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Monday, March 21, 2011
Thursday, March 17, 2011
Saturday, March 12, 2011
Ray Charles Can See It
A medic at work gave me this ekg and told me about this call he ran and that the STEMI was so obvious that Ray Charles could see it. Maybe he could, but if so, what would he be seeing? What do you see going on here with this pt?
This patient is 46 years old and has some cardiac history. He was awoken up from sleep with substernal chest pain. His skin was diaphoretic. He was given 4 NTG and morphine en route to the ER.
HR 75
BP 140/70
PR 176
QRS 119
QTC 433
Click on EKG’s to enlarge or press CTRL and + to zoom in on ekgs
Here is the 12 lead
This patient did make a trip to the Cath Lab shortly after arrival at the ER. Great Job to the Crew that ran this call and thanks so much for sharing.
This patient is 46 years old and has some cardiac history. He was awoken up from sleep with substernal chest pain. His skin was diaphoretic. He was given 4 NTG and morphine en route to the ER.
HR 75
BP 140/70
PR 176
QRS 119
QTC 433
Click on EKG’s to enlarge or press CTRL and + to zoom in on ekgs
Here is the 12 lead
This patient did make a trip to the Cath Lab shortly after arrival at the ER. Great Job to the Crew that ran this call and thanks so much for sharing.
Friday, March 4, 2011
It Must be Cardiac
by 12leadekg on March 4, 2011
81 year of Female altered mental status
What is going on with this patient?
Press CTRL and + putton on keyboard to zoom in on EKG strip to get a better look
The patient's ECG demonstrated a sinus rhythm at a rate of 60 bpm, with a markedly prolonged QT interval of 680 msec (normal range for females, 70% left anterior descending coronary artery stenosis at angiography.[9] Despite the association of this ECG pattern with significant coronary artery disease, in the setting of acute stroke this ECG pattern can be present without preexisting coronary artery disease.[1]
The determination of the causality of ECG changes seen in the patient described above requires careful attention to the neurologic and cognitive examination. Since patients who present with acute stroke also frequently have risk factors for the development of coronary artery disease, this ECG pattern can present a diagnostic dilemma. CNS-derived cardiac conditions can present with ECG changes mimicking cardiac ischemia and/or injury, focal wall motion abnormalities on echocardiography, and elevated biomarkers for cardiac injury. Therefore, these tests provide little diagnostic differentiation. Consequently, it is imperative to perform a rapid, but detailed, neurologic examination in patients who present to the ED with an ECG as described above in order to identify patients whose ECG changes may be related to an ongoing acute stroke. If the examination or clinical judgment warrants, rapid noncontrast CT scanning of the head or a magnetic resonance imaging (MRI) scan of the brain should be performed to evaluate for a CNS process.[1,2,3,4,6,10]
Once a patient has been identified as having ECG changes resulting from an acute stroke, it is reasonable for clinicians to perform echocardiography and serum biomarker analysis in order to potentially identify patients at a higher risk for cardiac adverse events. At a minimum, the presence of ECG changes during a CNS event warrants the placement of the patient on telemetry monitoring; however, given the frequency of ventricular arrhythmias (including ventricular tachycardia and fibrillation) in patients with acute stroke, placement of the patient in an intensive care unit solely for cardiac monitoring provides the highest level of safety. Treatments aimed at limiting adrenergic stimulation to the heart (beta-adrenergic receptor antagonists) can be given if the patient manifests evidence of cardiac dysfunction or injury. In cases of severe systolic dysfunction, supportive measures such as loop diuretics, supplemental oxygen, and/or endotracheal intubation may be necessary. While no randomized data support their use in stroke-mediated cardiac dysfunction, angiotensin-converting enzyme inhibitors (ACEI) and statin therapy are also reasonable options.[3,10]
Because of the overlapping risk profiles in patients with cerebrovascular and cardiovascular disease, once an acute CNS event has been treated, cardiac risk stratification with myocardial perfusion imaging may be performed. This serves to evaluate for potential underlying coronary artery disease that was "unmasked" by the stress of the CNS event. In the majority of patients with CNS-mediated ECG changes and cardiac dysfunction, however, the cause of their cardiac abnormalities is not significant coronary artery disease. Therefore, proceeding directly to coronary angiography in the absence of other compelling indicators is probably unwarranted.[10]
Despite the sometimes dramatic cardiac presentations in patients with acute stroke, the majority of these patients recover their cardiac function with supportive care. Patients should be monitored on telemetry until the ECG normalizes and the acute stroke symptoms stabilize. In patients with cardiac regional wall motion abnormalities, repeat echocardiography may be performed following normalization of the ECG to document resolution of the cardiac dysfunction.[10]
The patient in this case was admitted to the intensive care unit for cardiac monitoring, serial neurologic examinations, and further testing. An MRI of the brain confirmed a right-sided acute ischemic stroke, but the presence of the small subdural hemorrhages (likely the result of the patient's recurrent falls) prevented the use of antiplatelet therapy in this patient. The ECG changes normalized within 2 days and the cardiac enzymes remained within normal limits. An echocardiogram was performed on hospital day 2 which demonstrated moderate diastolic dysfunction, with no focal wall motion abnormalities. A repeat CT scan of the head on hospital day 4 showed no progression of the small subdural hemorrhages. The patient's neurologic exam did not change from her initial presentation and she was discharged to a skilled nursing facility on hospital day 5.
Special thanks are extended to Dr. John Vozenilek, MD, FACEP, for his contributions to the publication of this case
courtesy of Medscape
Tuesday, March 1, 2011
LBBB with MI present?
by 12leadekg on March 1, 2011
Is this a STEMI or is this normal for a LBBB?
There are several criteria s to determine if a BBB is present and if so which one, Left or Right? First QRS has to equal to or be > .12mm wide. We can use the turn signal method In lead V1 to see which way the QRS terminates. If it terminates down it would be a LBBB and if it terminated up it would be a RBBB. If you choose, you can use the rabbit-ear method to determine Left or Right BBB. If you see rabbit-ear patten (RSR’) in Leads V1 and V2 it would then most likely be a RBBB. If you were to see rabbit-ear pattern (RSR’) in leads V5 and V6 then it is most likely a LBBB. Although V1 is not shown here this is indeed a LBBB.
Now that we know we have a LBBB we now need to try to determine if we have a MI with this LBBB as well. One thing we know is that a LBBB is a huge STEMI Imposter. This means that there will probably be ST elevations present. What do you think about these elevations?
Saturday, February 26, 2011
Mouse heart 're-grows when cut', study shows
Scientists in the United States have found newborn mice can re-grow their own hearts.
The mice had a large chunk of their heart removed a day after birth, only for the heart to restore itself within three weeks.Fish and amphibians are known to have the power to re-grow heart tissue, but the study in Science is the first time the process has been seen in mammals.
British experts said understanding the process could help human heart care.
Narrow window The researchers at the University of Texas Southwestern Medical Center surgically removed what is known as the left ventricular apex of the heart (about 15% of the heart muscle) from mice just a day after birth.
The heart was then quickly seen to regenerate and was fully restored after 21 days. After two months, the organ still appeared to be functioning normally.
But when the same procedure was tested on mice aged one week, the heart failed to regenerate, suggesting this power of self-repair is extremely short-lived in mice.
The belief is that heart cells within the mouse have a narrow window after birth within which they can continue to replicate and repair. Subsequent tests suggested that these repair cells were coming from within the heart muscle.
"What our results show are that the new heart muscle cells which repair the amputated region of the heart came from proliferation and migration of pre-existing heart muscle cells," said Professor Eric Olson, who worked on the study.
