70 Year Old Male: Short of Breath

 

Good morning sports fans!

You are dispatched to the residence of a 70 year old male, complaining of “shortness of breath”.

You pull up to a well kept home, and are met at the front door by the patient’s wife. She tells you that her husband came home from the hospital yesterday after cosmetic eye surgery.

You are led into the kitchen, and find your patient sitting in a chair at the kitchen table. There is an eye patch over his right eye. He appears to be in moderate respiratory distress. His color is ok, but you note he can only speak in short sentences.

He tells you that he was fine until this morning when he suffered a sudden onset of shortness of breath. His wife describes it as “wheezing”. You ask about any Asthma/COPD history, and he says he has none. He also denies any cardiac history. He tells you he also had bouts of “coughing up phlegm”, and felt “very weak”.  As the day went on, his breathing worsened, so EMS was called.

You listen to his lungs and note basilar crackles. His history is significant for hypertension, repaired AAA, and skin cancer.

His vitals:

  • Pulse: 116 and weak
  • BP: 102/70 (patient states his systolic is normally in the 120-130 range)
  • RR: 24 and labored
  • SpO2: 92% on room air, and 97% on O2
  • Skin: unremarkable

Here is his rhythm strip:

rs4:4

and 12 Lead ECG:

ecg4:4

ECG interpretation?

What could be wrong with your patient?

How do you want to treat him, and where do you want to take him?

 

The nearest hospital is the local hospital 20 minutes away, and the nearest cardiac center is 50 minutes away.

Let’s hear it!

 

“Push Hard, Push Fast?”

“Push Hard, Push Fast”

We all know the mantra. It’s catchy.

Compressions not deep enough? Push hard.

CPR

Not fast enough? Push fast.

Great. Except… One thing many of us have learned as professional rescuers is that the bigger issue is not pushing too slow, but pushing too fast.

“But…push FAST!” I mean, faster has to be better right?

How many times have we witnessed CPR administered in a way that seems like a race to set the world record for fastest compression rate? How many times have we seen someone compress at an appropriate rate only to be chided to go faster?

While we know that compressing at a rate <100/min is too slow to provide effective CPR, how fast should we actually compress?

 At some point, can fast be too fast?

I did not find a lot of definitive research on this. What I did find indicates that the optimal rate of compressions are between 100-120 per minute. If the rate rises above 125, ROSC declines sharply (1). The classic law of diminishing returns kicks in, and bad things start to happen to decrease the chances of a successful outcome:

  • Increased rescuer fatigue
  • Compressions become more shallow and less effective
  • Full recoil of the chest is diminished

Clearly, these negative factors work against effective resuscitation and best practices. The only problem is that compression rates often reach the 140-180 range during resuscitative efforts.

I conducted an experiment a couple of years back utilizing an instrumented manikin. I’ll admit that the sample size was small, but I believe the results to be representative of the average rescuer. Compressors were told to provide guideline CPR,  and results were recorded. No metronome was utilized. The average rate delivered over the first two minutes was 140. As a BCLS/ACLS instructor, I have witnessed “too fast” compressions often, and I have heard of similar experiences elsewhere. Why does this happen? A few reasons are apparent to me:

  • Adrenaline surge
  • Poor temporal awareness
  • Gap in knowledge

Adrenaline Surge

The adrenaline surge is easy to understand. It makes us want to go fast, and leap tall buildings in a single bound.  Some of the fastest compression rates will be at the beginning of the code, just when we need effective compressions most. While it happens to all of us, not everyone has the same ability to control it, and prevent it from hindering our performance.

Poor temporal awareness

Related to the adrenaline surge, when under stress our ability to perceive time is distorted. Against our best efforts, time seems to slow down or speed up to the point where we can not accurately sense time lapses. It becomes difficult to effectively sense the difference between a compression rate of 110 and 140. This requires training, and even better the use of a metronome. This is akin to the problem of inadvertently over-ventilating patients at a too-fast rate.

