ECG Case 6
11/06/2012 by Leave a Comment
You respond to a 72 y/o female complaining of shortness of breath. Upon arrival you find an average sized elderly female with tachypnea and pale, moist skin. She states that she can’t do anything without feeling very short of breath. This is the ECG you obtain on the patient, what are you thinking at this point?
ECG 6 – Click to enlarge
Watch the video below for the full case review and interpretation.
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ECG Case 5
11/05/2012 by 2 Comments
You respond to a 65 y/o Male at his residence. His daughter, on scene, called 911 because she is worried about her father’s health. She states that he just hasn’t been acting right. “He is weaker than normal, and becomes short of breath very easily”. The patient himself is not thrilled about your presence. He is a rather obese man (about 400 lbs), and he is sitting in his recliner sans shirt or pants. His immediate area provides evidence that he doesn’t move
from that chair very often.
S – The patient states that he is always weak and it is normal for him to get short of breath when he gets up.
A – NKDA
M – Glucophage, Gabapentin, Albuterol, Singulair, Prevacid, Carevedilol, Enalapril, Digoxin, Aspirin, Oxygen
P – AMI, CHF, Asthma, Non-insulin dependent diabetes, AICD
L – Oreos and Orange Juice
E – Sitting in his chair
B/P: 61/37, Left Arm
SpO2: 83, on 2 lpm O2,
Pulse: 40 & regular
Resp: 30 & regular
Skin: Pale, cool, & clammy
You place your patient on the monitor and obtain the following 12-lead. What would you immediately ask your patient? What is your interpretation of the ECG? What treatments would you provide?
Understanding Bundle Branch Blocks
10/27/2012 by Leave a Comment
I’ve been at it again with the video tutorials. Here is a quick, two-part explanation of Bundle Branch Blocks. I explain what causes the ECG changes associated with bundle branch blocks to the best of my abilities within the short amount of time that Youtube allows.
Did you know that both types of bundle branch blocks require you to look at more than just lead V1 to truly identify them? If not, make sure you see part 2.
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The Capnography Tutorial
10/25/2012 by 1 Comment
I have put together a capnography tutorial for your education and enjoyment. The videos below are the capnography tutorial. There are 7 lessons, consisting of relatively short videos.
Enjoy.
Adam Thompson, EMT-P
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Inadequate needle thoracostomy rate in the prehospital setting for presumed pneumothorax: an ultrasound study – Full paper
02/10/2011 by 1 Comment
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Also posted over at Rogue Medic (now at EMS Blogs) and at Research Blogging.
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When I wrote Inadequate needle thoracostomy rate in the prehospital setting for presumed pneumothorax: an ultrasound study – abstract, I was only looking at the abstract. Now that I have seen the entire paper, I have not seen anything weaken the results of the study. There are plenty of points to discuss.
On the EMS Research Podcast Harry Mueller, Patrick Lickiss, Dr. Bill Toon, and I discuss this paper. In about half an hour, we go into the details. Here I will present the highlights. First, go listen to the podcast. Prehospital Needle Thoracostomy: EMS Research Episode4
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During the podcast, I suggested that Dr. Blaivas is a radiologist, or some other specialist in imaging medicine, as opposed to being an emergency physician. That is not correct. Dr. Blaivas is Professor of Emergency Medicine in the Department of Emergency Medicine at Northside Hospital Forsyth in Cumming, Georgia. Dr. Blaivas is also either the world’s first or second emergency ultrasound fellowship graduate. Therefore he is very well qualified to examine all aspects of emergency medicine and ultrasound.
Let’s look at the paper.
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An unstable trauma patient who is not oxygenating well or is hypotensive and has decreased breath sounds unilaterally on auscultation may be assumed by paramedics to have a PTX.2 Not unreasonably, with lack of a more definite way to rule in or rule out the presence of a PTX, needle thoracostomy is opted for to relieve the tension that is assumed to be present.[1]
Previous experience and this study lead me to the doubt this not unreasonable conclusion.
