59 year old male: chest pressure – Conclusion

This is the conclusion to 59 year old male: chest pressure, be sure to read the case study first!

When we left off, we’d loaded our 59 year old male patient with 10 of 10 chest pressure into the back of our unit with the help of a local volunteer EMT. The patient appeared acutely unwell and was hypotensive and bradycardic. We had the following initial ECG:

Uh Please Standby - Initial 12-Lead

Before we discuss this ECG in depth, let’s show a serial 12-Lead the crew obtained shortly after leaving the scene:

Uh Please Standby - 12-Lead 2

The importance of serial ECG’s cannot be understated. Using only one prehospital ECG could miss nearly 20% of all STEMI patients!

At this point we can see an obvious inferoposterior STEMI, likely due to an RCA occlusion. Also of note is a new right bundle branch block, which is an ominous sign. These changes were not lost on the crew, and the receiving facility, a PCI center, was made aware.

However, during their radio report a rhythm change was noted on the monitor:

Uh Please Standby - Rhythm Change

A single R-on-T PVC is seen initiating ventricular fibrillation. Thankfully, the crew elected to use a driver and had two sets of hands in the back. The defibrillator was charged while CPR was initiated, and a 200J shock was delivered after a period of chest compressions:

Uh Please Standby - Rhythm Defibrillation

A rhythm change was noted, however, as no pulses were present chest compressions were continued:

Uh Please Standby - Rhythm Post Defibrillation

Within a minute the patient awoke during CPR, and regained full consciousness. A repeat 12-Lead was obtained:

Uh Please Standby - 12-Lead 3

This ECG shows sinus tachycardia, right bundle branch block, and the evolving inferoposterior STEMI. Upon arrival at the PCI center, the patient was pit stopped in the ED’s resuscitation bay due to his recent ventricular arrhythmia. While there, he experienced another VF arrest. He was again resuscitated and moved to the cath lab for PCI.

Could we have predicted this series of events from the initial ECG? Yes and no.

Yes, the initial ECG provided all of the findings necessary to determine that the patient was experiencing a coronary artery occlusion. Reciprocal changes or T-wave inversion in aVL is an earlier and more sensitive finding than inferior ST-elevation during acute inferior STEMI.

No, the VF arrest is not as predictable. The R-on-T PVC which initiated ventricular fibrillation was the only PVC found on the full cardiac monitor report prior to the arrest! However, it is a best practice to place multifunction electrode pads on any STEMI patient in anticipation for these events.

Sometimes it pays off to read the computerized interpretation.

Sometimes it pays off to read the computerized interpretation.

Looking back the initial ECG we can see why the arbitrary criteria of 1 mm  ST-elevation is not nearly sensitive enough to catch every coronary artery occlusion:

  • Hyperacute T-waves dominate the inferior leads
  • T-wave inversion in aVL
  • ST-depression in I, V2, V3, and V4
  • Subtle ST-elevation relative to the PR-segment in III, aVF, and V6 (the actual isoelectric baseline)

Remember, ST-depression due to ischemia does not localize. Localized ST-depression is a reciprocal change until proven otherwise!

During PCI the patient was found to have a 99% occlusion of the LCX and received one stent.

99% occlusion of LCX

99% occlusion of LCX

Post pPCI.

Post pPCI.

Even with two VF arrests, the time from first medical contact to balloon was 61 minutes! If you do not believe in a system of care which begins with dispatchers, first responders, and EMS, travels through the hospital, and ends up back with EMS through continuous quality improvement feedback, perhaps this case can change your mind.

References

  • Verbeek PR, et al. Serial prehospital 12-lead electrocardiograms increase identification of ST-segment elevation myocardial infarction. Prehosp Emerg Care. 2012; 16(1):109-14. [PubMed]
  • Smith SW. Inferior Hyperacute T-waves. Dr. Smith’s ECG Blog, published 26 August 2009. [Free Full Text]
  • Smith SW. Inferior hyperacute T-waves. The clue is T-wave inversion in aVL. Serial ECGs evolve to ST Elevation. Dr. Smith’s ECG Blog, published 8 February 2011. [Free Full Text]
  • Smith SW. A Male in his 60s with Chest pain. What is the ECG Diagnosis? Dr. Smith’s ECG Blog, published 13 December 2013. [Free Full Text]
  • Smith SW. Five Primary Patterns of Ischemic ST depression, without ST elevation. Some are STEMI-equivalents. Dr. Smith’s ECG Blog, published 12 February 2012. [Free Full Text]
  • Hanna EB, Glancy DL. ST-segment depression and T-wave inversion: Classification, differential diagnosis, and caveats. Cleve Clin J Med. 2011; 78(6):404-14. [Free Full Text]

The Ventrogluteal IM injection site.