Think about it:  At a compression rate of 120/minute, at the edge of the effective zone, we are providing 2 compressions per second. At a rate of 150 compressions/minute, outside of the effective zone, we are giving 2.5 compressions per second. I don’t think it’s easy to perceive the difference between 2 and 2.5 compressions per second under non-stressful conditions, do you?  How do you think we do under stress? Without an effective mechanism to control this, we can easily slip outside the effective range.

Knowledge Gap

Many providers still do not realize that “push hard, push fast” has an upper limit, and that giving compressions at a rate > 125 can be detrimental to outcomes. “The faster the better” approach is still pervasive out in the field. More of an educational emphasis needs to be placed on the idea that faster isn’t always better.

Compression rates matter. While I would like to see more research in this area, for what we know now, we need to have a mechanism in place to prevent “over-compressing”. A metronome or similar device would seem to fit the bill. Simple, affordable, but still very under-utilized.

 

(1)    Study determines optimal chest compression rate (Idris, M.D.)
Image credit:  foxnews.com

 

When to stop: Termination of Resuscitation in Pediatric Traumatic Cardiac Arrest

Field termination of pediatric resuscitation is a difficult topic for EMS systems, prehospital providers, first responders, and the patient’s family. Clear guidelines exist for the termination of resuscitation of adults in cardiac arrest for both traumatic and non-traumatic etiologies, and routine transportation of adults in cardiac arrest all but guarantees poor outcomes. Unfortunately, for pediatric patients no clear guidelines exist to help drive the decision, so practically all pediatric patients suffering from traumatic cardiac arrest receive on-going resuscitation during transportation to hospital. 

In this month’s Annals of Emergency Medicine, the American College of Surgeons, American College of Emergency Physicians, National Association of EMS Physicians, and American Academy of Pediatrics released a joint statement providing general guidelines for withholding or terminating resuscitative efforts in out-of-hospital pediatric traumatic cardiac arrest [1]. This paper undertook a review of all available literature on the topic in an attempt to form evidence based guidelines.

In total, 27 articles were identified which were relevant to the topic and contained data applicable to the guideline being developed. No Class I evidence was found, which is unsurprising as it is difficult to perform large randomized controlled trials on adult OOHCA, let alone pediatric OOHCA. These 27 papers contained outcome data on 1114 patients, with only 60 survivors (5.4%). Of the 60 pediatric patients who survived to discharge, only 19 (1.2%) had a good neurological outcomes.

Table 1 adapted from Ann Emerg Med 2014;63:504-515

Table 1 adapted from Ann Emerg Med 2014;63:504-515

The fact that outcomes from pediatric traumatic OOHCA are dismal should not be surprising. Traumatic cardiac arrest often requires immediate surgical interventions not possible in most US EMS systems. Even among physician based EMS systems, the rapid availability of more advanced resuscitative measures has not improved survival to discharge neurologically intact.

Patients who had resuscitation efforts longer than 30 minutes had nearly universally poor neurological outcomes if they survived to hospital discharge. Most suffered devastating head injuries. Patients with good neurological outcomes were associated with early bystander CPR, signs of life prior to their cardiac arrest, and early ROSC. Epinephrine usage was not associated with improved ROSC or neurological survival.

The literature review identified key points which can help determine if field termination of pediatric traumatic arrest resuscitation is appropriate:

  • Patients with primary signs of futility such as injuries incompatible with life or obvious death (e.g. decapitation, traumatic amputations involving the thorax and abdomen).
  • Traumatic arrest with secondary signs of futility (e.g. dependent lividity, rigor mortis, and decomposition).
  • Victims of drowning or lightning strikes with primary or secondary signs of futility.
  • Unwitnessed traumatic cardiac arrest with prolonged resuscitation efforts (30 minutes) and no signs of life during the resuscitation.

