VOTW: Regional Wall Motion Abnormality

This weeks VOTW is brought to you by Dr. Eng and Dr. Xu!

An 82 year old male presented to the ED w/ confusion, slurred speech and fall. A stroke alert was called initially, however the EKG obtained showed deep inverted T-waves in the anterior leads as well as ST-elevation in I and aVL. A POCUS was performed which showed…

Clip 1 shows a parasternal short axis view of the heart. The septum, posterior and inferior walls appear to be contracting appropriately but the anterior and lateral walls appear akinetic. Clip 2 shows an apical 4 chamber view of the heart where again the septum appears to be contracting well but the apex and lateral walls appear to be akinetic. The area of akinesis correlates with the ST-changes seen on the EKG.

SALPI

Regional Wall Motion Abnormality

To evaluate for a regional wall motion abnormality (RWMA) remember the acronym SALPI (image 1). In the parasternal short axis view, starting at the septum, go clockwise to identify the anterior – lateral – posterior – inferior walls. To look for a RWMA, look closely at each wall during systole to see if:

1. The myocardium is moving in towards the center of the ventricle

2. The myocardium is increasing in thickness

The absence of these findings is concerning for a RWMA which may be indicative of an acute MI. Patients with old MIs may also have RWMAs - correlate with the EKG and old echos if available

The parasternal long axis view and apical 4 chamber views can also be used to evaluated for RWMA (image 2).

When to POCUS for RWMA

This may be especially helpful in patients w/ equivocal EKGs that you or cardiology is on the fence about activating the cath lab or when the symptoms are not quite consistent with an MI (as in this case). Finding a RWMA may expedite cath lab activation (1).

Pro Tip: Cover up the entire LV with your hand except the specific wall you’re looking at and look at each wall seperately.

Back to the patient

The patient did not have any active chest pain but the initial troponin returned at 27.

The patient was taken to the cath lab which showed triple vessel disease with 80% stenosis of mid-LAD, 95% stenosis of first diagonal, 95% stenosis of proximal circumflex. He was evaluated for CABG but ultimately chose medical therapy.

References:

(1) Xu C, Melendez A, Nguyen T, Ellenberg J, Anand A, Delgado J, et al. Point-of-care ultrasound may expedite diagnosis and revascularization of occult occlusive myocardial infarction. Am J Emerg Med. 2022;58:186–91.

Calcium and Sodium Bicarbonate Efficacy in Out of Hospital Cardiac Arrest

So not to harp on this too much, but also at the behest of our EMS colleagues, I wanted to share a brief lit review on the efficacy of out of hospital cardiac arrest (OHCA) use, or lack thereof, of sodium bicarbonate (SB) and calcium use. This post is *different* than the prior ones as it focuses on out of hospital care! There is a TLDR at the bottom if you're a "I'm happy for you, or sorry that happened" kind of reader. 

Calcium:

Calcium plays an important role in cardiac muscle contraction and is generally acknowledged for its inotropic and vasopressor effects. These effects could be beneficial in the setting of cardiac arrest. Two small, randomized trials from 1985, including a total of 163 patients, found that administration of calcium did not result in a significant increase in return of spontaneous circulation for patients with out-of-hospital cardiac arrest and asystole or pulseless electrical activity. However, both trials had point estimates that favored calcium. Since then there have been no randomized clinical trials assessing the effect of administration of calcium during cardiac arrest. 

A randomized control in Denmark was done in 2020-2021 by Vallentine et al. (citation is at bottom of this post), which asked is calcium administration in OHCA improved ROSC compared to saline. Known as the Calcium for Out-of-Hospital Cardiac Arrest, or COCA Trial, patients were randomized to receiving calcium or saline after their first dose of epi. Primary outcomes were sustained ROSC for 20 minutes, and secondary outcomes were survival to 30 days and survival with favorable neurological outcome at 30 days. 

This study found no significant difference between groups to get sustained ROSC. There was also no difference in survival or neurological outcomes at 30 days. Multiple follow up studies (also cited in the bottom of this post) were performed and found no improved outcomes at a year, and potential worse outcomes in the calcium group, suggesting harm. 

Sodium Bicarbonate:

Sodium bicarbonate (SB) administration has been considered an important part of treatment for severe metabolic acidosis in cardiac arrest. Administration of SB seems a reasonable intervention to counteract the severe metabolic acidosis caused by hypoxia, poor perfusion and increased lactate production in cardiac arrest, in an attempt to mitigate the adverse effects of acidosis. Correction of metabolic acidosis with SB was recommended by early advanced cardiac life support (ACLS) guidelines published in 1976 and SB was the medication most frequently used during cardiac arrest until the mid-1980s. Data published in the 1970s raised concerns that SB administration during cardiac arrest can worsen the outcome after cardiac arrest and emphasized the adverse effects of bicarbonates, including increased osmolality.