"We have no evidence they came from a stem-cell population." Many amphibians and fish, most famously the zebrafish, have the ability to renew heart muscle right into adulthood.
This new study suggests mammals too have such capacity for self-repair, if only for a limited time after birth.
Professor Olson believes future research will show humans have a similar capacity, although no experiments involving human heart tissue are currently planned.
"There's no reason to believe that the same window would not exist in the human heart.
"Everything we know about development and early function of the mouse heart is comparable to the human heart so we're quite confident that this process does exist in humans, although that of course still has to be shown."
Heart attacks The team's focus is now on looking at ways to "re-awaken" this capacity to self repair in adult mice, with the ultimate ambition to do the same in humans to repair damage sustained during heart attacks.
"We've identified a micro-RNA (a small piece of genetic material) which regulates this process so we're tying to use that as a way of further enhancing cardiac regeneration later in life and we're also screening for new drugs which can re-awaken this mechanism in adult mice," he said.
Professor Jeremy Pearson, associate medical director of the British Heart Foundation, said the study showed heart regeneration was not the exclusive preserve of zebrafish and newts, but said more work needed to be done to understand what was actually going on inside the healing heart.
"This exciting research shows for the first time that young mice, like fish and amphibians, can heal their damaged hearts," he said. "It strengthens the view that understanding how this happens could provide the key to healing adult human hearts."
Professor Olson concedes there will be problems ahead. What works in the low-pressured heart of a zebrafish, might not work in the high-pressured multi-chambered heart of humans.
Meddling with heart muscle cells could, for instance, trigger arrhythmias in the heart, he said.
Friday, February 25, 2011
U.K. Hospital Revives Man with No Heartbeat after 3.5 Hours on ZOLL AutoPulse and 20,000 Chest Compressions
CHELMSFORD, Mass.--(BUSINESS WIRE)--ZOLL Medical Corporation (Nasdaq GS: ZOLL), a manufacturer of medical devices and related software solutions, announced today that Croydon University Hospital in London successfully revived a 53-year-old man from sudden cardiac arrest (SCA) using the ZOLL AutoPulse® Non-invasive Cardiac Support Pump for 3.5 hours. The automated CPR machine performed nearly 20,000 chest compressions before the man’s pulse returned.
The patient, an East London engineer, was found lying unconscious in the street and hypothermic last month in temperatures of 14˚F (-10C) when he was rushed to Croydon, where he suffered a cardiac arrest. Fortunately for him, he came under the care of two of the leading resuscitation experts in England, Dr. Raghunath and Russell Metcalfe-Smith, Clinical Lead for Resuscitation at Coydon. The patient was placed on the AutoPulse, which delivered 80 compressions per minute, allowing the team of medics to perform other life-saving therapies.
“Even a fully-trained professional finds it hard to deliver consistent, high-quality chest compressions when attempting to resuscitate someone whose heart has stopped beating. A&E (Emergency Dept.) teams have a range of equipment available, but the AutoPulse means we can carry on helping someone’s heart to beat for much longer—improving blood flow to vital organs and increasing their chances of recovery,” said Dr. Raghunath.
“Without the AutoPulse, we would have needed relay teams of people continually performing chest compressions while we worked around them. With the clock approaching three and a half hours, the patient’s pulse returned and his heart flickered back to life,” said Metcalfe-Smith. “This is the stuff you read about in medical journals, but never expect to experience firsthand.”
Croydon was the first hospital in the United Kingdom to use the AutoPulse when it was installed four years ago, and the first in Europe to standardize on its use for every cardiac arrest in the facility. The hospital also experiences one of the highest cardiac arrest rates in London in the Emergency Department, according to Metcalfe-Smith, with around 350 cardiac arrest cases brought into the department each year and another 185 in-hospital arrests.
About the AutoPulse
The AutoPulse Non-invasive Cardiac Support Pump is an automated, portable device with an easy-to-use, load-distributing LifeBand® that squeezes the entire chest, improving blood flow to the heart and brain during sudden cardiac arrest (SCA). The AutoPulse may offer a significant advantage over manual CPR, moving blood more consistently than human providers. AutoPulse delivers high-quality, uninterrupted chest compressions to maintain myocardial and cerebral perfusion. Additionally, it offers the benefit of freeing up clinicians and rescuers to focus on other life-saving interventions.
Earlier this month ZOLL announced the successful completion of the international CIRC (Circulation Improving Resuscitation Care) trial when an analysis of the data by the independent Data Safety Monitoring Board (DSMB) showed the load-distributing band (AutoPulse) to be equivalent to manual chest compressions. The CIRC trial compared the rates of survival to hospital discharge from out-of-hospital cardiac arrest of patients treated with the load-distributing band device to those receiving manual CPR.
Nearly 6,000 AutoPulse devices are in use in hospitals and emergency service organizations worldwide.
About Sudden Cardiac Arrest
SCA, an abrupt disruption of the heart’s function, which causes a lack of blood flow to vital organs, claims more than 1 million lives globally each year. It is the leading cause of unexpected death in the world and strikes without warning. Survival is poor in most communities at less than eight percent and improvements in resuscitation practices could save as many as half of these victims.
About Croydon University Hospital
Croydon University Hospital (CUH) is the major hospital for Coydon Health Services NHS Trust, which serves Croydon, London’s largest borough with a population of 340,000 covering parts of southwest London and north Surrey. The Trust is responsible for planning and funding healthcare, and for public health in Croydon. CUH is a 500-bed hospital which treats over 120,000 patients a year, 41,000 of which are admitted for emergency care.
About ZOLL Medical Corporation
ZOLL Medical Corporation develops and markets medical devices and software solutions that help advance emergency care and save lives, while increasing clinical and operational efficiencies. With products for defibrillation and monitoring, circulation and CPR feedback, data management, fluid resuscitation, and therapeutic temperature management, ZOLL provides a comprehensive set of technologies that help clinicians, EMS and fire professionals, and lay rescuers treat victims needing resuscitation and critical care.
A NASDAQ Global Select company and a Forbes 100 Most Trustworthy Company in 2007, 2008, and 2009, ZOLL develops and manufactures its products in the United States, in California, Colorado, Illinois, Massachusetts, Pennsylvania, and Rhode Island. More than 400 direct sales and service representatives, 1,100 business partners, and 200 independent representatives serve our customers in over 140 countries around the globe. For more information, visit www.zoll.com.
Certain statements contained in this press release, including statements regarding the future business of the Company, and other statements contained herein regarding matters that are not historical facts, are “forward-looking” statements (as defined in the Private Securities Litigation Reform Act of 1995). Because such statements are subject to risks and uncertainties, actual results may differ materially from those expressed or implied by such forward-looking statements. Factors that could cause actual results to differ materially from those expressed or implied by such forward-looking statements include, but are not limited to, those factors discussed in the section entitled “Risk Factors” in the Company's Annual Report on Form 10-K filed with the SEC on December 17, 2010. You should not place undue reliance on the forward looking statements in this press release, and the Company disavows any obligation to update or supplement those statements in the event of any changes in the facts, circumstances, or expectations that underlie those statements.
Copyright © 2011 ZOLL Medical Corporation. All rights reserved. 269 Mill Road, Chelmsford, MA 01824-4105. AutoPulse and ZOLL are trademarks and/or registered trademarks of ZOLL Medical Corporation in the United States and/or other countries. All product names are the property of their respective owners.