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In the prehospital setting where external noise and distractions may be overwhelming, release of air is frequently not audible.[1]
This focus on decreased breath sounds may be one of the important factors in the misdiagnosis of tension pneumothorax.
How many medics are good at assessing lung sounds?
How many medics can tell the difference between the diminished lung sounds that are indicative of a tension pneumothorax and the diminished lung sounds that are consistent with any of the normal variations of lung sounds?
I would also change part of a sentence –
In the prehospital setting where external noise and distractions may be overwhelming, release of air is frequently not audible imaginary.
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Typically, in such critically ill patients, the chest tube is placed before review of a chest radiograph to confirm that the tension PTX has improved. The natural assumption is that regardless of whether a PTX was present, proper penetration of the chest wall would lead to a PTX even if it were not originally present.[1]
Should any doctor be using this logic to decide to place a chest tube without assessing the patient?
Should any doctor be placing a chest tube without assessing the patient?
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However, if the needle did not penetrate the lung and no PTX was initially present, a chest tube could be avoided.[1]
In the absence of a pneumothorax, a chest tube could should be avoided.
What justification is there for placing a chest tube in a patient with no indication for a chest tube?
Maybe the needle is in the chest because the medic has really scary IV skills. In this study, at least a quarter of the medics treating these patients (unless some are repeat offenders) have really scary needle decompression skills.
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The main outcome measure was whether a PTX was present. The secondary outcome measure was whether a PTX developed after catheter removal.[1]
There does not appear to be any discussion of whether a pneumothorax developed after catheter removal.
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Physicians performed the ultrasound examinations during the secondary survey. Chest radiographs were obtained immediately after the ultrasound examinations. Examiners were not blinded to physical findings or on which side needle thoracostomy was performed.[1]
blinding would have been nice, but this study seems to be more to demonstrate the concept that needle decompression may not even produce a simple pneumothorax. This can be left for a later study.
It would also be nice to follow up on the patients to find out if any showed any of the no pneumothorax patients showed any signs of pneumothorax later on, which could cast doubt on the ultrasound findings.
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A total of 57 patients were enrolled in the study over a 3-year period. Fifty-six patients had 1 needle thoracostomy performed, and 1 patient had 3 needle thoracostomy procedures on the same side for hypotension and persistent unilateral decreased breath sounds.[1]
It should not surprise anyone that the patient with the multiple stab wounds 3 attempts at needle decompression did not have any kind of pneumothorax.
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A tension PTX is a life-threatening process that must be treated immediately either through needle thoracostomy or tube thoracostomy. Despite frequent use of chest radiography on patient arrival to emergency departments, many PTXs are initially missed.[1]
It seems that a lot is missed.
Needles miss lungs.
Medics miss the absence of a tension pneumothoraces.
Doctors miss the presence of pneumothoraces.
If there is an important point to this, maybe it should be that we all need to improve our assessment for pneumothoraces and be more conservative in our treatment in the absence of unmistakable signs of a tension pneumothorax.
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The combination of unilateral decreased or absent breath sounds with instability is justifiably interpreted as the presence of a PTX. There is no way to verify or refute such a finding.[1]
Maybe.
Maybe not.
Should we assume that a tension pneumothorax is subtle?
I don’t think so.
Why do we teach about tension pneumothorax as if it is the same as an easily missed simple pneumothorax?
I think it is because we don’t realize just how unsubtle a tension pneumothorax is.
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This study had several limitations. The first was the small sample size. Second, the sonologists were not blinded to the side on which needle decompression was attempted. Third, it is possible that some patients did in fact have a PTX that was completely relieved by needle decompression, and no more air leaked after catheter removal. Thus, the CT scan would not show even a trace PTX. Although this is possible, it is clinically very unlikely.[1]
There are limitations, but are these results consistent with what we know about the shortcomings of EMS education and understanding of infrequently done procedures?
