Buddy

Still need to be more specific. There is a ton of info at: http://www.cdic.com/cdclin30.html There are also several recirded teleconferences with slides at: http://www.impedancecardiography.com We have yet to start field testing with Paramedics.

which specific area? On BNP?

ACE844: Keep trying. Are you sure you're dialing right? 888-309-4568. I have the phone on all day, whether I'm in a doctor's office or not. I didn't see any unknown calls come in, and actually answered it whenever it rang today. If you get VM, leave a message and I'll all you back.

ACE844- This is excellent information, thank you. It will help us put everything in context, with ICG having demonstrated more accurate identification and treatment of dyspnea in previous studies. The offer for your to call me still stands at 888-309-4568, when you get a chance.

Ace844: I'll try to address your questions and keep it short. First of all, they are good questions, and they are questions that we intend to try to answer with the pilot project. They might be better answered in detail in a phone conversation. I have a toll free number you can reach me at as well, 888-309-4568. I am not sure where I implied all failure was ischemic. There are several etiologies for heart failure, including, but not limited to various cardiomyopathies as well as ischemic heart damage. There is also right vs left heart failure. Right heart failure, or cor pulmonale, is not all that common in the general population. However, it is relatively more common in men over age 64. It is not uncommon for a COPD patient to develop right heart failure. The chronic hypoxemia most of these people live with, especially those with advanced COPD, is a factor. Hypoxemia is perhaps the most potent stimulator of pulmonary artery vasoconstriction. This in turn causes pulmonary hypertension. The right ventricle is not a powerhouse, and is not meant to pump against great pressure. As a result, the right ventricle begins to fail, causing a back up of fluid systemically, increasing preload (these are the people you will tend to see JVD in, along with distal edema). People with right heart failure may eventually develop left heart failure as well, as the left ventricle has to work harder to overcome the "backup" caused by the right heart failure. Some people have combined right and left heart failure, some only left heart. Regardless of the cause of heart failure, heart failure is still heart failure, along with all the attendant goodies. You are right in quoting me as saying treat the patient, not the monitor. This is certainly appropriate in the context of not relying on any monitor as the sole determinant of patient care. You can get false or unreliable ETCO2 readings from capnography in some patient types as discussed before. We all know a patient can have a really swell looking sinus rhythm on an EKG, yet be in EMD. Cookbook medicine, i.e. "treating the monitor not the patient" is not good in any situation; i.e. withholding nitrates in someone with elevated ST in II, III and aVF for fear that you will cause nitrate-induced hypotension in a patient with an inferior wall infarct. So long as the patient's systolic pressure is decent prior to administration and does not drop more than 10% post admin, then it is appropriate to treat that chest pain patient with nitro. Would it make sense to make someone suffer, withholding nitro because what a report said even if the patients pressure was stable? ICG is just one piece of the clinical picture that needs to be looked at in context with all other factors, both objective and subjective. There is great value in trending patients from one ICG report to another, just as there is value in trending EKG's. However, in theSpringfield study I referenced above, the physicians were blinded to the ICG data. Treatment was later reviewed and ICG determinants were compared to ED physician diagnosis to see which of the two was more accurate in differentiating cardiac vs pulmonary dyspnea. ICG demonstrated superior sensitivity, specificity, + predicitive values and - predicitive values. Sensitivity= The probability that a patient with a disease, condition or injury will test positive by a particular test for the problem. Specificity= The probability that patients without a particular disease, condition or injury will test negative for the problem by a particular test. Positive Predictive Value= The probability that the patient has the disease when restricted to those patients who test positive. Negative Predicitve Value= The probability that the patient will not have the disease when restricted to all patients who test negative. If you read the article, you will note that the readings they identified for cardiac index and systolic time ratio. If CI was <2.4, it was highly indicitive of a cardiac cause of dyspnea. If CI was less than 3.0 combined with STR>.55, this was also highly indicative of cardiac cause for dyspnea. ICG correctly identified more patients as cardiac cause as well as more patients with non-cardiac cause. In the ED-IMPACT trial, you will see that doctors given access to ICG after having made their initial diagnosis and treatment plan changed their diagnosis 12% of the time and changed treatment 39% of the time. Again, ICG is only one piece of the entire clinical picture, and of course sound clinical judgement, after consideration of all factors, should not be substituted for ICG alone, just as you should not rely on any other single test or reading when treating a patient. However, regardless of not having a baseline reading on the patients in the Springfield or ED-IMPACT studies, the retrospective analysis showed that ICG was highly accurate in it's identification of patients who had a cardiac cause of dyspnea. This bothers me, and I know bothers some physicians, especially medical directors who have medics in the field doing this under the medical director's license. Of course, physicians can do what they wish, regardless of indication or FDA approval, etc. However, if these clinicians had access to ICG data, they may not elect to give a beta agonist to a patient who is in acute failure. In my humble opinion, you are playing with fire by increaing myocardial oxygen demand in someone who is in acute failure. People tend to pigeon-hole COPD patients as "lung" only, when these people often have significant cardiac comorbidities and may be prone to a failure episode either due to cor pulmonale secondary to their COPD, or left heart failure due to a past ischemic event or other causes of left heart failure. Values from Swan's (thermodilution) are often operator dependant, and can vary greatly, even from measurement to measurement in the same patient. ICG has been shown to be highly reproducible to itself, moreso than thermodilution. ICG has also been studied in comparision to the gold standard for obtaining cardiac output values, the direct Fick method. R values, biases and other statistical measures showed that ICG correlates very well to values derived from direct fick. I encourage yo uto read the accuracy and reproducibility studies found at the following links: http://www.cdic.com/cdclin30.html#accuracy http://www.cdic.com/cdclin30.html#repro The ICG test was done right away, the physicians were just blinded to the results and had to diagnose and treat based solely on their clinical judgement.

