It looks like she's wet." I said before I even assessed the patient. After doing this job for so many years you become good at observations. However, a full assessment would be needed.

"That's what I was thinking." The nurse, Abba, was setting the pulse ox probe on the patient's finger. The sat read 86%. "Her blood pressure is also way high."

Peering up at the monitor, the BP read 192/124. I reached for my handy dandy stethescope and took a quick listen. Happy, the nurses supervisor, and a second nurse arrived and were now standing by my side.

"What do you think? Wet?" Abba asked. She was a good nurse. I had her trained well. A less worthy nurse would have said, "We need a treatment," without further assessment. This was working out just perfect. The way it should be done.

"Yep." I said.

"I think we should do an EKG, ABG and perhaps a treatment." Wow. It feels good using my brain.. A rush of joy filled my veins. Man, it feels so good to use my skills..

I paused a moment. I looked at the patient. Her head was now bowed between her arms so the back of her head stared at the ceiling. It's a miserable feeling not being able to breath. I understood completely.

I paused, however, because I wanted to make sure I wasn't overstepping my bounds. I didn't want to do a bunch of procedures that were not necessary. Rather, I didn't want the nurses in the room to think I was on a power trip like the Air-Flight nurse the other night. I looked at Happy. "Do you agree?"

"Oh, definitely," she said.

As per protocol, the doctor was called before the tests were completed. As I arrived back at the nurses station after running my ABG, the nurse set the phone on the receiver and peered over at me. "He said, 'Mumble, mumble, mumble, give her 20 of Lasix, mumble, mumble, mumble.'"

"As expected," I said, smiling.

"I told him that we did the treatment and the ABG, and he slammed the phone in my ear." She smiled as though she had expected as much. "I guess he doesn't care. So I'll write the order for those."

I said, "Hey, that's fine, because at least now we don't have to stress out about not knowing what her status is. We got all the test results done before the doctor was called. How many times do you sit and worry about a patient the doctor appears not to care about?"

"Not any more," she said, " But I'm glad we did the EKG at least, because her blood pressure is still in the 190s. He didn't seem to care at all about that. And I told him we did the ABGs and he still hung up the phone in my ear. It was almost as though he was annoyed that I even called."

"Well, perhaps we overstepped our bounds a bit. But I think it's great that we have this team. And I think we should always call the RRT before the doctor is called on these patients so we can do the tests we think are needed that the doctor won't order."

"I absolutely agree. I mean, we are the ones at the patient's bedside. We see right up close how the patient is doing, how she feels. The doctor just wants to get off the phone so he can get back to bed."

"Well, to be fair not all doctors are like that, but that one is."

I checked on the patient. She was snuggled under the blankets and the head of the bed was all the way down, a sure sign she was fine now. Despite that, I said, "Mrs. Beer, are you feeling better."

She nodded, turned to look at me, "Yes."

"Did the treatment work for you?"

"Yeah, I'm still a little short of breath, but I feel much more comfortable."

I know you guys are saying: "Why the hell did you give the breathing treatment when you figured the patient was wet? If a doctor did that you'd complain about it."

True. But sometimes pulmonary edema can cause bronchospasm, and sometimes a treatment can help treat that symptom. What I hate is when the treatment is ordered Q4 after the fact, when they are no longer needed. I have no problem trying one treatment.

I checked on her a few times the rest of the noc shift and she was sleeping comfortably each time, which meant the doctor was right on this one.

The patient gave us no further trouble, which was a good thing, because a half hour after I was finished with her, "SIGNAL ONE in CCU!" railed across the overhead speakers.

It was one busy night. But one in which I used my skills. It was awesome.

Bad news: Working nights linked with cancer; Good news: research may lead to cure for aging

Now we night shift hospital workers have yet another incentive to get off nights.

According to theAssociated Press, and research that shows an increase in cancer among night shift workers compared to people who work normal shifts, the World Health Organization is now including working night shift among its list of carcinogens. The American Cancer society states it will soon follow.

Some scientists say this is not necessarily true. However, based on my own research regarding melatonin, I'm leaning towards believing it.

Research on this is very new and quite vague, as researchers and scientists don't even know at what point working nights increases the risk of getting diseases, nor whether if one stops working nights his disease risk factors diminish or simply go away, nor if it's even linked to the disease process at all.

I wrote recently that I might try melatonin for my self diagnosed circadium rhythm sleep disorder, but instead of simply listening to my co-workers (and some of you bloggers) who told me it worked well, I decided to research it first. As it turns out, scientists have stated they know so little about melatonin that they really don't recommend that people take it more often than they really need it -- if at all.

The reason is because that while it may help you fall asleep, and while it may help you stay asleep, it's naturally produced by the body, and by you putting artificial melatonin in your body now who knows what effect that might have on your melatonin production in the future.

Not only that, but many studies have shown that people with neuro diseases, cardiac diseases and cancer have proven to have lower levels of melatonin. What they do not know is whether it is the disease process that causes the melatonin to decrease, or if it's low levels of melatonin that causes the disease states.

Older theories believed that melatonin decreased with age, and some scientists theorized that this might be what ultimately causes aging (and diseases). While melatonin is still considered to be linked with aging, it is no longer believed to decrease with age.

Thus, if someone has a low melatonin, something else must be going on other than that someone is just getting older, and lack of sleep might be one such causes of this.

Much research suggests that melatonin might be linked with aging and disease, and as further studies are completed, the study of melatonin might even lead to a cure to aging.

The reason they think this is because melatonin is an antioxident, which prevents the breakdown of cells. And, if we can prevent this from occurring, we can prevent cells from aging and diseases from forming.