ZOLL Medical Corporation
A. Ernest Whiton, +1 (978) 421-9655
Chief Financial Officer
or
MEDIA:
ZOLL Medical Corporation
Diane Egan, +1 (978) 421-9637
degan@zoll.com
“Without the AutoPulse, we would have needed relay teams of people continually performing chest compressions while we worked around them. With the clock approaching three and a half hours, the patient’s pulse returned and his heart flickered back to life”“He had no pulse or heartbeat when he arrived at the hospital, so it is amazing that we were able to resuscitate him. I’ve not seen anything like it in 15 years in the emergency department,” said Nigel Raghunath, M.D., who heads the hospital’s emergency unit.
The patient, an East London engineer, was found lying unconscious in the street and hypothermic last month in temperatures of 14˚F (-10C) when he was rushed to Croydon, where he suffered a cardiac arrest. Fortunately for him, he came under the care of two of the leading resuscitation experts in England, Dr. Raghunath and Russell Metcalfe-Smith, Clinical Lead for Resuscitation at Coydon. The patient was placed on the AutoPulse, which delivered 80 compressions per minute, allowing the team of medics to perform other life-saving therapies.
“Even a fully-trained professional finds it hard to deliver consistent, high-quality chest compressions when attempting to resuscitate someone whose heart has stopped beating. A&E (Emergency Dept.) teams have a range of equipment available, but the AutoPulse means we can carry on helping someone’s heart to beat for much longer—improving blood flow to vital organs and increasing their chances of recovery,” said Dr. Raghunath.
“Without the AutoPulse, we would have needed relay teams of people continually performing chest compressions while we worked around them. With the clock approaching three and a half hours, the patient’s pulse returned and his heart flickered back to life,” said Metcalfe-Smith. “This is the stuff you read about in medical journals, but never expect to experience firsthand.”
Croydon was the first hospital in the United Kingdom to use the AutoPulse when it was installed four years ago, and the first in Europe to standardize on its use for every cardiac arrest in the facility. The hospital also experiences one of the highest cardiac arrest rates in London in the Emergency Department, according to Metcalfe-Smith, with around 350 cardiac arrest cases brought into the department each year and another 185 in-hospital arrests.
About the AutoPulse
The AutoPulse Non-invasive Cardiac Support Pump is an automated, portable device with an easy-to-use, load-distributing LifeBand® that squeezes the entire chest, improving blood flow to the heart and brain during sudden cardiac arrest (SCA). The AutoPulse may offer a significant advantage over manual CPR, moving blood more consistently than human providers. AutoPulse delivers high-quality, uninterrupted chest compressions to maintain myocardial and cerebral perfusion. Additionally, it offers the benefit of freeing up clinicians and rescuers to focus on other life-saving interventions.
Earlier this month ZOLL announced the successful completion of the international CIRC (Circulation Improving Resuscitation Care) trial when an analysis of the data by the independent Data Safety Monitoring Board (DSMB) showed the load-distributing band (AutoPulse) to be equivalent to manual chest compressions. The CIRC trial compared the rates of survival to hospital discharge from out-of-hospital cardiac arrest of patients treated with the load-distributing band device to those receiving manual CPR.
Nearly 6,000 AutoPulse devices are in use in hospitals and emergency service organizations worldwide.
About Sudden Cardiac Arrest
SCA, an abrupt disruption of the heart’s function, which causes a lack of blood flow to vital organs, claims more than 1 million lives globally each year. It is the leading cause of unexpected death in the world and strikes without warning. Survival is poor in most communities at less than eight percent and improvements in resuscitation practices could save as many as half of these victims.
About Croydon University Hospital
Croydon University Hospital (CUH) is the major hospital for Coydon Health Services NHS Trust, which serves Croydon, London’s largest borough with a population of 340,000 covering parts of southwest London and north Surrey. The Trust is responsible for planning and funding healthcare, and for public health in Croydon. CUH is a 500-bed hospital which treats over 120,000 patients a year, 41,000 of which are admitted for emergency care.
About ZOLL Medical Corporation
ZOLL Medical Corporation develops and markets medical devices and software solutions that help advance emergency care and save lives, while increasing clinical and operational efficiencies. With products for defibrillation and monitoring, circulation and CPR feedback, data management, fluid resuscitation, and therapeutic temperature management, ZOLL provides a comprehensive set of technologies that help clinicians, EMS and fire professionals, and lay rescuers treat victims needing resuscitation and critical care.
A NASDAQ Global Select company and a Forbes 100 Most Trustworthy Company in 2007, 2008, and 2009, ZOLL develops and manufactures its products in the United States, in California, Colorado, Illinois, Massachusetts, Pennsylvania, and Rhode Island. More than 400 direct sales and service representatives, 1,100 business partners, and 200 independent representatives serve our customers in over 140 countries around the globe. For more information, visit www.zoll.com.
Certain statements contained in this press release, including statements regarding the future business of the Company, and other statements contained herein regarding matters that are not historical facts, are “forward-looking” statements (as defined in the Private Securities Litigation Reform Act of 1995). Because such statements are subject to risks and uncertainties, actual results may differ materially from those expressed or implied by such forward-looking statements. Factors that could cause actual results to differ materially from those expressed or implied by such forward-looking statements include, but are not limited to, those factors discussed in the section entitled “Risk Factors” in the Company's Annual Report on Form 10-K filed with the SEC on December 17, 2010. You should not place undue reliance on the forward looking statements in this press release, and the Company disavows any obligation to update or supplement those statements in the event of any changes in the facts, circumstances, or expectations that underlie those statements.
Copyright © 2011 ZOLL Medical Corporation. All rights reserved. 269 Mill Road, Chelmsford, MA 01824-4105. AutoPulse and ZOLL are trademarks and/or registered trademarks of ZOLL Medical Corporation in the United States and/or other countries. All product names are the property of their respective owners.
Contacts
INVESTORS:ZOLL Medical Corporation
A. Ernest Whiton, +1 (978) 421-9655
Chief Financial Officer
or
MEDIA:
ZOLL Medical Corporation
Diane Egan, +1 (978) 421-9637
degan@zoll.com
Tuesday, February 22, 2011
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Monday, February 21, 2011
What would you call this if you were running this call?
Here is another case study. This call was ran last week at 13:33 hours. What do you think about this 12 lead?
51 year old male patient working covered in black grease but Crew could tell that the patient appeared pale and diaphoretic. Skin was cool to touch. The patient tells the crew that it feels like something is setting on his chest. Pain is 9/10. He appears anxious but denies shortness of breath, nausea and vomiting, or weakness and dizziness. History of coronary issues with 9 to 10 stients and diabetes. BGL was checked 200mg/dl.
He was given ASA 324mg PO and NTG x 3 en route to ER. Pain down to 7/10. IV was established in AC.
V/S
BP 130/80
Pulse 89
Respirations 18-20
12 Lead EKG obtained and transmitted to ER. Is this EKG Normal/Not Normal? What is your interpretation?
Ok here is another 12 captured later in the call. The quality looks a little better. Does this change your mind?
51 year old male patient working covered in black grease but Crew could tell that the patient appeared pale and diaphoretic. Skin was cool to touch. The patient tells the crew that it feels like something is setting on his chest. Pain is 9/10. He appears anxious but denies shortness of breath, nausea and vomiting, or weakness and dizziness. History of coronary issues with 9 to 10 stients and diabetes. BGL was checked 200mg/dl.
He was given ASA 324mg PO and NTG x 3 en route to ER. Pain down to 7/10. IV was established in AC.
V/S
BP 130/80
Pulse 89
Respirations 18-20
12 Lead EKG obtained and transmitted to ER. Is this EKG Normal/Not Normal? What is your interpretation?
Ok here is another 12 captured later in the call. The quality looks a little better. Does this change your mind?