Absolutely.
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Click on the image to make it larger.
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From this study we cannot tell if the number that should be in the place of the double question marks is 42. Maybe it is 32. Maybe it is 22. Maybe it is 12. Maybe it is 2. Maybe it is zero. We don’t know and this study cannot tell us, which is not a fault of the study.
The same problem exists for trying to figure out the number that should be in the place of the single question mark.
We know that of the patients treated for claimed tension pneumothorax, 26% were treated by paramedics so poorly that the needle never even made it to the lung.
Should we assume that all of the patients treated with needles that actually reached the lung did have tension pneumothoraces?
There is nothing in this paper to suggest that.
There is no good reason to assume that all of the medics who missed the diagnosis also missed the lung. 26% missed the lung and missed the diagnosis.
It is reasonable to assume that some of the medics missed the diagnosis, but used a long enough needle to hit the lung. What we do not know is how many of those who hit the lung with a needle missed the diagnosis.
Another possibility is that the patient had a pneumothorax, most likely a simple pneumothorax, and the medic missed the lung with the needle, but since it was not a tension pneumothorax there was no dramatic deterioration of the patient. The needle decompression would be no more indicated for these patients than for those without any pneumothorax.
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Also covered at EMS Research Podcast Episode 4 at 510Medic.
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Footnotes:
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[1] Inadequate needle thoracostomy rate in the prehospital setting for presumed pneumothorax: an ultrasound study.
Blaivas M.
J Ultrasound Med. 2010 Sep;29(9):1285-9.
PMID: 20733183 [PubMed - in process]
Free Full Text from J Ultrasound Med.
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Blaivas M (2010). Inadequate needle thoracostomy rate in the prehospital setting for presumed pneumothorax: an ultrasound study. Journal of ultrasound in medicine : official journal of the American Institute of Ultrasound in Medicine, 29 (9), 1285-9 PMID: 20733183
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Some Food For Thought
11/04/2010 by 1 Comment
Some food for thought…
Controversial evidence & some reasoning.
Nitroglycerine is Contraindicated With Tachycardia?
- BP = Cardiac Output (CO) x Systemic Vascular Resistance
- CO = Stroke Volume x Heart Rate
An acute coronary event does not cause tachycardia. Tachycardia (without exertion) is almost always a result of decreased stroke volume. Stroke volume is dependant on venus return. So if stroke volume is down, and your body is trying to maintain normal cardiac output, so it may maintain a normal BP, the heart rate may be increased.
If the patient does not have pulmonary congestion (edema), nitro should be withheld if the patient is tachycardic. This is because the patient may be preload dependant as a result of dehydration, or some other hypovolemic condition. The tachycardia will most likely be compensatory, and the nitro will worsen the patients condition.
But anxiety can cause tachycardia…
Then console your patient and see if the tachycardia persists after they are calmed. If the tachycardia seems to accompany anxiety then nitrates may be acceptable. Be very weary of persistent tachycardia, whether they are anxious or not.
Patients Experiencing a Heart Attack Don’t Need O2?
Oxygen has recently shown to be much less benign a treatment than it was once thought to be. Hyperoxia leads to increased morbidity and mortality in stroke patients, post-arrest patients, head trauma patients, and it has most recently been discovered that hyperoxygenation may lead to poor outcomes in patients experiencing an AMI.
Why?
The answer isn’t so easy to understand. First of all, the research is still new. Just understand that these patients are not generally suffering from hypoxia. They are suffering from ischemic heart tissue, more specifically—myocardium. If their oxygen saturation is sufficient, than no additional O2 should be supplemented. Reasoning includes an elaborate explanation regarding free radicals. O2 is a free radical and may be toxic, leading to residual oxidative stress. This causes increased damage. Use of oxygen in MI patients questioned by new Cochrane review.
What is the Deal With Morphine?
