Cardiac vs Pulmonary Dyspnea - New tool to assess COPD/CHF

[Dustdevil]

I see the most potential for this technology being in rural areas where transport times are extended and the ability to get definitive therapy started half an hour earlier can make a big difference. Unfortunately, as with a lot of technology in EMS, those who need it most can afford it least.

[Buddy]

So while I am sure that this new monitoring tool will prove it's utility to a specific group of patients, how will it improve on a thorough history and physical exam?

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]

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

"Buddy,"

It's good to see a fellow EMS provider believe in something and to "get on board" to help improve pt care in the field!! I do have a few items to present for consideration as to your initial query on if this device may be "useful" in the field.

DISCLAIMER:: These opinions are my own and based on my own prejudice, insight, and info provided, etc.. and subject to change. This is MHLO/.02 and YMMV. Also I a personally a big "proponent" of new and emerging technologies "coming" to the field to help improve pt. care.

Having said that I have the following issues/opinions on this device and how it may or may not be useful "in the street".

1.) The vast majority of the studies posted did not use this device in the "initial assessment, test, decision making process" Thus the majority of Docs exposed to the products available info was only after the inital pt "workup" PE, and test results were back. Then the doc was provided with info from the device to see "if" this changed their decision making/Rx. Also, based on what i read there was no "chart/tree" to tell the physician or give them a measure of acute/chronic value for the indicies which the device measured and thus one can only assumed all info was against known physiologic norms. Because this device wasn't implemented "right away" in the acute patients care and assessment etc... One has to wonder the following things for the "in hospital" environment:"

A.) Because there was no "baseline" measure of the patient's studied to "match against the Md had to assume "physiologic norms" which most of these patient's most probably weren't at while at baseline.

B.) How long does it take to connect the device, how long was the pt monitored for before accurate values were obtained and how would this affect "acute/emergent" patient care

C.) The samples from the studies listed were all very small and very different between them all and very loosely homogenous, as well as mostly being performed on "stable" patients. Thus small population in these studies and the "data" obtained is questionable as to how representative/accurate it would be against a larger population

D.) How much did the corporation/funding have to do with the outcomes and how much input/influence did the company have on exclusion criteria, etc....

E.) There as I mentioned previously was no objective measure or method given to the clinicians to determine acute/chronic cardiac measures for the patient as well as acute/chronic measure states for the respiratory side. So as not to confuse I'll give a quick example. There alot of patients "nowa days" which are being D/c'd or being treated outpatient with the following PMHx's/comorbidities together: CHF, CAD/mi, Pulmonary edema (non-cardiac", Pulmonary Disease...

So if one was to encounter a patient with a known ef of say....30% and chronic cardiac issues (MI, CHF) as well as emphysema and a clinician were to "use the device" then the numbers would be "mixed" and "abnormal" thus leaving the clinician with the same issue you were trying to reslove wiht info from the device.....Not all Pulmonary edema is cardiogenic, not all wheezing is COPD/chronic resp dx related, etc .....

F.) It was studied as much or more so in the "primary care" environment as it was acute care and the majority of times "seemed" to have been used on "stable" patient's as opposed to "Acute/emergent" ones.

G.) I am leery of any device that has a relative sensitivity of a mere 63%, as a end all be all of a ceratin therepeutic measure

Now lets cover "pre-hospital" arena and issues there:

A.) Because I just mentioned it above see the issue from "E"

B.) Device size and time to apply

C.) How sensitive is the device and noting that you have approx 6 "electrodes" to obtain your "measures" how much artifact are you likely to experience

D.) Cost and Size

E.) Most prehospital providers haven't been educated to understand SVR, TFI, etc....so educational time and costs of the target population. as you I am sure noted by "browsing" the forums here education/trianing or lack there of is a big issue for "us" right now.

F.) To go with the artifact issue how often does/would the device need to be calibrated, and how susceptible/sensitive is it to a harsh environment

G.) In the street we don't have access to that all to valuable baseline info which will be critical to our decision making as far as patient treatment. This is one thing which the hospital has always had the benifit of which we don't have access to. In the ED or the hospital they can get old Mr's, and info as well as talk to the patient's PCP to get valuable info which will effect the ability of the clinician to be able to decide what is acute an what is not... this could also be a major factor in the effectiveness of this device "in the street"

This is just a few of the things that I encountered while reading the literature and your posts which made me go HMMMMM.....