If any of these criteria are met, discussions with the family should be made regarding the futility of resuscitation and the appropriateness of termination of resuscitation.

The literature review identified the following criteria for when resuscitation should be initiated or continued:

  • Witnessed traumatic arrest with prior signs of life and early CPR.
  • A mechanism of injury which does not correlate with a traumatic cardiac arrest.
  • Provider doubt as to the circumstances or timing of the traumatic cardiac arrest.
  • Prolonged traumatic cardiac arrest by drowning or lightning strike with hypothermia.
  • Consultation with family members or medical control recommends resuscitation.

If any of these criteria are met, immediate transportation of the patient should be made to the appropriate facility for pediatric traumatic cardiac arrest. Hemorrhage control and defibrillation should occur on scene. Treatments such as airway management and vascular access should be made enroute to the facility.

Pediatric cardiac arrest is a difficult topic and many providers may be unwilling to, “give up,” on resuscitation efforts. It is appropriate to terminate resuscitation efforts in both adult and pediatric cardiac arrests where efforts are futile. Recognizing futile efforts is important, so we can ensure families are not given a false sense of hope. Resuscitation of all patients in cardiac arrest, regardless of etiology, should be evidence based and free from emotion. However, the author recognizes that this is easier said than done.

1. American College of Surgeons, American College of Emergency Physicians, National Association of EMS Physicians, American Academy of Pediatrics. Joint Statement: Withholding or Termination of Resuscitation in Pediatric Out-of-Hospital Traumatic Cardiopulmonary Arrest. Ann Emerg Med 2014; 63(4):504–15.

Questions

  • Does your service have termination of resuscitation guidelines?
  • Do they include pediatric patients?
  • Are you willing to terminate the resuscitation of pediatric patients in cardiac arrest who meet these guidelines?
  • What can be done to improve provider willingness to acknowledge these difficult decisions?

Conclusion: 81 YOM with Chest Heaviness

This is the recap and conclusion for the previous case:

http://www.ems12lead.com/2014/03/11/81-yom-with-chest-heaviness/

Here’s the initial 12 lead ECG:

 

subendo1

What do we see?

 

- Sinus rhythm with 1Left Atrial Abnormality or “Enlargement”

- Wide complex QRS with a Right Ventricular Conduction Delay pattern or Right Bundle Branch Block (RBBB) morphology seen as rSR’ in V1 but abnormal S waves for a typical RBBB, therefore,  Intraventricular Conduction Delay (IVCD).

- Pathologic leftward frontal (limb leads) axis >-30 degrees (negative QRS in lead II) with two posibilities:

. Left Anterior Fascicular Block (LAFB)

. Left Ventricular Hypertrophy (LVH)

- Generalized ST segment depression

- ST segment elevation in aVR

There were 3 main causes suspected by most healthcare providers:

  1. Proximal LAD Occlusion
  2. Left Main Coronary Artery Occlusion
  3. 3 vessel disease

 

 Bottom line: DIFFUSE SUBENDOCARDIAL ISCHEMIA

 Now, some sources believe that elevation in aVR with generalized ST segment depression, a.k.a. Non-STEMI, indicate Left Main occlusion, however, in reality, the actual finding of a thrombus occluded Left Main artery is NOT that common.

Cases with these findings are more commonly the result of :

  • multi-vessel disease
  • severe atherosclerosis
  • catecholamine induced vasospasm

Either way, this is a STEMI equivalent which requires further investigation…

 

Based on the initial complaint of chest heaviness + vomiting, both being Acute Coronary Syndrome (ACS) signs, the patient was given 324 mg ASA and two repeated doses of .4 mg NTG tablet sublingual in a 5 minute interval. A serial 12 lead ECGs were obtained during transport:

 

sub-endo3

The patient was treated with a total of 4 NTG tablets, 1″ NTG paste on left chest wall and  4mg Zofran. Upon arrival to the initial receiving facility, the chest heaviness had decreased to 1/10 level and improved general appearance.