Sunday, February 20, 2011
Medical Review Date: August 5, 2009
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EKG's?
Ok folks I need new EKG's for some more discussions. Also if you have any questions ask. Send them to me. Thanks
Monday, February 14, 2011
A Broken Heart Mirrors Signs Of A Heart Attack Doctors Calls The Condition Broken Heart Syndrome
WATERBURY, Conn. -- Doctors call it the broken heart syndrome. A patient suffering from severe emotional stress has all the signs of a conventional heart attack. While rare, the syndrome, which is seen predominately in women, is brought on by severe emotional distress and physically alters the beating of a heart. “It is, by every measure, a heart attack. Patients come to the emergency room with chest pain. They do have EKG changes. They do have evidence in their blood that the heart muscle has been injured,” said Paul Kelly, a cardiologist at St. Mary’s Hospital in Waterbury. Kelly said when a patient found out that her mother had died 48 hours before her wedding, she was rushed to the hospital with what doctors thought was a heart attack. The severe emotional distress the patient experienced caused a surge of adrenaline in her body. “The heart is squeezing very vigorously from the front and on the underside. You can see it's contracting. It's almost super contracting, pushing very, very vigorously, “ Kelly said Unlike a heart attack, the symptoms of a broken heart come on very rapidly, within minutes of hearing bad news, and go back to normal almost as fast. Less than 1 percent of patients who go to the hospital with chest pains actually have broken heart syndrome, Kelly said. Therapy for a broken heart syndrome are beta blockers, medication that can shield some of the adrenaline and give the heart a chance to recover. The heart usually recovers within two days, Kelly said.. Kelly said chocolate also mends a broken heart. “Dark chocolate, and pounds of it,” he said.
What do you think? Next time you run that call to a family member who is hysterical and complaining of chest pain, because they just found out another family member or friend has died, may actually have a real medical situation.
Other interesting facts about Broken Heart Syndrome.
About 70-80% of cases of Tako-tsubo Syndrome (TTS) occur in post-menopausal women under some form of extreme, exceptional and prolonged mental stress,... with no good way out, no relief and often feeling deep resentment (such as the loss of a dear one...)
(Note: a word of caution... , in a minority of patients (<20%) the stress is physical (such as massive trauma, surgery or severe pain, or other type of stress. In very rare cases, no "cause" can be found).
Tako-tsubo Cardiomyopathy or Syndrome is also known as:
- neurogenic myocardial stunning,
- stress cardiomyopathy
- stress-induced cardiomyopathy,
- transient left ventricular apical ballooning,
- "ampulla" cardiomyopathy
- "broken heart syndrome".
"Tako-tsubo" is the japanese name for octopus traps that fishermen still use to catch octopus. In this syndrome, the heart (left ventricle) takes the shape of an octopus trap (tako-tsubo). How about that!
The shape that the left ventricle takes (tako-tsubo shape) is due to a state of complete exhaustion of the heart muscle (myocardial stunning) in the mid-section and tip of the heart. The fascinating part is that it occurs in patients without significant blockage (stenosis) of their coronary arteries (now: that is surprising and remarkable!).
A profound tako-tsubo syndrome is quite dangerous if not recognized as it can lead to transient but severe (occasionally lethal) cardiogenic shock. Electrocardiogram can show non-specific ST-T abnormalities, ST elevation, and/or QT prolongation with large negative T waves. Sometimes those changes occur in succession. And here is another surprise: the cardiac bio markers of heart damage (troponin, creatine kinase) are only very slightly elevated, confirming that there is not much heart muscle damage, but severe suffering (stunning) instead.
And that leads to the good news, Folks!
If this syndrome is recognized, over 95% of patients pull through that fairly easily (with most of the time complete recovery of the electrocardiographic changes and recovery of the cardiac shape and function. This may take a few weeks).
Suggestion: patients should be send to cardiac rehabilitation and if possible to a stress reduction clinic if the syndrome is complicated by continued stress or by a syndrome similar to "post-traumatic stress syndrome". If this syndrome is recognized, over 95% of patients pull through that fairly easily (with most of the time complete recovery of the electrocardiographic changes and recovery of the cardiac shape and function. This may take a few weeks).
The idea is to prevent recurrence (which is low but still exists) by indentifying and trying to eliminate or deflect stressors while educating patients how to counter and how to develop resilience to stress
Images on this site © Striped Giraffe Press, December 2005. All rights reserved.
Can Android teach EKG interpretation? An overview of three popular Android EKG apps
[Android medical app review]
Repetition, repetition, repetition. Most of the information I retained from the first few years of medical school is what I learned by repetition. Unless I use some bit of knowledge regularly, I tend to forget it. Reading an EKG is one of those skills in medicine that requires a lot of background knowledge, the ability to recognize patterns, and the clinical experience to know what looks “okay” and what looks “definitely not okay.” While no app or textbook can replace the practical skills that one acquires through months or years of interpreting real EKGs and seeing patients, it helps to have a quick reference of ground rules and basic pattern descriptions to refresh one’s mind on the basic reading rules of EKGs.Medical students and residents have been carrying around pocket-sized EKG manuals for decades. But over the past several months a few ECG/EKG apps have cropped up on the Android Market, hoping to fill the need for an electronic alternative.
Here I take a look at three EKG interpretation and learning tools for Android mobile devices: EKGdroid, EKG:Advanced, and EKG Calipers. Can Android really replace those pocket manuals and teach the next generation of doctors to read EKGs?
EKGdroid ($2.99) by Webpatient.net
EKGdroid is not a flashy app, but it has many of basic tools needed to interpret an EKG.. The interface is very basic in comparison to iPhone apps we have reviewed (ECG guide, Instant ECG, ECG Interpreter). But the learning curve to navigate the app is essentially zero. The user selects among the common normal and abnormal rhythms, and a zoom-able rhythm strip appears. The user can navigate among the sub-menus to learn about characteristics of that rhythm.
This app is not good for students who want to learn “from scratch” how to read EKGs. This app lacks information on basic EKG principles, like determining axis and rate. In general, the app does not teach how to understand EKGs, but rather how to identify common patterns of pathology on EKGs. This point might seem subtle, but trying to read EKGs without a basic understanding of the theory is an exercise in futility.
Finally, let it be known that EKGdroid is not an exhaustive manual of EKG interpretation. Only the most basic information about each rhythm is presented.
EKG: Advanced ($1.99) by simpaddico
For those who love flash cards, EKG:Advanced is a great app for a quick quiz of EKG knowledge. Like EKGdroid, this app is extremely easy to use and navigate. The app uses the Q&A style and quick-feedback that physical flashcard lovers enjoy. A Main Deck of cards contains all of the available questions, and the Faves menu allows the user to store wrongly-answered questions (or any set of cards) in another Faves Deck, which can be “flipped” through later. Alternatively, the Ignore function will remove cards from the deck. The Search function is useful – searching both questions and answers for the search term. Settings allow the user to shuffle the decks, or view the answers to each card first (presumably to guess the question – like Jeopardy?). I am still trying to figure out how one might use the Index.
Surprisingly, and unlike EKGdroid, there are no rhythm strips in this deck of flash cards.
In future versions, I would love to see a “make your own flashcard” function.
This app is not good for an organized approach to learning EKGs. The Main Deck is arranged in a seemingly random order, which is no way to learn EKG principles for the first time.
EKG Calipers ($0.99) by HC Dev
Trouble determining the heart rate on an EKG? EKG Calipers is a simple app that can be calibrated to estimate heart rate by holding the edge of the phone to an EKG. I guess the theory is that a caliper app reduces the need for (and cost of) another tool in the white coat.
Summary: Can Android teach EKG interpretation?