Some time ago a new-graduate nurse taught me how to give an intramuscular injection.
No, really….

After studiously watching one of our senior staff give an intramuscular (IM) injection, the new-grad informed us that, in fact, she was not taught to give injections into the upper-outer quadrant.
This is were I had been sticking my needles for many years now, and I have given thousands (if not millions) of injections this way.

But I was wrong. And I still see many (older) nurses who are continuing to administer intramuscular injections this way.
As complications from IM injections include abscess, cellulites, tissue necrosis, granuloma, muscle fibrosis, contractures, haematoma, injury to blood vessels, bones and peripheral nerves, it is important we follow best practice guidelines when delivering medications via this route.

OUT: The Dorsogluteal IM injection site.

This site been used by nurses for years as the target of choice for IM injections.
It is found in the area of the superior lateral aspect of the gluteal muscles, commonly known as the upper outer quadrant.
It is located by dividing the buttock into four equal quadrants. This is usually done by drawing an imaginary cross (bisecting it vertically and horizontally).

Problems that have been identified with using this site include:
  • Presence of major nerves and blood vessels in this area, including the sciatic nerve and superior gluteal artery.
    It has been taught that you will probably avoid this by further dividing the upper outer quadrant into another quadrant and giving the injection into the upper outer of the upper outer.
    Despite this, there have been reports of injuries to the sciatic nerve leading to problems ranging from foot drop to paralysis of the lower limb.
  • Thickness of fat in this area. A number of studies have found that the depth of muscle in the dorsogluteal region is often greater then the length of a standard needle used for IM injections, resulting in a failure to achieve intramuscular deposition of the medication.
    In fact, one study found the success rate of IM injections to be 32% (which fell to 8% in female patients)!
    With the increasing incidence of obesity amongst our patients we are probably going to be delivering subcutaneous injections if we choose this location.
  • Pain receptors are located in the subcutaneous layer, not in muscle tissues and so medication delivered into this area may be more painful.
  • Dorsogluteal site has a decreased absorption rate increasing the possibility of a depot effect with drug build up and potential for overdose.

IN: The Ventrogluteal IM injection site.

VGIM

 

The ventorgluteal (VG) site has less subcutaneous fat and a thicker muscle mass than the dorsogluteal site with an almost certain probability of penetrating muscle with a standard needle.
The VG site is also sparse of any major innervating nerves or blood vessels whilst remaining well perfused from smaller branches.

Locating the VG site.

The ventrogluteal site is located halfway between the hip and the head of the femur. One method to locate the correct site is:

  1. First, place the heel of your  hand (use your L hand if injecting into the patients R VG and vice-versa) over the patients greater trochanter, and feel for the anterior superior iliac spine with your index finger.
  2. The middle finger then slides across to make a peace-sign pointing up to the iliac crest.
  3. The injection site is in the middle of this peace-sign.
  4. Wipe site with alco-wipe in a circular motion and allow to dry.
  5. Use your peace sign to spread skin taut.
  6. Insert needle at 90 degree angle. Take care as you are inserting needle in proximity to your fingers.
  7. There is no evidence for the need to aspirate the plunger when using the VG site.
  8. Inject medication slowly (around 10 seconds per ml), remove needle quickly, and gently apply pressure to site for 10 seconds.

 

Still IN: the Z-track.

ZT

When delivering  medications via any IM route the technique of Z-tracking should be used.
This both reduces pain, and prevents dispersion of medication into subcutaneous tissue.

  1. Apply gentle traction on the skin to pull it away from the injection site (about 2-3 cm). Use your non-dominant hand.
  2. Inject (slowly) with needle at 90 degrees to skin surface.
  3. Withdraw needle quickly.
  4. Release skin.

 

Summary:

Whenever possible the VG site should be the preferred location for intramuscular injections.
The Z-Track method should be used for IM medication delivery.
The patient should be positioned so the target muscle is as relaxed as possible.