One last pre-hospital 12 lead ECG was obtained:

 

sub-endo2

Clinical outcome:

  • No thrombus (no occlusion)
  • Coronary Artery Disease (CAD) and severe stenosis
  • 100% Mid Left Anterior Descending (LAD) blockage
  • 75% Right Coronary Artery (RCA) blockage
  • 50% Distal LAD blockage
  • Troponin I = .07 ng/mL (.40-2.10 ng/mL normal range)
  • Creatine = 1.6 mg/dL (.10-9.0 mg/dL)

The patient was found to be with reduced Ejection Fraction (EF) of 35% during the initial hospitalization and was placed on Intra-aortic Balloon Pump at a 1:1 systolic ratio with improved EF of 50%.

sub-endo post

 

The patient was transferred the next morning to a higher level of care facility for Coronary Artery Bypass Graft (CABG) consult. During transport, the patient was on a Heparin drip at 1000 U/hr and NTG drip at 10 mcg/min. This 12 lead ECG was obtained prior transport:

 

sub-endo post3.

sub-endo post2

 

Conclusion:

CAD and severe stenosis are more common causes of Subendocardial Ischemia rather than an active occlusion of the Left Main Coronary Artery, which usually present with generalized ST segment elevation and patients often do not survive due to extensive Myocardial Infarct.

81 YOM with Chest Heaviness

It’s approximately 2000 hrs, right as you get comfortable in bed, when you are dispatched to a residence for Chest Pain (CP). You arrive on scene to find an 81 year old male, semifowler’s in bed, complaining of chest heaviness, 8/10, which started 2 hours ago, while in bed, watching tv. The patient also advised he has vomited twice since he called 911 less than ten minutes ago.

He is alert and oriented to person, place, time and event, GCS of 15, denies dyspnea with clear bilateral lung sounds, strong and regular radial pulses, warm to touch, diaphoretic and normal skin color.

Medical history:

  • Hypertension (HTN)
  • MI
  • Hyperlipidemia

Medications:

  • ASA
  • Metoprolol
  • Plavix
  • Pravachol

Vital sings:

  • BP: 160/87 mmHg
  • HR: 96 beats/min
  • RR: 18 breaths/min
  • SPo2: 94 RA
  • BGL: 104 mg/dL

You administer O2 at 2lpm via nasal canula and placed him on your cardiac monitor, then obtain the 12 lead ECG shown below:

subendo1edit

  • What is your ECG interpretation?
  • What would be your treatment?
  • Any concerns?

Understanding ECG Filtering

A common problem in ECG interpretation is the removal of unwanted artifact and noise. To help with this our cardiac monitors provide a means to filter the ECG recording.  Most cardiac monitors will choose the appropriate filter based on the situation. When performing routine monitoring, where only the cardiac rhythm is important, the filters applied are known as monitor mode filters. When performing a 12-Lead, which requires a high fidelity tracing, the filters applied are known as diagnostic mode filters. Beyond this, little emphasis is placed on understanding ECG filtering. This gap in education leads to problems for both experienced and inexperienced interpreters.

Signal Processing Basics

The frequency of a signal measures the cyclic rate or repetition, and is measured in Hertz (Hz). A frequency of 1 Hz means a signal repeats itself every one second. Our hearts produce electrical activity recorded by electrodes as a signal. The sinoatrial node fires at roughly 50 to 90 beats per minute, and for the sake of this post we will say 60 beats per minute is the happy median. This means the heart has a fundamental frequency of 1 Hz at this heart rate. Therefore, all of the ECG components (P, QRS, and T) will occur at or above this frequency.

Because the ECG signal repeats itself, each time the heart cycles through systole and diastole, we can break it down into individual waves or harmonics. This process of breaking down a signal into a series of sine waves is known as Fourier Analysis. Using the property of superposition, if you add together enough of these harmonics you can recreate the original signal.