In short… not yet. As compared to the iPhone apps we reviewed (see above links), these Android apps, as a group, fall short in three major areas.
1. No organized approach to learning EKG physiology, anatomy, and theory. None of these apps individually (or as a group) teach the basics of EKG interpretation in an organized manner. Without a great deal of prerequisite reading or background lectures to form a foundation of understanding, students will find these apps to be of little use.
2. Lacking depth. The information on these apps is, as you would expect from the price, only superficial, and does not compare to pocket EKG manuals or iPhone EKG apps.
3. Aesthetically blah. Like many of the medical apps currently available on the Android Market, these apps favor function over form. While not unattractive, these apps look… well… bland compared to the polish and prim of the iPhone competition.
So for now, Android users who want to use their mobile device to learn how to read an EKG have a few options: (1) buy an EKG textbook (or pocket manual), (2) call the nicest Cardiology fellow you know when reading EKGs, or (3) hope for further development of these and other EKG apps in the Android Market.
Defibrillator Implants: 1 In 5 Heart Could Be Unnecessary
CHICAGO — One in five heart defibrillators may be implanted for questionable reasons without solid evidence that the devices will help, according to a first-of-its-kind analysis.
Implanted defibrillators shock the heart back into a normal rhythm when it starts beating irregularly. They can prevent sudden death in people with advanced heart failure, but researchers haven't found a benefit for other patients.
Patients who've had a recent heart attack or recent bypass surgery aren't good candidates for defibrillators, for example. Guidelines don't recommend them for people newly diagnosed with heart failure either and those so sick that they have very limited life expectancies won't be helped.
But in the new study, which examined nearly four years of national data, 22 percent of the implant surgeries were in patients who fit one of those categories.
Some may have been appropriate, said lead author Dr. Sana Al-Khatib of Duke University School of Medicine in Durham, N.C., but it's likely that many were done despite the research evidence.
"It's lack of knowledge. It's ignorance. It's not keeping track of the guidelines," she said. "And we may have some physicians who don't agree with the guidelines or don't think the guidelines apply to their patients."
The study, appearing in Wednesday's Journal of the American Medical Association, examined national registry data from nearly 112,000 patients in 2006-2009.
The researchers found that the patients who got implants according to guidelines were less likely to die in the hospital and suffer complications than the patients whose surgeries clearly fell outside the guidelines. Fewer than 1 percent of either group died in the hospital.
The surgeries cost thousands of dollars, raising questions about wasted resources, Al-Khatib said. "It's all about improving the quality of care," she said.
Story continues below
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The 22 percent rate is disturbingly high, said Dr. Douglas Zipes of the Indiana University School of Medicine in Indianapolis. He wasn't involved in the study but has helped write research-based guidelines for the devices.
"If the patient is not benefiting, we shouldn't be doing it," Zipes said. He noted that doctors with special training in heart rhythms, had slightly better rates of evidence-based implants than did other types of doctors in the study.
Doctors should follow guidelines, he said, and patients should choose a specialist with training in heart rhythm problems.
___
Online:
JAMA: http://jama.ama-assn.org
Implanted defibrillators shock the heart back into a normal rhythm when it starts beating irregularly. They can prevent sudden death in people with advanced heart failure, but researchers haven't found a benefit for other patients.
Patients who've had a recent heart attack or recent bypass surgery aren't good candidates for defibrillators, for example. Guidelines don't recommend them for people newly diagnosed with heart failure either and those so sick that they have very limited life expectancies won't be helped.
But in the new study, which examined nearly four years of national data, 22 percent of the implant surgeries were in patients who fit one of those categories.
Some may have been appropriate, said lead author Dr. Sana Al-Khatib of Duke University School of Medicine in Durham, N.C., but it's likely that many were done despite the research evidence.
"It's lack of knowledge. It's ignorance. It's not keeping track of the guidelines," she said. "And we may have some physicians who don't agree with the guidelines or don't think the guidelines apply to their patients."
The study, appearing in Wednesday's Journal of the American Medical Association, examined national registry data from nearly 112,000 patients in 2006-2009.
The researchers found that the patients who got implants according to guidelines were less likely to die in the hospital and suffer complications than the patients whose surgeries clearly fell outside the guidelines. Fewer than 1 percent of either group died in the hospital.
The surgeries cost thousands of dollars, raising questions about wasted resources, Al-Khatib said. "It's all about improving the quality of care," she said.
Story continues below
Advertisement
The 22 percent rate is disturbingly high, said Dr. Douglas Zipes of the Indiana University School of Medicine in Indianapolis. He wasn't involved in the study but has helped write research-based guidelines for the devices.
"If the patient is not benefiting, we shouldn't be doing it," Zipes said. He noted that doctors with special training in heart rhythms, had slightly better rates of evidence-based implants than did other types of doctors in the study.
Doctors should follow guidelines, he said, and patients should choose a specialist with training in heart rhythm problems.
___
Online:
JAMA: http://jama.ama-assn.org
Saturday, February 12, 2011
Thursday, February 10, 2011
Q wave Time frame for STEMI's
A) Shows the normal QRS complex in a lead.
B & C) Within hours of the clinical onset of an MI, there is ST segment elevation. At this stage no QRS or T wave changes have occurred. This indicates myocardial damage only, not definitive evidence of infarction.
D) Within days, the R wave voltage falls and abnormal Q waves appear. This is sufficient evidence of an infarction. In addition, T wave inversion will also have appeared but the ST segment elevation may be less obvious than before.
E) Within one or more weeks, the ST segment changes revert completely to normal. The R wave voltage remains low and the abnormal Q waves persist. Deep, symmetrical T wave inversion may develop at this stage.
F) Months after the MI, the T waves may gradually return to normal. The abnormal Q waves and reduced R wave voltage persist.
Occasionally, all evidence of infarction may be lost with the passing of time; this is due to shrinkage of scar tissue.
B & C) Within hours of the clinical onset of an MI, there is ST segment elevation. At this stage no QRS or T wave changes have occurred. This indicates myocardial damage only, not definitive evidence of infarction.
D) Within days, the R wave voltage falls and abnormal Q waves appear. This is sufficient evidence of an infarction. In addition, T wave inversion will also have appeared but the ST segment elevation may be less obvious than before.
E) Within one or more weeks, the ST segment changes revert completely to normal. The R wave voltage remains low and the abnormal Q waves persist. Deep, symmetrical T wave inversion may develop at this stage.
F) Months after the MI, the T waves may gradually return to normal. The abnormal Q waves and reduced R wave voltage persist.
Occasionally, all evidence of infarction may be lost with the passing of time; this is due to shrinkage of scar tissue.
Another Version
Wednesday, February 9, 2011
Tuesday, February 8, 2011
Lets Talk Capnography
Capnography
10 Things Every Paramedic Should Know About CapnographyCapnography is the vital sign of ventilation.
By tracking the carbon dioxide in a patient’s exhaled breath, capnography enables paramedics to objectively evaluate a patient’s ventilatory status (and indirectly circulatory and metabolic status), as the medics utilize their clinical judgement to assess and treat their patients.
Part One: The Science
Definitions:Capnography – the measurement of carbon dioxide (CO2) in exhaled breath.
Capnometer – the numeric measurement of CO2.
Capnogram – the wave form.
End Tidal CO2 (ETCO2 or PetCO2) – the level of (partial pressure of) carbon dioxide released at end of expiration.
Oxygenation Versus Ventilation
Oxygenation is how we get oxygen to the tissue. Oxygen is inhaled into the lungs where gas exchange occurs at the capillary-alveolar membrane. Oxygen is transported to the tissues through the blood stream. Pulse oximetry measures oxygenation.