Even the best history and physical exam will not give you information on a patient's actual cardiac output, stroke volume, vascular resistance and thoracic fluid content. Aside from the utility in differentiating cardiac vs pulmonary causes of dyspnea utilizing in part live time cardiac output, there currently is no objective tool available to Paramedics that can give readouts on live time cardiac output, stroke volume and vascular resistance. We cannot lay hands on a patient and automatically know what their hemodynamic status is. We can make an educated guess, but that's what it is, a guess, and even some of the best physicians guess wrong in this regard. Believe me, I have seen many a doctor's eye's pop out of their head when they saw the true values on a patient that they were not expecting to see. Cardiac output is a function of heart rate x stroke volume. All we have that we can measure objectively is heart rate. As far as stroke volume, we have no idea what a patient's preload, afterload and contracility are. When it comes down to the very basics, it's all about oxygen delivery, which is a funtion of cardiac output, Hgb levels and SpO2. The latter two can be measured, cardiac output-- again, we're guessing. Just about every med we have in our boxes effects these parameters in some way shape or form. There should be an objective measure as to how these meds effect the patient (i.e. what is the patient's hemodynamic status on that dopamine drip? Some will say this is nice to know but... I say depending upon the med (i.e. dopamine and others that effect hemodynamics), it is beyond nice to know. We should know this and need to know this as paramedics if we are giving these medications to patients. As far as new technology, the sphygmomanometer met similar resistance to that experienced by the technologies you mentioned when it first was introduced! With regard to cost, this is a great concern of mine as it relates to practicality of bringing this technology into EMS. It is probably the most significant barrier. That is why I think ICG is best integrated into an existing platform, either OEM or as an add on module. That is why we are setting up this pilot. We need to first see how paramedics respond to the technology and if it is helpful and practical to use in the field. Once this is determined, they can look into product design and price points in line with EMS needs. Please read the clinical studies referenced earlier in this post. They will help you get a clearer picture of the clinical utility of ICG. If you have questions about this, or are interested in possibly becoming a pilot site, please feel free to contact me at 716-459-9566 or e-mail mbseak@verizon.net