Figure 1 from Buenda-Fuentes 2012

(a) The ECG which was used to obtain a sample of the signal, recording the coordinates of 514 points in one PP cycle. The cardiac frequency is 55 bpm, which implies an RR cycle or PP cycle of 1.08 s. The first harmonic represented in (b) and (c) in red colour has a frequency of 0.9Hz (1/1.08), and on the basis of this frequency the others are multiples (1.8, 2.7 Hz) of the first. (b) Spectrum of frequencies, by amplitude, corresponding to the 169 harmonics into which the signal was decomposed. The zone corresponding to the first 40 harmonics, which are those that contribute to the basic shape of the ECG signal, is shown—the harmonics beyond the first 25–30 having a very low amplitude. (c, d) Graphic and tabular presentation of the first 5 harmonics. Each one is composed of 514 coordinates corresponding to the PP cycle sample previously defined. Compare (b) and (c) (matching colors). The frequency spectrum is the amplitude
representation (peak-to-peak distance) of each one of the harmonics mentioned. The sum of the 5 waves in each one of the 514 points is presented in tabular form in the last column of (d) and in graphic form superimposed in red colour on the digitized ECG signal in (e). (Adapted from Figure 1 Buenda-Fuentes 2012)

Each of the harmonics (sine waves) have a certain amplitude, frequency, and phase. Amplitude is the magnitude of the signal, measured on the ECG in millivolts (mV). Frequency was discussed previously, and is the rate of repetition of the signal. Lower frequency harmonics have higher amplitudes, and higher frequency harmonics will have lower amplitudes. Therefore, the low frequency ECG components play the largest role in observed amplitude on the ECG.

Phase can be thought of as the delay before the signal begins. Think of a group singing Row Your Boat, where each person starts after the previous. We can say that if two singers match that they are in phase, and two who are at different parts of the song are out of phase:

What electrical signals are recorded by the ECG?

Like we said, the ECG signal is comprised of multiple sources. The recording is made through electrodes on the skin, which capture more than just the electrical activity of the heart. The primary electrical components captured are the myocardium, muscle, skin-electrode interface, and external interference.

ECG Component Frequencies

ECG Component Frequencies

The common frequencies of the important components on the ECG:

  • Heart rate: 0.67 – 5 Hz (i.e. 40 – 300 bpm)
  • P-wave: 0.67 – 5 Hz
  • QRS: 10 – 50 Hz
  • T-wave: 1 – 7 Hz
  • “High frequency potentials”: 100-500 Hz

The common frequencies of the artifact and noise on the ECG:

  • Muscle: 5 – 50 Hz
  • Respiratory: 0.12 – 0.5 Hz (e.g. 8 – 30 bpm)
  • External electrical: 50 or 60 Hz (A/C “mains” or “line” frequency)
  • Other electrical: typically >10 Hz (muscle stimulators, strong magnetic fields, pacemakers with impedance monitoring)

The skin-electrode interface requires special note, as it is the largest source of interference, producing a DC component of 200-300 mV. Compare this to the electrical activity of your heart, which is in the range of 0.1 to 2 mV! The interference seen from this component is magnified by motion, either patient movement, or respiratory variation.

How does Fourier Analysis relate to ECG filtering?

Filtering on an ECG is done four fold: high-pass, low-pass, notch, and common mode filtering.  High-pass filters remove low frequency signals (i.e. “only higher frequencies may pass”), and low-pass filters remove high frequency signals. The high-pass and low-pass filters together are known as a bandpass filter, literally allowing only a certain frequency band to pass through. The notch filter is used to eliminate the line frequency and is usually printed on the ECG (e.g. ~60 Hz). Common mode rejection is often done via right-leg drive, where an inverse signal of the three limb electrodes are sent back through the right leg electrode.