ACLS guidelines this past decade have made SB a class III drug in OHCA (not recommended). However it is a class IIB (mild recommendation to give) for TCA overdose, hyperkalemia. A lit review by Velissaris et al. (again linked in the bottom of this post) summarized recent literature on the use of SB, which essentially can be summed up as, SB increases intracellular acidosis, reduces cardiac output, shifts oxygen dissociation curve to the left, hypernatremia, and hyperosmolarity. The bicarb also breaks down into CO2 and worsens tissue acidosis. 

Another study, this by Kawano et al. examined the use of SB in OHCA, and found that its administration could worsen long term neuro outcomes. This was an observational study that included over 13,000 patients, and examined sustained ROSC, survival to 30 days, and favorable neurological outcomes at 30 days. SB groups had worse survival rates and worse neurological outcomes than the non-SB groups. Odds ratio for survival in SB group was 0.64, 95% CI 0.45-0.91, and the OR for favorable neuro outcome was 0.59, 95% CI 0.39-0.88. Obviously this is not a randomized control, but it does paint a poor picture of the use of this medication. 

TLDR: Sodium bicarb and calcium have a litany of evidence showing they do not provide any benefit in OHCA, and there is increasing evidence that they may actually cause harm to give. 

One final additional statistically tidbit I found fascinating while looking into these studies (which has less to do with SB and CC). A randomized control study on epi use in OHCA was performed in the UK by Perkins et al. This cited a number of other articles (all of which are cited below) to compare the number needed to treat for various interventions in ACLS. I wanted to present those here and let folks reflect on them.

NNT for epi in OHCA is 112

NNT for CPR by a bystander in OHCA is 15

NNT for early defibrillation in a shockable rhythm in OHCA is 5.

So second TLDR is early compressions and early application of pads during arrests are often the most life saving interventions we have! Happy reading and happy Tuesday!

Vallentin MF, Granfeldt A, Meilandt C, et al. Effect of Intravenous or Intraosseous Calcium vs Saline on Return of Spontaneous Circulation in Adults With Out-of-Hospital Cardiac Arrest: A Randomized Clinical Trial. JAMA. 2021;326(22):2268–2276. doi:10.1001/jama.2021.20929

Vallentin MF, Granfeldt A, Meilandt C, Povlsen AL, Sindberg B, Holmberg MJ, Iversen BN, Mærkedahl R, Mortensen LR, Nyboe R, Vandborg MP, Tarpgaard M, Runge C, Christiansen CF, Dissing TH, Terkelsen CJ, Christensen S, Kirkegaard H, Andersen LW. Effect of calcium vs. placebo on long-term outcomes in patients with out-of-hospital cardiac arrest. Resuscitation. 2022 Oct;179:21-24. doi: 10.1016/j.resuscitation.2022.07.034. Epub 2022 Jul 30. PMID: 35917866.

Vallentin MF, Povlsen AL, Granfeldt A, Terkelsen CJ, Andersen LW. Effect of calcium in patients with pulseless electrical activity and electrocardiographic characteristics potentially associated with hyperkalemia and ischemia-sub-study of the Calcium for Out-of-hospital Cardiac Arrest (COCA) trial. Resuscitation. 2022 Dec;181:150-157. doi: 10.1016/j.resuscitation.2022.11.006. Epub 2022 Nov 18. PMID: 36403820.

Velissaris D, Karamouzos V, Pierrakos C, Koniari I, Apostolopoulou C, Karanikolas M. Use of Sodium Bicarbonate in Cardiac Arrest: Current Guidelines and Literature Review. J Clin Med Res. 2016 Apr;8(4):277-83. doi: 10.14740/jocmr2456w. Epub 2016 Feb 27. PMID: 26985247; PMCID: PMC4780490.

Kawano T, Grunau B, Scheuermeyer FX, Gibo K, Dick W, Fordyce CB, Dorian P, Stenstrom R, Straight R, Christenson J. Prehospital sodium bicarbonate use could worsen long term survival with favorable neurological recovery among patients with out-of-hospital cardiac arrest. Resuscitation. 2017 Oct;119:63-69. doi: 10.1016/j.resuscitation.2017.08.008. Epub 2017 Aug 10. PMID: 28802878.