At the cellular level, oxygen and glucose combine to produce energy. Carbon dioxide, a waste product of this process (The Krebs cycle), diffuses into the blood.
Ventilation (the movement of air) is how we get rid of carbon dioxide. Carbon dioxide is carried back through the blood and exhaled by the lungs through the alveoli. Capnography measures ventilation.
Capnography versus Pulse Oximetry
Capnography provides an immediate picture of patient condition. Pulse oximetry is delayed. Hold your breath. Capnography will show immediate apnea, while pulse oximetry will show a high saturation for several minutes.
Circulation and Metabolism
While capnography is a direct measurement of ventilation in the lungs, it also indirectly measures metabolism and circulation. For example, an increased metabolism will increase the production of carbon dioxide increasing the ETCO2. A decrease in cardiac output will lower the delivery of carbon dioxide to the lungs decreasing the ETCO2.
“CO2 is the smoke from the flames of metabolism.”– Ray Fowler, M.D. Dallas, Street Doc’s Society
PaCO2 vs. PeTCO2
PaCO2= Partial Pressure of Carbon Dioxide in arterial blood gases. The PaCO2 is measured by drawing the ABGs, which also measure the arterial PH.
If ventilation and perfusion are stable PaCO2 should correlate to PetCO2.
In a study comparing PaCO2 and PetCO2 in 39 patients with severe asthma, the mean difference between PaCO2 and PetCO2 was 1.0 mm Hg, the median difference was 0 mm Hg. Only 2 patients were outside the 5 mg HG agreement (1-6, 1-12). -Jill Corbo, MD, et al, Concordance Between Capnography and Arterial Blood Gas Measurements of Carbon Dioxide in Acute Asthma, Annals of Emergency Medicine, October 2005
V/Q Mismatch
“Research has (also) shown good concordance…in patients with normal lung function, upper and lower airway disease, seizures, and diabetic ketoacidosis.” –ibid.
If ventilation or perfusion are unstable, a Ventilation/Perfusion (V/Q) mismatch can occur. This will alter the correlation between PaC02 and PetCO2.
This V/Q mismatch can be caused by blood shunting such as occurs during atelectasis (perfusing unventilated lung area) or by dead space in the lungs (Ventilating unperfused lung area) such as occurs with a pulmonary embolisim or hypovolemia.
Normal Capnography Values
ETCO2 35-45 mm Hg is the normal value for capnography. However, some experts say 30 mm HG – 43 mm Hg can be considered normal.
Cautions: Imperfect positioning of nasal cannula capnofilters may cause distorted readings. Unique nasal anatomy, obstructed nares and mouth breathers may skew results and/or require repositioning of cannula. Also, oxygen by mask may lower the reading by 10% or more.
Capnography Wave Form
The normal wave form appears as straight boxes on the monitor screen:
But the wave form appears more drawn out on the print out because the monitor screen is compressed time while the print out is in real time.
The capnogram wave form begins before exhalation and ends with inspiration. Breathing out comes before breathing in.
A to B is post inspiration/dead space exhalation, B is the start of alveolar exhalation, B-C is the exhalation upstroke where dead space gas mixes with lung gas, C-D is the continuation of exhalation, or the plateau(all the gas is alveolar now, rich in C02). D is the end-tidal value – the peak concentration, D-E is the inspiration washout.
Abnormal Values and Wave Forms
ETCO2 Less Than 35 mmHg = “Hyperventilation/Hypocapnia”
ETC02 Greater Than 45 mmHg = “Hypoventilation/Hypercapnia”
Caution:
“End Tidal CO2 reading without a waveform is like a heart rate without an ECG recording.” – Bob Page “Riding the Waves”
However, unlike ECGs, there are only a few capnography wave forms. The main abnormal ones — hyperventilation, hypoventilation, esophageal intubation and obstructive airway/shark fin — are described below.
Part Two: Clinical Uses of Capnography
1. Monitoring Ventilation
Capnography monitors patient ventilation, providing a breath by breath trend of respirations and an early warning system of impending respiratory crisis.
Hyperventilation
When a person hyperventilates, their CO2 goes down.
Hyperventilation can be caused by many factors from anxiety to bronchospasm to pulmonary embolus. Other reasons C02 may be low: cardiac arrest, decreased cardiac output, hypotension, cold, severe pulmonary edema.
Note: Ventilation equals tidal volume X respiratory rate. A patient taking in a large tidal volume can still hyperventilate with a normal respiratory rate just as a person with a small tidal volume can hypoventilate with a normal respiratory rate.
Hypoventilation
When a person hypoventilates, their CO2 goes up.
Hypoventilation can be caused by altered mental status such as overdose, sedation, intoxication, postictal states, head trauma, or stroke, or by a tiring CHF patient. Other reasons CO2 may be high: Increased cardiac output with increased breathing, fever, sepsis, pain, severe difficulty breathing, depressed respirations, chronic hypercapnia.
Some diseases may cause the CO2 to go down, then up, then down. (See asthma below).
Pay more attention to the ETCO2 trend than the actual number.
A steadily rising ETCO2 (as the patient begins to hypoventilate) can help a paramedic anticipate when a patient may soon require assisted ventilations or intubation.
Heroin Overdoses – Some EMS systems permit medics to administer narcan only to unresponsive patients with suspected opiate overdoses with respiratory rates less than 10. Monitoring ETCO2 provides a better gauge of ventilatory status than respiratory rate. ETCO2 will show a heroin overdose with a respiratory rate of 24 (with many shallow ineffective breaths) and an ETCO2 of 60 is more in need of arousal than a patient with a respiratory rate of 8, but an ETCO2 of 35.
2. Confirming, Maintaining , and Assisting Intubation
Continuous end-tidal CO2 monitoring can confirm a tracheal intubation. A good wave form indicating the presence of CO2 ensures the ET tube is in the trachea.
A 2005 study comparing field intubations that used continuous capnography to confirm intubations versus non-use showed zero unrecognized misplaced intubations in the monitoring group versus 23% misplaced tubes in the unmonitored group. -Silverstir, Annals of Emergency Medicine, May 2005
“When exhaled CO2 is detected (positive reading for CO2) in cardiac arrest, it is usually a reliable indicator of tube position in the trachea.” – The American Heart Association 2005 CPR and ECG Guidelines
Reasons ETCO2 is zero: The tube is in the esophagus.*
* True as a general rule, but may not hold for cases of greatly prolonged down time prior to initiation of CPR or cases of massive pulmonary embolism where blood flow to the lungs is completely blocked. Also, in patients in arrest, CPR is neccessary to generate a waveform.
Caution: In patients with a prolonged down time, the ETCO2 reading may be so low (sometimes less than 6mm HG) that some monitor’s apnea alarms may go off even though the monitor is still providing an ETCO2 reading and a small wave form. If the apnea alarm goes off and you continue to bag without resistance and have equal lung sounds and negative epigatric sounds, do not automatically pull your tube. A small but distinct square wave form along with even a marginal EtCO2 reading is still verification the tube is in the trachea.
ETCO2 can also be used to assist in difficult intubations of spontaneously breathing patients.
Paramedics can attach the capnography filter to the ET tube prior to intubation and, in cases where it is difficult to visualize the chords, use the monitor to assist placement. This includes cases of nasal tracheal intubation.
You’re out (missed the chords).
You’re in.
Paramedics who utilize this method during cardiac arrests with cardiac compressions continuing while they intubate may see CPR oscillations on the monitor screen immediately upon intubating, replaced by larger wave forms once the ambu-bag has been attached and ventilations begun. The oscillations provide proof that compressions alone can produce some ventilation.