All filters introduce distortion in the resulting output signal. This distortion can be in amplitude or phase. Filters found in cardiac monitors need to be real time and thus cannot tolerate delays. Because of this, the filter output exhibits non-linear characteristics due to their required shorter delays. Basically, they distort different frequencies differently causing phase distortion. If the filters were applied during post-processing, where real-time output of the signal is unnecessary, the design of these filters can be linear which minimizes phase distortion.

Low-pass filters on the ECG are used to remove high frequency muscle artifact and external interference. They typically attenuate only the amplitude of higher frequency ECG components. Analog low-pass filtering has a noticeable affect on the QRS complex, epsilon, and J-waves but do not alter repolarization signals.

High-pass filters remove low-frequency components such as motion artifact, respiratory variation, and baseline wander. Unlike low-pass filters, analog high-pass filters do not attenuate much of the signal. However, analog high-pass filters suffer from phase shift affecting the first 5 to 10 harmonics of the signal. This means that a 0.5 Hz high pass filter, which is a lower frequency than the myocardium produces, still can affect frequencies up to 5 Hz!

Compare the ST/T-waves between the raw V1 (blue) and filtered V1 (red). Common monitor mode 1 Hz analog high-pass filter was simulated using GNU Octave 3.6 and a 4th order Butterworth filter.

Compare the ST/T-waves between the raw V1 (blue) and filtered V1 (red). Common monitor mode 1 Hz analog high-pass filter was simulated using GNU Octave 3.6 and a 4th order Butterworth filter.

Remember that lower harmonics are of a larger amplitude than the higher harmonics, so any distortion to their phase is magnified on a real-time ECG. Studies have found that ECG’s with baseline alterations to the normal vectors of depolarization and repolarization feature greater distortion with high-pass filtering.

Compare the ST/T-waves between V1 (blue) and the filtered V1 (red). Diagnostic frequency response was used. Simulated using GNU Octave 3.6 and a 4th order Butterworth filter.

Compare the ST/T-waves between V1 (blue) and the filtered V1 (red). Diagnostic frequency response was used. Simulated using GNU Octave 3.6 and a 4th order Butterworth filter.

If a linear-phase high-pass filter is used, such as on a post-processed ECG, the frequency cutoff can be as high as 0.67 Hz without affecting ventricular repolarization at normal heart rates. However, because this filter design requires delays which do not permit real time display of the ECG signal, they are not commonly used in cardiac monitors. If a non-linear high-pass filter is used, the cutoff should be set to 0.05 Hz in order to minimize distortion to the ST-segment (10 times 0.05 Hz is 0.5 Hz, which is below physiological heart rates).

Putting it All Together

1. Use a frequency setting appropriate for your equipment and clinical setting. Most 12-Lead ECG’s should be acquired at 0.05 – 150 Hz for full fidelity ST-segments and late potentials (such as epsilon or J-waves). A decent compromise with 0.05 – 40 Hz or 0.05 – 100 Hz can be used if muscle artifact is severe, provided you’re aware of the amplitude distortions which will occur.

2. Always read the frequency settings and calibration pulse when interpreting an ECG. These provide valuable information in order to accurately interpret the ECG!

References

  • Buendía-Fuentes, F., Arnau-Vives, M., & Arnau-Vives, A (2012). High-Bandpass Filters in Electrocardiography: Source of Error in the Interpretation of the ST Segment. ISRN Cardiology.
  • Venkatachalam, K. L., Herbr, J. E., Herbrandson, J. E., son, & Asirvatham, S. J (2011). Signals and signal processing for the electrophysiologist: part I: electrogram acquisition Circulation. Arrhythmia And Electrophysiology, 4(6), 965-73. doi:10.1161/CIRCEP.111.964304
  • Venkatachalam, K. L., Herbr, J. E., Herbrandson, J. E., son, & Asirvatham, S. J (2011). Signals and signal processing for the electrophysiologist: part II: signal processing and artifact Circulation. Arrhythmia And Electrophysiology, 4(6), 974-81. doi:10.1161/CIRCEP.111.964973