ACE844- Yes, I do work in the field as a Paramedic one to two 12 hour shifts per week and I am also a preceptor and field training officer for new paramedics and paramedic students for an ambulance service in the Buffalo, NY area. I am also a certified ACLS and PALS instructor. I did take a position with CardioDynamics last month. One of the main reasons I sought them out was because I truly believe in this technology and that it is has amazing potential for the future of EMS. I actually had a very secure full time job in pharmaceutical sales prior to joining CardioDynamics, but I gave it up because I believe in this comapny and the benefits that this technology has to offer patients. I have not undertaken this EMS pilot project for financial gain-- my bread and butter right now with this device is in physician offices. If anything, it is additional work I have taken on with little hope of much return in the very near future, if ever. My idea with the pilot project is to first see how paramedics and EMS medical directors respond to the technology and if it is practical out in the field. We will also be exploring issues of billing and reimbursement for ambulance services for this procedure. We will be gathering data points similar to those found in the ED-IMPACT study. I have edited the links I provided in the original post so that people can find the relevant articles/studies on this technology, but here they are again: http://www.cdic.com/cdclin30.html#Dyspnea Two that are of high relevance found at this link are: Impedance Cardiography Changes Therapy in Dyspneic Patients: Results from the ED-IMPACT Trial. (Peacock et al.) and Utility of Impedance Cardiography to Determine Cardiac vs. Noncardiac Cause of Dyspnea in the Emergency Department. (Springfield et al.) Some studies were funded by the coporation, some were funded by other interests. The Mayo Clinic ran a study on hypertension on their own to try and "debunk" the technology and wound up determining that our device allowed for 70% better control of hypertension than specialist care alone! An article that describes all the hemodynamic parameters measured by the device and what they mean can be found at: http://www.impedancecardiography.com/icgprog10.html It is the one called: "A Clinical Guide to Interpreting ICG Hemodynamic Status Report" I personally think it would be fantastic if a version of this product could be developed for EMS that made it practical (i.e. size wise, or something where ICG was integrated into an existing monitor/defib platform). It would be great even if all it could do was help medics differentiate cardiac vs pulmonary dyspnea, but it can do so much more. The prospect of having live time readings on cardiac output, stroke volume, vascular resistance and thoracic fluid levels just boggles my mind. I know I would have use for it personally, the question is does EMS in general? That is where this pilot project comes in. Maybe it will be determined that it is not practical, or that EMS just isn't ready for this technology yet, but at least I will have tried, and I can live with that. Just so you understand the passion I have for EMS, I'll tell you the reason I became a paramedic. I was an 18 year old freshman in college. On April 19, 1990, at approximately 7:00pm, a class mate of mine collapsed in our Tae Kwon Do class. I was CPR trained from having been a lifeguard, so I initiated CPR and another trained classmate joined me and we performed CPR until the student and then vilage rescue squads arrived. Our classmate did not make it. All I can remember is the doctor at the hospital coming out to the waiting room to tell all of us. All I could do is stare at the floor through a flood of tears while everyone gathered around to tell me I did all I could. The village ambulance service where I went to college did not have defib capability at the time, who knows if it would have helped, it turned out he had a congenital heart defect. From that day on, I had a burning passion for EMS, especially in the area of defib access. I took that passion and my instructor group ran a pilot project to upgrade Certified First Responders to defib capability. We ran over 900 Buffalo Firefighters through our program in under 2 years. I now have the same passion for this technology. I have seen what it can do in hospitals and doctors offices, and I truly believe it is lifesaving technology. I have had physicians who have it tell me they would not dream of practicing without it now that it is available. Now I hope you can see where I am coming from. Feel free to contact me at 716-459-9566 or e-mail mbseak@verizon.net

Ruffems- Sorry about the problem with the links, when I roll the mouse over them on the website, the URL address that showed up on the bottom bar of my browser is what I put in. To access the articles I referred to, go to: http://www.cdic.com/cdclin30.html#Dyspnea The two I cited were: Impedance Cardiography Changes Therapy in Dyspneic Patients: Results from the ED-IMPACT Trial. (Peacock et al.) and Utility of Impedance Cardiography to Determine Cardiac vs. Noncardiac Cause of Dyspnea in the Emergency Department. (Springfield et al.) There are other clinical studies listed on the link above, just scroll up and down. There are plenty on Critical Care, ER, Dyspnea and Heart Failure. The article that describes al the hemodynamic parameters and what they mean can be found at: http://www.impedancecardiography.com/icgprog10.html It is the one called: "A Clinical Guide to Interpreting ICG Hemodynamic Status Report" As far as giving medics new, useful information-- Absolutely! In the Springfield article, they concluded that 2 parameters were key indicators as to whether or not dyspnea was cardiac or pulmonary in nature. If the cardiac index (the patient's cardiac output indexed to their body surface area-- CO/BSA in meters squared) was less than 2.4, or if the Systolic Time Ratio was greater than .55 with a cardiac index of less than 3.0, it was highly indicitive of a cardiac cause for the dyspnea. Systolic Time Ratio is a ratio between the Pre Ejection Period and the Left Ventricular Ejection Time. PEP is the time from the electrical stimulation of the ventricles to the opening of the aortic valve. LVET is the time from the opening of the aortic valve to the closing of the aortic valve. As a heart begins to fail, the PEP time lengthens, because it takes more time for the heart to generate enough pressure to open the aortic valve. LVET decreases, because the heart cannot maintain enough pressure to keep the aortic valve open for a long period of time. The result is a higher number (PEP) divided by a smaller number (LVET) in a failing heart and a resulting higher STR. This is valuable information for paramedics to know in the field, and it is not available through other means. If a paramedic chooses the wrong protocol to treat a dyspneic patient, say treating a CHF patient with albuterol as they would a COPD'er, the results can be disasterous. We all know albuterol is not terribly selective, having beta 1 and beta 2 effects. The beta 1 effects can increase myocardial oxygen demand and worsen an acute CHF event. Anything that can help medics in the field differentiate cardiac from pulmonary causes of dyspnea is a good thing. Also, changes in stroke volume/index are seen before you see a change in cardiac output/index and any clinical signs of failure. If you see stroke volume tanking, it may not be long before CO tanks and also the patient. This will not tell ejection fraction, but the device will help determine with a higher level of certainty if dyspnea is cardiac in nature. I believe in the future, ICG will be an invaluable tool in EMS. A lot of people were reticent about pulse oximetry, and now it is considered the 5th vital sign. I wish I could find the exact quote, but when the blood pressure cuff first came out, a well noted physician at the time commented on how awkward and time consuming the sphygmomanometer was and how in a busy physician office there was hardly time for such nonsense. Can you imagine not having blood pressure today? As for cost, billing and practicality, that is why we are doing the pilot project. In the ER, they bill it under APC code 0099, and I think the amount is around $26. Physicians in the ER can bill an interpretation fee, which I think is about $10. In a physician office, the amount averages $45-55 per test, CPT code 93701. Rather than a stand alone unit, it may make more sense to incorporate ICG monitoring into an existing monitor/defib design. If you are interested, perhaps your service can participate as part of the pilot. Call me at 716-459-9566, or e-mail mbseak@verizon.net.