Hope this helps,

Ace844

[Ace844]

"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 have noticed a trend in the billing in my area in which even with the new "EMS" ICD-9 codes there is a major lack of appropriate reimbursement for some theripies...I am sure this will be a big issue with this device as well.

Out here,

Ace844

[Buddy]

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.

Not all "failure" is ischemic related as "imply" above.

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.

B.) Some clinicians (Read doc's in the hospital) give a Beta agonist/Respiratory treatment to Pulmonary edema patients regardless of whether it is cardiac or not because the patient is in severe enough distress that they are willing to trade the "short term - effects" of the treatment for the "potential" beneifts that it may provide the patient in relation to a + change in their TV/Dead space/VQ/ MV/etc.....

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.

C.) Much like the debate in "IN house" critical care circles about the use, efficacy, and accuracy of a "Swan" in certain patient poulations, it seems to me that there would be a similar arguement about this device.

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

1.) The vast majority of the studies posted did not use this device in the "initial assessment, test, decision making process" Thus the majority of Docs exposed to the products available info was only after the inital pt "workup" PE, and test results were back. Then the doc was provided with info from the device to see "if" this changed their decision making/Rx. Also, based on what i read there was no "chart/tree" to tell the physician or give them a measure of acute/chronic value for the indicies which the device measured and thus one can only assumed all info was against known physiologic norms. Because this device wasn't implemented "right away" in the acute patients care and assessment etc... One has to wonder the following things for the "in hospital" environment:"

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.

B.) How long does it take to connect the device, how long was the pt monitored for before accurate values were obtained and how would this affect "acute/emergent" patient care ]

It takes about 3-5 minutes tops to apply the eletrodes and obtain the values.

Some studies were funded by the company, some were not. The inclusion/exclusion criteria are listed in the studies, and I am sure yo uwill find them reasonable. As a side note, the Mayo Clinic ran a hypertension study on its own, without the knowledge of the company in an attempt to "debunk" ICG, for lack of a better term.

The study is called: "Resistant Hypertension: Comparing Hemodynamic Management to Specialist Care" and can be found at this link:

http://www.cdic.com/cdclin30.html#Hypertension

There were two groups of nationally recognized hypertension specialists, one group with ICG and one without. The group with ICG had 70% greater hypertension control versus the group without ICG. Although this is not all that relevant to emergency care, it does speak to your inquiry about whether the studies were corporate sponsored or not. This study was not, and ICG came through with flying colors.

As mentioned above, in the ED-IMPACT trial, it resulted in a 12% change in diagnosis and a 39% change in treatment.

We will be looking into billing issues in the pilot project as well, as a part of determining the practicality of ICG for EMS. I would like to ask if anyone who has capnography in the field (my service currently does not) is able to bill separately for capnography. I suspect not, and if I am correct, it would appear that some services out there feel there is significant value in having capnography on board, so much so, they are willing to pay extra to have that option added to their LP 12. That is what we are looking to detemine in the pilot project-- is ICG practical in EMS, how does it perform in our environment and will it benefit patient care. If the answer is positive to all of these, perhaps it will be worth it to develop an EMS specific application for ICG that can be a low cost stand alone reporting only on the factors used in determining cardiac vs pulmonary dyspnea, or integrated into an existing monitor/defib platform, much the same as capnography, pulse oximetry, and external pacing have been integrated into existing monitor/defib platforms.

Other questions you had were on size-- it is a lot smaller and lighter than a LP 12! As far as how it responds in EMS, i.e. artifact, etc... these are things we will find out in the pilot. AS far as time, it takes 3-5 minutes from start to finish to obtain the values, and it can be left on for continuous monitoring, and the screen can be configured to show whichever values you wish to monitor.

ACE844- Please call me when you get a chance at 888-309-4568. I'd like to talk to you and get more input from you, plus I can answer your questions a little more effectively than going back and forth in posts.

[Ace844]

"Buddy"

Here's a semi-recent prehospital/ER study which is related to the topic at hand and may bring an interesting perspective...

Hope this helps,

Ace844

CONCORDANCE OF FIELD AND EMERGENCY DEPARTMENT ASSESSMENT IN THE PREHOSPITAL MANAGEMENT OF PATIENTS WITH DYSPNEA

Charles N. Pozner A1, Michael Levine A1, Nathan Shapiro A1, John P. Hanrahan A1

A1 Department of Emergency Medicine (CNP, NS, JPH), Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts; and Finch University and the Chicago Medical School (ML), North Chicago, Illinois.