Morphine is associated with an increase in morbidity when given to a patient experiencing an acute coronary event (an AMI).
Once again, there is no conclusive answer, but researchers from a CRUSADE study have three possible explanations.
- The first explanation is that patients treated with Morphine exhibit signs and symptoms of heart failure, and are treated as such. This isn’t really accepted as a plausible cause.
- The second, more widely accepted explanation is that Morphine masks symptoms of angina without correcting the underlined pathology. This means that caregivers may be less apt to provide follow-up treatments, procedures, and consults.
- The third explanation is that Morphine decreases the respiratory drive as well as causing CNS depression. Increased ischemia has been associated with these side effects, and extended infarction has been linked to Morphine itself.
| End point | No morphine
(n=40 036) |
Morphine
(n=17 003) |
Adjusted OR (95% CI) |
| Death (%) | 4.7 | 5.5 | 1.48 (1.33-1.64) |
| Death or MI (%) | 7.1 | 8.5 | 1.44 (1.34-1.56) |
| Postadmission MI (%) | 3.0 | 3.8 | 1.34 (1.22-1.48) |
Morphine has bad effects when administered to patients with CHF.
Yes, it is in most prehospital guidelines as a recommended treatment for congestive heart failure. This will soon change…
The Acute Decompenstated Heart Failure National Registry (ADHERE) conducted a study on patients admitted with CHF who received morphine and yielded important results. There was a five-fold increase in mortality (13% versus 2.4%), a five-fold increase in need for intubation and ventilation (39.7% versus 14.4%), the intensive care unit admission rate was (15% versus 3.0%), and those patients who were admitted had a prolonged hospital stay (5.6 days versus 4.2 days). Although this was an observational study, it has had a major impact on the use of morphine for CHF patients. We know that morphine causes histamine release and subsequent hypotheses have been made concluding that this may increase catecholamine release. This may be the link to the poor outcomes. Additionally, there is a lack of evidence that morphine is related to any clinically significant preload reduction.
No More Intubations?
There has been a new paradigm shift in the way we think of resuscitation. This has brought with it, some new terminology—cardiocerebral resuscitation (CCR). CCR is meant to replace CPR, or cardiopulmonary resuscitation. The focus is shifting from the lungs, or pulmonary system, to the brain, or cerebrum.
There have been suggestions from the result of much research, advocating CCR for witnessed cardiac arrest, and CPR for primary respiratory arrest. This makes perfect sense, considering the pathologies. Overall though, there has been much more success when emphasis has been on chest compressions, as opposed to airway management.
Blind insertion, supraglotic airways are now rapidly finding their way into prehospital cardiac arrest guidelines throughout the country. The Combitube, Laryngeal Mask, and King LT/LTD are a few of the most common devices being utilized. The big sell, is the ability to insert these devices without any pauses in chest compressions.
This emphasis on chest compressions comes from research showing the need to prime the pump during the circulatory phase of cardiac arrest. This basically means that the heart and brain need to be perfused as good as possible up until defibrillation. Immediate defibrillation is only indicated within the electrical phase; which only lasts for approximately the first five minutes of pulselessness.
Despite the turmoil and mixed opinions about ETI in cardiac arrest, the evidence is clear—survival is better when the main focus is on adequate chest compressions. By taking the ETI aspect, and all of the complications that accompany it, out of the equation, resuscitation efforts consequently improve.
We haven’t even gone to the extreme yet. One study has shown that by simply placing a non-rebreather mask on a cardiac arrest victim and providing high-quality chest compressions, they increased neurologically intact survival rates from 15 to 39%.
Remember: Nearly all-medical research is flawed. This is one reason why medicine will remain ever changing. Fortunately the good evidence usually trumps the biased or bad evidence. No single study should change anything.