Note: You must still assess for equal lung sounds. Capnography cannot detect right main-stem intubations.
Capnography can also be used for combitubes and LMAs.
Paramedics should document their use of continuous ETCO2 monitoring and attach wave form strips to their PCRs. Print a strip on intubation, periodically during care and transport, and then just prior to moving the patient from your stretcher to the hospital table and then immediately after transfer. This will timestamp and document your tube as good.
Continuous Wave Form Capnography Versus Colorimetric Capnography
In colorimetric capnography a filter attached to an ET tube changes color from purple to yellow when it detects carbon dioxide. This device has several drawbacks when compared to waveform capnography. It is not continuous, has no waveform, no number, no alarms, is easily contaminated, is hard to read in dark, and can give false readings.
Paramedics should encourage their services to equip them with continuous wave form capnography.
3. Measuring Cardiac Output During CPR
Monitoring ETC02 measures cardiac output, thus monitoring ETCO2 is a good way to measure the effectiveness of CPR.
In 1978, Kalenda “reported a decrease in ETC02 as the person performing CPR fatigued, followed by an increase in ETCO2 as a new rescuer took over, presumably providing better chest compressions.” –Gravenstein, Capnography: Clinical Aspects, Cambridge Press, 2004
With the new American Heart Association Guidelines calling for quality compressions (“push hard, push fast, push deep”), rescuers should switch places every two minutes. Set the monitor up so the compressors can view the ETCO2 readings as well as the ECG wave form generated by their compressions. Encourage them to keep the ETCO2 number up as high as possible.
“Reductions in ETCO2 during CPR are associated with comparable reductions in cardiac output….The extent to which resuscitation maneuvers, especially precordial compression, maintain cardiac output may be more readily assessed by measurements of ETCO2 than palpation of arterial pulses.” -Max Weil, M.D., Cardiac Output and End-Tidal carbon dioxide, Critical Care Medicine, November 1985
Note: Patients with extended down times may have ETCO2 readings so low that quality of compressions will show little difference in the number.
Return of Spontaneous Circulation (ROSC)
ETCO2 can be the first sign of return of spontaneous circulation (ROSC). During a cardiac arrest, if you see the CO2 number shoot up, stop CPR and check for pulses.
End-tidal CO2 will often overshoot baseline values when circulation is restored due to carbon dioxide washout from the tissues.
A recent study found the ETCO2 shot up on average 13.5 mmHg with sudden ROSC before settling into a normal range
.-Grmec S, Krizmaric M, Mally S, Kozelj A, Spindler M, Lesnik B.,Resuscitation. 2006 Dec 8
Note: Each bar represents 30 seconds.
“End-tidal CO2 monitoring during cardiac arrest is a safe and effective noninvasive indicator of cardiac output during CPR and may be an early indicator of ROSC in intubated patients.” – American Heart Association Guidelines 2005 CPR and ECG
Loss of Spontaneous Circulation
In a resuscitated patient, if you see the stabilized ETCO2 number significantly drop in a person with ROSC, immediately check pulses. You may have to restart CPR.
The graph below demonstrates three episodes of ROSC, followed by loss of circulation during a cardiac arrest:
4. End Tidal CO2 As Predictor of Resuscitation Outcome
End tidal CO2 monitoring can confirm the futility of resuscitation as well as forecast the likelihood of resuscitation.
“An end-tidal carbon dioxide level of 10 mmHg or less measured 20 minutes after the initiation of advanced cardiac life support accurately predicts death in patients with cardiac arrest associated with electrical activity but no pulse. Cardiopulmonary resuscitation may reasonably be terminated in such patients.” -Levine R, End-tidal Carbon Dioxide and Outcome of Out-of-Hospital Cardiac Arrest, New England Journal of Medicine, July 1997
Likewise, case studies have shown that patients with a high initial end tidal CO2 reading were more likely to be resuscitated than those who didn’t. The greater the initial value, the likelier the chance of a successful resuscitation.
“No patient who had an end-tidal carbon dioxide of level of less than 10 mm Hg survived. Conversely, in all 35 patients in whom spontaneous circulation was restored, end-tidal carbon dioxide rose to at least 18 mm Hg before the clinically detectable return of vital signs….The difference between survivors and nonsurvivors in 20 minute end-tidal carbon dioxide levels is dramatic and obvious.” – ibid.
“An ETCO2 value of 16 torr or less successfully discriminated between the survivors and the nonsurvivors in our study because no patient survived with an ETCO2 less than 16 torr. Our logistic regression model further showed that for every increase of 1 torr in ETCO2, the odds of surviving increased by 16%.” –Salen, Can Cardiac Sonography and Capnography Be Used Independently and in Combination to Predict Resuscitation Outcomes?, Academic Emergency Medicine, June 2001
Caution: While a low initial ETCO2 makes resuscitation less likely than a higher initial ETCO2, patients have been successfully resuscitated with an initial ETCO2 >10 mmHg.
Asphyxic Cardiac Arrest versus Primary Cardiac Arrest
Capnography can also be utilized to differentiate the nature of the cardiac arrest.
A 2003 study found that patients suffering from asphyxic arrest as opposed to primary cardiac arrest had significantly increased initial ETCO2 reading that came down within a minute. These high initial readings, caused by the buildup of carbon dioxide in the lungs while the nonbreathing/nonventilating patient’s heart continued pump carbon dioxide to the lungs before the heart bradyed down to asystole, should come down within a minute. The ETCO2 values of asphyxic arrest patients then become prognostic of ROSC
.-Grmec S, Lah K, Tusek-Bunc K,Crit Care. 2003 Dec
5. Monitoring Sedated Patients
Capnography should be used to monitor any patients receiving pain management or sedation (enough to alter their mental status) for evidence of hypoventilation and/or apnea.
In a 2006 published study of 60 patients undergoing sedation, in 14 of 17 patients who suffered acute respiratory events, ETCO2 monitoring flagged a problem before changes in SPO2 or observed changes in respiratory rate.
“End-tidal carbon dioxide monitoring of patients undergoing PSA detected many clinically significant acute respiratory events before standard ED monitoring practice did so. The majority of acute respiratory events noted in this trial occurred before changes in SP02 or observed hypoventilation and apnea.” – -Burton, Does End-Tidal Carbon Dioxide Monitoring Detect Respiratory Events Prior to Current Sedation Monitoring Practices, Academic Emergency Medicine, May 2006
In the graph below, the respiratory rate decreases as the ETCO2 rises, and the patient suffers apnea, all the while the SPO2 remains stable.
Note: Each bar represents thirty seconds.
Sedated, Intubated Patients
Capnography is also essential in sedated, intubated patients. A small notch in the wave form indicates the patient is beginning to arouse from sedation, starting to breathe on their own, and will need additional medication to prevent them from “bucking” the tube.
6. ETCO2 in Asthma, COPD, and CHF
End-tidal CO2 monitoring on non-intubated patients is an excellent way to assess the severity of Asthma/COPD, and the effectiveness of treatment. Bronchospasm will produce a characteristic “shark fin” wave form, as the patient has to struggle to exhale, creating a sloping “B-C” upstroke. The shape is caused by uneven alveolar emptying.
Multiple studies have confirmed the sloping shape correlates to bronchospasm and obstructive lung disease.
“The analysis of the capnogram’s shape is a quantitative method for evaluating the severity of bronchospasm.” –You, Expiratory capnography in asthma: evaluation of various shape indicies, European Respiratory Journal, Feb, 1994
Changing Asthma Values
Asthma values change with severity. With a mild asthma, the CO2 will drop (below 35) as the patient hyperventilates to compensate. As the asthma worsens, the C02 levels will rise to normal. When the asthma becomes severe, and the patient is tiring and has little air movement, the C02 numbers will rise to dangerous levels (above 60).