Abstract:

Objective. Dyspnea is a common complaint of patients treated by emergency medical services (EMS). Few studies have examined the ability of paramedics to distinguish between etiologies of dyspnea. The authors evaluated the degree of agreement related to cardiac versus noncardiac sources of dyspnea between field and emergency department (ED) assessment of patients transported at the advanced life support level. Methods. This was a retrospective, cohort study of consecutive patients aged ≥35 years transported by paramedics with dyspnea. The authors compared the concordance between the EMS and ED diagnoses. They also investigated whether patients whose assessments were discordant had worse outcomes. Results. Paramedics correctly assessed the cause of dyspnea in 172 of 222 (77%) patients (kappa = 0.60; 95% confidence interval [CI] = 0.51, 0.69). Among single-source (i.e., cardiac or noncardiac) dyspnea patients, prehospital providers correctly assessed 70 of 84 (83%) noncardiac causes and 98 of 114 (86%) cardiac causes (kappa = 0.69; 95% CI = 0.59, 0.79). When the ED diagnosis included both cardiac and noncardiac etiologies, paramedics treated seven of 24 (29%) patients as noncardiac, 13 of 24 (54%) as cardiac, and four of 24 (17%) as combined-source dyspnea.The authors did not observe any statistically significant differences in in-hospital mortality, intubation frequency, or hospital length of stay in patients whose prehospital dyspnea diagnosis was discordant. . Conclusion. The authors conclude that in this EMS system, field assessment of dyspnea by paramedics is in agreement with that arrived at in the ED in a high proportion of patients with dyspnea from a single source. However, field assessment of dyspnea from multiple etiologies is less concordant.

[Buddy]

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]

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.

"Buddy,"

I tried your number and keep getting V-mail, I will continue to do so...

out here,

Ace844

[Buddy]

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]

"Buddy@Everyone,"

Here's another study which you may find useful FYI...and which is quite relevant to our discussion here...

Utility of NT-proBNP for the Diagnosis of Congestive Heart Failure in Patients with Pulmonary Disease

Carlos A. Camargo, Jr., Roderick H. Tung, Daniel G. Krauser, Saif Anwaruddin, Aaron L. Baggish, Annabel A. Chen and James L. Januzzi, Jr.

Massachusetts General Hospital: Boston, MA

ABSTRACT

Background: The diagnosis of acute congestive heart failure (CHF) in patients (pts) with pulmonary disease can be challenging. Objective: We hypothesized that N-terminal proBNP (NT-proBNP) testing would prove useful for the diagnosis of acute CHF in pts with prior chronic obstructive pulmonary disease or asthma (COPD/asthma). Methods: We enrolled consecutive emergency department (ED) pts with COPD/asthma who presented with dyspnea to a large urban ED. Pts were analyzed according to their final diagnosis of acute CHF versus COPD/asthma exacerbation, as adjudicated by study physicians based on clinical data from ED presentation through 60 days. At enrollment, ED physicians gave a probability (0–100%) of acute CHF as the cause of dyspnea. NT-proBNP measurements were compared to clinician estimates using area under the receiver-operating characteristic curve (AUC) tests. Results: Among 216 pts with COPD/asthma, 164 (76%) did not have a prior history of CHF, while 52 (24%) did. In pts without prior CHF, median NT-proBNP levels were significantly higher in pts with (new-onset) CHF compared to those with COPD/asthma exacerbation (1,561 vs. 168 pg/mL, p < 0.001). High clinical suspicion for CHF (probability 80%) detected only 23% of pts with new-onset CHF. In pts with histories of both prior CHF and COPD/asthma, median NT-proBNP levels were significantly higher in those with acute CHF than in those with COPD/asthma exacerbation (4,435 vs. 536 pg/mL, p < 0.001). Using previously established cutoffs (>450 pg/mL for age < 50 years, >900 pg/mL for age 50 years), the overall sensitivity and specificity of NT-proBNP for acute CHF were both 83%. NT-proBNP outperformed clinical estimation (AUC 0.90 vs. 0.83; p = 0.02). The combination was best (AUC 0.94, with p = 0.05 for combo vs. NT-proBNP alone, and p = 0.01 for combo vs. clinical estimation alone). Conclusions: NT-proBNP testing in dyspneic pts with prior COPD/asthma helps clinicians to detect new-onset CHF in pts without prior CHF history and to better differentiate the cause of dyspnea in pts with histories of both CHF and COPD/asthma.