Differential Diagnosis: Headache
11/04/2010 by 3 Comments
Differential Diagnosis: Headaches
By Adam Thompson, EMT-P
Headaches account for a large volume of EMS responses. Most are benign, but a few could be an early symptom of a life-threatening cause. It may be beneficial to differentiate between the presentations. A good history is by far the most useful tool that any clinician has in determining a headache’s malignancy.
Common types of headaches:
- Tension-type headache
- Migraine headaches
- Cluster headaches
Tension-type the most common type of headache, and yet its causes aren’t well understood. A tension headache is generally a diffuse, mild to moderate pain that many people describe as feeling as if there’s a tight band around their head.It may feel as though muscle contractions are responsible for your head pain, but experts don’t think that’s the cause, which is why this type of headache is generally referred to as a tension-type headache. (from MayoClinic)
Migraine a common type of headache that may occur with symptoms such as nausea, vomiting, or sensitivity to light. In many people, a throbbing pain is felt only on one side of the head. Some people who get migraines have warning symptoms, called an aura, before the actual headache begins. An aura is a group of symptoms, usually vision disturbances, that serve as a warning sign that a bad headache is coming. Most people, however, do not have such warning signs. (from Google Health)
Cluster The term “cluster headache” refers to a type of headache that recurs over a period of time. People who have cluster headaches experience an episode one to three times per day during a period of time (the cluster period), which may last from two weeks to three months. The headaches may disappear completely (go into “remission”) for months or years, only to recur. A cluster headache typically awakens a person from sleep one to two hours after going to bed. These nocturnal attacks can be more severe than the daytime attacks. Attacks appear to be linked to the circadian rhythm (or “biological” clock). Most people with cluster headaches will develop cluster periods at the same time each year — either in the spring or fall or the winter or summer. (from WebMD)
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Symptom
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A
Tension |
B
Migraine |
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Intensity, Duration and Quality of Pain
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Mild or moderate pain intensity
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√
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√
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Severe
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√
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Duration of headache
30 min – 7 days
4-72 hours
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√
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√
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Intense pounding, throbbing and/or debilitating
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√
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Distracting but not debilitating
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√
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Steady ache
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√
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Location of Pain
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One side of head
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√
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Both sides of head
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√
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√
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Associated Symptoms
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Nausea/vomiting
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√
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Sensitivity to light and/or sounds
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√
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Aura before onset of headache such as visual symptoms
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√
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Table 1
Comparing benign headaches
90% of all headaches are benign. Tension headaches are muscle-contraction headaches, and migraine or cluster headaches are vascular headaches. Below is a table of accompanying symptoms with each type.
| CHARACTERISTICS | MUSCLE-CONTRACTION HEADACHES | VASCULAR HEADACHES |
|---|---|---|
| Incidence |
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| Precipitating factors |
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| Intensity and duration |
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| Associated signs and symptoms |
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Image 2 – Click the image above to enlarge
Quickie Definitions of Headaches You Never Knew Existed
- Weight-lifters: Just like you’d think, this is a headache that occurs after a strenuous weight-lifting regimen.
- Histamine: A headache caused by histamine overload, from a source such a histamine injection or certain wines.
- Coital: A headache that occurs suddenly during sex or after orgasm. As if couples nowadays didn’t have enough issues – thankfully, these are very rare and actually occur more often in men.
- Analgesic-rebound: That medication you’ve been taking for your headaches could now be the underlying cause of new headaches. Removal of the medication is required.
- Hypnic: This is an oddball headache that awakens people from sleep. Clusters can do this as well but the pain of hypnic headaches are not as intense and are not localized around the eye.
High Priority Symptoms
- The worst headache someone has ever had
- Headache with stiff neck (especially with a high grade fever)
- A headache associated with loss of consciousness or altered mental status.
- A headache accompanied by severe eye or ear pain.
- A headache that occurs in an individual who has experienced recent head trauma.
- A headache accompanied by sudden, disabling pain or convulsions.
- Headache with parasthesia or paralysis
References:
- American Headache Society – Table 1