Hello- If you copy and paste the links into your browser, you should be able to view them. They are PDF files, so you may need to get the free Adobe Acrobat reader at www.adobe.com. It is likely the same device. Yes, it is a non-invasive hemodynamic monitor. The trade name is BioZ. Yes, the cost is high, but in our pilot project, we are going to place one unit on a supervisor vehicle, and they will respond to all shortness of breath indicators for patients over a certain age, or where there is known cardiac and/or COPD history. One of the parameters, Systolic Time Ratio does have a general correlation to ejection fraction, but there is no direct conversion chart for STR to EF. Basically, if the STR is high, or has increased significantly in a patient, the likelihood is they have experienced a decrease in left cardiac function. If the results of the pilot project are favorable, the company who makes the monitor may be persuaded to develop an EMS specific product-- either a module to plug into a monitor/defib, a stand alone monitor/defib with ICG capability or maybe a small hand held device that would report only on the two parameters necessary to help differentiate cardiac vs pulmonary dyspnea.

We've all had the same call numerous times. A patient with mixed COPD and CHF/Cardiac history complaining of shortness of breath. Their lungs sound like garbage and the family may or may not know if any distal edema present is new, or increased from baseline. There is a tool available now that is being used in many emergency rooms, including the Cleveland Clinic, to assist clinicians in differentiating cardiac versus pulmonary causes of dyspnea. It is called Impedance Cardiography. The service I work for is in the process of developing a pilot project to see how paramedics respond to the technology and whether or not it would be practical to use in the field. Should the pilot work out, they may purchase some impedance cardiography devices for use in the field. Impedance Cardiography involves a device called the BioZ Monitor (Z is the symbol used to denote impedance) that utilizes impedance signals to track aortic blood flow. It is simlar to an EKG, but instead of electrical function/ryhthm, it gives readouts on the mechanical function of the heart such as cardiac output, stroke volume, vascular resistance and thoracic fluid levels, along with a number of other hemodynamic parameters (even some dealing with contractility). Studies have demonstrated that ICG has resulted in a significant change in ER physician diagnosis as to the cause of dyspnea, and a resulting significant change in course of therapy. It would seem there is a place for this technology in EMS. The value in determining cardiac vs pulmonary causes of dyspnea would certainly help avoid a patient in acute heart failure being treated with beta agonist bronchodilators that can increase heart rate and myocardial oxygen demand. I just wanted to put this out there to see what response there might be from other EMS professionals. If the pilot project is successful, and there is a demand, the company who produces the equipment might be persuaded to produce a device specific to the needs of EMS workers in the field. Here is a link to some articles on Impedance Cardiography used in dyspnea: http://www.cdic.com/cdclin30.html#Dyspnea Two that are of high relevance found at this link are: Impedance Cardiography Changes Therapy in Dyspneic Patients: Results from the ED-IMPACT Trial. (Peacock et al.) and Utility of Impedance Cardiography to Determine Cardiac vs. Noncardiac Cause of Dyspnea in the Emergency Department. (Springfield et al.) There are other clinical studies listed on the link above, just scroll up and down. There are plenty on Critical Care, ER, Dyspnea and Heart Failure. An article that describes all the hemodynamic parameters and what they mean can be found at: http://www.impedancecardiography.com/icgprog10.html It is the one called: "A Clinical Guide to Interpreting ICG Hemodynamic Status Report" If you have an interest in participating in or any questions about the pilot project, please feel free to contact me. My e-mail is mbseak@verizon.net. I can also be reached via pager at 716-459-9566. I truly believe that this technology can help save lives in the hands of paramedics.