Perkins GD, Ji C, Deakin CD, Quinn T, Nolan JP, Scomparin C, Regan S, Long J, Slowther A, Pocock H, Black JJM, Moore F, Fothergill RT, Rees N, O'Shea L, Docherty M, Gunson I, Han K, Charlton K, Finn J, Petrou S, Stallard N, Gates S, Lall R; PARAMEDIC2 Collaborators. A Randomized Trial of Epinephrine in Out-of-Hospital Cardiac Arrest. N Engl J Med. 2018 Aug 23;379(8):711-721. doi: 10.1056/NEJMoa1806842. Epub 2018 Jul 18. PMID: 30021076.

Berdowski J, Beekhuis F, Zwinderman AH, Tijssen JG, Koster RW. Importance of the first link: description and recognition of an out-of-hospital cardiac arrest in an emergency call. Circulation 2009;119:2096-2102.
Hasselqvist-Ax I, Riva G, Herlitz J, et al. Early cardiopulmonary resuscitation in out-of-hospital cardiac arrest. N Engl J Med 2015;372:2307-2315.

Kitamura T, Kiyohara K, Sakai T, et al. Public-access defibrillation and out-of-hospital cardiac arrest in Japan. N Engl J Med 2016;375:1649-1659.

Frostbite

Frostbite is a condition that occurs when skin and underlying tissues freeze due to exposure to cold temperatures. It occurs due to vasoconstriction, resulting in decreased blood flow (which would deliver heat) to tissues, and this leads to ice crystal formation. Frostbite most often occurs due to exposure at temperatures of less than -20°C (that includes wind chill). Freezing alone typically does not cause tissue damage. Thawing is what worsens the damage by disrupting the endothelium of cells. The blood flow of skin is normally around 250 ml/min, but in tissue damaged by frostbite, drops to 20-50 ml/min. This endothelial damage leads to swelling, platelet aggregation, and potentially thrombosis (in the form of microthrombi due to decreased intravascular flow). 

Exposed and wet skin are the most likely to be damaged. Most likely areas are feet, hands, ears, lips, and nose. Risk factors for frostbite include patients that are colder temperatures, wind chill, no shelter, prolonged exposure, exposure while wet, patients with EtOH use. Patients with medical conditions that impact vasculature are also at increased risk, including diabetes, PVD, and smokers.

Classifications of Frostbite:

1. First Degree: Involves superficial skin freezing, causing redness and irritation, but usually has good recover

   • Symptoms include stinging and burning, eventually throbbing

   • Patients typically develop erythema, swelling, and have desquamation later

2. Second Degree: Involves freezing of the skin and deeper tissues, resulting in blistering and swelling, but usually has good recovery

   • Symptoms include numbness, then followed by aching and throbbing

   • Patients typically have extensive edema for hours, then develop blisters after that, and desquamate over the course of days

3. Third Degree: Involves freezing extending to subcutaneous tissues, leading to deep tissue damage, usually has poor recovery

   • Symptoms include extremities feeling heavy, then burning, throbbing, and shooting pains

   • Patient with third degree frostbite will develop hemorrhagic blisters

4. Fourth Degree: The most severe form, involving freezing of muscles, tendons, and bone, often leading to irreversible damage

   • Symptoms include a deep, aching pain

   • Skin becomes mottled, and deep eschar forms

Management:

• Treat hypothermia first! Rewarm core temperature, otherwise at risk of reinjuring the patient if their extremities are re-exposed to cold again

• Remove wet clothing

• Place extremities in a 40-42°C bath for 20-30 min

  • Care should be made to not rewarm too quickly, otherwise you risk worsening reperfusion injuries

  • For areas that can not be placed in a bath (nose, ears, etc) can use a warm, wet towel

• Rewarming is considerably painful and should be treated with aggressive pain control

• Wound care should be undertaken

  • Wrap wounds with sterile, dry gauze

  • Keep effected extremities elevated

  • Do not remove blisters

  • Have a high clinical suspicion for possible compartment syndrome

• Patients with full thickness injuries and no evidence of reperfusion after rewarming should be considered for tPa therapy which may reduce the risk of digital amputation

• Patients should receive tetanus vaccination

Complications of frostbite

Patients can develop hypersensitivity to the cold with pain and ongoing numbness. Many patients can develop arthritis, can have loss of nails, cracked skin, atrophy of muscles. If tissue ischemia is severe, debridement may end up being necessary for extreme cases.

Example of Stage 3 injury

Basit H, Wallen TJ, Dudley C. Frostbite. [Updated 2023 Jun 26]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-Available from: https://www.ncbi.nlm.nih.gov/books/NBK536914/

Handford C, Thomas O, Imray CHE. Frostbite. Emerg Med Clin N Am. 2017;35(2):281–299.

Frostbite. Orthobullets. (n.d.). https://www.orthobullets.com/hand/12105/frostbite