If this leads in the direction we hope, this could result in major scientific breakthroughs that will benefit millions of people. Who knows, maybe it will put some of us medical workers out of jobs.

One expert suggested that you get your melatonin tested, because if it's normal you shouldn't take synthetic melatonin pills, because if your body thinks it is making too much melatonin, it will shut down production of natural melatonin. And when you stop taking synthetic melatonin, your body won't know enough to continue making its own.

Another expert wrote that melatonin can't be tested, because levels vary at different times of the day. So, as you can see, the experts vary in opinion regarding how to prescribe melatonin.

My thinking is, if you work a swing shift and are rarely getting enough sleep, you might as well assume your melatonin is low and take a small dose of melatonin to help you sleep. If nothing else, perhaps it will keep your melatonin levels closer to a normal level so you (hopefully) decrease your chances of getting lack of sleep related diseases.

Still, while scientists note that melatonin does not have the side effects of other sleep aids for most people, they still do not know the long term implications of using it.

One site I found had complicated recommendations for using melatonin, and recommend using it every day at different times of day. I'm not a fan of taking it that often.

Another site I found seemed more realistic, and stated that it's best to take melatonin the first day you are trying to adjust to sleeping days. This should allow your body to adjust back to sleeping days, and no further melatonin should be needed to help you sleep.

You should therefore not use it again until you want to adjust back to nights, and then you should (ideally) not need it again until you need to adjust back to a normal schedule.

My thinking is if your miserable due to lack of sleep, you might as well try it. Because having a little synthetic melatonin in your system a few days a week and risking whatever long term implications might result from this is far better than all the negative side effects that come from not sleeping at all.

In a way, it's kind of like giving small doses of steroids to asthma and COPD patients. While the small dose increases the quality of their life, studies have shown that having a small dose of synthetic steroid in your body is relatively safe.

That's my take on it. Let me know if you think otherwise.

Circadian rhythm sleep disorder: I have it

Until a few days ago I thought I only had one disease -- asthma. Now I've learned that the 12 hour shifts I work three nights a week have caused me to develop a new disease -- Circadian rhythm sleep disorder.

From what I've read, Circardian rhythms are the signals you get during the day from the sun light that tell your body what time of day it is. Your body actually increases or decreases hormones based on the time of day.

If you work night you screw this whole process up. So, when you're night shift friends tell you you're chemically screwed up, they are right.

So my being completely exhausted at around 3 a.m. is due to the fact that I'm supposed to be in deep REM sleep at that time. Then, when I get home, I am in and out of sleep all day. I cannot sleep for five straight hours. When I wake up it takes me hours to get back to sleep. Then, when I start my six day off in a row stretch, I can't seem to adjust to a regular sleep pattern.

That's a sign of insomnia. What I have, according to what I've read, is a classic sign of a sleep/awake disorder called Circadian rhythm sleep disorders. (I think I have that right.)

Over time us night shifters become more and more sleep deprived and symptoms start to develop:

• Headaches (absolutely)


• Increased irritability & being moody (I have to admit it)


• Overly emotional (snapping or losing your temper. Just ask my son.)


• Too sensitive and defensive (getting all worked up over nothing)


• Contrary behavior (seeing problems that aren't really there)


• Forgetful (My wife will contend to this)

Who would have imagined there would be a whole scientific effort to study nothing but us poor night shifters, and that they'd even have a disease named in our honor. I don't know if I feel better now or worse.

I suppose I feel a little better because since it's a disease experts have an actual list of things one can do to make it all better. I'll get to that in a bit. But What I'm most concerned about are all the side effects to working nights:

• Fatigue/ tiredness (Yep, had that)


• Loss of energy (have this)


• Loss of sex drive (ummm)


• Broken sleep after shift (definitely)


• Constipation (never had that)


• Stomach problems (I'm on Provoloc)


• Dehydration (yes)


• Cardiovascular disorders (I'm not there yet)


• stymied career advancement (no energy)


• Eating more junk food junkies (can't keep the weight off)


• Increased obesity (always having pot-lucks)


• Staying out of social loop (Never feel like doing anything)


• increased medical errors (50% caused by lack of sleep)


• Miscarriage


• Getting injured at work (I've been lucky)

Dehydration they said is another problem for us night shifters. So I drink a lot of water. Now I have to get up every two hours even when I am sleeping good to go pee. We just can't win .

Serotonin is an important chemical in our bodies that allows us to control our moods and emotions. Research shows that night shifters produce a lower level of serotonin than normal people, because serotonin is only produced during sleeping hours. And, as we get older, our body becomes slower at producing serotonin as it is, which doesn't help. (No, Melitonin won't help either.)

So no wonder we're so out of wack.

What can we do to help ourselves improve our sleep habits. Unlike my asthma the problem would simply go away if I went to days. But that's not an option right. I've tried all these at one time or another, and some work and some don't; and sometimes it doesn't matter what I do. Anyway, here's what the experts recommend to resolve this disease:

1. Go to days (I've been next in line for 8 years)


2. Keep room dark (no problem there)


3. Avoid caffeine (haven't had any in 4 years)


4. Eat healthy (I am, but don't know how long it will last)


5. Exercise (I do)


6. Avoid sedatives (I do)


7. Try to keep sleep patterns consistent


8. Pay attention at work (I keep double checking myself)

Good news guys. My friend Milt was wrong, and I will not have 7 years cut off my life. Studies show there is no evidence that working nights has an effect on lifespan or cancer. Yipee.