Successful treatment will lessen or eliminate the shark fin shape and return the ETCO2 to normal range (Patient below: capnogram on arrival, after start of 1st combi-vent, after two combivents).
Hypoxic Drive
Capnography will show the hypoxic drive in COPD “retainers.” ETCO2 readings will steadily rise, alerting you to cut back on the oxygen before the patient becomes obtunded. Since it has been estimated that only 5% of COPDers have a hypoxic drive, monitoring capnography will also allow you to maintain sufficient oxygen levels in the majority of tachypneic COPDers without worry that they will hypoventilate.
CHF: Cardiac Asthma
It has been suggested that in wheezing patients with CHF (because the alveoli are still, for the most part, emptying equally), the wave form should be upright. This can help assist your clinical judgement when attempting to differentiate between obstructive airway wheezing such as COPD and the “cardiac asthma” of CHF.
(wave form of patient with cardiac asthma)
7. Ventilating Head Injured Patients
Capnography can help paramedics avoid hyperventilation in intubated head injured patients.
“Recent evidence suggests hyperventilation leads to ischemia almost immediately…current models of both ischemic and TBI suggest an immediate period during which the brain is especially vulnerable to secondary insults. This underscores the importance of avoiding hyperventilation in the prehospital environment.” –Capnography as a Guide to Ventilation in the Field, D.P. Davis, Gravenstein, Capnography: Clinical Perspectives, Cambridge Press, 2004
Hyperventilation decreases intracranial pressure by decreasing intracranial blood flow. The decreased cerebral blood flow may result in cerebral ischemia.
In a study of 291 intubated head injured patients, 144 had ETCO2 monitoring. Patients with ETCO2 monitoring had lower incidence of inadvertant severe hyperventilation (5.6%) than those without ETCO2 monitoring (13.4%). Patients in both groups with severe hyperventilation had significantly higher mortality (56%) than those without (30%). –Davis, The Use of Quantitative End-Tidal Capnometry to Avoid Inadvertant Severe Hyperventilation in Patients with Head Injury After Paramedic Rapid Sequence Intubation, Journal of Trauma, April 2004
8. Perfusion Warning Sign
“A target value of 35 mmHg is recommended…The propensity of prehospital personnel to use excessively high respiratory rates suggests that the number of breaths per minute should be decreased. On the other hand, the mounting evidence against tidal volumes in excessive of 10cc/kg especially in the absence of peep, would suggest the hypocapnia be addressed by lower volume ventilation.” – –Capnography as a Guide to Ventilation in the Field, D.P. Davis, Gravenstein, Capnography: Clinical Perspectives, Cambridge Press, 2004
End tidal CO2 monitoring can provide an early warning sign of shock. A patient with a sudden drop in cardiac output will show a drop in ETCO2 numbers that may be regardless of any change in breathing. This has implications for trauma patients, cardiac patients – any patient at risk for shock.
In the study cited below, 5 pigs had hemorrhagic shock induced by bleeding, 5 pigs had septic shock induced by infusion of e-coli, and 6 pigs had cardiogenic shock induced by repeated episodes of v-fib. The pigs’ cardiac output was continuously measured as well as their PETCO2.
“Cardiac output and PetCO2 were highly related in diverse experimental models of circulatory shock in which cardiac output was reduced by >40 % of baseline values… measurement of PetC02 is a noninvasive alternative for continuous assessment of cardiac output during low flow circulatory shock states of diverse causes.” -Xiahua, End-tidal carbon dioxide as a noninvasive indicator of cardiac index during circulatory shock, Critical Care Medicine, 2000, Vol 28, No 7
“A patient with low cardiac output caused by cardiogenic shock or hypovolemia resulting from hemorrhage won’t carry as much CO2 per minute back to the lungs to be exhaled. This patient’s ETC02 will be reduced. It doesn’t necessarily mean the patient is hyperventilating or that their arterial CO2 level will be reduced. Reduced perfusion to the lungs alone causes this phenomenon. The patient’s lung function may be perfectly normal.” –Baruch Krauss, M.D, JEMS, November 2003
9. Other Issues:
DKA – Patients with DKA hyperventilate to lessen their acidosis. The hyperventilation causes their PAC02 to go down.
“End-tidal C02 is linearly related to HC03 and is significantly lower in children with DKA. If confirmed by larger trials, cut-points of 29 torr and 36 torr, in conjunction with clinical assessment, may help discriminate between patients with and without DKA, respectively.” –Fearon, End-tidal carbon dioxide predicts the presence and severity of acidosis in children with diabetes, Academic Emergency Medicine, December 2002
Pulmonary Embolus – Pulmonary embolus will cause an increase in the dead space in the lungs decreasing the alveoli available to offload carbon dioxide. The ETCO2 will go down.
Hyperthermia – Metabolism is on overdrive in fever, which may cause ETCO2 to rise. Observing this phenomena can be live-saving in patients with malignant hyperthermia, a rare side effect of RSI (Rapid Sequence Induction).
Trauma – A 2004 study of blunt trauma patients requiring RSI showed that only 5 percent of patients with ETCO2 below 26.25 mm Hg after 20 minutes survived to discharge. The median ETCO2 for survivors was 30.75. -
Deakin CD, Sado DM, Coats TJ, Davies G. “Prehospital end-tidal carbon dioxide concentration and outcome in major trauma.” Journal of Trauma. 2004;57:65-68.
Field Disaster Triage – It has been suggested that capnography is an excellent triage tool to assess respiratory status in patients in mass casualty chemical incidents, such as those that might be caused by terrorism.
“Capnography…can serve as an effective, rapid assessment and triage tool for critically injured patients and victims of chemical exposure. It provides the ABCs in less than 15 seconds and identifies the common complications of chemical terrorism. EMS systems should consider adding capnography to their triage and patient assessment toolbox and emphasize its use during educational programs and MCI drills.”- Krauss, Heightman, 15 Second Triage Tool, JEMS, September 2006
Anxiety- ETCO2 is being used on an ambulatory basis to teach patients with anxiety disorders as well as asthmatics how to better control their breathing. Try (it may not always be possible) to get your anxious patient to focus on the monitor, telling them that as they slow their breathing, their ETCO2 number will rise, their respiratory rate number will fall and they will feel better.
Anaphylaxis- Some patients who suffer anaphylactic reactions to food they have ingested (nuts, seafood, etc.) may experience a second attack after initial treatment because the allergens remain in their stomach. Monitoring ETCO2 may provide early warning to a reoccurrence. The wave form may start to slope before wheezing is noticed.
Accurate Respiratory Rate – Studies have shown that many medical professionals do a poor job of recording a patient’s respiratory rate. Capnography not only provides an accurate respiratory rate, it provides an accurate trend or respirations.
10. The Future
Capnography should be the prehospital standard of care for confirmation and continuous monitoring of intubation, as well as for monitoring ventilation in sedated patients. Additionally, it should see increasing use in the monitoring of unstable patients of many etiologies. As more research is done, the role of capnography in prehospital medicine will continue to grow and evolve.
***
10 Things Every Paramedic Should Know About Capnography
Peter Canning, EMT-P
December 29, 2007 (Version 6.3)
Disclaimer: The information in this paper is gathered from textbooks, research articles, web sites, lectures and my own experiences. Paramedics should consult their medical directors and protocols for approved uses.
***
For more information on capnography, go to the site:
Capnography for Paramedics
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