 


References:

Featured image via: zaldylmd

  1. Intramuscular injections: a rev… [J Psychiatr Ment Health Nurs. 2008] – PubMed – NCBI [Internet]. [cited 2014 Apr 23]. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18454829
  2. Are techniques used for intramuscular injection based on research evidence? | Practice | Nursing Times [Internet]. [cited 2014 Apr 23]. Available from: http://www.nursingtimes.net/1952004.article
  3. Large-volume IM injections: 
A review of best practices – ONA [Internet]. [cited 2014 Apr 23]. Available from: http://www.oncologynurseadvisor.com/large-volume-im-injections-a-review-of-best-practices/article/281208/
  4. Recognizing the evidence and changing pr… [Br J Nurs. 2010 Oct 14-27] – PubMed – NCBI [Internet]. [cited 2014 Apr 23]. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20948472

 

 

 

Lab Case 14

A 28 year old man presents to your Emergency Department with epigastric pain. Describe and Interpret his  ABG on room air pH 7.65   (7.36-7.44)                                                                Na 140 (136-145) pCO2 16  (36-44)                                                                      K 3.8 (3.3-5) pO2 130                                                                                    Cl 110 HCO3 19 (24+/-2)                                                                     Gluc 6.9 Lactate … Continue reading

More about phenibut

phenibut_23.5 out of 5 stars

Phenibut (β-Phenyl-GABA): A Tranquilizer and Nootropic Drug. Lapin I. CNS Drug Rev 2001;7:471-481.

Abstract

Since posting about phenibut yesterday, I wondered how much medical literature existed describing its pharmacology and toxicology. This paper — not included in the  the initial accepted manuscript of O’Connell et al but referenced in the Wikipedia entry on phenibut — is the most complete discussion I found. However,  phenibut was first synthesized and used medically in the Soviet Union half a century ago and there undoubtedly is considerable literature published in Russian that I can’t access.

Here are some key points from this paper:

  • Phenibut (PB) is a GABA agonist, mostly at the GABAB receptor but to some extent also at GABAA receptors as well.
  • In addition, PB increases release of dopamine.
  • PB has no appreciable anticonvulsant effect.
  • Users quickly develop tolerance to the effects of PB.
  • In volunteers given a single oral dose, the plasma half-life of PB was 5.3 hours.
  • PB is excreted predominantly unchanged in the urine.

Wikipedia also referenced a 2008 abstract from the NYC Poison Control Center describing a case of PB withdrawal. a 40-year-old man presented to hospital with agitation, psychosis, hallucinations, and insomnia. He had stopped using PB 3 days previously. His vital signs were unremarkable except for a pulse rate of 110/min.

The patient required sedation with lorazepam βand intubation for chemical restraint. When he was extubated 4 days later his mental status had returned to baseline and there was no evidence of psychosis.
 

More about phenibut

phenibut_23.5 out of 5 stars

Phenibut (β-Phenyl-GABA): A Tranquilizer and Nootropic Drug. Lapin I. CNS Drug Rev 2001;7:471-481.

Abstract

Since posting about phenibut yesterday, I wondered how much medical literature existed describing its pharmacology and toxicology. This paper — not included in the  the initial accepted manuscript of O’Connell et al but referenced in the Wikipedia entry on phenibut — is the most complete discussion I found. However,  phenibut was first synthesized and used medically in the Soviet Union half a century ago and there undoubtedly is considerable literature published in Russian that I can’t access.

Here are some key points from this paper:

  • Phenibut (PB) is a GABA agonist, mostly at the GABAB receptor but to some extent also at GABAA receptors as well.
  • In addition, PB increases release of dopamine.
  • PB has no appreciable anticonvulsant effect.
  • Users quickly develop tolerance to the effects of PB.
  • In volunteers given a single oral dose, the plasma half-life of PB was 5.3 hours.
  • PB is excreted predominantly unchanged in the urine.

Wikipedia also referenced a 2008 abstract from the NYC Poison Control Center describing a case of PB withdrawal. a 40-year-old man presented to hospital with agitation, psychosis, hallucinations, and insomnia. He had stopped using PB 3 days previously. His vital signs were unremarkable except for a pulse rate of 110/min.

The patient required sedation with lorazepam βand intubation for chemical restraint. When he was extubated 4 days later his mental status had returned to baseline and there was no evidence of psychosis.
 

This Ophthalmologist Collected $21,000,000 in 2012 From Medicare?

The article below in the NYT is an interesting one for EM physicians. Guess who makes a lot of money? Yep, opthalmologists, radiation oncologists, and a few others. Here’s a quote:

“In 2012, 100 doctors received a total of $610 million, ranging from a Florida ophthalmologist who was paid $21 million by Medicare to dozens of doctors, eye and cancer specialists chief among them, who received more than $4 million each that year.”

$21 million dollars collected by ONE eye doc. Huh? there are some subtleties but interesting nonetheless.

http://nyti.ms/1hqBVxh